Vol. 125 - 1-2 Novembre 2014

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Archivio di Ortopedia e Reumatologia BOARD SCIENTIFICO Direttore Responsabile A. Tropiano, Milano Direttori Scientifici G. V. Mineo, Milano P. Meroni, Milano   Vice Direttori Scientifici G. M. Calori, Milano B. M. Marelli, Milano  Comitato Scientifico R. Buly, New York R. Capanna, Firenze F. Catani, Modena P. Cherubino, Varese S. Giannini, Bologna P. Giannoudis, Leeds P. Rossi, Torino G. Zatti, Monza Comitato Editoriale E. Biffi, Milano  G. Cornaggia, Milano C. Crapanzano, Milano C. Cucciniello, Milano M. Dall’Aglio, Milano P. A. Daolio, Milano G. Di Luca, Milano M. Gallazzi, Milano V. Gerloni, Milano A. Guarino, Milano M. Loiero, Milano V. Massari, Milano A. Memeo, Milano B. Misaggi, Milano

L. Panella, Milano A. Parafioriti, Milano L. Sinigaglia, Milano A. L. Tassi, Milano R. Viganò, Milano Comitato di Redazione G. Bernabè, Milano M. Berruto, Milano S. Brambilla, Milano C. Corradini, Milano U. Dacatra, Milano U. De Bellis, Milano A. D’Aloia, Milano S. Failoni, Milano M. Franceschini, Milano L. Galdi, Milano A. Marchesoni, Milano E. Mazza, Milano V. Pedrini, Milano A. Pellegrini, Milano D. Peroni, Milano L. Pierannunzi, Milano A. Ventura, Milano, F. Tramontana, Milano M. Varenna, Milano E. Vignali, Milano S. Zeni, Milano A. Wolf, Milano Commissione ECM   G. V. Mineo, Milano P. Meroni, Milano B. M. Marelli, Milano G. M. Calori, Milano Segreteria di Redazione N. Zerbi, Milano

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Vol. 125 - 1-2 Novembre 2014

EDITORIALE

T

he ARCHIVIO DI ORTOPEDIA E REUMATOLOGIA is an historic scientific magazine that for our Institute has always had a major role in helping to spread experiences and knowledges in the fields of orthopaedics and reumathology. This first issue after a lack of pubblications due to a change of editor, is presented in a graphic totally renewed, more usable and now similar to the most famous scientific international publications. This issue, first with the new format, is totally dedicated to degenerative shoulder that is represented by all shoulder diseases that slowly appear after 40yo and then evolve after 50yo and especially after 60yo. The index of the present issue follows the stages of a conference held two years ago in Milan for which I worked in co-operation with Pierluigi Gambrioli and Alessandro Castagna, two friends of mine and celebrated shoulder surgeons. The former idea was to build the congress following a theoretical evolution of the degenerative shoulder disease in which the anatomical damage becomes gradually more and more serious. Then we will start from basic science and biology, trying to understand how and why rotator cuff tendinopathy begins. At the same time we will discuss two particular shoulder diseases that not infrequently affect the shoulder like adhesive capsulitis and calcifying tendinopathy. After the beginning of a real tendinopathy, tendon fibers deteriorate and torn leading to a partial tear or, in some case of no-treatment, to a full thickness tendon tear. A lot of papers will be focused on rotator cuff tear talking from modern suture techniques to the possibilities that modern biological science offer in order to improve rotator cuff healing after surgical repair. We will also discover that not all kind of ruptures can be treated arthroscopically, like a complete full thickness subscapular tear, that requires open surgery, or like massive irreparable cuff tear requiring latissimus dorsi or teres major tendon transfer that should be isolated via open surgery. Another kind of degenerative shoulder disease affects cartilage layer. In this case we recognise a shoulder arthropathy that can be primitive or secondary to a fracture or to a serious rotator cuff tear that have been never treated before. When degenerative disease lead to an arthropathy the treatment can be a modern shoulder prosthesis that is generally widely adaptable to the anatomy of the patient and to the pathology. Last but not least an adequate space has been left to rehabilitation even in the field of tendinopathy than in shoulder prosthesis field. In this issue the reader will find a reference in modern approaches to surgical treatment and in rehabilitation of degenerative shoulder. Roberto LEO n

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SOmmarIO

2.

Editoriale

.

Roberto Leo

5.

Tendon disease and rotator cuff tears

.

.

A. Castagna, V. Fogliata, R. Garofalo

8.

Calcific tendinitis of the shoulder

58. Platelet rich plasma in rotator cuff disease

.

P. Randelli, V. Ragone, R. D’Ambrosi, F. Randelli, P. Cabitza

13 . Adhesive capsulitis: clinical aspects and treatment

.

R. Leo, PL. Gambrioli

16. Biological enhancement in rotator cuff repairs .

53. Platelet Rich Plasma in Arthroscopic Rotator Cuff Repair: State of the Art

P. Randelli, V. Ragone, A. Menon, R. D’Ambrosi, F. Randelli, P. Cabitza

.

U.G. Longo, A. Berton, G. Rizzello, G. Salvatore, V. Denaro

61. Biology of rotator cuff tendinopathy .

A. Murgo, O. De Lucia, C. Crotti, PL. Meroni

64. Scaffold augmentation in rotator cuff tears repairs

.

A. Castagna, V. Fogliata, R. Garofalo, E. Cesari

R. Rotini, A. Marinelli, E. Guerra, G. Bettelli, M. Cavaciocchi, L. Zaccarelli, M. Fini, E. Bondioli

23. Partial-thickness rotator cuff tear. Surgery:

72. Rational approach to the irreparable cuff tears -

.

.

when and how

M. Rebuzzi, P. Baudi, M. Gialdini, C. Rovesta,

from “functional” repair to muscle transfer

F. Catani

29. Rotator cuff rehabilitation .

in reparable rotator cuff tears. Actual standards and limitations

.

G. Merolla, G. Porcellini

76. Arthroscopically-assisted latissimus dorsi transfer

M. Conti, R. Garofalo

35. Modern technique of arthroscopic suture

.

E. Gervasi, A. Spicuzza

81. The rotator cuff irreparable tears: latissimus round muscle transfer

R. Leo, V. Fogliata, A.M. Querenghi, M. Pivetta,

.

B.M. Marelli

85. Reverse shoulder arthroplasty with and without

43. Subscapularis tendon tear.

F. Odella, S. Odella

tendon transfer for arthropathy with massive rotator cuff tear: personal experience and critical analysis of the literature

Modern surgical approach

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F. Campi, P. Paladini, C. Buononato, A. Tartarone,

D. Petriccioli, G. Marchi, C. Bertone

47. Painful shoulder:

.

the Rheumatologist’s point of view

92. Shoulder arthroplasty’s rehabilitation

.

L. Sinigaglia, F. Zucchi, M. Varenna

.

N. Ivaldo, G. Caione, M. Rossoni

R. Costantino, L. Panella, E. Prisco

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Tendon disease and rotator cuff tears Alessandro Castagna, Valentina Fogliata*, Raffaele Garofalo** Unità di chirurgia della spalla e gomito, IRCCS Istituto Humanitas, Milano * Dipartimento di Ortotraumatologia Generale e Chirurgie Ortopediche Specialistiche, Struttura Semplice Dipartimentale Chirurgia Spalla e Gomito, Istituto Ortopedico G. Pini, Milano **Servizio Chirurgia della spalla Ospedale F. Miulli, Acquaviva delle Fonti, Bari

INTRODUCTION

ABSTRACT

In 1972, Neer coined the term of subacromial impingement to indicate a pathologic condition characterized by an extrinsic compression of the supraspinatus tendon in particular by the anterior margin of the acromion, the coracoacromial ligament, and also by acromioclavicular joint osteophytes 1. This chronic, compression associated with microtrauma, firstly implied an inflammatory-reactive framework and therefore a progressive degeneration until the rupture of the tendon itself, with consequent pain syndrome and shoulder functional impotence. However, in 1922 Meyer had already suggested that capsular and tendinous shoulder injuries were the result of the contact between the greater tuberosity and the acromion2. In support of this theory Bigliani had described 3 different acromion morphologies: type I (flat), type II (curved), and type III (hooked acromion). This author suggested that 70% of rotator cuff lesions were associated with a type III acromion 3. Later, Nyffeler has shown how not only the acromion shape but also its lateral extension could be responsible for an impingement subacromial syndrome and a consequent lesion of the rotator cuff 4. In recent years, however, there has been a considerable incentive to the study of the rotator cuff pathology basis. In particular, these studies have revealed that the injury of the cuff tendons is the result of a tendon desease that is associated with specific extrinsic situations (impingement) and microtrauma. This paper aims to analyze the literature for intrinsic aspects that could contribute in causing rotator cuff injuries.

Shoulder impingement syndrome was originally introduced by Neer in 1972, when he described the compression of the supraspinatus tendon against the anterior edge of the acromion, the coracoacromial arch and the acromioclavicular joint. As a result, for long rotator cuff tendons lesions were believed to be caused by extrinsic factors and in particular by subacromial impingement. Recent studies on rotator cuff pathology reveal that, actually, most of these injuries result from a multifactorial process in which the intrinsic factors play a key role. The recognition of these different factors is very important in order to improve the approach to this disease. The hope is that, in the future, prevention and treatment of rotator cuff diseases could be optimized even with pharmacological interventions.

ROTATOR CUFF TENDONS STRUCTURE The rotator cuff is represented by 4 tendons that are the supraspinatus, the infraspinatus, the teres minor and the subscapularis. Each of these tendons is inserted at the level of the proximal humerus. In particular, the subscapularis inserts on throchine (lesser tuberosity) and the other three tendons are inserted on the throchite (greater tuberosity). Of these tendons, supraspinatus is the most vulnerable; the cause of this condition is attributed to the fact that this tendon is located below the coracoacromial arch and also to the fact that it presents an abnormal vascularization. The type I collagen accounts for about 85% of the dry weight of the rotator cuff tendons. In supraspinatus there is a significant proportion of type III collagen and a relatively high content of glycosaminoglycans (GAGs). The supraspinatus undergoes significant compression because

of its location and biomechanics, and expressed proteins of the extracellular matrix (ECM) that are often found in the cartilage (decorin, biglycan and aggrecan). Since the most anterior region of the supraspinatus is that which most frequently undergoes breakage, it is easy understand how the concentration of proteoglycans at the level of this region is important. At tendon to bone interface (entheses) there is an interdigitation of several layers of longitudinally oriented fibers of type I collagen which are inserted in a gradual manner on the humerus5. The number of vessels and their size gradually decrease getting closer to the bone5. At the level of this junction 4 zones are distinguished: tendon, non-mineralized fibrocartilage, mineralized fibrocartilage, and bone. Type I collagen predominates in zones 1 and 4, while zones 2 and 3 contain mainly collagen I, II and X, as well as ECM with proteoglycans. With the aging process, the level of vascularization in this area tends to decrease progressively, altering the intrinsic structure of the tendon to bone interface. ECM is constantly being reshaped itself and this is possible thanks to the delicate balance between collagenase and collagenase inhibitors themselves. This balance is influenced by genetic factors, functional overload and extrinsic factors that can influence the activity of these enzymes. Many studies have emphasized the importance of ECM in connective tissue homeostasis. Physiological and pathological ECM changes appear to be involved in tendinopathy and tendon lesions. From the biomechanical point of view the articular portion of the supraspinatus is the one that has the highest modulus of elasticity. Tendon longitudinal bursal bundles

Archivio di Ortopedia e Reumatologia

are better able to disperse the tensile loads than the thinner fibers present at the level of the articular portion. This effect is most noticeable during abduction of the arm. Mathematical models confirm these data and show that the concentration of stress is greater in articular insertional area and increases with abduction.

TENDON DISEASE AND ROTATOR CUFF TEARS Recent scientific evidence shows that the majority of rotator cuff tears (RCTs) are caused by a degenerative disease intrinsic in the tendon.

VASCULAR THEORY One of the causes of this degeneration would be represented by the particular vasculature of certain tendons, especially the supraspinatus tendon. In particular, an hypoperfusion area was described at about 10-15 mm from the insertion of the supraspinatus tendon. However it is not clear whether the hypoperfusion could really contribute to the tendon degeneration. Furthermore some authors have studied the capillaries distribution in cadaver cuff samples, and have concluded that hypovascularization area does not exist 6. Other authors have revealed that at the cuff tendon rupture margin there is not an hypovascular reaction but an hyperemic response. Goodmurphy says that the reduced vascularity that can be seen at the criticism zone may be an artifact of the technique used7. Taking account of the above, the etiopathogenetic vascular hypothesis is currently in steep decline.

DEGENERATIVE THEORY In the 30s, Codman had already suggested the degenerative theory as an RCTs cause 8. This theory was recently confirmed by a series of pathological studies performed on the edge of the tendinous lesion. These studies, in fact, confirm the presence of thinning of the tendon, disruption of the collagen fibers, myxoid degeneration, hyaline degeneration, chondroid metaplasia, calcification, angiogenesis and fatty infiltration at the margin of the injured tendon 9. Other authors have also shown how the degenerative process involves not only the edge of breakage, but also a medial part of the tendon (1 cm) which apparently shows to be healthy. This data is very important in consideration of the cuff tendon repair 10. The degeneration of the tendon appears to be closely correlated with the age of the patient. Yamaguchi et al. in a retrospective study showed a difference of about 10 years among patients without rotator cuff lesion (48.7 years) in comparison with those with partial lesion (58.7 years), and patients with full-thickness lesion (67.8 years). Also in this study is shown that 35.5% of patients with a symptomatic rotator cuff lesion had a non-symptomatic lesion in the contralateral limb11.

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ECM and metalloprotease Tenocytes taken from a tendon inveterate tear are not capable of synthesizing a normal ECM. ECM is the substrate on which the cells adhere, migrate and differentiate. An alteration of the ECM seems to be one of the most important factors involved in tendinopathy and tendon tears. The ECM turnover in a normal tendon is mediated by matrix metalloproteinases (MMPs) 12. In particular, MMP-1, MMP-2 and MMP-3 seem to be the most involved. An increase in the activity of MMP-1 leads to a degradation of the network of collagen fibrils with a consequent weakening of the tendon matrix. The tendon in this manner becomes less stable from a mechanical point of view and this can contribute to the rupture of the tendon itself. Some authors have shown that at the level of the edge of a damaged tendon there is an increased activity of MMPs (MMP 1,2,3) and a decreased activity of their inhibitors. Moreover, since even more interesting, this alteration even manifested itself in the most medial portion of the tendon that appeared to be intact13. This data shows how likely the biological degradation processes precede macroscopic morphostructural alterations and are not a consequence. Apoptosis Yuan et al. were the first authors to recognize a role of apoptosis in rotator cuff pathology14. Apoptosis is a physiological process that leads to a mechanism of programmed cellular suicide. This process is regulated by a family of proteases, in particular by caspases. The role of apoptosis in determining an RCT is not yet completely clear. However, what is certain is that an increase in apoptosis at the level of the tendon tissue can result in a reduction of the cell population, the collagen synthesis and in a progression to tendon degeneration. It is interesting to note that caspases can also be activated by oxidative stress derived from overuse and from reduced vascularity of the tendon itself. The same caspases alter the ECM composition, weakening the tendon and there is a stimulus to the increase of MMPs activity, which (in turn) weakens the tendon itself. In this manner a sort of vicious circle that leads to the tendon tear is created. Recently some authors have shown that, in the case of tendon rupture, the caspases activity is not increased only at the level of the broken margin of the tendon, but also 1 cm medial to the break15. This is important not only to understand the tendon degenerative disease, but also for the considerations that follow for the surgical treatment of lesions. Metabolic disorders and RCT Symptomatic lesions of the rotator cuff have been more commonly observed in patients with type I and II diabetes and in patients with glucose intolerance16. In asymptomatic diabetic patients, there were an increased thickness of the supraspinatus tendon and the long-head biceps tendon and a higher prevalence of RCT. Recently, Abboud et al. have found a correlation between hypercholesterolemia and RCT. In particular it has been found that the levels of total cholesterol, triglycerides and LDL, were higher in patients with RCT17. It is unclear, however, whether this represents an indepen-

Archivio di Ortopedia e Reumatologia

dent risk factor for rotator cuff injury or whether it represents an aspect of concomitant disease related to aging of the patient.

CONCLUSIONS In light of recent studies it appears that the majority of RCT are the result of a multifactorial process, where there is probably not a single cause capable of determining the wear, and then the rupture of the tendon. Both the patient’s age and the degenerative tendinous intrinsic process associated with it, are certainly the basis on which may contribute also external factors such as overuse and impingement, as well as the responsible lifestyle for metabolic diseases. In choosing the appropriate plan of treatment of this disease, the clinician must be very careful to specifically assess the various factors that contribute to the pathology of the patient. It is to be hoped that, in the future, a prevention and treatment of RCT can be optimized with pharmalogical treatments that can avoid surgery or improve the results of the latter.

REFERENCES 1. Neer CS II Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J Bone Joint Surg 1972; 54-A:41-50 2. Meyer AW Further observations on use-destruction in joints. J Bone Joint Surg. 1922; 4:491–511 3. Bigliani LU, Morris DS, April EW The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 1986; 10:216 4. Nyffeler RW, Werner CM, Sukthankar A et al. Association of a

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large lateral extension of the acromion with rotator cuff tears. J Bone Joint Surg Am 2008; 88:800-5 5. Uhthoff HK, Seki M, Backman DS et al. Tensile strength of the supraspinatus after reimplantation into a bony trough: An experimental study in rabbits. J Shoulder Elbow Surg 2002; 11:504–509 6. Moseley HF, Goldie I The arterial patterns of the rotator cuff of the shoulder. J Bone Joint Surg Br 1963; 45:780-89 7. Goodmurphy CW, Osborn J, Akesson EJ et al. An Immunocytochemical analysis of torn rotator cuff tendon taken at the time of repair. J Shoulder Elbow Surg 2003; 12:368-374 8. Codman EA The shoulder. Rupture of the supraspinatus tendon, Boston, Thomas Todd, 1934: 123-177 9. Chillemi C, Petrozza V, Garro L et al. Rotator cuff re-tear or nonhealing: histopathological aspects and predictive factors. Knee Surg Sports traumatol Arthrosc 2011; 19:1588-96 10. Longo UG, Franceschi F, Ruzzini L et al. Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med 2008; 36:533-8 11. Yamaguchi K, Ditsios K, Middleton WD et al. The demographic and morphological features of rotator cuff disease. A comparison of asymptomatic and symptomatic shoulders. J Bone Joint Surg Am 2006; 88:1699-1704 12. Garofalo R, Cesari E, Vinci E, Castagna A. Role of metalloproteasi in rotator cuff tear. Sports Med Arthrosc 2011; 19:207-12 13. Castagna A, Cesari E, Garofalo R et al. Matrix metalloproteases and their inhibitors are altered in torn rotator cuff tendons, but also in the macroscopically and histologically intact portion of those tendons. Muscles Ligaments Tendons J 2013; 3:132-8 14. Yuan J, Murrell GA, Wei AQ, Wang MX Apoptosis in rotator cuff tendinopathy. J Orthop Res 2002; 20:1372–1379 15. Lee HJ, Kim YS, OK JH, Song HJ. Apoptosis occurs throughout the diseased rotator cuff. Am J Sports Med 2013; 41: 2249-2255 16. Longo UG, Franceschi F, Ruzzini L et al. Higher fasting plasma glucose levels within the normoglycaemic range and rotator cuff tears. Br J Sports Med 2009; 43:284–7 17. Abboud JA, Kim JS. The effect of hypercholesterolemia on rotator cuff disease. Clin Orthop Relat Res 2010; 468:1493-97

PRESERVATION. FIXATION. CONVERSION. PERFORMANCE.

TORNIER. WE EXPECT MORE THAN OTHERS THINK IS POSSIBLE. www.tornier.com

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Calcific tendinitis of the shoulder Pietro Randelli, Vincenza Ragone, Riccardo D’Ambrosi, Filippo Randelli, Paolo Cabitza Dipartimento di Scienze Medico-Chirurgiche, Università degli Studi di Milano, IRCCS, Policlinico San Donato, Milano

Introduction Calcium deposits within the tendons of the rotator cuff are a common shoulder disorder 1. The incidence in the healthy population is 2.7%, rising to 6.8% in patients with shoulder pain 2. The predominant age is 30–60 years and women are affected slightly more often than men. Bilateral involvement is not uncommon (in 10% to 25% of patients). Calcifications occur commonly in the supraspinatus tendon (51%–90%) and least commonly in the subscapularis tendon (3%) 3. Up to 50% of cases are asymptomatic and run a self-limiting course 4-5. Two different etiological processes have been proposed. The first is degenerative calcification, in which Codman6 proposed that degeneration within the tendon fibers precedes calcification. This was later adopted by Moseley and Goldie, 7 who defined the tendon-bone insertion area as the ‘‘critical zone’’. The second cause proposed is reactive calcification within a healthy tendon 8. Other theories have been introduced in recent years involving chemical factors causing the deposit of calcium, cell proliferation and production of inflammatory agents, metabolic factors and genetic predisposition to the formation of calcific deposits.

formative phase, the deposits exhibit a chalk-like consistency. b) Resting phase: occurs when fibrocollagenous tissue borders the foci of calcification without evidence of inflammation, thereby indicating termination of deposition. c) Resorptive phase: is marked by the appearance of thin-walled vascular channels at the periphery of the deposit. Macrophages and multinucleated giant cells then surround the deposit and phagocytose debris with calcium removal. In this phase the deposit exhibits a thick, creamy, or tooth- paste-like material that is often under pressure. 3) Postcalcific stage: as the tissue undergoes healing during the post-calcific stage, new vascular channels promote fibro- blasts to form type III collagen that becomes replaced by type I collagen. The tendon is healed subsequently with fiber realignment and resolution of the calcium deposit.

Clinical presentation Classification There are numerous classifications that have been proposed by various authors. Anatomical9: small (< 0.5 cm), medium (from 0.5 to 1.5 cm) and large (>1.5 cm). Patte and Goutallier10 have distinguished calcifications in localized and diffuse. Clinical: depending on the symptomatology can be divided into acute, subacute and chronic. Pathological: Uhthoff 8 proposes that the evolution of the disease can be divided into three distinct stages: 1) precalcific, 2) calcific, and 3) postcalcific. 1) Precalcific stage: fibrocartilaginous transformation begins within the tendon at the site of predilection for calcification. This metaplasia of tenocytes into chondrocytes is accompanied by metachromasia, indicating the elaboration of proteoglycan.

The onset of symptoms is chronic, with very low noise and discomfort content. The initial state of formation of the deposits has no vascular neo-formation, cellular reaction and there is no change in tension of the tendon tissue. The clinical presentation becomes very painful, however, in the phase of resorption because the vascular neoformation, together with the exudative state, can bring a substantial increase in the volume of tissue with consequent increase of intratendinous pressure. The pain typically exacerbates overnight, radiates to the outside face of the ipsilateral arm, with the forearm extension. In some cases, this is also reflected radiation to the cervical region. Symptoms are accompanied by functional impotence of variable degree in relation to pain. Three symptomatic phases can be distinguished: 1. The acute phase may occur in 1 to 5-6 weeks. In this phase an intense pain causes important discomfort and loss of function.

2) Calcific stage that follows is subdivided into three phases 11: a) formative, b) resting, and c) resorptive.

2. The chronic phase can occur for many months with a continuous, dull and of fixed intensity pain. This pain is significantly lower than the acute form.

a) Formative phase: separated by chondrocytes and fibrocartilaginous tissue septae, calcium crystals are deposited primarily in matrix vesicles that coalesce to form large foci of calcification. In this

3. Persistent chronic phase characterized by periods of pain and periods of complete well-being. Its minimum duration of 1-2 months can extend for more than 6 months.

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Figure 1: Rx anterior-posterior left shoulder. Clearly visible calcification in the context of the supraspinatus tendon.

Several methods of treatment are listed in the literature. Among the most known are Shockwaves, US lavage, Needling and Arthroscopy (Figure 2).

Imaging Calcium deposits can be seen on plain radiographs with a full series of shoulder films that include AP, (Figure 1), internal and external rotation, scapular Y, and axillary lateral views. These views help to localize the deposit to a specific tendon and show signs of possible impingement. For the recognition of calcifications is also very useful ultrasound examination. Hartig and Huth12 have shown that ultrasound allows to detect the totality of calcifications while radiography permits only in 90% of cases. Magnetic resonance imaging (MRI) evaluation can lead to diagnostic errors and it is not indicated routinely.

Extracorporeal shock wave therapy In the last two decades, several studies have demonstrated the effectiveness of extracorporeal shockwave therapy (ESWT) in treatment of calcifying tendinitis of the rotator cuff15-18. One study even stated that ESWT should be preferred to arthroscopy due to its non-invasiveness at equivalent outcome. A single high-level middle-energetic ESWT was found as effective as two applications of a lower-dosed middle-energetic ESWT for calcifying tendinitis of the rotator cuff after failure of other conservative treatment options (physiotherapy, infiltrations or NSAIDS)19. A literature review20 suggests that ESWT is moderately effective in reducing pain and improving function in individuals with chronic shoulder calcific tendinitis, for up to a year after its application. Although satisfaction results are been associated to this treatment there is no clear evidence regarding the optimal dosage in energy level, intervals between sessions, and number of sessions required for optimal recovery from the condition. Clinicians should also record the intervention parameters because these provide important clinical audit information for future investigations. Future studies of level 1 of evidence are needed to dry definitive conclusions on ESWT treatment for shoulder calcific tendinitis. Needling Needle lavage has been described as an effective treatment that can be performed either in the operating room or in the radiology suite. This technique is best used in patients

Treatment The choice of treatment should be evaluated and placed in relation to each other the medical history, symptoms and radiographic findings. In some cases, calcifications will resorb during the natural progression of disease. Gärtner13 followed the natural evolution of calcific deposits, finding that radiologically dense deposits disappeared in 33% compared with 85% of fluffy deposits over 3 year. Unfortunately it’s known that up to 38% of the calcification do not disappear with time5. In particular medial and anterior localization of the calcification is a negative prognostic factor for self reabsorption of the deposit14. The persistence of the calcification is detrimental to the tendon biology and resistance. Thus is mandatory to follow-up the calcification and to treat it in case it would not reabsorb spontaneously.

Figure 2: Arthroscopic image. Removal of calcification of the supraspinatus tendon.

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with an acutely painful shoulder in the resorptive phase, and it can help decrease the intratendinous pressure. Clinical studies that have analyzed the US-guided percutaneous treatment of calcific tendonitis have reported generally satisfactory results. Serafini et al.21 compare short and long term outcomes of patients with rotator cuff calcific tendonitis who did and did not undergo ultrasonographically (US)-guided percutaneous treatment. Of 219 patients referred for US-guided treatment of rotator cuff calcific tendonitis, 68 patients refused treatment and served as control subjects. Compared with control group, treated patients reported a significant decrease in symptoms at 1 month, 3 months and 1 year. Clinical scores were not significantly different between the two groups at 5 years and 10 years. The authors conclude that US-guided percutaneous treatment facilitated prompt shoulder function recovery and pain relief. Another study22 compares 2 regularly applied calcific rotator cuff treatments: ultrasound (US)–guided needling and lavage combined with a US-guided corticosteroid injection in the subacromial bursa (barbotage group) versus an isolated subacromial bursa injection (control group). Patients were randomly assigned to the 2 groups. Shoulder function was assessed before treatment and at regular follow-up intervals (6 weeks and 3, 6, and 12 months). Additionally, calcification location, size, and Gärtner classification were assessed on radiographs. On average, there was improvement at 1-year follow-up in both treatment groups, but clinical and radiographic results were significantly better in the barbotage group. Furthermore ultrasound-guided needling in combination with high-energy shock-wave therapy (treatment group) was found more effective than shock-wave therapy alone (control group) in patients with symptomatic calcific tendonitis23. A higher rate of elimination of the calcium deposits was seen in treatment group (60%) than in control group 2 (32.5%) (p < 0.05). Arthroscopic removal of the deposit was avoided in 32 patients of treatment group and in 22 of control group (p < 0.05) .

Platelet-rich plasma therapy Platelet-rich plasma therapy (PRPT) has been advocated for the treatment of muscle, tendon as well as joint pathologies24. Seijas et al.25 reported the use of PRPT in a 44year-old female with chronic calcific tendinopathy of the supraspinatus that was nonresponsive to traditional conservative therapy. The patient received three treatments at 2-week intervals. After 6 weeks, the patient was reportedly asymptomatic. Follow-up at 1 year confirmed the patient remained pain-free and was able to return to unrestricted activities. This isolated case study (level V) suggests PRPT may be of value for intractable cases of calcific tendinopathy. However evidence from clinical studies of Level 1 are required. Surgery Surgery is indicated for patients who have progression of their symptoms, constant pain that interferes with activities of daily living, and absence of improvement after conservative therapy. Surgical treatment is helpful for the chronic formative phase patients (radiological dense calcification

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and sharp edges) and especially those with impingement symptoms. Harrington and Codman performed the first operative procedure for removal of calcific deposit in 1902 6. Since the 1930s many investigators have supported this procedure 26--28. Rochwerger et al.29 reported on 22 patients who underwent open removal of a calcific deposit and acromionplasty and found the Constant-Murley assessment score was increased 23 months after the treatment. They concluded that the most favorable results are obtained in patients with the longest interval between onset of the disease and intervention (more than 1 year) and with a progressive course of the disease. Arthroscopic treatment has been shown to have outcomes that are equivalent to those of open procedures, and it has the added benefits of improved cosmesis and possibly a shorter hospital stay, which leads to decreased cost (Figure 2). Rehabilitation consists of a simple home exercise program to regain muscle tone and to prevent adhesive capsulitis. In 1987 Ellman30 first described his arthroscopic technique, involving blind needle aspiration to locate the deposit, followed by excision, and the acromionplasty. Jerosch et al.31 evaluated 48 patients treated arthoscopically with deposit removal, resection of the coracoacromial ligament and acromionplasty. Results showed patients with post-operative radiographic elimination or reduction of the deposits had significantly better outcomes than those without radiographic change and that acromionplasty did not improve the results. Even more recent studies support the arthroscopic technique in patients with persistence or progression of symptoms and constant pain. Seil et al.32 have analyzed the outcome of arthroscopic removal of calcifying tendinitis of the rotator cuff on 58 patients. Every patient was evaluated by using the Constant score, pre and post-operative radiographs and ultrasonoography to assess integrity of rotator cuff. Shoulder function improved according to Constant score, and ultrasonography revealed minor structural changes of the supraspinatus in 66% patients. 92% of the patients were very satisfied. The study confirmed previously reported successful results of arthroscopic treatment of calcifying tendinitis of the rotator cuff. El Shewy33 studied the results of arthroscopic removal of the calcium deposits within the rotator cuff, without rotator cuff repair after a minimum follow-up of 7 years. On 56 patients everyone improved their shoulder’s activity (measured by ASES, UCLA and Costant). Only 3.7% of cases developed rotator cuff tears over the period of follow-up. The author concludes that arthroscopic removal of as much as possible of symptomatic calcium deposits of the rotator cuff is a safe and effective treatment when nonoperative methods fail. Yoo et al.34 also substained that complete removal of calcium deposits in tendon cuff provides good clinical results and earlier pain relief when it was compared to previous literature of minimal removal technique. Porcellini et al.35 demonstrated results of arthroscopic removal of calcifications and an acromioplasty only when

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the coracoacromial ligament was rough and the acromion was exposed. They concluded that a successful outcome seemed strongly related only to the absence of calcium deposits in the tendon cuff. Other studies have advocated the surgical removal of deposits, either by an open or artrhoscopic procedure. Balke et al.36 reported the results on 70 shoulders of 62 patients with a mean age of 54 years, after arthroscopic removal of calcium deposits of the supraspinatus tendon. In 44 shoulders, additional subacromial decompression was performed. After a mean follow-up of 6 years, patients were clinically investigated, and function was statistically evaluated using Constant and ASES scores. Affected and contralateral shoulders were examined by ultrasound in 48 shoulders, and rotator cuff tears were documented. The mean Constant scores of the operated shoulders were significantly lower than those of the healthy shoulders. The ASES scores significantly increased after surgery but were still lower than the ASES scores of the healthy shoulders. Pain was found significantly better in patients with the subacromial decompression. Ultrasound examination at last follow-up showed a partial supraspinatus tendon tear in 11 operated and 3 contralateral shoulders. The results of this study indicate that although the good clinical results after arthroscopic treatment of calcifying tendinitis of the shoulder persist midterm, the affected shoulders present significantly lower clinical scores than healthy shoulders. The rate of partial supraspinatus tendon tears seems to be higher after calcium removal. Additional subacromial decompression seems to reduce postoperative pain. Tillander and Norlin37 compared two groups with an impingement syndrome, one group showing deposits in the rotator cuff and the other not showing such deposits. Both groups performed arthroscopic acromioplasty, with no difference in results or calcification dissolution. They suggested that calcifications may not cause pain and are an insignificant observation on radiographic evaluation regarding treatment indication. Hofstee and collagues38 evaluated two groups of patients after 3 years. The first group treated with acromioplasty and removal of calcification, the second only with acromioplasty. There was no difference in clinical outcomes between surgical subacromial decompression with or without removal of the calcifications.

Treatment Algorithm Calcific Tendinitis represent a treatment challenge since there is no consensus on its treatment. Most studies concerning treatment of rotator cuff calcifications are uncontrolled. Moreover, most studies focus on symptom disappearance, more than calcification disappearance, after conservative or operative therapy. Therefore, although symptoms may improve, the pathology (intratendinous degeneration and calcification) remains. Patients compliance is the key in the treatment algorithm for this disease. As a matter of fact shockwaves are not well tolerated by patients, as like as the surgical treatment is not well perceived. Recently US guided lavage offers

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an easy way of treatment of the tendinitis, washing out the entire deposit. Unfortunately US lavage is suitable only in acute calcific tendinitis when the deposit is pretty fluid. On the other hand the arthroscopic treatment allows to repair a cuff tear related to a chronic calcific tendinitis. A practical Treatment Algorithm has been developed following the main concepts of: 1) reduce the pain, 2) treat the tendon avoiding a subsequent cuff tear. 1. In case of acute onset of calcific tendonitis diagnosed by X-Rays, the patients are sent to the radiology dept for US lavage. The lavage is performed in local anesthesia and in an outpatient way. 2. Two days after the treatment the patients start physical therapy, for passive range of motion (ROM) exercises, with a full ROM recovery at 7 days after treatment. Active ROM exercises will start only 1520 days after treatment depending on the residual pain. 3. The patients will repeat an X-rays at 2 months after treatment plus an MRI in case of persistent pain. If the tendon is torn the patients are scheduled for surgery, if not they continue follow-up surveillance. 4. In case of Chronic calcific tendonitis we suggest an arthroscopic treatment with/out rotator cuff repair.

Conclusions The calcific tendonitis is a cell-mediated pathology, multiphasic, which creates a calcium deposit particularly in the supraspinatus tendon, or subacromial bursa, and a subsequent resorption. Most cases resolve spontaneously. In the literature, several conservative treatments have been reported with varying levels of evidence on their effectiveness. A very well accepted and successful technique is the US lavage. The arthroscopic surgery is the last option available to the orthopedic specialist; should be noted that the post-surgical pain may be present for several weeks after surgery. Arthroscopic treatment should be reserved for chronic cases or for cuff ruptures due to the deposit.

References 1) Lippmann RK. Observations concerning the calcific cuff deposit. Clin Orthop 1961; 20:49-60 2) Bosworth BM. Calcium deposits in the shoulder and subacromial bursitis; a survey of 12122 shoulders. JAMA 1941; 116:2477–82 3) Editorial. Calcific tendonitis of the shoulder. New Engl J Med 1999; 340:1582–4 4) Hedtmann A, Fett H. So-called humero-scapular periarthropathy: classification and analysis based on 1,266 cases. Z Orthop Ihre Grenzgeb. 1989; 127:643-649 5) Uhthoff HK, Loehr JF. Calcifying tendinitis. In: Rockwood CA, Matsen FA, eds. The Shoulder. Philadelphia: Saunders; 1998:9891008 6) Codman EA. On stiff and painful shoulders. Boston Med Surg J. 1906; 154:613-620

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7) Moseley HF, Goldie I. The arterial pattern of the rotator cuff of the shoulder. J Bone Joint Surg Br. 1963; 45:780-789 8) Uhthoff HK, Loehr JW. Calcific tendinopathy of the rotator cuff. J Am Acad Orthop Surg. 1997; 5:183-191 9) Bosworth BM. Calcium deposits in the shoulder and subacromial bursitis: A survay of 12122 shoulders JAMA 1941; 116: 2477-2482 10) Patte and Goutalier D. Calcifications. Rev Chir Orthop 1988; 74: 277-278 11) Gosens T, Hofstee DJ. Calcifying tendinitis of the shoulder: advances in imaging and management. Curr Rheumatol Rep. 2009; 11:129-34 12) Hartig A and Huth F. Neue Aspekte zur Morphologie und Therapie der Tendinosis calcarea der Schultergelenke. Artroskopie 1995; 8: 117-122 13) Gärtner J. Is tendinosis calcarea associated with HLA-A1? Z Orthop Ihre Grenzgeb 1993; 31:461–469 14) Ogon P, Suedkamp NP, Jaeger M, Izadpanah K, Koestler W, Maier D. Prognostic factors in nonoperative therapy for chronic symptomatic calcific tendinitis of the shoulder. Arthritis Rheum 2009; 60:2978–2984 15) Loew M, Daecke W, Kusnierczak D, Rahmanzadeh M, Ewerbeck V. Shock-wave therapy is effec- tive for chronic calcifying tendinitis of the shoulder. J Bone Joint Surg Br 1999; 81:863–867 16) Gerdesmeyer L, Wagenpfeil S, HaakeM MM, Loew M, Wörtler K, Lampe R, Seil R et al. Extracorporeal shock wave therapy for the treatment of chronic calcifying tendonitis of the rotator cuff. JAMA 2003; 290:2573–2580 17) Ogden JA, Toth-Kischkat A, Schultheiss R. Principles of shock wave therapy. Clin Orthop Relat Res 2001; 387:8–17 18) Speed CA, Richards C, Nichols D, Burnet S, Weiss JT, Humphreys H, Hazleman BL () Extracorporeal shock wave therapy for tendonitis of rotator cuff. J Bone Joint Surg Br 2002; 84-B:509–512 19) Farr S, Sevelda F, Mader P, Graf A, Petje G, Sabeti-Aschraf M. Extracorporeal shockwave therapy in calcifying tendinitis of the shoulder. Knee Surg Sports Traumatol Arthrosc 2011; 19:2085-9 20) Lee SY, Cheng B, Grimmer-Somers K. The midterm effectiveness of extracorporeal shockwave therapy in the management of chronic calcific shoulder tendinitis. J Shoulder Elbow Surg 2011; 20:845-54 21) Serafini G, Sconfienza LM, Lacelli F, Silvestri E, Aliprandi A, Sarda- nelli F. Rotator cuff calcific tendonitis: short-term and 10-year out- comes after two-needle US-guided percutaneous treatment. Nonrandomized controlled trial. Radiology 2009; 252:157-164 22) de Witte PB, Selten JW, Navas A, Nagels J, Visser CP, Nelissen RG, Reijnierse M. Calcific tendinitis of the rotator cuff: a randomized controlled trial of ultrasound-guided needling and lavage versus subacromial corticosteroids. Am J Sports Med 2013; 41:1665-73 23) Krasny C, Enenkel M, Aigner N,  Wlk M,  Landsiedl F. Ultra-

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sound guided needling combined with shock-wave therapy for the  treatment  of  calcifying tendonitis of the shoulder. J Bone Joint Surg Br. 2005; 87:501-7 24) Podd D. Platelet-rich plasma therapy: origins and applications investigated. JAAPA 2012; 25:44-49 25) Seijas R, Ares O, Alvarez P, et al. Platelet-rich plasma for calcific tendinitis of the shoulder: a case report. J Orthop Surg 2012; 20:126-130 26) Bosworth BM. Examination of the shoulder for calcium deposits. Technique of fluoroscopy and spot film roentgenography. J Bone Joint Surg 1941; 23:567-77 27) Harmon PH. Methods and results in the treatment of 2580 painful shoulders with special reference to calcific tendinitis and the frozen shoulder. Am J Surg 1958; 95:527-44 28) McLaughlin HL. The selection of calcium deposits for operation: the technique and resultant operations. Surg Clin N Am 1963;43:1501-4 29) Rochwerger A, Franceschi JP, Viton JM, Roux H, Mat- tei JP. Surgical management of calcific tendinitis of the shoulder: an analysis of 26 cases. Clin Rheumatol 1999; 18:313-6 30) Ellman H. Arthroscopic subacromial decompression. Analysis of one- to three-year results. Arthroscopy 1987; 3:173-81. 31) Jerosch J, Strauss JM, Schmiel S. Arthroscopic treat- ment of calcific tendinitis of the shoulder. J Shoulder Elbow Surg 1998; 7:30-7 32) Seil R, Litzenburger H, Kohn D, Rupp S.Arthroscopic treatment of chronically painful calcifying tendinitis of the supraspinatus tendon. Arthroscopy 2006; 22:521-7 33) El Shewy MT. Arthroscopic removal of calcium deposits of the rotator cuff: a 7-year follow-up. Am J Sports Med 2011; 39:1302-5 34) Yoo JC, Park WH, Koh KH, Kim SM. Arthroscopic treatment of chronic calcific tendinitis with complete removal and rotator cuff tendon repair. Knee Surg Sports Traumatol Arthrosc. 2010; 18:1694-9 35) Porcellini G, Paladini P, Campi F, Paganelli M: Arthroscopic 
treatment of calcifying tendonitis of the shoulder: clinical and ultrasonographic follow-up findings at two to five years. J Shoulder Elbow Surg 2004; 13:503-508 36) Balke M, Bielefeld R, Schmidt C, Dedy N, Liem D. Calcifying tendinitis of the shoulder: midterm results after arthroscopic treatment. Am J Sports Med 2012; 40:657-61 37) Tillander BM, Norlin RO. Change of calcifications after arthroscopic subacromial decompression. J Shoulder Elbow Surg 1998; 7:213–217 38) Hofstee DJ, Gosens T, Bonnet M, De Waal Malefijt J. Calcifications in the cuff: take it or leave it? Br J Sports Med. 2007; 41:832-5

Si

ze

s

NOT ALL GLENOID IMPLANTS ARE CREATED EQUAL | PARTICULARLY IN CHALLENGING CASES

>REAL VERSATILITY
RELIABLE FIXATION
PATIENT SPECIFIC TREATMENT
6 mm) and grade 2 and 3 bursal sided (> 3 mm) shoul be repaired.

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Figure 2: Articular sided tear targeting by spinal needle for visualization from subacromial space

Trans-tendon repair Some surgeons prefer intra-tendinous repair techniques, that have been reported with good clinical results and biomechanical properties 2, 6. In particular a proposed advantage is the maintenance of the rotator cuff footprint still attached, which allows for a more accurate anatomic repair and so minimizing any length-tension mismatch created by repair 2, 20, 34. Trans-tendon repairs believe that provide a more accurate restoration of the footprint, increasing the mechanical strength 32. If an articular partial thickness cuff tear is found, a gentle debridement of the torn surfaces is needed, to evaluate the real extent of the tear. Then arthroscope can pass in the subacromial space and the bursa must be completely excised, so that the sutures can be easily visualized subacromially without having to shave around. To localise the joint tear from the bursal side, use a spinal needle (18 gauge) for marking on the bursal surface the partial tear as the technique developed by Snyder et al 16 (Figure 2). This spinal needle becomes also the guide to percutaneous suture anchor placement through the intact bursal side into the medial portion of the great tuberosity 6. Prepare the footprint, then place one or two anchors according to the anterior-posterior size. Ide et al 35 used a single anchor when tear size was less than 1.5 cm, and two anchors when was more. Use a suture passer to pass suture limbs from the anchor through rotator cuff, tie the sutures subacromially searching the best angle of approach, a supero-lateral portal near to the acromion 27. In this way you performed a sort of double-row repair, exploiting the tendon yet attached. To judge the final outcome you have to assess two features: subacromial, the good indentation of the tendon by knots; intra-articular, the good restoration of the footprint 27. If a bursal partial thickness cuff tear is found, a gentle debridement of the torn surfaces is anyway necessary. Palpate the defect to assess and confirm the intact medial wall of cuff, prepare the footprint to a bleeding base and perform a single or double row repair 27. Use suture passer for antegrade or retrograde passage of sutures.

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Figure 3: Articular tear completion before repair

Completion tear and repair Some surgeons prefer tear completion and more traditional repair techniques, that have been reported with good clinical results too. In case of an articular or bursal partial thickness cuff tear, the torn poor quality tissue must be excised by shaver to complete tear to a full thickness (Figure 3): the palpation of tissue is necessary to judge which kind of repair carry out. The bone bed at footprint should be prepare until bleeding removing residual soft tissue all the way to the cartilage margin27. The repair both of articular or bursal sided could be execute using a single (Figure 4) or double row, a suture bridge or a transosseous repair technique. Intra-tendinous partial tear: pearls and pitfalls Their diagnosis is quite difficult: the key is the assessment of cuff surface from the joint and bursal points of view by palpation searching if tissue plane is entered by probe and if relative motion between layers is present. If you suspect this tear, connect a syringe with saline to a spinal needle and put the tip in this defect: as the cuff defect fills with fluid (1-2 ml saline), it forms a dome shaped “bubble” 27. Another important possible sign is the capsular “dimple” at rotator crescent portion. Often these intratendinous laminations are associated with bursal or articular partial tears 36. After diagnosis you have to debride the torn tissue and complete the tear. The laminations have not been excised totally, as demonstrated by Sonnabend et al 37, who suggest to remove only the synovial lining. Then you should perform the repair with single or double row techniques. Treatment in over-head athlete The partial thickness cuff tear of an overhead athlete is often associated with other pathologies. The approach should be an aggressive trial of nonoperative management. If this conservative course fails, cuff debridement with the treatment of concurrent symptomatic pathologies is indicated 2, 10. The subacromial decompression is rarely needed 3. In general, the outcome of cuff tears re-

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B Figure 4 A-B: Ellman 3 bursal partial tear. A) prepared footprint; B) repair after completion with single row

pair in overhead athletes have been discouraging, with few athletes able to return to the same or higher level of competition 2.

Discussion All treatment resulted in significant improvement in shoulder pain and function. However a 6.5 to 34.6% of tear progression to full-thickness tears is present6 regardless operative or not operative treatment. The patients with tear progression had poorer outcomes6, and retear rate increases with time 4. There is no reliable report on the conservative treatment of partial thickness, because real incidence of diagnosis is unknown. For partial thickness less than 50% subacromial decompression does not lead to better outcomes when compared to debridement alone 2, 6, and the results of debridement alone are quite variable 3. The literature suggests that there is no significant difference between transtendon and tear-completion repair, as reported also in a prospective comparative study by Castagna et al 38. In this study they noted only one difference not statistical significant: an higher improvement in strength in tear-completion repair group, and they have just reported a 41% incidence of persistent shoulder pain after trans-tendon repair 39. In articular partial tears trans-tendon repairs require the placement of anchors through a tissue that is already poor in quality and thinned, moreover the anchor positioning is more difficult 32. On the other hand this surgical technique provides the avoidance of potential length-tendon mismatch 20, 34. Both repairs have been shown effective in restoring the anatomic footprint: a recent study reported that using a magnetic resonance arthrography to assess cuff structural integrity the rate of retear was not significantly different between articular and bursal sided tears at 6 months, respectively 8% and 11% 40. Another more recent study by

Kim KC et al 41 showed post operative rate of retear that differs but not significantly between high grade articular 0% and bursal 9.5% sided tears treated with full thicknessconversion and repair at 35.5 months mean follow up. Another complication mentioned in some studies is that of stiffness: partial thickness cuff tear repairs seem to lead a higher incidence of stiffness if compared with full-thickness repairs, 18% to 8%, but only few cases need capsular arthroscopic release4. Comparing the post operative clinical outcomes between articular and bursal sided tears it seems that there is no significant difference regard to pain and functional scores, and both guarantee a good to excellent result ranging from 86% to 94.1% 6.

Conclusion There is to date no evidence to support a treatment algorithm for partial thickness tears: surgical techniques provide good to excellent clinical results. We need prospective studies with long-term follow up: these kind of tears may be complicated by progression in long term, regardless of a correct and adequate treatment.

References 1. Fukuda H. Partial-thickness rotator cuff tears: A modern view on Codman’s classic. J Shoulder Elbow Surg 2000; 9:163-8 2. Finnan RP, Crosby LA. Partial-thickness rotator cuff tears. Review article. J Shoulder Elbow Surg 2010; 19: 609-616 3. Fukuda H. The management of partial-thickness tears of the rotator cuff: Review article. J Bone Joint Surg [Br] 2003; 85-B:3-11 4. Peters KS, McCallum S, Briggs L, et al. A Comparison of Outcomes After Arthroscopic Repair of Partial Versus Small or Medium-Sized Full-Thickness Rotator Cuff Tears. J Bone Joint Surg Am 2012; 94:1078-85 5. Sher JS, Uribe JW, Posada A, et al. Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg [Am] 1995; 77-A:10-5 6. Strauss EJ, Salata MJ, Kercher J, et al. The Arthroscopic Management of Partial-Thickness Rotator Cuff Tears: A Systematic Review of the Literature. Arthroscopy: The Journal of Arthroscopic and Related Surgery 2011; 27: 568-580

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7. Liem D, Buschmann VE, Schmidt C, et al. The Prevalence of Rotator Cuff Tears: Is the Contralateral Shoulder at Risk? Am J Sports Med 2014; 42:826-830 8. Ruotolo C, Fow JE, Nottage WM. The supraspinatus footprint: An anatomic study of the supraspinatus insertion. Arthroscopy 2004; 20:246-249 9. Nakajima T, Rokuuma N, Hamada K, et al. Histologic and biomechanical characteristics of the supraspinatus tendon: reference to rotator cuff tearing. J Shoulder Elbow Surg 1994; 3:79-87 10. Reilly P, Amis AA, Wallace AL, et al. Supraspinatus tears: Propagation and strain alteration. J Shoulder Elbow Surg 2003; 12:134138 11. Andarawis-Puri N, Ricchetti ET, Soslowsky LJ. Rotator cuff tendon strain correlates with tear propagation. J Biomech 2009; 42:158-163 12. Mazzocca AD, Rincon LM, O’Connor RW, et al. Intra-articular partial-thickness rotator cuff tears: Analysis of injured and repaired strain behavior. Am J Sports Med 2008; 36:110-116 13. Frisch KE, Marcu D, Baer G, et al. The Influence of Partial and Full Thickness Tears on Infraspinatus Tendon Strain Patterns. J Biomech Eng 2014; 136:051004 14. Ozaki J, Fujimoto S, Nakagawa Y, et al. Tears of the rotator cuff of the shoulder associated with pathologic changes in the acromion: a study in cadavera. J Bone Joint Surg Am 1988; 70:122430 15. Ellman H. Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res 1990; 254:64-74 16. Snyder SJ, Pachelli AF, Del Pizzo W, et al. Partial thickness rotator cuff tears: results of arthroscopic treatment. Arthroscopy 1991; 7:1-7 17. Conway JE. Arthroscopic repair of partial-thickness rotator cuff tears and SLAP lesions in professional baseball players. Orthop Clin North Am 2001; 32:443-456 18. Walch G, Boileau P, Noel E, et al. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg 1992; 1:238-45 19. Jobe CM. Superior glenoid impingement. Orthop Clin North Am1997; 2:137-43 20. Tokish JM, Ponce BA. Management of Partial-Thickness Rotator Cuff Tears. Oper Tech Sports Med 2005; 13:206-211 21. Gotoh M, Hamada K, Yamakawa H, et al. Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J Orthop Res 1998;16:618-21 22. Wolff AB, Sethi P, Sutton KM, et al. Partial-thickness rotator cuff tears. J Am Acad Orthop Surg 2006; 14:715-725 23. Yamanaka K, Matsumoto T. The joint side tear of the rotator cuff. A followup study by arthrography. Clin Orthop Relat Res 1994: 304:68-73 24. Brenneke SL, Morgan CJ. Evaluation of ultrasonography as a diagnostic technique in the assessment of rotator cuff tendon tears. Am J Sports Med 1992; 20:287-9 25. Reynolds SB, Dugas JR, Cain EL, et al. Debridement of small partial-thickness rotator cuff tears in elite overhead throwers. Clin Orthop Relat Res 2008; 466:614-621

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26. Budoff JE, Rodin D, Ochiai D, et al. Arthroscopic rotator cuff debridement without decompression for the treatment of tendinosis. Arthroscopy 2005; 21:1081-1089 27. Burkhart SS, Lo IKY, Brady PC. Rotator Cuff. In Burkhart’s view of the shoulder: A cowboy’s guide to advanced shoulder arthroscopy. Lippincott Williams & Wilkins, 2006 28. Park JY, Yoo MJ, Kim MH. Comparison of surgical outcome between bursal and articular partial thickness rotator cuff tears. Orthopedics 2003; 26:387-90 29. Cordasco FA, Backer M, Craig EV, et al. The partial-thickness rotator cuff tear: is acromioplasty without repair sufficient? Am J Sports Med 2002; 30:257-60 30. Liem D, Alci S, Dedy N, et al. Clinical and structural results of partial supraspinatus tears treated by subacromial decompression without repair. Knee Surg Sports Traumatol Arthrosc 2008; 16:967-972 31. Kartus J, Kartus C, Rostgard-Christensen L, et al. Long-term clinical and ultrasound evaluation after arthroscopic acromioplasty in patients with partial rotator cuff tears. Arthroscopy 2006; 22:44-49 32. Porat S, Nottage WM, Fouse MN. Repair of partial thickness rotator cuff tears: A retrospective review with minimum two year follow-up. J Shoulder Elbow Surg 2008; 17:729-731 33. Budoff JE, Nirschl RP, Guidi EJ. Debridement of partial thickness tears of the rotator cuff without acromioplasty. Long-term follow-up and review of the literature. J Bone Joint Surg Am 1998; 80:733-748 34. Lo IK, Burkhart SS. Transtendon arthroscopic repair of partialthickness, articular surface tears of the rotator cuff. Arthroscopy 2004; 20:214-220 35. Ide J, Maeda S, Takagi K. Arthroscopic transtendon repair of partial-thickness articular-side tears of the rotator cuff: Anatomical and clinical study. Am J Sports Med 2005; 33:1672-1679 36. Fukuda H, Hamada K, Nakajima T, et al. Partial thickness tears of the rotator cuff: a clinicopathological review based on 66 surgically verified cases. Int Orthop 1996; 20:257-65 37. Sonnabend DH, Yu Y, Howlett CR, et al. Laminated tears of the human rotator cuff: a histologic and immunochemical study. J Shoulder Elbow Surg 2001; 10:109-15 38. Castagna A, Borroni M, Garofalo R, et al. Deep partial rotator cuff tear: transtendon repair or tear completion and repair? A randomized clinical trial. Knee Surg Sports Traumatol Arthrosc 2013; May 21 [Epub ahead of print] 39. Castagna A, Delle Rose G, Conti M, et al. Predictive factors of subtle residual shoulder symptoms after transtendinous arthroscopic cuff repair: A clinical study. Am J Sports Med 2009; 37:103-108 40. Kim SJ, Kim SH, Lim SH, et al. Use of magnetic resonance arthrography to compare clinical features and structural integrity after arthroscopic repair of bursal versus articular side partial-thickness rotator cuff tears. Am J Sports Med 2013; 41:2041-7 41. Kim KC, Shin HD, Cha SM, et al. Repair integrity and functional outcome after arthroscopic conversion to a full-thickness rotator cuff tear: articular- versus bursal-side partial tears. Am J Sports Med 2014; 42:451-6

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Rotator cuff rehabilitation Marco Conti, Raffaele Garofalo* Unità di Riabilitazione Funzionale, Istituto Clinico “Humanitas”, Milano * Unità Chirurgia della Salla, Ospedale “F. Miulli”, Acquaviva delle Fonti, Bari

In the framework of shoulder pathologies the rotator cuff tendon lesions are pathology frequently found [1], especially among patients aged over 45. However younger people are increasingly subjecting their scapular-humeral joints to significant stress and can therefore suffer from this type of lesion, especially in sports and overhead working activities, but the presence of a rotator cuff tendon lesion does not necessarily suggest the need for surgical operations [2–5]. There is in fact increasing agreement that surgery is indicated after failure of preventive rehabilitation treatment carried out for a period of at least 3–4 months, or in the cases in which significant and progressive rotator cuff tendon insufficiency occurs [6], or in relationship with dimension of lesions related to the patients expectations or needs. The progression of technology allows surgeon to perform today surgical repair of a rotator cuff tendon tear (RCT) using a variety of methods, open, mini-open and arthroscopic techniques [7], and the post-op results are generally good and substantially comparable [8–11]. A great topics of discussion is not therefore today the surgical technique to use but rather post-surgery recurrence. When minor re-ruptures occur, patients may still show improvement of the clinical symptoms compared with the pre-operative period, while patients with massive re-ruptures do not benefit in any way from the surgical operation [5–12]. Therefore the level of healing of the repaired tendon [13], seems to be increasingly the key point for therapeutic success and clinical result. Many factors can influence The healing of the repaired tendon seems to be influenced by many factors [14, 15]: we can in fact distinguish between surgical factors associated with recognition of the type of lesion (forms and number of tendons involved), the size of the lesion, the technique such as the mobilisation of the tendon tissue that was possible to obtain intra operatively, the tendon quality, the degree of muscular hypo-atrophy, as well as adequate subacromial decompression, correct preparation of the humeral tuberosity, and the anchoring and suturing method. Then a series of factors related to the patient such as age, lifestyle and the presence of other shoulder complaints or systemic illnesses [7] that either must be taken in account (such as diabetes, thyroid pathologies, hormonal imbalances). In this light, the post-surgery rehabilitative treatment assumes great importance as it must be able to protect the repair in the early stages, to prevent post-op stiffness and then restore the function of the scapular-humeral joint [15, 16].

Abstract A variety of types or extensions of cuff lesions in patients from a wide range of age groups who have different kinds of jobs and participate in different kinds of sports, and who have widely different expectations in terms of recovery of functions and pain relief can be today addressed by advances in techniques and materials for rotator cuff surgery. Instead a large number of factors must be taken into account before implementing a rehabilitation protocol after rotator cuff surgery. Mainly the surgery technique (materials and procedure) used by the surgeon. Moreover, tissue quality, retraction, fatty infiltration and time from rupture are important biological factors while the patient’s work or sport or daily activities after surgery and expectations of recovery must also be assessed. A tailored rehabilitation protocol should also take into account the timing of biological healing of bone to tendon or tendon to tendon interface, depending on the type of rupture and repair. This timing should direct the therapist’s choice of correct passive or assisted exercise and mobilisation manoeuvres and the teaching of correct active mobilisation movements the patient has to do. Following accepted knowledge about the time of biological tissue healing, surgical technique and focused rehabilitation exercise, a conceptual protocol in four phases could be applied, tailoring the protocol for each patient. It starts with sling rest with passive and small self-assisted arm motion in phase one, to prevent post-op stiffness. In phase two passive mobilisation by the patient dry or in water, integrated with scapular mobilisation and stabiliser reinforcement, are done. Phase three consists of progressive active arm mobilisation dry or in water integrated with proprioceptive exercise and “core” stabilisation. In phase four full strength recovery integrated with the recovery of work or sports movements will complete the protocol. Because of the multi-factorial aspects of the problem, the best results can be obtained through a full transfer of information from the surgeon to the therapist to optimise timing and sizing of the individual rehabilitation protocol for each patient.

Many rehabilitation protocols have been proposed, often based only on empirical experiences, without fully taking into account biological aspects relative to the healing steps of the repaired tendon [17-19-44-49]. Furthermore post-surgical rehabilitation of the suture of rotator cuff tendons can vary from patient to patient, bearing in mind (all together in the same time) the surgical technique, the patient’s expectations and functional demands, the number of tendons repaired and therefore the grade of the lesion, the quality of the tissue and any associated surgical actions [16].

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Tendon healing

Immobilisation and sling

The biological time for the tendon to heal must be taken as the one of the most important aspects the rehabilitation protocol must take into account is. This process involves tendon healing at the bone footprint if the tendon has been reinserted into its anatomical place using a technique with anchors and sutures or trans osseous suture technique or alternatively tendon with tendon healing if a suture technique with latero-lateral stitches has been carried out. The reparative phenomena follow a cascading series of mechanisms one after another in healthy individuals [20]. The first stage is the inflammatory one: during the first week it is characterised by an increasing number of inflammatory cells like leukocytes, lymphocytes and monocytes, which release histamine and bradykinin, which increase vascular permeability and therefore allow the plates to reach the level of the repair site. The fibrin with the fibronectin form a fragile scar which reduces the haemorrhagy process without any real adhesion between tendon and bone. The inflammatory stage lasts for a period which varies between 1and 2 weeks and which is generally transformed into the proliferative stage. During the proliferative stage a tighter adhesion between the tendon and the bone surface is obtained thanks to the inflammatory tisssue that is gradually replaced by fibroblasts, myofibroblasts and endothelial cells, which organise themselves with a new extracellular matrix to form a granulation tissue which guarantees the adesion between two so different tissues. Then the fibroblasts starts to produce type III collagens fibers , which are therefore immature, and glycosaminoglycans; then there is significant neoangiogenesis. This stage lasts about 10 days and commences after the first 15 days after surgical repair. The last stage of maturing and remodelling then follows, which therefore begins around the third week and is characterised by maturing of the scar tissue. The immature type III collagen is replaced by type I with the formation of dense connective tissue. By now the fibroblastic cells will have replaced the inflammatory cells. The process continues during the following weeks until the tendon is completely integrated with the bone surface. Tendon healing studies have mainly been carried out on animal models and therefore the remodelling and maturing stages have been seen to vary in duration depending on the animal model used. Some authors have described periods of 12–16 weeks for the tendon to recover its tensile strength [20], while other authors who have studied sheep models have reported times of as much as 26 weeks (4 months) [21]. These studies obviously reveal a set of limits linked to the model studied while, furthermore, human ruptured tendons reveal a series of degenerative alterations which can negatively influence and therefore prolong the healing time. The recognition of the role of the biological timing is very important and must be properly recognised by the doctor and the therapists to modulate the rehabilitative timing.

On the basis of the biological healing stages of the repaired cuff tendon tissue, it is clear that precocious and aggressive mobilisation or violent muscular contraction can exceed the mechanical strength of the repair and damage it, even though precocious mobilisation could reduce the risks of articular stiffness. The purpose of a reasoned rehabilitative process after a rotator cuff repair is therefore to obtain cuff tendon healing by recovering mobility and shoulder function gradually. From this starting point an adequate immobilisation of the limb is crucial during the initial post-operative stage in order to guarantee effective tendon healing. Study on rats highlighted that the cuff tendons that were immobilised after surgical suturing revealed excellent orientation of the collagen fibres and enhanced organisation of the extracellular matrix compared with rats that were left free after the repair [22]. Adequate immobilisation must however take into account the vascular and biomechanical characteristics of the rotator cuff [23]. The use of an abduction sling during the early weeks seems capable of reducing tension at suture level and improving vascularisation of the scar. In fact we know that the hypovascular zone of a healthy supraspinatus tendon is about 1.5 cm from the greater tuberosity of the humerus and the position of the head of the humerus influences tendon vascularisation significantly [24]. Assessing tendon microcirculation in relation to the head position, Rathbun and Macnab showed that there is a reduction of the haematic flow to the tendon when the arm is in a total adduction position [25]. Based on these observations, it seems prudent to recommend post-op immobilisation in a sling with the arm abducted at least to 30 for the first 4–6 post-operative weeks in order to improve microcirculation and reduce the stress on the operated tendon, especially in the case of a repair carried out on an inveterate tendon lesion [26, 27]. A recent study of our group (still in printing at this time) compared, in patients treated for RCT repair for the same lesion with the same type of repair, the use of a sling in abduction 30° and external rotation 15° with a sling in abduction 30° and internal rotation 15°. The data demonstrated in the group of Abd 30° and ER 15° sling a significantly greater passive mobility at 1 and 3 months, a significantly greater Constant score at 3 months and a minor VAS for pain still at 3 months. Same results for the two groups at 6 months. This study suggest that the use of a sling in Abd 30° and ER 15° seems to be more suitable for the patient.

Continuous passive mobilisation Few studies in the literature help us to understand if this therapeutic aid (obtained today with electronically controlled automatic programmable mobiliser) can be of benefit in the rehabilitation of patients operated by suturing the rotator cuff. As a general rule this continuous passive mobilisation (CPM) can be applied in the immediate postop period applying a low mechanical stress on the repair. Hatakeyama et al. have shown that the safety position after

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this surgery is 30° of elevation on the scapular plane with an external rotation range between 0 and 60° [28]. In a double-blind randomised study of patients treated with repair of the cuff and subacromial decompression, Raab et al. [29] showed that three months after the surgical operation there were no differences in the various scores between patients treated with physical therapy and CPM and those treated with physical therapy only; however the range of movement and pain level were better in patients in the first group. Recently, Michael et al. [30] seemed to confirm these data and also showed how the recovery of the range of movement is faster in patients treated with CPM in the post-operative period. In another randomised prospective study on 31 patients operated for repair of the rotator cuff, Lastayo et al. [31] compared 2 groups, one treated with CPM in the first 4 weeks while the other was subjected in the same period of time to a physical therapy programme with passive recovery of mobility. A follow-up carried out after 22 months found that there were no statistically significant differences in the scores of the two groups or in pain and isometric muscular strength. Our figures [32] relating to a randomised prospective study on 100 patients seem to indicate that the precocious use of CPM for at least two hours daily overall, for one month after the operation, can permit better recovery of the passive ROM in both abduction and external rotation and in forward flexion with significant data already at two and a half months. It therefore seems, from the analysis of the literature, that in the medium and long term, CPM succeeds in substantially influencing the recovery of the range of movement only, while it remains to be seen whether it can have a positive effect on faster recovery of working activities or of common everyday activities. It is also not yet known if the use of CPM can influence healing of the repaired tendons to any extent. Certainly, however, this method can be used in patients who have a cuff lesion associated with adhesive capsulitis in the pre-operative period and who can therefore benefit from a recovery, or at least from a non-loss, of the range of movement already gained during the surgical operation.

Post-operative functional rehabilitation Multiple factors, which the surgeon and rehabilitation therapist must share, are the variables that, from what we have said so far, the rehabilitative management after RCT repair must take into account. On top of the processes and biological timing of tendon healing also must be taken in account the size of the tendon lesion treated, the quality of the treated tendon, the type of repair made (type of cuff suture made, if partial or total, if a mono or pluri-tendon suture, and if the repair is tendon–tendon or tendon–bone type; knowledge of the type of implant used – reabsorbable or not reabsorbable – is also important), any associated surgical actions (acromion plastic surgery, resection of the distal clavicle or, in younger patients, repair of an associated lesion of the SLAP type, tenotomy or tenodesis of the long end of the biceps and possibly knowledge of the type of tenodesis technique – whether static or dynamic – to the soft parts of the cuff), the physiological age and

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expectations of the patient, and the range of pre-op movement of the operated shoulder. The degree of fatty degeneration of the tendon and of muscular atrophy, the size of the lesion treated and the extent of reduction of the range of movement in the pre-op period In particular, must be also seen with particular attention because of the fact that the prognosis after repair can be significantly related to [12, 13, 35]. In this sense, communications and coordination between the surgeon, physiatrist and physiotherapist are fundamental in order to obtain an optimum result for the patients themselves. The current general consensus in the literature [14, 15, 19, 36–39] is to subdivide the post-operative rehabilitative treatment into four stages, each one with different aims. The aim of the first stage is to prevent articular stiffness because of post-surgical adherences by means of exercises of the passive type, which help to minimise loading at the repair site. The aim of the second stage is the progressive recovery of the passive range of movement without scapular compensation by means of exercises of the assisted /active type which begin gradually to apply work loads on the repaired tendons. The aim of the third stage is to recover strength and physiological scapular-humeral rhythm by means of toning exercises focusing on the recovery of power and the strength of the rotator cuff tendons. The aim of the fourth stage is the best recovery of the strength and normal actions for both work and sports. These stages naturally interweave and overlap without any break and it is possible, in the same stages, to find a series of variables linked to all the conditions regarding the patient and type of lesions treated and to the type of surgical technique used. The first rehabilitation stage runs from the immediate post-op period until the 4th–6th week. During this stage the patient will be asked to wear the abduction/er sling (up to 5-6 weeks for complete lesions; up to 4-5 weeks for partial and incomplete lesions) and it is only removed 3–4 times per day to carry out passive abduction, front flexion and external rotation mobilisation exercises, as pendulum exercise. During this stage the loads on the repair made must be minimal and, in fact, this stage is characterised biologically by a slight coagulation of fibrin with type III collagen; therefore exercises with active muscular contraction on the operated limb must be avoided at this stage. The recovery of the passive movement must be carried out inside a safety range and the patient must work without pain and with the avoidance of maximum stretching. In the case of an associated subscapular repair, external passive rotation must be limited to 0°. Therefore patients can make active movements of the wrist, hand and elbow. The active flexion–extension of the elbow must be modulated and limited in this stage if a tenodesis of the long end of the biceps has been carried out, especially if of the dynamic type at the rotator cuff. Pendulum exercises are useful at this stage, to be carried out with extreme relaxation of the musculature and with the trunk tilted 30° forward. Furthermore, preference must be given to active and proprioceptive work of the scapular/thoracic joint. Once the

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skin suture stitches have been removed the passive mobilisation and slight stretching exercises can also be carried out in a pool [26]. Ice is an useful anti-inflammatory aid for use in this stage, especially in the first 10–15 days and after the physiotherapy sessions [39]. Also CPM can be useful in this stage, particularly with patients who have had a reduction of the physiological range of movement or capsulitis in the pre op phase. The second stage runs from the 4th–6th week until the end of 3rd month. This is because, from the 6th week after the operation, the extent of healing of the tendon to the bone and of the tendon to tendon begins to be sufficient to allow the introduction of active movements at a minimum load. The mobilisation exercises can also be carried out by a therapist at this stage and it is possible to begin greater and greater stretching, with decoaptation of the humeral head in order to begin to recover the range of movement towards the greatest angles without inducting a subacromial iatrogenous conflict. It is possible at this stage to begin to use aids such as pulleys and sticks. In this case too it is necessary to continue to take care of some strategies. If, for example, the top fibres of the subscapular muscle have been sutured, the recovery of external rotation should preferably be obtained by means of an abduction of the limb to 45° (and with the elbow raised 4–6 cm from the couch to reduce stress on the sutures to a minimum if the execution is carried out in a supine position). Hydrotherapy is very useful from the 6–8 weeks to begin the active mobilisation exercises in a condition of reduced mechanical stress for the repair because the reduced force of gravity. The patient can be allowed to swim breaststroke and when front passive flexion reaches around 130° some modified backstroke can be added, without submerging the limb but ending the movement at surface level. At this stage, therefore, it is possible to start active movements without important loads and therefore the use of the arm is permitted in everyday activities. The proprioceptive exercises on the scapularthoracic joint are intensified as the active toning of the active scapular stabilizer muscles. Particularly important at this stage is the use of neuromuscular biofeedback systems which, help the therapist to get the patient to “relearn” the ability of voluntary and coordinated control of the fundamental muscle groups for scapulo-humeral stabilization and which, have been mal-functioning for some time because the profound alteration of the motor patterns induced by the cuff lesion, by the pain and by the compensation mechanisms implemented instinctively to permit the spatial positioning of the hand on the basis of living needs. At the end of the third month (10th–12th week) can start the third stage : is the muscular toning stage with progressive functional recovery. The start of this stage obviously depends on various factors. As we have already said, one of the most important factors is the type of lesion repaired. This is because more serious is the tendon lesion repaired, more this stage is delayed. Furthermore, the start of this rehabilitation stage is secondary to recovery of a satisfactory range of active movement of the operated limb, especially in terms of front flexion and external rotation. This is because repeated

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attempts to tone a shoulder which is still stiff can give rise to pain, subacromial conflict and excess stress on the repair itself. Patients who are still unable to actively raise the arm against gravity at this stage should begin to carry out reinforcement exercises without resistance in a supine position that virtually eliminate the gravity weight and the patient can begins to raise the limb over 90° and reinforce the deltoid. This exercise can be carried out at the beginning with the elbow flexed and then gradually increasing the lever arm by extending the elbow progressively with a small weight in the hand or using an elastic resistance system [40]. At this rehabilitation stage it is important to respect the pain while the intensity of the exercises must be properly monitored staring with submaximal isometric contractions which permit the application of controlled force through the repaired tendon. If the supraspinatus has been repaired, toning must be carried out first attempting to reinforce the pair of front (subscapular) and rear (subspinatus) forces by means of exercises with the limb abducted to 30°– 45° and then 60°, to limit the possibility of a subacromial conflict that can entail pain as well as mechanical stress on the repair made. Isometric reinforcement is followed by a isotonic reinforcement stage with elastic bands initially concentrate on the execution of many repetitions with low loads. Remembering that muscular toning is dependent on the articular angle, it is necessary to seek different angular positions of the humerus at which to carry out the same exercises so that with each exercise all fibers of the involved muscle will be involved then changing the exercise and the humerus spatial position the infraspinatus, the teres minor, the subscapular, the deltoid (first front and then rear), the mid and inferior parts of the trapezius and the rhom- boideus or costoscapularis muscles could be progressively involved [45]. The exercises must be modulated to spare the repaired tendon as much as possible at the beginning. Takeda et al. [41] have shown that with the arm abducted on the scapular plane the supraspinatus is isolated and that this would therefore be the ideal position for the reinforcement of this tendon, if not involved in the repair or in the late stages of the process of healing. However it is necessary to be very careful with the humeral rotation in this position. Some NMR studies have shown that in the abduction and internal rotation position the subacromial space is reduced in a dynamic manner and gives rise to stress on the repair [42], and this is why abduction positions of less than 90° are recommended if internal or external rotations are associated with them [26] . At this stage it is also necessary to continue to improve the range of movement with exercises for stretching the capsulo-ligamentous structures, in particular on the antero-inferior and postero-inferior capsule that is always stiff at this stage. The proprioceptive work of the scapular stabilisers must be intensified without forgetting “core” stabilisation (the muscular system of the abdominal, oblique, dorsal and gluteus muscles), fundamental for correct positioning of the scapula [48]. A crucial role in progressive functional recovery is played by proprioceptive exercises in a closed kinetic chain first below and then above the breast .

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Around the 16th week, and always on the basis of the functional recovery attained by each patient, generally begins the fourth and last rehabilitation stage of the rehabilitation process that last until the 6th month. This stage is a progression of the third stage, and its end point is different depending on the type of patient [43]. This is because at this stage a patient with a low functional demand will continue to improve in a progressive manner in a programme of exercises prevalently home based with an increasingly complete recovery of the normal activities of everyday life and the resumption, with great caution, of overhead activities. With regard to young patients and athletes [47], generally more high demanding, these last stage begin with exercises first in an open kinetic chain with increasing ARoM and velocity and then go on to specific sports recovery exercises first for the gesture and then with force applied to the specific sports gesture itself, while workers begin to carry out activities which simulate the working activity in a specific and progressive manner. Is a therapist’s job to teach patients appropriate strategies for limiting at the minimum the stress on the repaired tendon during the sports or work activities.

Conclusions Evident is the consensus about how post-operative rehabilitation is a progressive, integrated and tailored process (rather than a “protocol”) in which a fundamental role is played by the passage of information between the surgeon and the physiotherapist, as well as the sharing of knowledge regarding the characteristics of each individual operation both in terms of surgical technique and in terms of the biological and anatomical characteristics of the repaired tissues. Only through the integration of this information with data regarding the patient’s lifestyle and expectations it will be possible to establish a tailored rehabilitation programme which can not ignore the times and processes of biological tissue healing in order to achieve the best possible result both in terms of functional recovery and of management of the symptoms.

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Modern technique of arthroscopic suture in reparable rotator cuff tears. Actual standards and limitations Roberto Leo, Valentina Fogliata, Amos Maria Querenghi, Marco Pivetta, Bruno Michele Marelli Dipartimento di Ortotraumatologia Generale e Chirurgie Ortopediche Specialistiche, Struttura Semplice Dipartimentale Chirurgia Spalla e Gomito, Istituto Ortopedico G. Pini, Milano

INTRODUCTION

ABSTRACT

The treatment of rotator cuff lesions got great improvements through the decades. In fact, before 1970s these lesions weren’t treated surgically. Afterwards, between 1970s and 1980s, open surgical treatment of rotator cuff tears was the gold standard for treating this kind of lesion. More recently, from 1990s and the beginning of the new century, open surgical treatment was slowly and progressively replaced by the new mini-invasive arthroscopic treatment. Over the years, several studies compared the outcomes of open-surgical technique and arthroscopic one1,2,3 demonstrating that there is no difference between the two techniques, considering both the possibility of repairing wide lesions and the quality of tendon-to-bone fixation4. The effectiveness of tissue repair, apart from biological responses, depends also on the mechanical resistance of the construct including anchor fixation, knot reliability, stability of the suture loop, and suture configuration. All of these are key points in a good tendon healing process. The aim of this paper is to describe how the modern arthroscopic surgery developed in order to achieve results comparable to the one of the traditional open techniques. First of all, we’ll analyse the tools used by the surgeon to obtain the suture, considering hardware and materials. Then we will also analyse suture techniques used to achieve the best tendon-to-bone repair.

The aim of this paper is to describe how the modern arthroscopic surgery developed in order to achieve results comparable to former traditional open techniques. New materials available in shoulder surgery, new surgical tools and new suture techniques developed by surgeons lead today to better final outcomes than at the beginning of arthroscopic surgery. For this reason in our paper we described the main used suturing techniques (single row, double row, transosseous equivalent suture bridge, triple row, and transosseous) comparing their virtues and vices. Finally me must conclude that modern mini-invasive techniques are based not only on the surgeon learning curve but also on the improvement of suture materials and tools that are available for surgery. In the future, by one side better understanding of the biological processes causing tendon damage and, in the other side, better knowledge of the processes that lead to tendon to bone reparation after surgery seems to be the key for improving clinical results and then patient satisfaction.

EVOLUTION OF SURGICAL TOOLS AND MATERIALS The evolution of materials comprises: 1) Surgical tools; 2) Anchors; 3) Sutures.

Figure 1: Single step suture passer

1) Surgical tools There are mainly 3 kind of suture passing instruments: - Single step suture passer: it is a tool that grasps the tissue and, at the same time, thanks to a needle, it passes the suture through the tendon. Nowadays, this 3rd generation of suture passer is available and it increases the rate of success in passing the suture through the tendon (Figures 1, 2),

Figure 2: Single step suture passer perforating tendon

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Figure 4: Perforating tool

Figure 3: Double step suture passer

- Double step suture passer (for example Spectrum® - Conmed TM or Accu-Pass® Suture Shuttle – Smith & Nephew): it is a perforating tool that, after passing through the tendon, releases a shuttle suture wire that works as a real shuttle for anchorwire (Figure 3). - Perforating tool (also called ‘Bird beak’): it is a tool that penetrates the tissue, grasps the suture and makes it passing through the tendon with a retrograde movement. In the beginning this tool was straight or slightly curved but, nowadays, ‘bird beaks’ are available curved in different directions, in order to make this device suitable for almost all cases (Figure 4). Each surgeon has his favourite set of tools, so an ideal instrumentations for performing a suture doesn’t exist. However, it is compulsory to understand all the characteristics, indications and limitations of every single tool to make possible the best repair of every kind of lesion.

2) Anchors Different kinds of anchor exist, from metallic to entirely resorbable ones. This evolution is due to the need to improve the tendon-to-bone healing5. The first models of anchors produced were made up of metallic alloy with non-resorbable suture-wires and, in the beginning, they made possible to achieve good results even if further studies demonstrated presence of complication such as incarceration or migrations of the anchors6-8. For that reason non-resorbable anchors were produced9,10. The materials with the greatest history and most commonly used are polyglycolic acid (PGA) with a degradation time of 3 to 4 months and polylactic acid enantiomers (PLA, naming levo-stereoisomer PLLA and dextro-stereoisomer PDLA) with a degradation time between 10 to over 30 months. One of the first use of this anchors was Suretac® system, made of PGA and used in arthroscopic Bankart repair. Even if a few authors describe a good long term results using this device,9 there are several studies that showed as it produced massive synovitis, loose fragments spread in joint cavity and induced a foreign-body reaction11,12. After this one, PLLA anchors were presented; they showed a longer time of reabsorption. Several studies, e.g. Dejong et al.13, stated that the reabsorbable PLA suture anchor construct, tested in an in vivo intra-articular model, had similar strength over a 12-week period of implantation with a comparable metal anchor construct. So they showed that resorbable anchors are a good alternative to metallic ones, since they have a function and a pull-out resistance comparable to metallic ones, in addition to the advantage linked to the resorbable materials (e.g. no interference to MRI). But we must notice that using this biomaterial there were concerns that an excessively long period of degradation would not allow a complete osseous replacement leading potentially to complications similar to metallic anchors 14. In order to reduce the anchor degradation time, the amorphous nature of PLLA has been increased, using copolymers of the levo- and dextro-stereoisomers of lactic acid and PGA the polylactide-co-glycolide (PDLLA-co-PGA) or PLGA, in which the composition range of the polymers can be variable15-17. This evolution led to the introduction of biocomposite anchors made by new generation materials, improving

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stimulation of reabsorption and subsequent stimulation of bone ingrowth. They are generally a blend of tricalcium phosphate (TCP) and PLA. One of this copolymer is composed by 30% TCP and 70% PLGA. Another one copolymer of this family is composed by 15% TCP and 85% PLA. Both are reported to produce a few tissue reaction and sub sequential good bone ingrowth. Polyetheretherketone (PEEK) is a stable material, highly unreactive, that is resistant to chemical, thermal, and radiation-induced degradation. It has been widely used in trauma and orthopedics. PEEK-based anchors are strong, relatively inert, radiolucent, and can be easily removed during revision surgery 18.. More recently have been introduced the so-called “soft anchors” made by all-soft flat-braided high-strength polyester non resorbable suture wire (for example JuggerKnot®, Biomet - Y-knot®, Conmed Linvatec - Suturefix Ultra®, Smith&Nephew). In these devices the construct does not require a rigid body for bone engagement. In fact after they are inserted into the pilot hole, as soon as they are released, the suture wire forms a “ball” inside the tunnel immediately under the humeral cortical layer. This “ball” can function as a real biosorbable stiff anchor. The key point in these types of anchors is that they eliminate every kind of tinny and stiff material inside the joint. All these great new anchors biomechanical properties are suitable for several cases in arthroscopic shoulder surgery.

3) Sutures The ideal suture wire would be strong but biologically inert and must simply dissolve in body fluids loosening resistance at the same time that repaired tissue gains mechanical resistance. Modern sutures are close to the above mentioned ideal suture. At the same time we must say that even if there have been great improvements in suture materials, no single suture can be perfect in all circumstances. We must distinguish from absorbable and non-absorbable suture noticing that in any case suture wire act as a foreign body inside our tissues. Talking about rotator cuff surgery the most used sutures are yet the non-absorbable ones who keep the same resistance for all the period during which the tendon is repairing on the bone. One of the most famous non-absorbable suture is Ethibond®. Ethibond® is a ���������������������������������������� non-absorbable, braided and sterile surgical suture composed of Polyethylene terephthalate. It is prepared from fibers of high molecular weight, longchain, linear polyesters. It is uniformly coated with polybutilate and this highly adherent coating acts as a lubricant to mechanically improve the physical properties of sliding and flexibility, improving in this way his handling qualities. The pitfall of this suture is the lower mechanical resistance during the knot tightening and, sometimes, the suture is sheared by using the knot pusher. Nowadays companies improved the quality of sutures used in rotator cuff repair and so now they offer high resistance wires that are able to withstand much better to the strength applied while tightening the knot. In fact the

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resistance of the construct and consequently the quality of the repair depend on the reliability of the knot and on the elongation of the system (suture and loop); therefore, the increased material resistance may minimize suture breakage due to either “sharp” devices or overthightenig19. Biomechanical tests made by companies demonstrate that the resistance to traction of the knot pusher in this new kind of suture is doubled than in Ethibond®. As following, we analize the characteristics of four kind of high-resistance sutures produced by four of the main companies: - Orthocord® (De Puy Mitek): it’s a braided and synthetic suture composed of resorbable polydioxanone (PDS®) and non-resorbable non-colored polyethylene fibers. The suture is covered by a partially resorbable copolymer (90% Polycaprolactone and 10% Glycolide) to facilitate the sliding during the tightening of the knot. - FiberWire® (Arthrex): it’s a multi strand structure suture composed by a central core of ultra high molecular weight polyethylene (UHMW) covered in a braided coating composed of fibers of ultra high density polyester and polyethylene. This pattern gives a high resistance to rupture and friction. However, this suture has a high stiffness that must be considered in case of tendon-to-bone suture since the excessive tightening of the knots could reduce the tissue blood supply and so worsen the healing process. - Hi-Fi® (Conmed Linvatec): it’s a braided suture composed of ultra high molecular weight poly ethylene fibers without central core. It offers high resistance to the rupture caused by the knot pusher and it is mainly non-resorbable. - Ultrabraid Suture® (Smith&Nephew): It’s once again a non-absorbable suture composed of a special ultra high molecular weight (UHMW) polyethylene fiber featuring a unique braid configuration without central core.

SUTURE TECHNIQUES One of the most important thing to consider in arthroscopic repair is to understand the shape of the lesion: partial (articular or bursal) or complete, usually divided in crescentshaped, U-shaped, L-shaped and massive tears20. In fact, understanding the shape of the lesion allow the surgeon to use the most reliable and suitable technique to restore the normal anatomy of rotator cuff if possible. The main purpose of the surgical procedure is to re-attach tendons to������������������������������������������������� the bone ��������������������������������������� at their anatomical insertion.��������� The �������� stability of the tendon-to-bone fixation and its tight contact (a so called ‘watertight cuff repair’) are the essential assumptions for an appropriate tendon-to-bone healing and so for good clinical outcomes. For this reason in arthroscopic surgery there has been an evolution of the technique, both considering the devices, the wires and the surgical managing, in order to adapt����� surgery to the anatomy of the��������������������������������� tendinous lesion, after evaluating its shape, width and the quality of the tissue.

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Figure 5: Single row construct

Figure 6: Mason Allen stitch modified for arthroscopy

The main used suturing techniques could be divided into 5 types: - single row, - double row, - transosseous equivalent suture bridge, - triple row, - transosseous.

Single Row In this technique the surgeon implant��������������������� s�������������������� a single row of anchors parallel to each others and perpendicular to the glenoid articular surface. ����������������������������������� As in other techniques ������������ right placement of the anchor is very important for the biomechanics of the final construct. Firstly, considering the superior surface of the great��������� er������� tuberosity, the inclination of the angle should comply the concept

of the ‘deadman angle’ by Burkhart21. Also the distance from the articular humeral cartilages must be considered and it depends on the grade of retraction of the tendon: the more is the tendon retracted, the more the anchor should be medialized. There are different ways of passing suture wire through the tendon: ‘simple’ (only a wire into the tendon – Figure 5), ‘double’ or ‘mattress’ (both sides of the suture pass through the tendon), and more complex ones, such as the arthroscopic Mason-Allen (Figure 6) or the Italian modification of the latter, the Alex stitch22. Usually, this technique doesn’t need high duration of surgery and it has lower costs compared to the techniques described below. In our experience, we get very good outcomes, even though several studies23,24 demonstrated that not always this technique achieves a good tendon-to-bone fixation on the anatomical footprint if compared to double row or transosseous equivalent technique.

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Figure 7: Double row construct

Figure 8: Suture bridge transosseous equivalent

Double Row This kind of suture is performed using 2 rows of anchors, one near to the articular border of the humeral head and the other one������������������������������������������� more�������������������������������������� lateral������������������������������ near������������������������� to the ����������������� top of the ������ greater tuberosity. It is possible to perform simple knots for every anchors or to perform simple knots for the medial anchors and a mattress knot for every lateral anchor, as described by Lo and Burkhart25 (Figure 7). In this way, every anchor acts like an independent point of support with the advantage of increasing the area of tendon-tobone contact and, as a consequence, the process of tendon-to-bone healing. Disadvantages of this technique are higher costs (it needs a doubled amount of anchors than single row technique) and higher duration of surgery. Another disadvantage is that the high number of sutures could excessively increase the compression of the tendon resulting in a ������ poten-

tial decrease of blood supply and, as a consequence, of all growth factors involved in the process of tendon-to-bone healing. There are several studies that compared single row to double row techniques. Kim et al26 evaluated both techniques in terms of cyclic loading, gap formation and failure loads and they stated that double row technique got 42% less gap formation, 46% more stiffness and 48% higher ultimate load to failure. The strain experienced in the footprint of double-row repair was 1/3 of that seen in single row. In their study, Saridakis and Jones27 stated that doublerow sutures get a more stable structural repair than single row, but there isn’t a significant statistical difference in term of clinical outcomes in lesion of less than 3 cm if compared with single-row suture. Instead, Duquin et al28 stated that in case of lesions of more than 1 cm, double-

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Figure 9: Triple row construct

row technique has a much lower rate of recurrence of lesions if compared to single-row technique. In their study, Ma et al29 showed that patients with lesions of more than 3 cm repaired with a double-row suture have a higher value of strength if compared with a repair with a single-row suture; however, after repairing every kind of lesions, they didn’t find a significant statistical difference in rotator cuff integrity at a 2-years follow-up.

Transosseous equivalent suture bridge In this technique, presented by Park et al.30, the surgeon knots the sutures of the medial anchors at the lateral ones after crossing them (Figure 8 - Transosseous equivalent suture bridge). In this technique simple knots are performed at the medial anchors and then the insertional part of the tendon is pulled till the great tuberosity and it is fixed here by special anchors (like for example PushLock® by Arthrex) that lock the terminal part of the sutures into the holes inside the anchors without further knots . Nasson et al.31 demonstrated that this technique brings to a more water-tightening repair if compared with single row technique. The main pitfalls are the increase of surgical time and of costs of the procedure. Triple Row This technique was introduced by Ostrander and McKinney32 in 2012 considering that the most anatomical repair could lead to a decrease of recurrence in massive lesions. This technique, a sort of suture bridge-modified, requires a further anchor in median position between the row of medial anchors and the row of the lateral ones (Figure 9). Ostrander and McKinney32 demonstrated that this technique showed a higher pressure at the area of contact with a larger tendon-to-bone area at the footprint if compared to double rows and to suture bridge techniques. However this technique needs a longer duration of the surgery and it is burdened by considerable costs. Furthermore, from our point of view, the use of 5 anchors for performing this technique could considerably weaken the bone increasing the risk of iatrogenic or late fractures.

Arthroscopic transosseous technique The transosseus repair of rotator cuff lesions was largely used when it was performed with open surgery. Since this technique is able to achieve a good seal respect���������� ing������� anatomy without using anchors, a specific tool was developed to perform the arthroscopic transosseous suture33. Recently, Garofalo et al.34 tested a new device (ArthroTunneler® device by Tornier) that makes possible to perform an arthroscopic transosseous tendon repair taking advantage of mini-invasive surgery and the reliability of transosseous open repair. Furthermore, without using anchors, this technique avoids all complication linked to it, such as pullout or osteolysis of great tuberosity. Moreover, Park et al. (2007) demonstrated that all techniques of tendon repair with anchors lead to an increase of circumferential tension but a low compression at the tendon-bone interface35. In this technique, the lateral tunnel is performed 1,5 cm distally to the superior border of the great tuberosity but,

Figure 10: Schematic drawing of the suture wire through the tendon and inside the transosseus tunnels

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Figure 11: Transosseous construct

in order to increase the mechanical strength of the transosseous suture of the tendon, this tunnel could be performed at more than 10 mm far from the extremity of the great tuberosity36 (Figure 10, 11). This technique represents surely an effective alternative to the use of anchors for the treatment of rotator cuff lesions but, nowadays, biomechanical and clinical evaluations should be performed again. Several authors described different techniques for arthroscopic transosseous repair such as Fleega37, Fox38, Frick39 et al. whom presented techniques in which they used needle of great dimension to perform the transosseous suture. The pitfalls of these techniques are the reproducibility, the possible breakdown of the bone-tunnel, the rupture of the needle inside the tunnel and possible lesions of the axillary nerve depending on the angle of insertion used by the surgeon that is very variable. Indeed, this new device (ArthroTunneler® device – Tornier) could perform the transosseous tunnels in a very reproducible way avoiding most of the pitfalls and complications caused by the free-hand techniques previously presented.

CONCLUSIONS In the last 40 years, the surgery of the tendinous lesions got a significant evolution and nowadays the shoulder surgeon performers arthroscopically almost all kind of cuff repair with the same reliability �������������������������������������������� of the older�������������������� open surgical techniques. The only lesion that already requires, in the majority of the cases, an open technique is the traumatic complete full thickness subscapularis tendon tear. In any case one can say that modern arthroscopic techniques are based not only by the completion of the surgeon learning curve but also by the improvement of suture materials and tools������������������������������������������������������ now�������������������������������������������������� available. ������������������������������������������������� The surgeon skills lead today to realize even more effective sutures that increase tendon-to-bone adhesion minimally affecting tendon vascularisation. Last but not least, we must consider the increased knowl-

edge about biological mechanisms that are at the base of tendon-to-bone healing processes, that is essential for good clinical outcomes. In the future better understanding of the biological processes that lead to tendinous rupture and then that lead to restoration of the cuff anatomy after surgery seems to be the key for improving clinical results and then patient satisfaction.

REFERENCES 1. Walton JR, Murrell GA. A two-year clinical outcomes study of 400 patients, comparing open surgery and arthroscopy for rotator cuff repair. Bone Joint Res 2012; 1: 210-217 2. Kim SH, Ha KI, Park JH et al. Arthroscopic versus mini-open salvage repair of the rotator cuff tear: outcome analysis at 2 to 6 years’ follow-up. Arthroscopy 2003; 19: 746-754 3. Severud EL1, Ruotolo C, Abbott DD, Nottage WM. All-arthroscopic versus mini-open rotator cuff repair: A long-term retrospective outcome comparison. Arthroscopy 2003; 19: 234-238 4. Buess E1, Steuber KU, Waibl B. Open versus arthroscopic rotator cuff repair: a comparative view of 96 cases. Arthroscopy 2005; 21: 597-604 5. Mueller MB, Fredrich HH, Steinhauser E et al. Biomechanical evaluation of different suture anchors for the stabilization of anterior labrum lesions. Arthroscopy 2005; 21: 611-619 6. Kaar TK, Schenck RC Jr, Wirth MA, Rockwood CA Jr. Complications of metallic suture anchors in shoulder surgery: A report of 8 cases. Arthroscopy 2001; 17: 31-37 7. Silver MD, Daigneault JP. Symptomatic interarticular migration of glenoid suture anchors. Arthroscopy 2000;16: 102-105 8. Gaenslen ES, Satterlee CC, Hinson GW. Magnetic resonance imaging for evaluation of failed repairs of the rotator cuff. Relationship to operative findings. J Bone Joint Surg Am 1996; 78: 1391-1396 9. Marquardt B, Witt KA, Götze C et al. Long-term results of arthroscopic Bankart repair with a bioabsorbable tack. Am J Sports Med 2006; 34: 1906-10 10. Tan CK, Guisasola I, Machani B et al. Arthroscopic stabilization of the shoulder: a prospective randomized study of absorbable versus nonabsorbable suture anchors. Arthroscopy 2006; 22: 716-720

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11. Burkart A1, Imhoff AB, Roscher E. Foreign-body reaction to the bioabsorbable suretac device. Arthroscopy 2000; 16:91-95 12. Edwards DJ, Hoy G, Saies AD, Hayes MG. Adverse reactions to an absorbable shoulder fixation device. J Shoulder Elbow Surg 1994; 3:230-233 13. Dejong ES, DeBerardino TM, Brooks DE, Judson K. In vivo comparison of a metal versus a biodegradable suture anchor. Arthroscopy 2004; 20: 511-516 14. Ticker JB, Lippe RJ, Barkin DE, Carroll MP. Infected suture anchors in the shoulder. Arthroscopy 1996; 12: 613-615 15. Middleton JC, Tipton AJ. Synthetic biodegradable polymers as orthopedic devices. Biomaterials 2000; 21: 2335-2346 16. Athanasiou KA, Agrawal CM, Barber FA, Burkhart SS. Orthopaedic applications for PLA-PGA biodegradable polymers. Arthroscopy 1998; 14:726-737 17.��������������������������������������������������������������� �������������������������������������������������������������� Ciccone WJ 2nd, Motz C, Bentley C, Tasto JP. Bioabsorbable���� ��� implants in orthopaedics: New developments and clinical applications. J Am Acad Orthop Surg 2001; 9:280-288 18. Kurtz SM, Devine JN. PEEK biomaterials in trauma, orthopedic, and spinal implants. Biomaterials 2007; 28:4845-4869 19. Li X, King M, MacDonald P. Comparative study of knot performance and ease of manipulation of monofilament and braided sutures for arthroscopic applications. Knee Surg Sports Traumatol Arthrosc. 2004; 12:448-452 20. Burkhart SS, Lo IK.Arthroscopic rotator cuff repair. J Am Acad Orthop Surg 2006; 14:333-346 21. Burkhart SS, The deadman theory of suture anchors: observations along a south Texas fence line. Arthroscopy 1995; 11:119123 22. Castagna A, Garofalo R, Conti M et al. Arthroscopic rotator cuff repair using a triple-loaded suture anchor and a modified Mason-Allen technique (Alex stitch). Arthroscopy 2007; 23:440 23. Ma CB, Comerford L, Wilson J, Puttlitz CM. Biomechanical evaluation of arthroscopic rotator cuff repairs: double-row compared with single-row fixation. J Bone Joint Surg Am 2006; 88:403410 24. Baums MH, Spahn G, Steckel H et al. Comparative evaluation of the tendon-bone interface contact pressure in different singleversus double-row suture anchor repair techniques. Knee Surg Sports Traumatol Arthrosc 2009; 17: 1466-1472 25. Lo IK, Burkhart SS. Double-row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy 2003; 19:1035-1042

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26. Kim DH, Elattrache NS, Tibone JE et al. Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med 2006; 34:407-414 27. Saridakis P, Jones G. Outcomes of single-row and double-row arthroscopic rotator cuff repair: a systematic review. J Bone Joint Surg Am 2010; 92:732-742 28. Duquin TR, Buyea C, Bisson LJ. Which method of rotator cuff repair leads to the highest rate of structural healing? A systematic review. Am J Sports Med 2010; 38:835-841 29. Ma HL, Chiang ER, Wu HT et al. Clinical outcome and imaging of arthroscopic single-row and double-row rotator cuff repair: a prospective randomized trial. Arthroscopy 2012; 28:16-24 30. Park MC, Elattrache NS, Ahmad CS, Tibone JE. “Transosseousequivalent” rotator cuff repair technique. Arthroscopy 2006; 22:1360 31. Nassos JT, ElAttrache NS, Angel MJ et al. A watertight construct in arthroscopic rotator cuff repair. J Shoulder Elbow Surg 2012; 21:589-596 32. Ostrander RV 3rd, McKinney BI. Evaluation of footprint contact area and pressure using a triple-row modification of the suturebridge technique for rotator cuff repair. J Shoulder Elbow Surg 2012; 21:1406-1412 33. Rossouw DJ, McElroy BJ, Amis AA, Emery RJ. A biomechanical evaluation of suture anchors in repair of the rotator cuff. J Bone Joint Surg Br 1997; 79:458-461 34. Garofalo R, Castagna A, Borroni M, Krishnan SG. Arthroscopic transosseous (anchorless) rotator cuff repair. Knee Surg Sports Traumatol Arthrosc 2012; 20:1031-1035 35. Park MC, ElAttrache NS, Tibone JE et al. Part I: Footprint contact characteristics for a transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg 2007; 16:461-468 36. Caldwell GL, Warner JP, Miller MD et al. Strength of fixation with transosseous sutures in rotator cuff repair. J Bone Joint Surg Am 1997; 79:1064-1068 37. Fleega BA Arthroscopic transhumeral rotator cuff repair: Giant needle technique. Arthroscopy 2002; 18:218-223 38. Fox MP, Auffarth A, Tauber M et al. A novel transosseous button technique for rotator cuff repair. Arthroscopy 2008; 24:10741077 39. Frick H, Haag M, Volz M, Stehle J. Arthroscopic bone needle: a new, safe, and cost-effective technique for rotator cuff repair. Tech Should Surg 2010; 11:107–112

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Subscapularis tendon tear. Modern surgical approach Dario Petriccioli, Giacomo Marchi, Celeste Bertone Department of Orthopedics, Istituto Clinico Città di Brescia, Brescia

For a long time, the subscapularis tendon, was not considered as a basic structure in the shoulder biomechanics, gaining the term “forgotten tendon” with a high percentage of unrecognized injuries (hidden lesion) 1. Over the past 10 years, thanks to authors like Walch, Gerber, Bennet and others, we realized its real importance and considerable disability in the case of its breakage2,3. The etiology can be both traumatic and degenerative, often in association with LHB instability, dislocations or impingement, mainly with coracoid process. We can find isolated lesions or in association with other rotator cuff tendons in percentages ranging from 3.5 to 20.8%4. A correct and modern surgical approach to the subscapularis lesions, needs their systematic staging through the many classifications that literature offers. Generally we use the 2007 Lafosse classification (CT or MRI) to select an appropriate surgical treatment:5

ABSTRACT Operative treatment on the subscapularis tendon tears has become more minimally invasive and selective over the past decade. This requires high-quality preoperative imaging evaluation for better knowledge of the relevant anatomical considerations. Arthroscopic repair has become the operation of choice for most patients presenting with small and not retracted tear. In case of larger tears the open operative treatment remains the unique solution, especially in irreparable tears who requires a tendon transfer.

STAGE I-II 6, 7, 8 (PIC. 1) I Partial lesion of superior one-third II Complete lesion of superior one-third III Complete lesion of superior two-thirds IV Complete lesion of tendon but head centred and fatty degeneration classified as less than or equal to Goutallier stage III V Complete lesion of tendon but eccentric head with coracoid impingement and fatty degeneration classified as more than or equal to Goutallier stage III

we can summarize the surgical protocol that we have chosen, in the following way: STAGE I-II: Arthroscopic repair or conservative treatment, in elderly patients with low functional demands and limited pain STAGE III: Arthroscopic or open repair with possible reinforcement using pectoralis minor transfer (Wirth procedure) STAGE IV: Open repair and, if necessary, augmentation with synthetic scaffold or pectoralis minor transfer STAGE V: lesions that tend to be non-repairable requiring pectoralis major transfer (Gerber or Resch technique)

The arthroscopic approach can be made in lateral decubitus, with about 40° limb abduction, or in beach chair position (best technique for the author) with back reclined approximately 60° and in general anesthesia associated with interscalene block. The technique involves first posterior portal, approximately 1 cm medial and 1 cm under rear corner of the acromion, and anterior-superior and lateral portals. Sometimes it can be useful an antero-medial portal near the lateral margin of the conjoint tendon. The next step is the intra-articular evaluation of capsuleligament and tendon structures with particular attention to the subscapularis insertion, sometimes can be useful internal rotation motion to relax the foot-print fibers and obtain better visualization. Particular attention must be paid to the biceps tendon and its groove, trying medial and lateral dislocation with a probe. In instability situation (Walch classification), is necessary LHB tenotomy or tenodesis, in order to improve the visualization of the subscapularis and to protect its suture. In frying situations (partial tear) we do a simple debridement of the tendon top edge and lesser tuberosity in the footprint area; in the case of superior one-third tear, its repair through a double suture anchor in the bicipital groove is performed. (Figure 1)  Sometimes a triple suture anchor can be used to realize both subscapularis repair and LHB tenodesis.9

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Figure 1: Arthroscopic surgical repair of subscapularis tendon superior one-third. Once the tenotomy of the biceps has been done, the visualization for subscapularis repair is greatly improved (A). Using traction sutures to pull the subscapularis as far laterally as possible (B), the tendon is fixed on the lesser tuberosity.

Figure 2: Open subscapularis repair with synthetic augmentation. The biceps tendon is found medially subluxed out of its groove with subscapularis complete ruptures (A). The subscapularis is fixed on the lesser tuberosity using simple transosseous sutures (B, C) and then reinforced with a synthetic augmentation (D)

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STAGE III 10, 11 (PIC. 2) In this situation it is essential to evaluate the tendon quality and muscle trophism at the pre-operative exams (usually MRI). In situations of good tendon and muscle quality, with preserved thickness and trophism, we prefer to perform an arthroscopic approach, always in the beach chair position. Always evaluate and eventually treat LHB tendon pathology. In the upper two thirds tears is crucial evaluate the possibility of a proper reduction of the tendon to avoid any tensions; in this case it may be necessary its release with detachment of LGOM from the subscapularis deep surface, and remove any adhesions with the conjoined tendon superficially. In this case, it is recommended to pay special attention medial to the conjoined tendon, for the presence of the circumflex and musculo-cutaneous nerve, axillary artery and the cords of the brachial plexus. The repair is carried out, generally, using 2 double suture anchors. First one with “U” stitches to fix the lower part of the tendon, and the second one, always in correspondence of the bicipital groove for its upper third. In the case the MRI showing a poor quality tendon or muscle we prefer an approach in open surgery (deltoid-pectoral), always in the beach chair position, in order to perform a best release of the tendon and a fixation with multiple trans-osseous stitches, using synthetic augmentation, to

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increase the tightness of the suture in a poor tissue. In a poor and atrophic muscle, at the end of the subscapularis repair, we perform pectoralis minor transfer sec. Wirth as a biological augmentation 12.

STAGE IV 10,11 In the case of the full subscapularis tendon tear (all thickness and all length) our choice is always directed towards an open deltoid-pectoral approach. The surgical technique is the same described in stage III, with multiple trans-osseous stitches and synthetical augmentation (Figure 2) or pectoralis minor transfer. At this stage it’s not always possible direct repair, especially in advanced tendon retraction (over the glenoid). The open surgery technique permits more chance of mobilization and release of muscle-tendon complex and, in a case of failure, allows us to perform pectoralis major transfer, to supply the lack of the subscapularis tendon, reducing the progressive anterior displacement of the humeral head, and its arthropathy.

STAGE V 10,11,12 (PIC. 3) These lesion are generally old, previously unrecognized, with important tendon retraction and fatty infiltration of

Figure 3: Subscapularis Reconstruction with Pectoralis Major Transfer over (Gerber technique, A) or under (Resch technique, B) the conjoined tendon.

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muscle. These are non-repairable lesions and our choice is directed to the palliative treatment of pectoralis major transfer in an attempt to reduce the inevitable and progressive anterior humeral head displacement and arthropathy, improve active intrarotation and strength. Surgery is performed in beach chair position (30 ° of back flexion), with general anesthesia and interscale brachial plexus block. Using a delto-pectoral approach we detach the 2/3 of pectoralis major sternal part from the humerus. The transfer to the less tuberosity can be performed in according to the Gerber technique13, above the conjoint tendon or (author favorite), as in Resch technique14, under the conjoint tendon after isolation and protection of the musculocutaneous nerve (Figure 3). In way you can create a pulley effect that permits (especially in male) to reach​ strength values slightly higher. The humeral fixation is obtained using trans-osseous stitches or charging high resistence wires used to prepare the tendon, in one or more impact anchors. The treatment algorithm just described, required a correct “timing” in diagnostic and surgical path. After the literature and our daily evaluation, the subscapularis tendon should always be repaired in a short time, especially in young patients with traumatic injuries. This problem is an urgent surgery situation, because the fast retraction of the tendon can lead to a not raparable tear. In this case is necessary, in young and adult patients, a tendon transfer to supply the subscapularis actions.

REFERENCES 1) C.Gerber, R.J.Krushel Isolated rupture of the tendon of the subscapularis muscle. Clinical features in 16 cases. J Bone Joint Surg Br 1991; 73:389-394 2) Bennett WF Subscapularis, Medial, and Lateral Head Cora-

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cohumeral. Ligament Insertion Anatomy: Arthroscopic Appearance and Incidence of “Hidden” Rotator Interval Lesions. Arthroscopy 2001; 17: 173–180 3) Walch G, Nove-Josserand L, Levigne C, Renaud E. Complete ruptures of the supraspinatus tendon associated with “hidden lesions” of the rotator interval. J Shoulder Elbow Surg 1994; 3:353-360 4) Lo IK, Burkhart SS The Etiology and Assessment of Subscapularis Tendon Tears: A Case for Subcoracoid Impingement, the RollerWringer Effect, and TUFF Lesions of the Subscapularis. Arthroscopy 2003; 19:1142-1150 5) L. Lafosse, B. Jost, Y.Reiland et al. Subscapularis Tear Classification. J Bone Joint Surg Am. 2007; 89:1184-1193 6) Adams CR, Schoolfield JD, Burkhart SS The Results of Arthroscopic Subscapularis Tendon Repairs. Arthroscopy 2008; 24:1381-1389 7) Burkhart SS, Brady PC Technical Note. Arthroscopic Subscapularis Repair: Surgical Tips and Pearls A to Z. Arthroscopy 2006; 22:1014-1027 8) Lafosse L, Jost B, Reiland Y et al. Structural Integrity and Clinical Outcomes after Arthroscopic Repair of Isolated Subscapularis Tears. J Bone Joint Surg Am 2007; 89:1184-93 9) Walch G, Nové-Josserand L, Boileau P, Levigne C Subluxation and dislocation of the tendon of the long head of the biceps. 1998; 7:100-108 10) Sewick A, Kelly JD, Leggin B Subscapularis Tears: Diagnosis and Treatment. University Of Pennsylvania Orthopaedic Journal. 2011; 21:25-30 11) Edwards TB, Walch G, Sirveaux F et al. Repair of Tears of the Subscapularis. J Bone Joint Surg Am 2006; 88:1-10 12) Wirth MA, Rockwood CA Operative treatment of irreparable rupture of the subscapularis. J Bone Joint Surg Am. 1997; 79:722-31 13) Jost B, Puskas GJ, Lustenberger A, Gerber C Outcome of Pectoralis Major Transfer for the Treatment of Irreparable Subscapularis Tears. J Bone Joint Surg Am. 2003; 85:1944-51 14) Resch H, Povacz P, Ritter E, Matschi W Transfer of the Pectoralis Major Muscle for the Treatment of Irreparable Rupture of the Subscapularis Tendon J Bone Joint Surg Am 2000; 82:372-382

TOPICS LESIONI TRAUMATICHE E POST-TRAUMATICHE DEL POLSO E DELL’AVAMBRACCIO ALL AROUND THE WRIST AND FOREARM

Convegno Internazionale

Wrist trauma ‹

TRAUMI DEL POLSO

Forearm fractures ‹

FRATTURE DELL'AVAMBRACCIO

Interosseous membrane ‹

LA MEMBRANA INTEROSSEA LA RADIOULNARE PROSSIMALE

Proximal radio-ulnar joint ‹ Distal radio-ulnar joint ‹

LA RADIOULNARE DISTALE ARTROSCOPIA

Arthroscopy ‹

OSTEOSINTESI

Internal fixation ‹ Arthroplasty ‹

PROTESICA

SEGRETERIA SCIENTIFICA U. Dacatra S. Odella P. Del Bò

Presidenti Onorari Bruno Marelli Giuseppe V. Mineo

Presidenti Jane Messina Virgilio Pedrini

SEGRETERIA ORGANIZZATIVA !"#$%&'(")*+,!"#$%&'&(")&$*#+)"+"$,$-$./0.1$*"2#+&$-$34#25 672$/.89:0..90,$;#0$ 7-?#"2@$"+A&BC75D&E'7FE&G#H)&? !!!"#$%!&'($)'&*+",&-

PRIMO ANNUNCIO Aula Magna - Istituto Ortopedico Gaetano Pini

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Painful shoulder: the Rheumatologist’s point of view Luigi Sinigaglia, Francesca Zucchi, Massimo Varenna Division of Rheumatology DH, Gaetano Pini Orthopedic Institute, Milan

Inflammatory arthritides affecting the shoulder

Introduction Shoulder pain is one of the most common musculoskeletal complaints and may arise from diverse causes. Accurate diagnosis of shoulder pain is made difficult by the unique anatomy and position of the shoulder, which serves as a link between the upper extremity and the thorax. A variety of Rheumatological conditions can affect the shoulder and when examining the patient , a preliminary approach includes topography of pain, mono or bilateral localization, circumstances of occurrence of pain ( inflammatory or mechanical pain), existence of accompanying pain related to other structures of the musculoskeletal system and the presence of constitutional signs and symptoms which can drive the clinician to a definitive diagnosis. Such a preliminary approach can help the clinician in the differential diagnosis of shoulder pain which includes not only common local disorders but also consideration of etiologies arising from distant anatomic sites by referred pain-mediated pathways. Furtherly, systemic arthropathies can occasionally present with shoulder disease and often involve the shoulder over time. Early assessment in these patients is essential in order to reach a definitive and correct diagnosis, thus avoiding waste of time and therapeutic unfinalized efforts. This paper provides a practical overview of painful shoulder disorders that may be encountered in a rheumatology or general practice. The majority of these clinical entities are as well commonly encountered by the Orthopedic, suggesting that a combined approach, when directed by a high level of suspicion, can be the best way to diagnose ad treat the patient.

Rheumatoid Arthritis (RA) of the shoulder not only affects synovium within the gleno-humeral joint but also involves the distal third of the clavicle and various bursae and rotator cuff. Usually shoulder involvement is seen preferably in the most severe forms of the disease. Pain in the shoulder(s) is a common onset in elderly patients with RA. Severe shoulder pain is often bilateral and can lead to sleep disorders because of difficulty to find a comfortable position. In a series of 200 consecutive patients with RA studied by arthrography, 21% had rotator cuff tears and an additional 24% had evidence of frayed tendons 1. The most likely mechanism leading to rotator cuff tears is that tendon insertion is vulnerable to erosion by the proliferative synovitis. Marked soft tissue swelling of the anterolateral aspect of the shoulders commonly accompanying RA may be caused by chronic subacromial bursitis rather than by glenohumeral joint effusions. Synovial proliferation of the subdeltoid bursa might explain the resorption of the distal end of the clavicle. Rarely the shoulder joint may rupture, with symptoms resembling those of obstruction of venous return from the arm. A true gleno-humeral involvement in Psoriatic Arthritis (PsA) is rare. PsA should be suspected in a patient with an asymmetric joint involvement who may have additional clinical features such as dactylitis, enthesitis or inflammatory type back pain and who is negative for rheumatoid factor. Since PsA presents a prominent entheseal involvement, rotator cuff enthesitis can be a manifestation of the disease. The girdle or “root” joints (hips and shoulders) are the most frequently involved extra-axial joints in Ankylosing Spondylitis (AS), and pain in these areas is the presenting symptom in up to 15% of patients. Shoulder involvement may cause considerable physical disability. Hips and shoulders are involved in the course of the disease in up to 35% of patients. In these patients coexisting inflammatory back pain is the usual clue to the early diagnosis of AS or of axial spondyloarthritis.

except in elderly women. ���������������������������������� It is the joint site with the oldest age of onset in OA. Apart from age and sex there are no obvious associations, except with the link with rotator cuff damage which is also very common in the elderly. Most OA of the shoulder presents with pain on movement and a restricted range of motion, especially external rotation and elevation. The radiograph shows evidence of OA, with joint space narrowing, subchondral sclerosis, cysts in the glenoid and often large inferior osteophytes on the glenoid.

Osteoarthritis

Septic arthritis

The shoulder is a common source of pain in patients with Osteoarthritis (OA), although the symptoms are more often due to osteophytosis and narrowing of the acromioclavicular and/or sternoclavicular joints than the glenohumeral joint itself. Primary OA of the shoulder joint is uncommon,

Septic arthritis of the shoulder can mimic any of the conditions affecting gleno-humeral joint. Sepsis must be included in any differential diagnosis of shoulder pain because early recognition and prompt treatment are mandatory to achieve a good functional result. The diagnosis is con-

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firmed by joint aspiration with synovial fluid analysis and culture. Cultures should include aerobic, anaerobic, mycobacterial and fungal studies.

Milwaukee shoulder syndrome Milwauke shoulder syndrome was first described by Robert Adams in 1857, subsequently well defined and called “chronic rheumatic arthritis of the shoulder”2 and later on also named l’épaule sénile hémorragique 3, cuff-tear arthropaty 4, idiopathic destructive arthritis 5, apatite associated destructive arthritis 6, arthropatie destructrice rapide de l’épaule 7. It is a destructive shoulder arthropathy associated with deposition of basic calcium phosphate (BCP) crystals, characterized by the presence of large amount of synovial fluid and a complete rotator cuff tear. It is predominantly found in elderly women and is bilateral in more than 50% of cases 8, predominantly affecting the dominant side. Some predisposing factors have been demonstrated, as high energy trauma or recurrent microtrauma, recurrent sub-luxations, concurrent calcium pyrophosphate dehydrate (CPPD) crystal deposition, neurological diseases (syringomyelia, cervical root compression) or renal failure with hemodialysis 9-12, but a lot of cases are idiopathic. The incidence in the general population is not known as well as the pathogenesis. Some Authors speculated that BCP crystals are phagocytosed by synovial lining cells stimulating them to produce metalloproteinase (MMP), and also causing them to proliferate, which contribute to progressive joint damage 13. In vitro studies have shown that calciumcontaining crystals contribute to mitogenic and inflammatory responses in various cell types 14. BCP and CPPD crystals can also stimulate fibroblast to produce various MMP; matrix metalloproteinase-8 has now been identified as another enzymatic product of fibroblast stimulation by calcium-containing crystals 15. The patient generally refers moderate shoulder pain lasting several months or years, but in some cases the pain may be acute and rapidly progressive, usually most apparent at night and on joint use with functional impairment. Characteristically, large joint effusion is present extending into the subdeltoid region and the synovial fluid is frequently blood tinged, containing low, predominantly monuclear, cells count. Rupture of the effusion can lead to a massive extravasation of blood and synovial fluid into the surrounding tissue. The extensive destruction of periarticular tissue, including the rotator cuff, leads to instability of the shoulder. Although the shoulder predominates, knees, hips, elbows and other joints may be involved 6, 16. Generally, the plain radiograph findings can be sufficient for the diagnosis, showing upward subluxation of the homerus, causing subcromial impingement that in time can erode the anterior portion of the acromion and the acromion-clavicular joint. Other findings may include cystic degeneration of the humeral tuberosities, erosion of cortical bone at the side of insertion of rotator cuff, degenerative changes of the humeral head and/or glenoid of the scapula, degenerative changes of the acromion-clavicular joint and calcifications of the tendineous rotator cuff. Eventually the soft, atrophic homerus head can collapse and an extensive

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atrophic destruction and loss of bone of both the acromion and the glenohumeral joint can be recognized 4,17. Further imaging tools as ultrasound and MRI can provide more information about cartilage damage, bone marrow edema, synovial hypertrophy, joint effusion, calcifications, tendineous and soft tissue damage 18. The natural history of this condition has not a standard feature, but many cases seem to stabilize after a year or two, with reduction of symptoms, joint effusions and no further radiographic changes. No specific therapies are nowadays available 19 and the treatment of symptomatic phase is generally unsatisfactory. A conservative approach, including analgesics and NSAIDs, repeated shoulder aspirations followed by injection of methylprednisolone acetate 20 can be sometimes useful. As pain subsides, functional rehabilitation must be started. Anatomic damage of the joint needs an orthopedic evaluation for surgical approach.

Osteonecrosis Osteonecrosis of the humeral head is seen in association with a variety of conditions. Apart from traumatic causes, the commonest condition leading to this complication is steroid therapy provided in conjunction with organ transplantation, systemic lupus erythematosus, systemic vasculitides, miscellaneous steroid-sensitive diseases or asthma. Other conditions associated with necrosis of the humeral head include hemoglobinopathies, pacreatitis, hyperbarism or alcohol abuse. Symptoms arise from synovitis and joint incongruity resulting from resorption, repair and remodeling. Early diagnosis is difficult because the presence of symptoms is often delayed. Magnetic Resonance Imaging is highly sensitive and more specific than scintigraphy. Plain radiographs show progressive phases of necrosis and repair. In early stages the x-ray may be normal or may show osteopenia or bone sclerosis. A crescent sign representing subchondral fracture ( Fig. 1) or demarcation of the necrotic segment appears during the reparative process. Patients who fail to remodel show collapse of the humeral

Figure 1: Osteonecrosis of the humeral head (Crescent sign)

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head with secondary degenerative changes. A considerable discrepancy is usually noted between symptoms and radiographic involvement.

Polymialgia Rheumatica Polymialgia Rheumatica (PMR) is a syndrome of unknown etiology characterized by aching in the proximal portions of the extremities, often involving the neck and girdles. There are no specific diagnostic tests or pathologic findings, so that the syndrome is defined on a clinical ground. PMR is relatively frequent with an average annual incidence rate of 52.5 cases per 100.000 persons aged 50 years or older 21. The prevalence of PMR (active plus remitted cases) is approximately 600 per 100.000 persons aged 50 years and older. The features included in most definitions of PMR are as follows: (1) aching and morning stiffness lasting half an hour or longer in the shoulders, hip girdle, neck or some combination; (2) duration of these symptoms for 1 month or longer; (3) age older than 50 years; (4) laboratory evidence of systemic inflammation with increase in acute phase reactants; (5) rapid response to small doses of glucocorticoids such as prednisone 10 mg per day. Nearly half of the patients have systemic manifestations such as malaise, low-grade fever and weight loss at disease onset. Pain may develop abruptly or evolve insidiously over weeks or months. In most patients the shoulder girdle is the first to become symptomatic. The discomfort may arise in one shoulder or hip but usually becomes bilateral within weeks. Symptoms are located at proximal limbs, axial musculature and tendon attachments. Morning stiffness resembling that of RA and “gelling” after inactivity are usually prominent. Distal joint pain and swelling occur only in some cases. Pain at night is extremely common and movement during sleep usually awakens the patient. Muscle strength is generally unaffected. Pathogenesis include bursal inflammation and synovitis. Diagnostic and classification criteria for PMR have been proposed in 1982 22, reviewed in 1984 23 and recently redeveloped to

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incorporate informations provided by ultrasound evaluation 24 (Table 1). Diagnostic criteria underscore that the diagnosis of PMR is clinical and depends on eliciting symptoms. Distinguishing PMR from early RA with proximal joints onset can be difficult especially in patients who are rheumatoid factor negative and in those who have not yet developed prominent synovitis of the small joints of the hands and feet. Furtherly, distal joint pain and swelling occur in some cases of PMR including diffuse distal extremity swelling with pitting edema. Patients with polymiositis complain much more of weakness than pain. Although patients with neoplasms may have generalized musculoskeletal aching, there is no association between PMR and malignancy. Therefore a search for an underlying tumor is not necessary except in cases of “atypical PMR” and poor response to low-dose prednisone. This therapeutic approach is usually sufficient to control pain and leads to normalization of laboratory tests. Usually prednisone must be tapered slowly, according to acute phase reactants and a full drug-free recovery is achievable in 9-12 months. Flares are common, and are seen in 30% of cases necessitating dose increase to achieve remission. Some, but not all, studies suggest that oral Methotrexate can reduce the long-term need for corticosteroids. A large body of evidences support the idea that PMR is related to Giant Cell Arteritis (GCA). Since these patients are considered at high risk for vascular complications such as vision loss or ischemic events including irreversible blindness, stroke or large artery disease, a high index of suspicion must be kept in mind since early treatment of this disease can prevent these dramatic complications. Between 30 and 50% of patients with GCA develop PMR and approximately 10 to 15 % of patients with PMR have positive temporal artery biopsies. For these reasons a temporal artery biopsy is strongly recommended in the presence of accompanying symptoms such as headache, jaw claudication, visual symptoms or high fever. Color duplex ultrasonography can be of aid in these situations, showing abnormalities of the temporal artery with a sensitivity of 93%. Glucocorticoid therapy must be commenced as soon

Table 1. PMR classification criteria scoring algorithm. Pre-required criteria: age ≥50 years, bilateral shoulder aching and abnormal CRP and/or ESR 24

Points without US (0-6)

Points with US (0-8)*

Morning stiffness duration >45 minutes

2

2

Hip pain or limited range of motion

1

1

Absence of RF or ACPA

2

2

Absence of other joint involvement

1

1

At least 1 shoulder with subdeltoid bursitis and/or biceps tenosynovitis and/or glenohumeral synovitis (either posterior or axillary) and at least 1 hip with synovitis and/ or trochanteric bursitis

NA

1

Both shoulders with subdeltoid bursitis, biceps tenosynovitis, or glenohumeral synovitis

NA

1

A score of 4 or more is categorized as Polymyalgia Rheumatica (PMR) in the algorithm without ultrasound (US) and a score of 5 or more is categorized as PMR in the algorithm with US. CRP = C-reactive protein; ESR = erytrocyte sedimentation rate; RF = Rheumatoid Factor; ACPA = anti-cytrullinated protein antibody; NA = not applicable *optional US cyteria

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as the diagnosis of GCA is strongly suspected with prednisone doses between 40 and 60 mg/day in order to prevent loss of vision.

Neuralgic Amyotrophy (Parsonage-Turner syndrome) Neuralgic Amyotrophy (NA) was first clinically defined by Parsonage and Turner in 1948 25 and is typically characterized by attacks of neuropathic pain and subsequent patchy paresis in the upper extremity. The reported incidence is 2-3 per 100,000 individuals per year in the general population but the true annual incidence, considering underdiagnosis and misdiagnosis, seems to be 20 to 30 cases per 100.000 26,27,28; the highest incidence is between the third and seventh decades of life and male are predominantly affected 26,29. The cause of NA is still unknown but the available evidences suggest that neuralgic amyotrophy has a complex pathophysiology that includes an underlying predisposition, a susceptibility to dysfunction of some peripheral nerve structures, and an autoimmune trigger for attack 30. Available literature suggests that possible triggers include viral infections, immunization, and the perioperative and peripartum periods as well as a previous period of strenuous exercise 26, 31. The few histological studies have demonstrated evidence of an autoimmune etiology, with mononuclear inflammatory infiltrates in the brachial plexus biopsies 32,33 or increase in complement-fixing antibodies to peripheral nerve myelin in the acute phase of the disease 34. NA occurs in both idiopathic and hereditary forms; the second one, ten times less common than the first one, is an autosomal dominant monogenic disorder with high but incomplete penetrance, caused by mutation in the gene septin 9 on chromosome 17q23 35,36. In most cases patients affected by NA present acute, severe shoulder pain that radiates to the arm or neck and lasts for several hours to weeks; the pain frequently can awaken patients from sleep and may be exacerbated by shoulder and elbow motion. As the pain subsides, a flaccid paralysis with muscle weakness, muscle atrophy, and sensory loss of shoulder girdle and arm develops, with a characteristic patchy distribution. The most common sites of sensory loss are over the deltoid, the lateral aspect of upper arm, and the radial aspect of the forearm. Bilateral brachial plexus involvement occurs in 10 to 30% of cases, although symptoms are usually asymmetric 25,37-39. In about 17% of sporadic NA and 56% of hereditary NA, involvement of nerves outside brachial plexus can occur, most commonly the lumbosacral plexus, phrenic nerve and/or recurrent laryngeal nerve and occasionally the facial, hypoglossus or intercostal nerves 26,31. In approximately 15% of patients signs of involvement of the peripheral autonomic nervous system were documented, such as vegetative and trophyc skin changes, edema in the involved extremity at the onset of the attack, temperature dysregulation, increased sweating, and changes in nail growth 31. At the beginning, clinical presentation of NA is not specific; the differential diagnosis must include not only neurologic and orthopaedic condition, but also thorax diseases.

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Despite of a complete clinical examination, no currently available tests can unequivocally confirm or exclude the diagnosis of NA. MRI can demonstrate edema involving one or more muscles innervated by brachial plexus in early phase of the disease, and signal suggesting atrophy with fatty infiltration in one ore more muscle groups of the shoulder in the late phase 38,40. EMG examination can be abnormal and suggesting NA revealing acute denervation (with positive sharp waves and fibrillation potential) 3 to 4 weeks after the onset of the disease, present in both a peripheral nervs and nerve root distribution 37; an EMG performed 3 to 4 months after the onset of initial symptoms may show chronic denervation and early reinnervation with polyphasic motor unit potentials 26,37. No specific treatment is nowadays available; early corticosteroids therapy may have a positive effect on pain in some patient as well as opioid in combination with longacting NSAIDS 36 . The patient should be encouraged to use the affected limb as fully as possible. The disease can last 2-3 years before symptoms and impairment fully disappear.

Shoulder-hand syndrome Complex regional pain syndrome type I (CRPS-I), formerly known as reflex sympathetic dystrophy, is a severely disabling pain syndrome characterized by sensory and vasomotor disturbance, edema and functional impairment 41 that in most cases developed following a trauma or surgery42. The pathogenesis is still unknown and no specific test is currently available for the diagnosis. Recently updated Budapest Criteria are widely accepted to make a clinical diagnosis 43, 44 (Table 2). In 1947 Steinbrocker first described the shoulder-hand syndrome 45, a CRPS-I involving the shoulder and the hand. The clinical course was historically described as divided in three main stages, according to the clinical manifestations: stage 1, lasting 3-6 weeks to 6 months, with painful shoulder, swelling, pain and stiffness in the hand; stage 2, lasting from 3 to 6 months, with gradual lessening of shoulder pain and resolution of the swelling at the hand with increasingly stiff with flexion deformity of the fingers and atrophy of subcutaneous tissue and thickening of the palmar fascia; stage 3, that may last many months, characterized by a smooth, glossy skin with trophic changes and atrophy with thickened palmar fascia and Dupuytren-like contracture. The main predisposing factor to hand-shoulder syndrome is stroke (12.5%-27%) 46 but also other conditions are recognized (myocardial infarction, thoracic disease, injury as glenohomeral subluxation, Herpes Zoster infection) 45 . The relationship with shoulder-hand syndrome and the assumption of Phenobarbital is historically important. Pathology, patient’s age, prior motor deficit, and duration from onset of stroke may affect the appearance of this syndrome. Diagnosis of CRPS in stroke patients is more difficult than in other diseases since the paretic upper limb is frequently painful, edematosus, with altered heat and tactile sensitivity and slight dystrophic skin secondary to non-use syndrome. Conventional radiology may reveal the classic patchy os-

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Table 2. Proposed clinical diagnostic criteria for CRPS type I

To make the clinical diagnosis, the following criteria must be met: 1. Continuing pain, which is disproportionate to any inciting event 2. Must report at least one symptom in three of the following categories: Sensory: Reports of hyperesthesia and/or allodynia Vasomotor: Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry Sudomotor/Edema: Reports of edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin) 3. Must display at least one sign at time of evaluation in two or more of the following categories: Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or temperature sensation and/or deep somatic pressure and/or joint movement) Vasomotor: Evidence of temperature asymmetry (>1°C) and/or skin color changes and/or asymmetry Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/ or trophic changes (hair, nail, skin) 4. There is no other diagnosis that better explains the signs and symptoms

teoporosis at the shoulder and/or at the hand that may appear generally within 4-8 weeks or later, after the onset of the disease, a feature present in only 40% of patients. Three-phase scintigraphy with technetium has been reported to have high sensivity but low specificity. At MRI bone marrow edema is the most frequent finding, with soft tissue anomalies and skin thickening, subcutaneous edema and muscular atrophy. Several therapeutic approaches have been employed in CRPS-1 with different results but recent studies provide conclusive evidence that the use of i.v. bisphosphonate is the treatment of choice 47. A well-planned physiotherapy program after stroke can help to prevent the late complications of the disease 48.

Miscellaneous conditions affecting the shoulder In the increasing group of patients undergoing chronic hemodyalisis, a shoulder pain syndrome known as Dyalisis Shoulder Arthropathy (DSA) has been described. It is characterized by shlouder pain, weakness, loss of motion and functional limitation. The pathogenesis of this condition is not fully elucidated although rotator cuff disease, pathologic fracture, bursitis and local amyloid deposition have been implicated as causative factors. Patients generally respond poorly to local steroid injections or NSAIDs, but their condition may improve with the correction of underlying metabolic disorders such as ostemalacia or secondary hyperparathyroidism. Primary neoplasms can cause shoulder pain by direct invasion of the musculoskeletal system or by compression with referred pain. Primary tumors are more likely to occur in younger individuals. More common lesions have a typical distribution such as the predilection of a chondroblastoma for the proximal humeral epiphysis or an osteogenic sarcoma for the metaphysis. Neoplasms also may involve the shoulder through metastases to the region. Pancoast tu-

mor may manifest as shoulder pain or cervical radiculitis caused by invasion of the brachial plexus or invasion of the last cervical roots. Cervical pathology may manifest with associated shoulder pain. The area of referred pain has a dermatomal pattern, consistent with the distribution of dermatomal nerve roots. Because conditions causing cervical neck pain and conditions causing shoulder pain may coexist it is often difficult to distinguish which lesion is responsible for the symptoms. The thoracic outlet syndromes often manifest as a vague shoulder pain and deserve a deep clinical evaluation. Finally, from a clinical standpoint, it must be remembered that shouder pain may be unrelated to musculoskeletal diseases and can be a manifestation of referred pain linked to a variety of visceral causes. The main gastrointestinal diseases causing shoulder pain are gallstone disease, liver cancer or abscess and splenic breakage. In all of these cases pain referral depends on the innervation of the diaphragm. Furtherly, the most common cardiological causes of shoulder pain are related to myiocardial ischaemia, pericarditis, aortic dissection and pulmonary embolism. These conditions underscore the value of a full-blown clinical evaluation of the patient with shoulder pain which represent a true critical challenge in clinical practice.

REFERENCES 1. Ennevaara K. Painful shoulder joint in rheumatoid arthritis: a clinical and radiological study of 200 cases with special reference to arthrography of the glenohumeral joint. Acta Rheumatol Scand 1967; 11:1-116 2. McCarty DJ. Robert Adams’ rheumatic arthritis of the shoulder: “Milwaukee shoulder” revisited. J Rheumatol 1989; 16:668-70 3. Lamboley C, Bataille R, Rosemberg F et al. L’épaule senile hémorragique: à propos de 9 observations. Rheumatologie 1977; 29:323-30 4. Neer CS, Craig EV, Fakuda H. Cuff-tear arthropathy. J Bone Joint Surg 1983; 65A:1232-44

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5. Campion GV, McCrae F, Alwan W et al. Idiopathic destructive arthritis of the shoulder. Semin Arthritis Rheum 1988; 17:232-45 6. Dieppe PA, Doherty M, MacFarlane DG et al. Apatite associated destructive arthritis. Br J Rheumatol 1984; 23:84-91 7. Lequesne M, Fallut M, Couloumb R. L’arthropathie destructrice rapide de l’épaule. Rev Rheum 1982; 49:427-37 8. Halverson PB, Carrera GF, McCarty DJ. Milwaukee shoulder syndrome: Fifteen additional cases and description of contributing factors. Arch Intern Med 1990; 150:677-82 9. Dieppe PA, Doyle DV, Huskisson EC et al. Mixed crystal deposition disease and osteoarthritis. Br Med J 1978 1:1-15 10. Halverson PB, McCarty DJ. Patterns of radiographic abnormalities associated with basic calcium phosphate and calcium pyrophosphate dehydrate crystal deposition in the knee. Ann Rheum Dis 1986; 45:603-5 11. Yano E, Takeuchi A, Yoshioka M. Hydroxyapatite associated arthritis in a patient undergoing hemodialysis. Int J Tissue React 1985; 7:527-34 12. Bonavita JA, Dalinka MK. Shoulder erosions in renal osteodystrophy. Skeletal Radiol 1980; 5:105-8 13. Dieppe PA, Watt I. Crystal deposition in osteoarthritis. An opportunistic event. Clin Rheum Dis 1985; 11:367-91 14. Halverson PB, McCarty DJ, Cheung HS et al. Milwaukee shoulder syndrome: eleven additional cases with involvement of the knee in seven (basic calcium phosphate deposition disease). Semin Arthritis Rheum 1984; 14:36-44 15. Pons-Estel BA, Gimenez C, Sacnum M et al. Familial osteoarthritis and Milwaukee shoulder associated with calcium pyrophosphate and apatite crystal deposition. J Rheumatol 2000; 27:47180 16. Alverson PB. Arthropathies associated with basic calcium phpsphate crystals. Scanning Microscopy 1992; 6:791-7 17. McCarthy GM. Crystal-related arthropathies. In Klippel JH, Dieppe PA. Rheumathology (second ed.). Mosby, London, 1998, 8(17.1)-8(17.8) 18. Seibold CJ, Mallisee TA, Erikson SJ et al. Rotator cuff: evaluation with US and MR imaging. Radiographics 1999; 19:685-705 19. Ea HK, Liote F. Calcium pyrophosphate dehydrate and basic calcium phosphate crystal-induced arthropathies: update on pathogenesis, clinical features and therapy. Curr Rheumatol Rep 2004; 6:221-7 20. Caporali R, Rossi S, Montecucco C. Tidal irrigation in Milwaukee shoulder syndrome. J Rheumatol 1994; 21:1781-2 21. Salvarani C, Gabriel SE, O’Fallon WM et al. Epidemiology of polymyalgia rheumatica in Olmsted County, Minnesota, 1970-1991. Arthritis Rheum 1995; 38:369 22. Chuang T-Y, Hunder GG, Ilstrup DM et al. Polymyalgia rheumatica: a 10-years epidemiologic and clinical study. Ann Intern Med 1982; 97:672 23. Healey LA. Long-term follow-up of polymialgya rheumatica: evidence for synovitis. Arthritis Rheum 1984; 13:322 24. Dasgupta B, Cimmino MA, Kremers HM et al. 2012 provisional classification criteria for polymyalgia rheumatica: a European League Against Rheumatism/American College of Rheumatology collaborative initiative. Arthritis Rheum 2012; 64:943-954 25. Parsonage MJ, Turner JW. Neuralgic amyotrophy: The shouldergirdle syndrome. Lancet 1948; 1(6513):973-978 26. Stutz CM. Neuralgic amyotrophy: Parsonage-Turner syndrome. J Hand Surg Am 2010; 35:2104-2106 27. van Alfen N. Clinical and pathophysiological concepts of neuralgic amyotrophy. Nat Rev Neurol 2011; 7:315-322

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28. Watts G, Falder S, Rea S, Silbert P, Wood F. Parsonage-Turner syndrome in a major burns patients. Burns 2009; 35:1038-1041 29. Sathasivam S, Lecky B, Manohar R et al. Neuralgic amyotrophy. J Bone Joint Surg Br 2008; 90:550-553 30. van Alfen N. The neuralgic amyotrophy consultation. J Neurol 2007; 254:695-704 31. van Alfen N, van Engelen BG. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain 2006; 129:438-450 32. Cusimano MD, Bilbao JM, Cohen SM. Hypertrophic brachial plexus neuritis: a pathological study of two cases. Ann Neurol 1988; 24:615-622 33. Suarez GA, Giannini C, Bosh EP et al. Immune brachial plexus neuropathy: suggestive evidence for an inflammatory-immune pathogenesis. Neurology 1996; 46:559-561 34. Vriesendorp FJ, Dmytrenko GS, Dietrich T et al. Anti-Peripheral nerve myelin antibodies and terminal activation products of complement in serum of patients with acute brachial plexus neuropathy. Arch Neurol 1993; 50:1301-1303 35. Husson M, Goizet C, Rivera S et al. Hereditary neuralgic amyotrophy: a pediatric and familial presentation of Parsonage-Turner syndrome. Arch Pediatr 2004; 11:1336-1338 36. van Alfen N, van Engelen BG, Hughes RA. Treatment for idiopathic and hereditary neuralgic amyotrophy (brachial neuritis). Cochrane Database Syst Rev 2009; 3:CD006976 37. Dillin L, Hoaglund FT, Scheck M. Brachial neuritis. J Bone Joint Surg Am 1985; 67(6):878-880 38. Gaskin CM, Helms CA. Parsonage-Turner syndrome: MR imaging findings and clinical informations in 27 patients. Radiology 2006; 240:501-507 39. Van Tongel A, Schreurus M, Bruyninckx F et al. Bilateral Parsonage-Turner syndrome with unilateral brachialis muscle wasting: a case report. J Shoulder Elbow Surg 2010; 19:e14-e16 40. Squintani G, Mezzina C, Lettieri C et al. ���������������������� MRI findings of 26 patients with Parsonage-Turner syndrome. Am J Roentgenol 2007; 189:W39-W44 41. Merskey H, Bogduk N. Classification of chronic pain; descriptions of chronic pain syndromes and definition of pain terms, 2nd edn. Seattle: IASP Press, 1994 42. de Mos M, de Bruijn AG, Huygen FJ et al. The incidence of complex regional pain syndrome  : a population-based study. Pain 2007; 129:12-20 43. Harden RN, Bruehl S, Stanton-Hicks M et al. Proposed new diagnostic criteria for complex regional pain syndrome. Pain Med 2007; 8:326-31 44. Harden RN, Bruehl S, Perez RS et al. Validation of proposed diagnostic criteria (the “Budapest criteria”) for complex regional pain syndrome. Pain 2010; 150:268-74 45. Steinbrocker O. The shoulder-hand syndrome; associated painful homolateral disability of the shoulder and hand with swelling and atrophy of the hand. Am J Med 1947; 3:402-7 46. Davis SW, Petrillo CR. Shoulder-hand syndrome in a hemiplegic population, a 5-years retrospective study. Arch Phys Med Rehabil 1977; 58:353-6 47. Varenna M, Adami S, Rossini M et al. Treatment of complex regional pain syndrome type I with Neridronate: a rondomized, double-blind, placebo-controlled study. Rheumatology 2013; 52:534-42 48. Kondo I, Hosokawa K, Soma M et al. Protocol to prevent shoulder-hand sindrome after stroke. Arch Phys Med Rehabil 2001; 82:1619-23

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Platelet Rich Plasma in Arthroscopic Rotator Cuff Repair: State of the Art Pietro Randelli, Vincenza Ragone, Alessandra Menon, Riccardo D’Ambrosi, Filippo Randelli, Paolo Cabitza Dipartimento di Scienze Medico-Chirurgiche, Università degli Studi di Milano; IRCCS, Policlinico San Donato, Milano

Clinical evidence Surgical use of PRP in arthroscopic rotator cuff repair The rotator cuff literature has shown that PRP can be applied by either direct injection or physical application of a PRP matrix scaffold to repaired tissues. The main characteristics of clinical studies analyzed in this paper are reported in Table 1. Randelli and colleagues6 demonstrated in a pilot study of 14 patients who underwent arthroscopic repair of the rotator cuff, that the use of PRP in combination with autologous thrombin, injected locally in the surgical repair is a safe procedure and effective, no side effects. Later the same authors published7 the results of a randomized controlled trial on the effectiveness of the use of PRP in the intraoperative arthroscopic repair of rotator cuff injuries. The pain in the treatment group was significantly lower compared to the control group at 3, 7, 14 and 30 days after surgery. The clinical scores were significantly better in the treatment group compared to the control group at 3 months after surgery. There was no difference between the two groups after 6, 12 and 24 months. The MRI performed 12 months after surgery showed no significant difference in the rate of re-injury of rotator cuff (treatment group: 40%, control group: 52%). Ruiz-Moneo and colleagues8 using a different technology for the preparation of platelet concentrate, at clinical evaluation did not observe any difference between the group treated with the platelet preparation in the absence of leukocytes (N = 32) and the control group (N = 31). Patients of both groups were subjected to arthroscopic repair of lesions with the difference that in patients randomized to the treatment group the plasma rich in growth factors was injected at the site of repair. The healing of the repair of the cuff occurred in 34% of cases in the treatment group and in 25% of cases in the control group (p > 0.05). 9

Antuna and colleagues have recently investigated whether the platelet-rich fibrin improves healing of arthroscopic repair of massive cuff lesions (> 50 mm). The authors applied the fibrin rich in platelets at the site of repair of the lesion in 14 patients and compared the clinical and radiological results with a control group of 14 patients. The clinical score and the rate of re-injury (71% in the treatment group versus 64% in the control group) were similar in the two groups at 24 months after surgery.

Introduction Rotator cuff tendinopathies represent the vast majority of shoulder injuries in adult patients and are a common contributing factor to shoulder pain and occupational disability, which prevalence in the population is rising 1. The use of platelet-rich plasma (PRP) as a biological solution to improve rotator cuff tendon healing has gained popularity over the last several years. Platelet rich plasma (PRP) is a whole blood fraction containing high platelet concentrations that, once activated, provides a release of various growth factors that participate in tissue repair processes: transforming growth factor beta (TGF-b), fibroblast growth factor (FGF), platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), connective tissue growth factors, and epidermal growth factor (EGF) 2. Platelets also have dense granules that contain a variety of important bioactive molecules. These proteins function in an autocrine or paracrine fashion to modulate cell signaling and chemotaxis promoting tendon healing 3. There are clear differences in PRP formulations in terms of growth factor concentration and catabolic enzyme content4. A PRP classification system exists which is based on the presence or absence of white blood cells and whether the PRP is used in an activated or unactivated form. PRP may be prepared via centrifugation as a pure platelet concentrate suspended in plasma (leukocytepoor PRP) or as a mixture with white blood cells (leukocyte-rich PRP)5. Platelets can be activated ex-vivo with thrombin and/or calcium. Use of PRP in an unactivated manner, without thrombin or calcium relies on in-vivo activation via endogenous collagen. This paper discuss and explores the available evidence to determine the efficacy of the PRP in treatment of rotator cuff injuries. Emphasis will be placed on published, peer review data investigating the role of this biologic tool in rotator cuff tendon healing.

Gumina and colleagues10 have more recently evaluated the clinical results obtained from the magnetic resonance of the arthroscopic repair of rotator cuff with and without the use of a membrane enriched of platelets and leukocytes in patients with a large posterior-superior cuff tear. Eighty consecutive patients were randomized to treatment with membrane-enriched leukocytes and platelets (PRP group: 40 patients) or without (control group: 40 patients) inserted between the tendons of the rotator cuff and its insertion. At a follow-up post-operative mean of

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Authors

Evidence

PRP formulation

Surgical technique

No. patients

Randelli et al. (2011)

Level 1 Randomized controlled

Injectable PRP (GPS system)

Single row

53

Ruiz-Moneo et al. (2013)

Level 1 Randomized controlled

Injectable PRP (PRGF Endoret System)

Double row

63

Antuna et al.. (2013)

Livello 2 Randomized controlled

Injectable PRP (Vivostat system)

Single row

28

Gumina et al. (2012)

Level 1 Randomized controlled

Suturable PRP (RegenKit-THT system)

Single row

76

Jo et al. (2011)

Livello 2 Prospective cohort

Suturable PRP (COBE spectra system)

Transosseous equivalent

42

Jo et al. (2013)

Level 1 Randomized controlled

Suturable PRP (COBE spectra system)

Transosseous equivalent

48

Zumstein et al. (2014)

Level 1 Randomized controlled

Suturable PRP (PRF Process)

Transosseous equivalent

20

Castricini et al. (2010)

Level 1 Randomized controlled Livello 2 Randomized controlled

Suturable PRP (Cascade system)

Double row

88

Suturable PRP (Cascade system)

Single OR Double row/ Transosseous-equivalent

67

Barber et al. (2011)

Livello 3 Case control study

Suturable PRP (Cascade system)

Single row

40

Bergeson et al (2012)

Livello 3 Cohort study

Suturable PRP (Cascade system)

Single OR Double row

37

Weber et al. (2013)

Level 1 Randomized controlled

Suturable PRP (Cascade system)

Single row

60

Rodeo et al. (2012)

Table 1: Studies investigating the use of PRP in arthroscopic rotator cuff repair.

13 months, were observed re-cuff lesions only in the control group. A prospective level II cohort study11 has shown that PRP application during arthroscopic rotator cuff repair did not accelerate recovery with respect to pain, range of motion, strength, functional scores, or overall satisfaction when compared with controls at any follow- up time point. The investigators did, however, note a reduced retear rate in the PRP group compared with the control group, but this difference did not reach statistical significance. The same authors12 have recently published the results of a randomized controlled trial on the use of 3 platelet rich fibrin clots in the arthroscopic repair of massive cuff lesions (lesion size:> 30 mm). The rate of re-injury was 20% (4/20) in the group treated with PRP and 55.6% (10/18) in the control group (p=0.02). Recently Zumstein et al.13 hypothesized that arthroscopic rotator cuff repairs using leukocyte- and platelet-rich fibrin (L-PRF) results in a higher vascularization response and watertight healing rate during early healing. They have treated 20 patients, 10 with arthroscopy plus L-PRF and 10 only with arthroscopy. Clinical examinations including visual analogic scale (VAS), Constant, and Simple Shoulder Test scores and measurement of the vascularization with power Doppler ultrasonography

were made at 6 and 12 weeks. The study concludes that arthroscopic rotator cuff repair with the application of LPRF is technically feasible and yields higher early vascularization. Increased vascularization may potentially predispose to an increased and earlier cellular response and an increased healing rate. Several authors used the Cascade Autologous Platelet System (Cascade Medical Enterprises, Wayne, NJ) to create a platelet rich plasma from autologous blood. Castricini and colleagues14 conducted a study in prospective randomized controlled double-blind trial of 88 patients who underwent arthroscopic repair of the rotator cuff with the addition of platelet-rich fibrin matrix autologous (43 patients) and without (45 patients). The autologous fibrin membrane was integrated into the suture and placed at the interface between the tendon and the greater tuberosity under continuous arthroscopic lavage. For an evaluation of 16 months follow-up, there was no statistically significant difference in terms of Constant and magnetic resonance imaging. However, the rate of re-injury resulted of 10.5% in the control group compared to 2.5% in the treatment group with a trend curve which approaches the significance. Arnoczky15 has re-evaluated the data of magnetic resonance imaging in this work using the chi-square test for binomial and concluded that

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PRP improved the results of cuff repair compared to control. Using the same technology for the preparation of the fibrin matrix rich in platelets autologous Weber and colleagues16 have revealed no statistical difference in the percentage of re-injury between the treatment group and the control group (43% and 29%, respectively) after an average of 3-5 months after surgery. A randomized controlled study from Rodeo et al.17 supported the work of Castricini and questioned the early healing benefits of PRP by showing no differences between repairs augmented with autologous fibrin membrane and the control group in terms of vascularity and clinical outcomes. In addition, the authors found that 67% of the repairs in the PRP group were intact compared with 81% of the repairs in the control group (p=0.2) which suggests that autologous fibrin membrane may in fact be detrimental to tendon healing in the rotator cuff. In a case-control study performed by Barber and colleagues18 clinical outcomes were no difference between the PRP-augmented arthroscopic rotator cuff repair group and the control group. This study did find, interestingly, that the observed incidence of retears on magnetic resonance imaging was significantly lower in the PRP group than in the control repairs. Of note, a total of 3 and 2 PRP fibrin gels were used in each study, respectively. A similar cohort study performed by Bergeson and colleagues19 showed no improvement in terms of retear rates or functional outcomes in the PRP-augmented repair group compared with controls. Two platelet-rich fibrin matrix (PRFM) clots were used to augment cuff repair of 16 patients with rotator cuff tears at risk for retears inserted into the repair site in this study. The PRP group was compared to a historical control group of 21 patients with similar at risk tears who underwent standard repair without PRP augmentation. Single or double row techniques were performed at the discretion of the surgeon in both the PRP and control group. Passive range of motion was started at 4 to 6 weeks postoperatively. MRI studies at a minimum of one year follow-up showed a significant difference in the re-tear rate in favor of the control group (PRP group: 56%, Control group: 38%, p=0.024). The significant difference remained when double row repairs were removed from the analysis (PRP group: 62%, Control group: 40%, p=0.022).

PRP injections for rotator cuff tendinopathy Rha and colleagues20 reported a study comparing PRP injection (Prosys PRP Platelet Concentration System) with dry needling in patients with  tendinosis or a partial tear less than 1.0 cm, but not a complete tear. Two procedures in both groups were applied at a 4-week interval. The injection of PRP was superior to dry needling with respect to pain, function, and range of motion over a 6-month period. These findings suggest that treatment with plateletrich plasma injections is safe and useful for rotator cuff disease.

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Kesikburun and colleagues21 investigated the effect of PRP injections on pain and shoulder functions in patients with chronic rotator cuff tendinopathy. Forty patients were randomized to a PRP group (n = 20) or placebo group (n = 20). Patients received an ultrasound-guided injection into the subacromial space that contained either 5 mL of PRP prepared from autologous venous blood (GPS system) in ��������������������������������������� an unactivated manner��������������� or 5 mL of saline solution. All patients underwent a 6-week standard exercise program. Clinical outcomes were assessed at baseline and at 3, 6, 12, and 24 weeks and 1 year after injection. This study sustains a PRP injection is no more effective in improving quality of life, pain, disability, and shoulder range of motion than placebo in patients with chronic rotator cuff tendinopathy. Recently Scarpone and colleagues22 recruited from an outpatient sports medicine clinic patients with rotator cuff tendinopathy refractory to physical therapy and corticosteroid injection. They received one ultrasound-guided injection of 3.0 mL of 1% xylocaine followed by 3.5 mL of PRP at the lesion and surrounding tendon. The authors found that a single ultrasound-guided, intralesional injection of PRP resulted in safe, significant, sustained improvement of pain, function, and MRI outcomes.

Discussion Surgical use of PRP in arthroscopic rotator cuff repair Clinical studies have produced conflicting results on the effectiveness of the use of PRP in tendon repair of the rotator cuff, making it now difficult to draw definitive conclusions. The clinical studies published to date have different experimental designs and with a level of evidence that varies from 1 to 3. Moreover 7 different systems of preparation of PRP were used between studies (Table 1). The experimental protocol presents variations between different, as regards the volume of autologous blood, speed and time of centrifugation, method of administration, activating agent, the presence of leukocytes, the final volume of PRP and final concentrations of platelets and factors growth. The surgical technique (transosseous equivalent, single or double row) and the rehabilitation protocol (standard or rapid) were not the same among the different studies. Despite the differences in surgical techniques, in the formulation of the PRP, the sizes of the lesions, the reinjury rate has been recalculated by combining the available data from studies in order to determine the potential of the PRP to improve the healing of surgical repair of the rotator cuff. The analysis of all 12 studies examined showed that there was no significant difference in the rate of re-rupture between the PRP and the control group. The re-injury rate was 31% (90 of 292) and 36.6% (103 of 281), respectively (p-value > 0.05). Three studies have identified small and medium tears of rotator cuff such as those measuring less than 3 cm in length11,14,18. Randelli and colleagues7 have classified

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the lesions according to the amount of retraction. If the lesion exposed the head of the humerus, but the tendon retraction did not come to the surface of the glenoid, was defined as a small or medium injury. A significant difference was found when a stratified analysis was performed to analyze the results of small and medium lesions of the rotator cuff. The rate of re-injury was 7.9% among patients treated with PRP compared to 26.8% of those treated without PRP (p-value = 0.002, Chi-square test). It is important to emphasize that with the exception of two cases of infection, has not been reported any complication from the use of PRP. Bergeson and colleagues19 showed an infection rate of 12% among patients treated with fibrin matrix rich in platelets (Cascade Autologous Platelet System) compared to 0% in the control group. However, this difference did not reach statistical significance, and no difference in the rates of infection or complication rates was found in the remaining studies. Although clinical studies have produced conflicting results, the data on PRP suggest a beneficial effect on the healing process when applied during the repair of the rotator cuff. The stratified analysis of small or medium lesions showed a significant rate of re-injury overall lower in the group PRP. Therefore currently it seems the PRP can improve the healing of arthroscopic repair of small and medium lesions that seem more prone to a biological response to treatment with growth factors. Namazi has recently highlighted the main mechanisms by which PRP can reduce the rate of re-injury of the rotator cuff 23. The level of interleukin 1������������������� β������������������ (IL-1������������ β����������� ) is correlated with the degeneration of the tendons of the cuff. In contrast, TGF-β can improve the strength of the repair of these tendons. Recent studies have shown that the PRP can not only inhibit the inflammatory effects of IL-1β, but also enhance the production of TGF-β24,25. A recent in vitro studies on the effect of PRP on human tenocytes from rotator cuff with degenerative lesions, have shown that the growth factors released by platelets may enhance cell proliferation of tenocytes and promote the synthesis of extracellular matrix tendon26,27. Furthermore an in vivo animal study has shown than that the type of application, injection or absorption from a sponge did not influence the effect of PRP on rotator cuff healing28. The PRP is certainly a source of bioactive growth factors, however the optimal preparation, activation, as well as the quantification of the various growth factors present in the PRP is a controversial subject. Further prospective randomized controlled trials (level 1 evidence) will be necessary.

PRP injections for rotator cuff tendinopathy Injections of PRP have gained popularity in the treatment of tendinopathy based on its promoting effects on tendon cell proliferation, collagen synthesis, and vascularization, which have been shown in animal and in vitro studies29,30. As regards the use of PRP for chronic rotator cuff tendinopathy there is a limitation of well designed studies

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testing the effectiveness of PRP injections in the subacromial space. In a systematic review of the literature we have found only two randomized controlled trials evaluating the use of PRP injections in rotator cuff tendinopathy20,21. These studies have reported controversial results on the effectiveness of the use of PRP injection in chronic cuff tendon diseases. The systems of preparation of PRP were not the same across the trials and different treatment protocols were used (single or double PRP injections). Furthermore the presence of some bias including the concomitant standard exercise program and the needle stimulus effect can have influenced the results of studies. Furthermore rotator cuff tendinopathy has a multifactorial origin. Extrinsic factors including anatomic problems and alterations in kinematics of the joint or intrinsic factors including age-related degenerative changes and vascularity changes may play a role in developing such disease. The effect of PRP can change according to different mechanisms underlying rotator cuff tendinopathy. The nature of rotator cuff disease was not the same across the studies and patients who didn’t respond to physical therapy and corticosteroid injection seem to be advantaged from the PRP use. Whether PRP may be beneficial in a more specific group of patients ��������������������� refractory ���������� to a standard exercise therapy needs of additional research. More studies with a high level of evidence are required to justify PRP injections in rotator cuff tendinopathy.

References 1. Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB. Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am 1995;77:10-5 2. Eppley BL, Woodell JE, Higgins J. Platelet quantification and growth factor analysis from platelet-rich plasma: implications for wound healing. Plast Reconstr Surg 2004; 114:1502-8 3. Coppinger JA1, Cagney G, Toomey S, Kislinger T, Belton O, McRedmond JP, Cahill DJ, Emili A, Fitzgerald DJ, Maguire PB. Characterization of the proteins released from activated platelets leads to localization of novel platelet proteins in human atherosclerotic lesions. Blood. 2004;103:2096-104 4. Sundman EA, Cole BJ, Fortier LA. Growth factor and catabolic cytokine concentrations are influenced by the cellular composition of platelet-rich plasma. Am J of Sports Med 2011; 39:21352140 5. Dohan Ehrenfest DM, Bielecki T, Mishra A, Borzini P, Inchingolo F, Sammartino G, Rasmusson L, Evert PA. In Search of a Consensus Terminology in the Field of Platelet Concentrates for Surgical Use: Platelet-Rich Plasma (PRP), Platelet-Rich Fibrin (PRF), Fibrin Gel Polymerization and Leukocytes. Curr Pharm Biotechnol. 2012;13:1131-7 6. Randelli PS, Arrigoni P, Cabitza P, Volpi P, Maffulli N. Autologous platelet rich plasma for arthroscopic rotator cuff repair. A pilot study. Disabil Rehabil 2008; 30:1584-9 7. Randelli P, Arrigoni P, Ragone V, Aliprandi A, Cabitza P. Platelet rich plasma in arthroscopic rotator cuff repair: a prospective RCT study, 2-year follow-up. J Shoulder Elbow Surg 2011; 20:518-28 8. Ruiz-Moneo P, Molano-Munoz J, Prieto E, Algorta J. Plasma rich in growth factors in arthroscopic rotator cuff repair: a randomized, double-blind, controlled clinical trial. Arthroscopy 2013; 29:2-9

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9. Antuna S, Barco R, Martinez Diez JM, Sanchez Marquez JM. Platelet-rich fibrin in arthroscopic repair of massive rotator cuff tears: a prospective randomized pilot clinical trial. Acta Orthop Belg 2013; 79:25-30 10. Gumina S, Campagna V, Ferrazza G, et al. Use of platelet-leukocyte membrane in arthroscopic repair of large rotator cuff tears: a prospective randomized study. J Bone Joint Surg Am 2012; 94:1345-52 11. Jo CH, Kim JE, Yoon KS, et al. Does platelet-rich plasma accelerate recovery after rotator cuff repair? A prospective cohort study. Am J Sports Med 2011; 39:2082-90 12. Jo CH, Shin JS, Lee YG, et al. Platelet-rich plasma for arthroscopic repair of large to massive rotator cuff tears: a randomized, singleblind, parallel-group trial. Am J Sports Med 2013; 41:2240-8 13. Zumstein MA, Rumian A, Lesbats V, Schaer M, Boileau P. Increased vascularization during early healing after biologic augmentation in repair of chronic rotator cuff tears using autologous leukocyte- and platelet-rich fibrin (L-PRF): a prospective randomized controlled pilot trial. J Shoulder Elbow Surg. 2014; 23:3-12 14. Castricini R, Longo UG, De Benedetto M, et al. Platelet-rich plasma augmentation for arthroscopic rotator cuff repair: a randomized controlled trial. Am J Sports Med 2011; 39:258-65 15. Arnoczky SP. Platelet-rich plasma augmentation of rotator cuff repair: letter. Am J Sports Med; 2011:NP8-9; author reply NP11. 16. Weber SC, Kauffman JI, Parise C, Weber SJ, Katz SD. Platelet-rich fibrin matrix in the management of arthroscopic repair of the rotator cuff: a prospective, randomized, double-blinded study. Am J Sports Med 2013; 41:263-70 17. Rodeo SA, Delos D, Williams RJ, Adler RS, Pearle A, Warren RF. The effect of platelet-rich fibrin matrix on rotator cuff tendon healing: a prospective, randomized clinical study. Am J Sports Med 2012; 40:1234-41 18. Barber FA, Hrnack SA, Snyder SJ, Hapa O. Rotator cuff repair healing influenced by platelet-rich plasma construct augmentation. Arthroscopy 2011; 27:1029-35 19. Bergeson AG, Tashjian RZ, Greis PE, Crim J, Stoddard GJ, Burks RT. Effects of platelet-rich fibrin matrix on repair integrity of atrisk rotator cuff tears. Am J Sports Med 2012; 40:286-93 20. Rha DW1, Park GY, Kim YK, Kim MT, Lee SC. Comparison of the

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therapeutic effects of ultrasound-guided platelet-rich plasma injection and dry needling in rotator cuff disease: a randomized controlled trial. Clin Rehabil. 2013; 27:113-22 21. Kesikburun S, Tan AK, Yilmaz B, Yaşar E, Yazicioğlu K. Platelet-rich plasma injections in the treatment of chronic rotator cuff tendinopathy: a randomized controlled trial with 1-year follow-up. Am J Sports Med. 2013; 41:2609-16 22. Scarpone M, Rabago D, Snell E, Demeo P, Ruppert K, Pritchard P, Arbogast G, Wilson JJ, Balzano JF. Effectiveness of Platelet-rich Plasma Injection for Rotator Cuff Tendinopathy: A Prospective Open-label Study. Glob Adv Health Med. 2013; 2:26-31 23. Namazi H. Rotator cuff repair healing influenced by platelet-rich plasma construct augmentation: a novel molecular mechanism. Arthroscopy; 2011:1456; author reply -7 24. Kakudo N, Minakata T, Mitsui T, Kushida S, Notodihardjo FZ, Kusumoto K. Proliferation-promoting effect of platelet-rich plasma on human adipose-derived stem cells and human dermal fibroblasts. Plast Reconstr Surg 2008; 122:1352-60 25. Savitskaya YA, Izaguirre A, Sierra L, et al. Effect of angiogenesisrelated cytokines on rotator cuff disease: the search for sensitive biomarkers of early tendon degeneration. Clin Med Insights Arthritis Musculoskelet Disord 2011; 4:43-53. 26. Hoppe S, Alini M, Benneker LM, Milz S, Boileau P, Zumstein MA. Tenocytes of chronic rotator cuff tendon tears can be stimulated by platelet-released growth factors. J Shoulder Elbow Surg 2013; 22:340-9 27. Jo CH, Kim JE, Yoon KS, Shin S. Platelet-rich plasma stimulates cell proliferation and enhances matrix gene expression and synthesis in tenocytes from human rotator cuff tendons with degenerative tears. Am J Sports Med 2012; 40:1035-45 28. Ersen A1, Demirhan M, Atalar AC, Kapicioğlu M, Baysal G. Arch Orthop Trauma Surg. Platelet-rich plasma for enhancing surgical  rotator cuff  repair: evaluation and comparison of two application methods in a rat model. 2014;134:405-11 29. Jo CH, Kim JE, Yoon KS, Shin S. Platelet-rich plasma stimulates cell proliferation and enhances matrix gene expression and synthesis in tenocytes from human rotator cuff tendons with degenerative tears. Am J Sports Med. 2012; 40:1035-1045 30. de Mos M, van der Windt AE, Jahr H, et al. Can platelet-rich plasma enhance tendon repair? A cell culture study. Am J Sports Med. 2008; 36:1171-1178

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Platelet rich plasma in rotator cuff disease Umile Giuseppe Longo, Alessandra Berton, Giacomo Rizzello, Giuseppe Salvatore, Vincenzo Denaro Department of Orthopaedic and Trauma Surgery, Campus Bio-Medico University, Roma

Abstract Platelet-rich plasma (PRP) is an emerging strategy to enhance tendon healing. Its increased used in the clinical setting is due to its safety. However, definitive evidence on PRP potentiality still need to be clarified. Only some molecular mechanisms have been described and many others need to be studied. The knowledge of the healing process will also help to identify optimal formulations and protocols for the clinical use. The available clinical studies on PRP for rotator cuff disease not only reported conflicting results but they are difficult to compare because of different experimental designs, level of evidence, PRP formulations, surgical technique, rehabilitation protocol, size of the lesion or nature of the disease. To date, clinical benefits of PRP are not demonstrated and powered randomized controlled trials are necessary.

PRP BIOLOGY Platelet-rich plasma (PRP) gained popularity over the last years thanks to its potential as a biological solution to improve rotator cuff tendon healing. It is a blood fraction containing high platelet concentrations, high density of growth factors and structural proteins. PRP acts upon tendon healing by modulating inflammation, activating fibroblast migration, promoting angiogenesis, and increasing cell proliferation1. Platelets become activated at the site of tissue injury and release intracellular stores. They are predominantly alphagranules (50-80 alpha-granules per platelet), dense granules (3-5 granules per platelet) and lysosome 2. Alfa-granules contain more than 300 proteins. Basic growth factors identified include PDGF, TGF, FGF, endothelial growth factor (EGF), hepatocyte growth factor (HGF), connective tissue growth factor (CTGF) and VEGF. Those play important roles in cell proliferation, chemotaxis, cell differentiation, and angiogenesis. Specifically, TGF-β promotes matrix synthesis PDGF, together with platelet factor-4 and CXCL7, activates fibroblasts’ migration3, PDGF-B, bFGF and CXCL5 are involved in the homing of precursor cells4, HGF is a potent antifibrotic that may help to reduce scar formation around tendon tissues5 and, together with VEGF promote angiogenesis6. The role of platelets in angiogenesis is complex because a-granules also contain anti-angiogenic proteins such as Thrombospondin-1 (TSP-1), angiostatin, endostatin, fibronectin and the tissue inhibitors of metalloproteinases (TIMPs -1 to -4)7. They are stored separately and should

be released differentially thanks to an agonist-specific mechanism 8. Platelets also modulate inflammation by secreting high levels of chemokine such as CXCL1/GRO, ENA78/ CXCL5, monocyte chemoattractant protein-1 (MCP-1), CCL5, IL8 9. Moreover, platelets secrete platelet basic protein (PBP) and connective tissue activating peptide-III (CTAP-III)). Those are precursors of b-thromboglobulin [(CXCL7 or neutrophil activating peptide-2, (NAP-2)], a strong chemoattractant and an activator for neutrophils. Dense granules contain bioactive factors that have important effects on biologic aspects of wound healing. Histamine and serotonin increase capillary permeability, allowing inflammatory cells to migrate toward the area of inflammation. Moreover, they activate macrophages10,11. Studies show that the nature of the stimulants or the combination of stimulants on macrophage can lead to different kind of activation. ‘classical’ macrophage activation may determine an anti-inflammatory environment compared to ‘innate” activation 12. PRP therapies also contain cell adhesion molecules including fibronectin, fibrin, and vitronectin. Those add to the potential biologic activity of PRP by forming threedimensional scaffolds where cells can adhere and begin the wound healing process.

PRP COMPOSITION PRP therapies includes several formulations that differ in their pharmacological and material characteristics. Those characteristics influence the biology and potential effects. The main difference between plasma concentrates is leucocytes content and fibrin network. Four categories have been identified: leucocyte-poor or pure platelet-rich plasma (P-PRP), leucocyte- and platelet-rich plasma (L-PRP), leucocyte-poor or pure platelet-rich fibrin (P-PRF), leucocyte- and platelet-rich fibrin (L-PRF). A further division is between activated (ex vivo activation with thrombin and/or calcium) and unactivated form (in vivo activation via endogenous collagen)13,14. There are no definitive data to support the use of L-PRP or PRP. Studies showed L-PRP had pro-inflammatory effect when injected in rabbits15 and increased the levels of MMPs when assayed in tenocyte cultures compared with pure PRP16. On the other hand, leucocyte in PRP has a positive role as anti-infectious and immune regulatory agents 17-20. Studies showed decreased pain and inflammation when used for treatment of tendonitis 21,22.

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The ratio between fibrinogen and thrombin concentrations is another aspect that ���������������������������������������� is still under-researched. It is responsible for fibrin polymerization and its biochemical architecture that represent the support cytokine enmeshment and cellular migration23-25. Further studies are needed define the optimal PRP formulation to manage rotator cuff lesions.

Clinical studies on PRP in rotator cuff lesions and tendinopathy There are still many questions about the biologic mechanisms of the action of PRP, however the safety and feasibility of PRP therapies allowed clinical studies and patientoriented research to be performed. PRP has been used both on acutely injured tendon and degenerative tendon. The underlying cellular and molecular processes are quite different between these two disparate clinical conditions, thus they should be considered separately. Clinical studies on PRP in rotator cuff lesions not only reported conflicting results but they are difficult to compare because of different experimental designs, level of evidence, PRP formulations, surgical technique, and the rehabilitation protocol. At the moment, studies that have been published are: seven level 126-32 and two level 233,34 randomized controlled trials , one level 2 prospective cohort study 35, two Level 3 case control studies 36,37 and one level 3 cohort study38. Four of them investigated the effect of injectable PRP in arthroscopic rotator cuff repair26,27,33,36 while the others applied suturable PRP28-32,34,35,37,38. Plasma products were heterogenic, in terms of volume of autologous blood collected, speed and time of centrifugation, method of administration, activating agent, presence of leukocytes, final volume of PRP, and final concentration of platelets and growth factors. The surgical technique was single row26,28,32-34,37,38, double row27,31,34,36 or transosseous equivalent29,30,35. The rehabilitation protocol was could be standard or rapid. All those factors might have important implications for clinical outcomes and arise the need for comparative effectiveness research. Clinical outcomes were no different between PRP group and control group in all studies. Only Randelli et al26 detected a statistically significant improvement in the Constant, SER, UCLA, SST at the 3 month follow-up and Barber et al37 detected a statistically significant difference in the Rowe score (mean follow-up of 31 months). Postoperative tendon healing showed no significant difference both at MRI26,31,37 or ultrasound34 imaging. Re-rupture rates between PRP and control group was not significantly different in all studies. However, Barber et al37 showed a statistically significant difference in the rates of tendon re-rupture (60% vs 30%; P = 0.03) at 4 months from surgery. Moreover, a stratified analysis the results of small and medium lesions of the rotator cuff showed lower rate of reinjury (7.9%) among patients treated with PRP, compared to those treated without PRP (26.8%)39. To date, there are not definitive evidence to support the routine use of PRP in rotator cuff repair. ������������� Further randomized prospective trials are necessary to achieve definitive answers in this field.

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Clinical studies on PRP injections for rotator cuff tendinopathy are just few despite the great popularity in the clinical setting40,41. Also in this case there are methodological limitations and difficulties in comparisons. There are two randomized controlled trials on PRP injections for rotator cuff tendinopathy, one supporting PRP superiority with respect to pain, function, and range of motion over a 6-month period40, the other showing no difference for quality of life, pain, disability, and range of motion at 1 year41. They used different treatment protocols, Rha et al.40 used 2 PRP (3 mL) injections at a 4-week interval, and Kesikburun et al.41 used 1 injection of PRP (5 mL) with concomitant standard exercise program. Moreover the nature of the disease was not the same, maybe influencing the results. Further studies are needed to acquire higher level of evidence and define the role of PRP injection for rotator cuff tendinopathy.

CONCLUSION Platelet-rich plasma (PRP) ������������������������������ is an emerging strategy to enhance tendon healing42-46. Its increased used in the clinical setting is due to its safety. However, definitive evidence on PRP potentiality still need to be clarified. Only some molecular mechanisms have been described and many others need to be studied. The knowledge of the healing process will also help to identify optimal formulations and protocols for the clinical use. The available clinical studies on PRP for rotator cuff disease not only reported conflicting results but they are difficult to compare because of different experimental designs, level of evidence, PRP formulations, surgical technique, rehabilitation protocol, size of the lesion or nature of the disease. To date, clinical benefits of PRP are not demonstrated and powered randomized controlled trials are necessary.

REFERENCES 1. Gulotta LV, Wiznia D, Cunningham M et al. What’s new in orthopaedic research. J Bone Joint Surg Am 2011; 93:2136-2141 2. Blair P, Flaumenhaft R. Platelet alpha-granules: basic biology and clinical correlates. Blood Rev 2009; 23:177-189 3. Senior RM, Griffin GL, Huang JS et al. Chemotactic activity of platelet alpha granule proteins for fibroblasts. J Cell Biol 1983; 96:382-385 4. Nedeau AE, Bauer RJ, Gallagher K et al. A CXCL5- and bFGFdependent effect of PDGF-B-activated fibroblasts in promoting trafficking and differentiation of bone marrow-derived mesenchymal stem cells. Exp Cell Res 2008; 314:2176-2186 5. Anitua E, Sanchez M, Nurden AT et al. Autologous fibrin matrices: a potential source of biological mediators that modulate tendon cell activities. J Biomed Mater Res. Part A. 2006; 77:285-293 6. Bates DO, Harper SJ. Regulation of vascular permeability by vascular endothelial growth factors. Vascul Pharmacol 2002; 39:225-237 7. Nurden AT, Nurden P, Sanchez M, Andia I, Anitua E. Platelets and wound healing. Front Biosci 2008; 13:3532-3548 8. Villeneuve J, Block A, Le Bousse-Kerdiles MC, et al. Tissue inhibitors of matrix metalloproteinases in platelets and megakaryo-

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cytes: a novel organization for these secreted proteins. Exp Hematol 2009; 37:849-856 9. Flad HD, Harter L, Petersen F et al. Regulation of neutrophil activation by proteolytic processing of platelet-derived alphachemokines. Adv Exp Med Biol 1997; 421:223-230 10. Bennett NT, Schultz GS. Growth factors and wound healing: biochemical properties of growth factors and their receptors. Am J Surg 1993; 165:728-737 11. Los G, De Weger RA, Van den Berg DT et al. Macrophage infiltration in tumors and tumor-surrounding tissue: influence of serotonin and sensitized lymphocytes. Cancer Immunol Immunother 1988; 26:145-152 12. Menzies FM, Henriquez FL, Alexander J, Roberts CW. Sequential expression of macrophage anti-microbial/inflammatory and wound healing markers following innate, alternative and classical activation. Clin Exp Immunol 2010; 160:369-379 13. Mishra A, Randelli P, Barr C et al. Platelet-rich plasma and the upper extremity. Hand Clin 2012; 28:481-491 14. Dohan Ehrenfest DMB, T. Mishra, A. et al. In search of a consensus terminology in the field of platelet concentrates for surgical use: Platelet-Rich Plasma (PRP), Platelet-Rich Fibrin (PRF), fibrin gel polymerization and leukocytes. Curr Pharm Biotechnol 2012; 13:1131–1137 15. Loftus ML, Endo Y, Adler RS. Retrospective analysis of postinjection ultrasound imaging after platelet-rich plasma or autologous blood: observational review of anatomic distribution of injected material. AJR. Am J Roentgenol 2012; 199:W501-505 16. Carofino B, Chowaniec DM, McCarthy MB, et al. Corticosteroids and local anesthetics decrease positive effects of platelet-rich plasma: an in vitro study on human tendon cells. Arthroscopy 2012; 28:711-719 17. Dohan DM, Choukroun J, Diss A et al. Platelet-rich fibrin (PRF): a second-generation platelet concentrate. Part III: leucocyte activation: a new feature for platelet concentrates? Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2006; 101:e51-55 18. Moojen DJ, Everts PA, Schure RM et al. Antimicrobial activity of platelet-leukocyte gel against Staphylococcus aureus. J Orthop Res 2008; 26:404-410 19. Cieslik-Bielecka A, Gazdzik TS, Bielecki TM, Cieslik T. Why the platelet-rich gel has antimicrobial activity? Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2007; 103:303-305; author reply 305-306 20. El-Sharkawy H, Kantarci A, Deady J et al. Platelet-rich plasma: growth factors and pro- and anti-inflammatory properties. J Periodontol 2007; 78:661-669 21. Everts PA, Devilee RJ, Brown Mahoney C et al. Exogenous application of platelet-leukocyte gel during open subacromial decompression contributes to improved patient outcome. A prospective randomized double-blind study. Eur Surg Res 2008; 40:203-210 22. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am J Sports Med 2006; 34:17741778 23. Mosesson MW, Siebenlist KR, Meh DA. The structure and biological features of fibrinogen and fibrin. Annals NY Acad Sci 2001; 936:11-30 24. Clark RA. Fibrin and wound healing. Annals NY Acad Sci 2001; 936:355-367 25. van Hinsbergh VW, Collen A, Koolwijk P. Role of fibrin matrix in angiogenesis. Annals NY Acad Sci 2001; 936:426-437. 26. Randelli P, Arrigoni P, Ragone V et al. Platelet rich plasma in arthroscopic rotator cuff repair: a prospective RCT study, 2-year follow-up. J Shoulder Elbow Surg 2011; 20:518-528 27. Ruiz-Moneo P, Molano-Munoz J, Prieto E, Algorta J. Plasma rich in growth factors in arthroscopic rotator cuff repair: a randomized, double-blind, controlled clinical trial. Arthroscopy 2013; 29:2-9

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28. Gumina S, Campagna V, Ferrazza G et al. Use of platelet-leukocyte membrane in arthroscopic repair of large rotator cuff tears: a prospective randomized study. J Bone Joint Surg Am 2012; 94:1345-1352 29. Jo CH, Shin JS, Lee YG, et al. Platelet-rich plasma for arthroscopic repair of large to massive rotator cuff tears: a randomized, single-blind, parallel-group trial. Am J Sports Med 2013; 41:22402248 30. Zumstein MA, Rumian A, Lesbats V et al. Increased vascularization during early healing after biologic augmentation in repair of chronic rotator cuff tears using autologous leukocyte- and platelet-rich fibrin (L-PRF): a prospective randomized controlled pilot trial. J Shoulder Elbow Surg 2014; 23:3-12 31. Castricini R, Longo UG, De Benedetto M et al. Platelet-rich plasma augmentation for arthroscopic rotator cuff repair: a randomized controlled trial. Am J Sports Med Feb 2011; 39:258-265 32. Weber SC, Kauffman JI, Parise C et al. Platelet-rich fibrin matrix in the management of arthroscopic repair of the rotator cuff: a prospective, randomized, double-blinded study. Am J Sports Med 2013; 41:263-270 33. Antuna S, Barco R, Martinez Diez JM, Sanchez Marquez JM. Platelet-rich fibrin in arthroscopic repair of massive rotator cuff tears: a prospective randomized pilot clinical trial. Acta Orthop Belg 2013; 79:25-30 34. Rodeo SA, Delos D, Williams RJ et al. The effect of platelet-rich fibrin matrix on rotator cuff tendon healing: a prospective, randomized clinical study. Am J Sports Med 2012; 40:1234-1241 35. Jo CH, Kim JE, Yoon KS, et al. Does platelet-rich plasma accelerate recovery after rotator cuff repair? A prospective cohort study. Am J Sports Med 2011; 39:2082-2090 36. Charousset C, Zaoui A, Bellaiche L, Piterman M. Does autologous leukocyte-platelet-rich plasma improve tendon healing in arthroscopic repair of large or massive rotator cuff tears? Arthroscopy 2014; 30:428-435 37. Barber FA, Hrnack SA, Snyder SJ, Hapa O. Rotator cuff repair healing influenced by platelet-rich plasma construct augmentation. Arthroscopy 2011; 27:1029-1035 38. Bergeson AG, Tashjian RZ, Greis PE et al. Effects of platelet-rich fibrin matrix on repair integrity of at-risk rotator cuff tears. Am J Sports Med 2012; 40:286-293 39. Chahal J, Van Thiel GS, Mall N, et al. The role of platelet-rich plasma in arthroscopic rotator cuff repair: a systematic review with quantitative synthesis. Arthroscopy 2012; 28:1718-1727 40. Rha DW, Park GY, Kim YK et al. Comparison of the therapeutic effects of ultrasound-guided platelet-rich plasma injection and dry needling in rotator cuff disease: a randomized controlled trial. Clin Rehabil 2013; 27:113-122 41. Kesikburun S, Tan AK, Yilmaz B et al. Platelet-rich plasma injections in the treatment of chronic rotator cuff tendinopathy: a randomized controlled trial with 1-year follow-up. Am J Sports Med 2013; 41:2609-2616 42. Maffulli N, Longo UG, Hüfner T, Denaro V. [Surgical treatment for pain syndromes of the Achilles tendon]. Unfallchirurg 2010; 113:721-725 43. Forriol F, Longo UG, Concejo C et al. Platelet-rich plasma, rhOP-1 (rhBMP-7) and frozen rib allograft for the reconstruction of bony mandibular defects in sheep. A pilot experimental study. Injury 2009; 40:S44-49 44. Longo UG, Lamberti A, Maffulli N, Denaro V. Tendon augmentation grafts: a systematic review. Br Med Bull 2010; 94:165-188 45. Longo UG, Lamberti A, Maffulli N, Denaro V. Tissue engineered biological augmentation for tendon healing: a systematic review. Br Med Bull 2011; 98:31-59 46. Maffulli N, Longo UG, Loppini M et al. Tissue engineering for rotator cuff repair: an evidence-based systematic review. Stem Cells Int 2012; 2012:418086

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Biology of rotator cuff tendinopathy Antonella Murgo, Orazio De Lucia, Chiara Crotti, Pier Luigi Meroni Divisione e Cattedra di Reumatologia, Istituto Ortopedico Gaetano Pini, Milano

Genetic associations

Introduction

Although it has been suggested that some individuals display a genetic predisposition to the development of tendinopathy (variants of tenascin-C gene with 12 and 14 guanine-thymine repeats or COL5A1 BstUI restriction fragment length polimorphisms), a specific genetic association is still matter of research. The difficulty in finding such association may be explained by the existence of a complex interactions between multiple genes 3.

Tendinopathy is a frequent condition and cause for referral to orthopedics and rheumatologists. Rotator cuff tendons (especially the supraspinatus) are the most vulnerable and commonly involved structure; the incidence increases with age up to 40% in subjects aged >70 years 1. The etiopathogenesis of the rotator cuff tendinopathy is still poorly defined despite its high frequency. Better understanding of the biological processes lying behind the tendon-bone junction damage is needed in order to have more therapeutical options. The clinical syndrome characterized by pain, impaired performance and swelling due to the increased thickness of tendons and/or the surrounding structures, is called tendinopathy. Because of the presence of symptoms usually related to inflammation, the term “tendinitis” had been used to describe this condition for long time. However, the evidence of degenerative lesions, characterized by disorganization of tendon ultrastructure, not always accompanied by a significant inflammatory component, has led to prefer the generic term tendinopathy 2. Rotator cuff tendinopathy is mediated by extrinsic mechanisms (i.e. anatomical, biomechanical) and intrinsic processes (i.e. alterations in biological and mechanical properties, in morphology, in vascularization), both responsible for the possible damage of the whole tendon. It is commonly described as a progressive disorder, beginning with an acute phase followed by a condition in which degenerative aspects are prevalent and potentially ending in a complete rupture.

Cellular and molecular pathogenesis Cell infiltrates, thinning and disorganization of the tendon fibers, granulation tissue and fibrocartilage alterations have been described in rotator cuff tendinopathy and linked to tension force decrease and rupture tendency 4. Histopathological changes are consistent with a generalized hypoxia. Immunohistochemical and microarray studies have demonstrated the presence of neo-vascularization and the increase of neurotransmitters (in particular substance P), which would partially explain the origin of chronic pain in tendinopathy 5. The definition of cellular infiltrate is a milestone in the acknowledgment of rotator cuff tendinopathy. The early stages of tendon damage could result from an inflammatory response to a mechanical stress. The difficulty in achieving appropriate experimental models leads to a lack of information concerning the role of inflammatory cells and mediators. A significant increase of neutrophils, macrophages and mast cells can be found in the early stages of tendinopathy; inflammatory cells produce different angiogenic, pro-inflammatory and degenerative factors, that promote degenerative and reparative processes into the extracellular matrix 6. An increasing number of studies suggest that cytokines (TGF-β, IL1, IL6, IL15, IL18) are active in various steps of tendinopathy, affecting cell-chemotaxis, proliferation and differentiation, matrix synthesis throught an autocrine or paracrine signaling. These effects are particularly remarkable under the influence of transforming growth factor β (TGF-β) produced by macrophages. The family of TGF-β is required for proper fetal development of tendons and plays a major role in the healing process. It has been shown that TNF-β increases the production of collagen and proteinase activity 7, with the result of stimulating the formation of small fibrovascular scars. This event initially would play a protective and reparative role, but later it could cause a weakening of the structure,

facilitating tendon rupture. TGF-β helps the production of matrix proteins (fibronectin, glycosaminoglycans) and the maturation of monocytes into macrophages, amplifying the inflammatory response. The role of IL-6 has been recently investigated: its expression is up-regulated in pathological tendons. IL-6 has both pro-inflammatory and anti-inflammatory effects and its expression, as a mediator of cyclooxygenase-2 (COX2) in pathological tendon, its expression does not necessarily support an inflammatory state. IL-6 expression is different in the Achilles and posterior tibial tendinopathy; it remains unclear whether this finding is related to differences in load, structure or progression of tendinopathy 8. Although this study does not analyze the rotator cuff tendons, in our opinion, it suggests the complexity of tendinopathy biomechanical processes. IL-1β increases the synthesis of COX-2, PGE2 production and matrix metalloproteinases (MMP-1, MMP-3, MMP13) which cause matrix destruction, a loss of tendon biochemical properties. Moreover IL1β displays pro-apop-

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totic activity and strongly down regulates several gene expression 9.

The role of the extracellular matrix Extracellular matrix (ECM) is a complex entity that surrounds and supports the tendon cells; it is composed by collagen fibers and elastin. In addition to structural proteins it contains specialized proteins (eg fibronectin and fibrillin) and proteoglycans. In order to play its physiological role, ECM undergoes to a continuous remodeling process, mediated by some enzymatic activities (mainly MMP). Since the interaction between cells and matrix is bi-directional, extracellular changes may arise from cellular processes (proliferation, migration, apoptosis, and morphogenesis), or may originate from extracellular microenvironment 10. According to several Authors, the imbalance between synthesis and degradation of ECM components would lead to the deterioration and degeneration of the tendon structure. The balance between MMP and their inhibitors is essential in the maintenance of tendon ECM homeostasis and an imbalance may result in uncontrolled tendon damage. These enzymes play a major role in the matrix degradation during development, repairing process and may play a key role in the pathogenesis of tendinopathy. An in vitro study demonstrated that MMP inhibitors can prevent the activation of MMp-13 and inhibit pericellular matrix degeneration and the loss of material properties associated with stress deprivation 10. Collagen is the main component of the tendon. The collagen portion is made up of 95% type I collagen with small amounts of 27 other types of collagen. Following TGF-β1 secretion, there is an increase in collagen production, especially in favor of less represented variants (type I, III, V) and of “altered” forms (high percentage of denatured collagen) 11. The loss of balance between synthesis and degradation of ECM has also a negative impact on proteoglycans, which are protein/polysaccharide complexes. Proteoglycans, and their constituent glycosaminoglycans (GAGs), are involved in several physiological processes and may display both a structural and signaling role. Unfortunately the changes occurring in proteins different from collagen are still poorly known in tendinopathies. It has been documented that some GAGs, such as fibronectin and tenascin-C, promote the migration of fibroblasts and their adherence to fibrin. A persistent increase in expression of fibronectin and tenascin-C has been reported in tendinopathies and may contribute to the pathogenic remodeling 12. A disintegrin-like and metalloprotease with thrombospondin motifs (ADAMTS), a novel family of extracellular proteases, seems to play an important role in proteoglycan turnover in tendon, although the informations on this mechanism are not enough 13. Tenocytes, a fibroblast-like cell type, are the regulators of the ECM remodeling process. Before the development of tendinopathy, tenocytes undergo significant changes in morphology and proliferation, become necrotic or apoptotic and increase the local expression of insulin-like growth factor (IGF-1) 10. IGF-1 increases DNA synthesis

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in tenocytes, GAG production and collagen synthesis; its stimulating effects affect other cell types such as cartilage, bone and muscular cells. It has been observed that rotator cuff tendon cells display a fibrochondrogenic phenotype nearby the affected areas. An increased expression of cartilage genes, such as COL2A1, SOX9 and aggrecan, has been described in animal models of supraspinatus tendinopathy 9.

The role of apoptosis Apoptosis, or programmed death of tenocytes, plays a definite role in the genesis of rotator cuff tendinopathy. Apoptosis is triggered and tuned by intrinsic and extrinsic mechanisms. Fibroblast or fibroblast-like apoptosis may play a critical role in the maintenance of the extracellular matrix of rotator cuff tendons. BNip3, a pro-apoptotic member of the BcL-2 family, has been specifically linked with hypoxia and inflammation-induced apoptosis. Benson et al. reported an almost 3-fold increase in apoptosis within full-thickness rotator cuff tears compared with control groups 14.

Mechanical causes Repetitive microtraumas/stressing conditions are thought to play a main pathophysiological role in tendinopathies. More recently it has been demonstrated that repeated traumas and the related stromal tissue damage can affect cell responses through the receptor recognition of intracellular proteins released by necrotic cells. Among them, heat shock proteins (HSPs), also called damage-associated molecular patterns (DAMPs), are rapidly released following non-programmed cell death, are key effectors of the innate immune system and restore homeostasis of the tissue. HSPs, released from stressed tenocytes, play a role in early tendon damage as they regulate both the tissue healing response and the inflammatory reaction with a fine balance between reparative versus degenerative changes 6. Repetitive micro-traumas/stresses are also responsible for ischemia, and consequent hypoxia, which represents potential trigger and cause of rotator cuff tendinopathy, recently correlated with an increased apoptosis. Cytokines play a key role in oxidative stress-induced cellular apoptosis, which is mediated by the activation of caspases (cysteine-dependent aspartate-directed proteases, a group of proteolytic enzymes) 15. Hypoxia also triggers the expression of vascular endothelial growth factor (VEGF), which promotes angiogenesis and increases the expression of MMPs. Both these events can cause weakening of the tendon structure. VEGF and von Willebrand factor messenger RNA (mRNA) expression levels were significantly increased in a rat model of sovraspinatus tendon overuse injury, but it is unclear whether the increase in these angiogenic cytokines is part of the early healing response cascade or just reflects the response to injury 16. Hypoperfusion is also responsible for the increase of free radicals, which can cause a direct cell damage. In fact, the

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expression of peroxiredoxin 5, an antioxidant enzyme that protects cells from free radicals- induced damage, is increased in tenocytes during tendinopathy. However small amounts of free radicals can be harmless and stimulate the fibroblast proliferation. For example, nitrix oxide (NO), can enhance tendon healing. NO is synthesized by a family of enzymes, the nitric oxide synthases (NOSs) that can be induced by bacterial cell wall products and proinflammatory cytokines (eg. IL-1 and TNF). Three NOS isoforms are expressed by fibroblasts during tendon healing and NO production increase seems to be related to an improvement in mechanical properties of damaged tendons, through the stimulation of fibroblast proliferation and ECM synthesis. Existing data indicate that several proinflammatory agents (e.g. cytokines, prostaglandins, growth factors and neuropetides) may initiate rotator cuff tendinopathy and that apoptosis play a key role in the development and progression of the process. Our understanding of the biology of tendinopathy is poor, mainly because of the difficulties in defining the sequence and chronology of the pathogenic events taking place in such a complex process.

References 1. Meislin RJ, Sperling JW, Stitik TP. Persistent shoulder pain: epidemiology, pathophysiology and diagnosis. Am J Orthp 2005; 34:5-9 2. Maffulli N, Kahn KM. Clinical nomenclature for tendon injuries. Medicine and Science in Sports and exercise 1999; 31:352-3 3. Mokone GG, Schwellnus MP et al. The COL5A1 gene and Achilles tendon pathology. Scand J Med Sci Sports 2006; 16:19-26

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4. Blevins FT, Djurasovic M, Flatow EL, Vogel KG. Biology of the rotator cuff tendon. Orthop Clin North Am 1997; 28:1-16 5. Schubert TE, Weidler C, Lerch K, Hofstadter F, Straub RH. ������ Achilles tendinosis is associated with sprouting pf substance P positive nerve fibres. Ann Rheum Dis. 2005; 64: 1083-1086 6. Millar NL, Wei AQ, Molloy TJ, Bonar F, Murrell GA. Cytokines and apoptosis in supraspinatus tendinopathy. J Bone Joint Surg Br 2009; 91:417-24 7. Hays PL, Kawamura S, Deng XH, Dagher E, Mithoefer K, Ying L, et al. The role of macrophages in early healing of a tendon graft in bone tunnel. J Bone Joint Surg Am 2008; 90:565-79 8. Legerlotz K, Jones ER, Screen HRC, Riley GP. Rheumatology 2012; 51:1161-1165 9. Archambault JM, Tsuzaki M, Herzog W, Banes AJ. Stretch and interleukin-1beta induce matrix metalloproteinases in rabbit tendon in vitro. J Orthop Res 2002; 20: 36-39 10. Arnoczky SP, Lavagnino M, Egerbacher M. The mechanobiological aetiopathogenesis of tendonpathy: is it the over-stimolation or under-stimulation of tendon cells? Int J Exp Pathol 2007; 88:217-226 11. Riley G. The pathogenesis of tendinopathy. A molecular perspective. Rheumatology 2004; 43:131-142 12. Xu Y, Murrel GAC. The Basic science of Tendinopathy. Clin Orthop Relat Res 2008; 466: 1528-1538 13. Jones GC, Riley GP, ADAMTS proteinases: a multi-domain, multifunctional family with roles in extracellular matrix turnover and arthritis. Arthritis Res Ther 2005; 7:160-169 14. Benson RT, McDonnell SM, Knowles HJ, Rees JL, Carr AJ, Hulley PA, Tendinopathy and tears of the rotator cuff are associated with hypoxia and apoptosis. Journal of bone and joint surgery. 2010; 92B:448-53 15. Yuan J, Murrell GAC, Trickett A, Wang MX. Involvment of cytochrome c release and caspase-3 activation in the oxidative stress-induced apoptosis in human tendon fibroblasts. Biochimica et Biophysica Acta. 2003; 1641:35-41 16. Perry SM, McIlhenny SE, Hoffman MC, Soslowsky LJ. Inflammatory and angiogenic mRNA level are altered in a supraspinatus tendon overuse animal model. J Shoulder Elbow Surg 2005; 14:79S-83S

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Scaffold augmentation in rotator cuff tears repairs Roberto Rotini, Alessandro Marinelli, Enrico Guerra, Graziano Bettelli, Michele Cavaciocchi, Lorenzo Zaccarelli, Milena Fini*, Elena Bondioli** Shoulder and Elbow Unit, Rizzoli Orthopaedic Institute, Bologna * Laboratory of Preclinical and Surgical Studies, Rizzoli Orthopaedic Institute, Bologna ** Burn Intensive Care Unit and “Regione Emilia Romagna” Skin Bank, Bufalini Hospital, Cesena

Abstract The high incidence of recurrent tendon tears after repair of massive cuff lesions is prompting the research of materials aimed at mechanically or biologically reinforcing the tendon. Among the materials studied so far, the Extracellular Matrix (ECM) scaffolds of human origin have proved to be the safest and most efficient, but the current legislations on grafts and transplants preclude their use in Europe. In order to overcome this condition in 2006 we started a project on the production of an ECM scaffold of human origin which could be implanted in Europe too. In 2009 the clinical study began with the implantation of dermal matrix scaffolds in 7 middle-aged patients affected with wide/ massive cuff lesions and tendon degeneration. Out of 5 cases followed for at least 1 year in which the scaffold was employed as an augmentation device, there were 3 patients with complete healing, 1 partial re-tear and 1 total recurrence. The absence of adverse inflammatory or septic complications allows to continue this research line with a prospective controlled study in order to define which might the real advantages and correct indications offered by scaffold application.

Introduction The lesion of the rotator cuff is present in 40% of patients over the age of sixty, in a high percentage, the injury causes disability due to pain and functional limitation or because it demonstrates evolutionary causing a progressive loss of strength.1 Remarkable advances in the surgical technique of rotator cuff tears over the last 15 years offer nowadays the opportunity to effectively repair most of the lesions. Progress has either involved manufacturing suture anchors that now present higher pull-out strength and are treated with multiple reinforced sutures, as well as improvement in repair techniques.2-6 In particular margin convergence techniques, that allow to reduce the stress of the repair, better “suture grasping” techniques and double row or transosseous equivalent repair techniques, that permit to widen the contact surface between tendon and foot-print, allow to obtain suture repairs mechanically stronger than in the past.7 However there are still several conditions where limits of reparative surgery are evident. A high incidence of failure follows repair of wide/massive lesions, particularly when the lesion is old and the tendon shows degenerative changes.8 Failure can happen after a time (re-tear), but in many of

these cases it can be the effect of missed healing. The main factors that can cause a missed tendon-to-bone healing are mechanical (low strength of the tendon or of the suture, excessive tension on the repair) or biological (low quality and vitality of tendon and bone). Recently, in order to overcome the limits of traditional reparative surgery, techniques of regenerative medicine are under investigation; they are aimed at enhancing and directing the tissue repair with formation of a tendon tissue having histological and mechanical properties resembling those of the native tendon. Most of the research studies are focused on obtaining scaffolds able to provide an initial mechanical augmentation to the repaired cuff, absorbing part of the stresses and thereby protecting the suture. At the same time the scaffold should be, already in the initial phases, a ground for hosting cells colonization, leading to the formation of a tendon structure with the same histological, architectural and mechanical features of the native one, but with a higher thickness. Additional requisites for these scaffolds should be a full biocompatibility and tolerability, a complete resorption at the end of the healing process, high suture retention properties and being easily to handle and fit for arthroscopical application. The materials that have been studied and employed as augmentation devices can be divided into synthetic and biologic (Tab. 1). A. Synthetic scaffolds, as Mersilene meshes or Polytetrafluoroethylene patches, have been used for rotator cuff repair, but regardless of their excellent tensile strength9-10 they are not recommended due to the lack of biological properties, the possibility to obstacle the tissue tendon growth and the risk of foreign body reactions. In recent years the novelty among synthetic scaffolds has been the development of absorbable materials obtained through the electrospinning techniques (electrospinning). This method, through the processing of synthetic nanofibers, allows to create a three dimensional structure that mimics the normal orientation of collagen fibers;11 on these materials, so far only tested in vitro, can also be applied growth factors or stem cells. B. Biologic scaffolds can be classified into: B1) autologous tissues from fascia lata 12 or biceps tendon; 13-15 B2) homologous tissues from rotator cuff 16-17 or patellar tendon allografts, Achilles tendon allografts and quadriceps tendon allografts18 that were used to treat massive, irreparable rotator cuff tears have been associated with unsatisfactory or variable not reproducible results; B3) allografts or xenograft from extracellular matrices (ECM scaffolds) obtained through decellularization pro-

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Table. 1 Materials employed as augmentation devices for rotator cuff repair.

A. SYNTHETIC: Use regulated by FDA (USA) or CE (Europe)

Product Tissue type & Source

SportMesh Soft Tissue Reinforcement X-Repair

Poly (urethanaeurea) Poly-L-Lactide

Company Biomet Sports Medicine Synthasome

B. BIOLOGIC: 1) Autografts (Long Head fo the Biceps, Fascia Lata) 2) Allografts unprocessed tissues (Rotator cuff, Achilles, Cutis, Fascia Lata) 3) Allograft or Xenograft decellularized tissues (Small Intestinal Submucosa, Derma, Pericardium, Fascia Lata)

a) Xenografts Use regulated by FDA (USA) or CE (Europe) Product Tissue type & Source

Company



Restore CuffPatch Conexa TissueMend Permacol Bio-Blanket OrthADAPT bioimplant

Depuy Orthopaedics Biomet Tornier Stryker Orthopaedics Zimmer Kensey Nash Pegasus Biologics

SIS-Porcine SIS Porcine Dermis Porcine Fetal Dermis Bovine Dermis Porcine Dermis Bovine Pericardium Equine

b) Allograft Use regulated by National Transplantation Centers Product Tissue type & Source

Company



Wright Medical Technology Muskulosk. Foundation

Graft Jacket Allopatch

Human Dermis Human Fascia Lata

cesses. This group is nowadays the most extensively studied to obtain biologic scaffolds. The decellularization process based upon chemical or physical processes eliminates the cellular DNA containing the immunogenic components, but preserves unaltered the extracellular matrix with its threedimensional structure and its content in collagen fibres. The three-dimensional architecture, the presence of collageneous and not collageneous proteins and growth factors (GFs) are fundamental to create an adequate environment for cell adhesion, proliferation and differentiation. During the healing process the progressive degradation of the scaffold releases molecules that also play a role in determining the recruitment and proliferation of appropriate cell types during tissue remodeling. ECM scaffolds available on the market for surgical repair of cuff lesions can be divided into: B3.a) Xenografts – membranes deriving from animal dermis, intestine, pericardium B3.b) Allografts – membranes deriving from human dermis or fascia lata Scaffolds from animal origin (B.3a) meet the criteria dictated by FDA; the EU approve which approves their use as devices for reinforcement after tendon repair (augmentation), but not as devices to patch the rotator cuff hole (bridging).

In some cases this kind of scaffolds has proven to be immunogenic, so their use in cuff repair surgery is now discouraged (Fig. 1).19-23 Human-derived membranes (B.3b), like the human dermal matrix - Graft Jacket (GJA) or Allopatch, are classified as human tissues for transplantation and each Country has to follow National Regulatory Transplantation Center rules for the control of human-derived tissue transplants. Due to the differences between transplant laws between Europe and USA, commercial membranes derived from human tissue and produced in USA currently cannot be implanted all over Europe. In 2005, before Italian and European laws forbid its use, we obtained good results in some patients treated with GJA (unpublished data). Confirmations on the effectiveness of acellular human dermal matrix come from several researches. A study performed at our Istitute confirms that GJA presents suitable biological properties for in situ tissue engineering and in vitro bioengineering of rotator cuff tendons24 and has been shown to increase the mechanical strength of the repair.25 In two different animal studies where GJA was used to bridge large full thickness tendon tears, Adams and Ide noted the histological evidence of native cell infiltration and neotendon development already at 6 weeks; moreover in few months after surgery histological incorporation of the acellular dermal matrix graft into a structure resembling

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A

B Figure 1. MRI image DP Fat Sat, coronal oblique, sagittal and axial. Patient of 28 aa with important inflammatory arthrosynovitis 6 months after implantation of a scaffold equine that required a re-operation for removal of the membrane in arthroscopy and joint lavage.

normal tendon was evident.26-27 Even if no one is a casecontrol study, in all clinical studies published so far GJA showed good results either if used asaugmentation28, or as bridging29-31 device. Snyder led in 2010 a clinical study of 45 patients with massive and irreparable rotator cuff tear treated with arthroscopic implantation of Graft Jacket used as bridging, resulting in more than two years of follow-up significant clinical improvement in the absence of inflammatory reactions and discards.31 In one of his histological study on a biopsy specimen taken from a rotator cuff augmented 3 months earlier with GJA scaffold, incorporation and remodelling was demonstrated, with alignment of collagen fibers, presence of revascularization signs, repopulation with host cells and little or no inflammatory response.32

Methods and Materials The need to have a decellularized bioactive collagenic membrane available in our clinical practice for the treatment of large/massive rotator cuff lesions with high risk of retear induced us in 2006 to organize a multidisciplinary group aimed at its production. This led to a cooperation between the Rizzoli Orthopedic Institute in Bologna and the Cutis Bank of the Burns Unit of the Bufalini Hospital in Cesena. From 2008 this activity is included in the Research Program Regione Emilia Romagna-University 2008-2011: “Regenerative Medicine in Osteoarticular Disease”.33 The study included 4 steps: 1) Development of a proprietary decellularization technique of dermis coming from multiorgan and multitissue donors. Such technique is protected by an international patent of AUSL Cesena and Rizzoli Orthopedic Institute and allows to produce an Acellular Human Dermal Matrix (AHDM) that fits the indications of the Italian and European laws about grafts and transplants.

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C

2) Evaluation of the biologic properties and features of the membrane:24, 35 - the product was analyzed with optic and electronic microscopy techniques to confirm the conservation of the tridimensional collagenic structure which is necessary for tendon tissue regeneration - optic and electronic microscopy techniques as well as biochemical tests were employed to rule out the persistence of residual vital cells, an important aspect to avoid possible immunological reactions - the anabolic activity of tenocytes grown on the AHDM was investigated through the analysis of Cell Proliferation (WST-1), the ECM production tissue, Collagen I (CICP), Proteoglycans (PG), Fibronectin (FBN), and Transforming Growth Factor β1 (TGFß1), Interleukin 6 (IL-6) evaluation. From a comparison between AHDM and control cultures a significant higher amount of collagen I, fibronectin, proteoglycans, and TGFβ1 was observed in AHDM cultures.34 3) Evaluation of adequate mechanical properties: - through traction test (Sintech-1/M, MTS Adamel Lhomargy, Ivry sur Seine, France) both the direct resistance and the resistance between suture stitch and AHDM were tested (Fig. 2). A comparison with some other commercially available membranes showed that AHDM had a failure mode similar to other membranes as described in literature and has superposable mechanical properties. 4) Evaluation of the membrane histocompatibility by implantation of membrane samples in rats subcutis. No inflammatory reaction was observed. After obtaining these laboratory results and with the approval of the Hospital Ethical Committee, in 2009 we started the clinical application of the AHDM in a selected group of patients. The study was aimed at reporting the preliminary results of our experience with AHDM membrane implanted as augmentation in a subset of rotator cuff lesions having a high recurrence risk. This group consisted of middle-aged high-demand patients affected with large/massive and old postero-superior cuff lesions. Patients were controlled both clinically and with imaging techniques to evaluate safety, excluding adverse reaction of inflammatory or septic nature,

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Figure 2. Mechanical Test of tensile strength between suture and membrane AHDM (Instron machine).

and efficacy of the membrane.36 Between March 2009 and December 2010 in our Shoulder and Elbow Unit about 400 surgical procedures of cuff repair have been performed. In 7 patients with specific clinical and imagine characteristics we employed the AHDM, as an augmentation in 6 cases and as a bridging device in 1 case with the cuff proved to be irreparable. One of the 6 augmentation cases was excluded due to insufficient follow-up. The remaining 5 cases satisfied the following pre-operative selection criteria. Inclusion criteria: - healthy subjects with high functional requests - age below 55, affected with large to massive lesion according to Gerber involving supraspinatus and infraspinatus tendons, tendon retraction ≤ 3 according to Thomazeau and fatty degeneration ≤ 3 according to Goutallier, with possibility at surgery to obtain tendon reduction. - Follow-up 1 year or more Exclusion criteria: - arthritic degeneration even mild according to Samilson - frozen shoulder - symptomatic acromioclavicular arthritis - inability to cope with an adequate post-operative rehabilitation regimen - autoimmune connective tissue disease - allergy for penicillin and pork meat The patients had the same preoperative workout and the same postoperative regimen that we use for normal cuff repair surgery. Preoperative study included standard clinical examination, x-ray and MRI. Anaesthesia consisted of interscalenic block and intraoperative sedation. Antibiotic prophylaxis was done with single shot cefazolin administration.

Figure 3a, 3b. Implantationof AHDM in open surgery after rotator cuff repair

A

AHDM harvesting, processing and distribution was performed according to national rules on tissues for transplantation. Then sample of human dermis 1.5-mm thick was first taken from multi-organ and/or multi-tissue donors and then transported to the Skin Bank of Bufalini Hospital, CesenaItaly for processing; here the tissues were processed to dermis separation from epidermidis, decellularization and storage in nitrogen vapors at -180 °C. Twenty-four hours before surgical implantation a sample of tissue of requested sizes was prepared, and then sent in a sterile condition from Skin Bank of Bufalini Hospital to our Hospital, and here conserved at a temperature of 4° C until its use.

Surgical technique The tendon repair and scaffold implantation was performed with an open technique in 3 cases and with arthroscopic technique in 2 cases. In all cases Peek (Poly-Eter-Eter-Keton) anchors were employed, to allow better MRI visualization at follow-up controls. The anchors were in 3 cases a 5.5 mm Healix anchor [DePuy Mitek, Raynham, MA] loaded with 3 Orthocord sutures and in 2 case a 4.5 mm CrossFT anchor [ConMed Linvatec, Largo, FL] loaded with 3 Hi-Fi sutures. The surgical technique was the same for open and arthroscopic repair (Fig. 3a, 3b), with two of the three anchor sutures

B

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Results and complications

Figure 4. Arthroscopic surgical technique: the scaffold is sutured with STIK (Short-Tailed Knotted Interference), nodes for the transport of the membrane within the shoulder.

used for the rotator cuff repair and the other suture used to fix laterally the scaffold. Additional stitches were used to fix the scaffold to the cuff medially, as well as anteriorly and posteriorly. In arthroscopy for the transport of the scaffold within the shoulder was used the Snyder’s technique (Fig. 4).31 The patients wore an abduction pillow sling for 30 days and then started gentle rehabilitation, with standard rehabilitation protocol for the repairs of the rotator cuff. Patients were seen at follow up at 1, 3, 6 and 12 months. Clinical evaluation was done by the Constant-Murley scoring system. A control MRI was performed at about 12 months after surgery in all cases.

All 5 patients were male with mean age 48 years old (range from 37 to 55). At the latest follow up of at least 1 year all the patients showed symptoms improvement after surgery. The average Constant score raised from 64 pts (range 55-75) in the preoperative evaluation to 87 pts (range 77-95) postoperatively, with an average increase of 23 pts (range 20-30). None of the 5 patients treated with AHDM showed adverse inflammatory or septic reactions. Between 3 and 5 months all the patients, in spite of prudential recommendations, took on again full heavy work or sport activity. On the basis of MRI study and clinical evaluation in 3 cases it was possible to assist to a tendon repair integrity (Fig. 5a, 5b), with patients showing excellent shoulder function with also strength recovery; 1 patient, agonist yachtsman, felt a tear sensation during a sailing competition at 4 months postoperatively, with shoulder ache for 2 weeks. In the MRI at 1 year it is possible to observe a partial lesion with MRI images showing substantial scaffold integrity and presence of re-tear of the tendon cuff (Fig. 6a, 6b). In one case, without any history of trauma postoperatively, a complete re-tear was present; this case was the only one with pre-operative Goutallier stage 3 muscle-fatty degeneration. The patients data are summarized in Table 2.

Conclusions The research on materials capable of increasing the biological and mechanical response of the tendon after the repair is in continuous development. Indeed, the repair of lesions of the rotator cuff is often a challenge both mechanical and biological healing. It is increasingly clear that a thinned and

Table 2. Patients treated data Patient

Age

Shoulder trauma

Preop Test

Pre-oper MRI

Surgery

Activity resumption

F.U.

SCORE Preop to postop

Postop MRI

Opposite shoulder

R.S.

37

2005

Jobe + Patte +

T 2/3 G1

Open repair, large lesion, thin tendon, LHB tenodesis, 1 anchor

4 months

18 months

75 à 95

Repair integrity, scaffold incorporation

Tendinopathy

Jobe + Patte +

T3 G3

Scope repair, massive lesion, sub-optimal tendon repairability: 2 anchors, LHB ok and untreated

4 months

13

55 à 77

Complete rerupture

Partilal lesion

T 2/3 G1

Scope repair, massive lesion, complete reducibility: 2 anchors, LHB tenotomy

5 months

13

66 à 90

Repair integrity, scaffold incorporation

Partial lesion

5 months

12

55à85 ERLS – Jobe e Patte +

Repair integrity, scaffold incorporation

Tendinopathy

3 months (trauma at 4th month)

12

70 à 95

Partial tendon rerupture, graft incorporation

Partial lesion

B.R.

R.C.

50

2008

55

2005

Patte +

F.G.

54

No trauma reported

Jobe + Patte +, ERLS +

T3 G2

Open repair, large lesion, degenerative tendon, complete reducibility, 1 anchor LHB tenotomy

M.V.

48

2008

Jobe +

T2G 2 LHB spontaneous tenotomy

Open repair, large lesion, degenerative tendon, complete reducibility, 1 anchor

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A

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B Figure 5a. 3 months follow up Magnetic Resonance paracoronal image, T2-weighted Fast Spin-Echo Fat Suppression: integrity of the repair with integration between tendon and scaffold;

degenerated tendon cannot heal even if is performed a technically correct repair and mechanically valid. If the failure in elderly patients can be tolerated, in young patients with high functional demands the problem remains open. In the past 15 years have been studied and tested various materials to improve healing of the tendon repaired by moving gradually attempts to stimulate a biological response of host tissues. The ideal scaffold for rotator cuff repair should comply with the following ten characteristics: - Biologically active - Biocompatible - Absorbable - No risk of disease transmission - Mechanically resistant to traction - High resistance to seal the suture - Available in different sizes (size and thickness) - Easy to handle both in arthroscopic surgery and in open surgery - Can be used as augmentation that as bridging - ready available in the operating room Among the various materials studied, the human-derived dermal matrices (AHDM) now appear to be able to get closer to the ideal characteristics of the scaffold while the scaffold of animal origin and the scaffolds of synthetic origin produced disappointing results due to frequent tissue reaction events. Preclinical studies on the AHDM confirmed excellent biologic characteristics as scaffolds, mechanical tests confirmed good mechanical strength and suture retention quali-

Figure 5b. 1 year follow up Magnetic Resonance paracoronal image, T2-weighted Fast Spin-Echo Fat Suppression: Integrity of the repair.

ty, animal studies showed excellent tolerability. MRI studies showed the reabsorption of the material with an incorporation with the native tendon. Differently from animal scaffold, the human one can be also used for bridging, if needed. Even if the possibilities to transmit infectious diseases is extremely low, either for the strict control of the human donors and for the physical and chemical treatments of processation and conservation, a blood control after 6 months from operation is mandatory to rule out infectious diseases, like B or C hepatitis or HIV infection. All the analyses conducted on the patients treated until now gave negative response. At the moment the AHDM is available in different sizes, but not in different thicknesses. Another negative aspect is that AHDM needs to be prepared 24 hours before surgery, and this aspect can condition and limit the use of that scaffold. The use of scaffolds with feature augmentation is in our opinion indicated in the young patient (under age 55) who has a lesion of the rotator cuff large or massive but repairable (negative hornblower’s signs), with high functional demands and poor quality of the tendon, in this group of patients alternative “replacement” surgeries like tendon transfers or shoulder prosthesis have no indication; in our experience we have observed that a case with muscle atrophy of the supraspinatus Goutallier 3° prematurely failed and is currently considering candidates for this surgery only patients with fatty degeneration with Goutallier 65/70 ys

Partial

Conservative treatment*

Conservative treatment *

Conservative treatment *

Small

Repair

Large/massive

Repair Augmentation° Margin convergence

Irreparable

Tendon transposition Bridging

Conservative treatment * Repair Repair

Margin convergence Bridging

* at least for a period non less than 6 months ° chronic lesion, degenerative and thin tendon, hypotrophic muscle, Goutallier < 3

Conservative treatment * Conservative treatment * Repair Conservative treatment * Reverse arthroplasty if arthropathy

Archivio di Ortopedia e Reumatologia

pear to be the most useful; anchor made ​​of PEEK compared to titanium allow you to see better the MRI healing signs of the repaired tendon and the incorporation of the scaffold. Only through close cooperation between research and surgery will be possible to produce a scaffold well tolerated able to promote tendon healing. Multicentre randomized controlled studies will clarify the many questions still open about the type of scaffold to be used, indications and the surgical technique of application.

BIBLIOGRAPHY 1. K.A. Derwin, S.F. Badylak, S.P. Steinmann, J. P. Iannotti. Extracellular matrix scaffold devices for rotator cuff repair. J Shoulder Elbow Surg 2010; 19:467-476 2. Burkhart SS, Athanasiou KA, Wirth MA. Margin convergence: a method of reducing strain in massive rotator cuff tears. Arthroscopy 1996; 12:335-338 3. Baleani M, Schrader S, Veronesi CA, Rotini R, Giardino R, Toni A. Surgical repair of the rotator cuff: a biomechanical evaluation of different tendon grasping and bone suture fixation techniques. Clin Biomech 2003; 18:721-729 4. Ma CB, MacGillivray JD, Clabeaux J, Lee S, Otis JC. Biomechanical evaluation of arthroscopic rotator cuff stitches. J Bone Joint Surg Am 2004; 86:1211-1216 5. Bungaro P, Rotini R, Traina F, Baleani M, Antonioli D, Fini M, Castagna A. Comparative and experimental study on different tendinous grasping techniques in rotator cuff repair: a new reinforced stitch. Chir Organi Mov 2005; 90:113-119 6. Baleani M, Ohman C, Guandalini L, Rotini R, Giavaresi G, Traina F, Viceconti M. Comparative study of different tendon grasping techniques for arthroscopic repair of the rotator cuff. Clin Biomech 2006; 21:799-803 7. Lo IK, Burkhart SS. Double-row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy 2003; 19:1035-42 8. Matthews, T.J.W. et al. Pathology of the torn rotator cuff tendon: reduction in potential for repair as tear size increases. J Bone Joint Surg Br. 2006; 88:489-95 9. Audenaert E, Van Nuffel J, Schepens A, Verhelst M, Verdonk R. Reconstruction of massive rotator cuff lesions with a synthetic interposition graft: a prospective study of 41 patients. Knee Surg Sports Traumatol Arthrosc 2006; 14:360-364 10. Hirooka A, Yoneda M, Wakaitani S, Isaka Y, Hayashida K, Fukushima S, Okamura K. Augmentation with a Gore-Tex patch for repair of large rotator cuff tears that cannot be sutured. J Orthop Sci 2002; 7:451-456 11. Hakimi O, Mouthuy P-A, Carr. A Synthetic and degradable patches: An emergingsolution for rotator cuff repair. Int J Exp Pathol 2013; 4:287-292 12. Heikel HV. Rupture of the rotator cuff of the shoulder. experiences of surgical treatment. Acta Orthop Scand 1968; 39:477-492 13. Neviaser JS. Ruptures of the rotator cuff of the shoulder. new concepts in the diagnosis and operative treatment of chronic ruptures. Arch Surg 1971; 102:483-485 14. Rhee YG, Cho NS, Lim CT, Yi JW, Vishvanathan T. Bridging the gap in immobile massive rotator cuff tears: augmentation using the tenotomized biceps. Am J Sports Med 2008; 36:1511-1518 15. Cho NS, Yi JW, Rhee YG. Arthroscopic biceps augmentation for avoiding undue tension in repair of massive rotator cuff tears. Arthroscopy 2009; 25:183-191 16. Neviaser JS, Neviaser RJ, Neviaser TJ. The repair of chronic massive ruptures of the rotator cuff of the shoulder by use of a freezedried rotator cuff. J Bone Joint Surg Am 1978; 60:681-684 17. Nasca RJ. The use of freeze-dried allografts in the manage-

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ment of global rotator cuff tears. Clin Orthop Relat Res 1988; (228):218-226 18. Moore DR, Cain EL, Schwartz ML, Clancy WG Jr. Allograft reconstruction for massive, irreparable rotator cuff tears. Am J Sports Med 2006; 34:392-396 19. Sclamberg SG, Tibone JE, Itamura JM, Kasraeian S.Sixmonth magnetic resonance imaging follow-up of large and massive rotator cuff repairs reinforced with porcine small intestinal submucosa. J Shoulder Elbow Surg 2004; 13:538-541 20. Iannotti JP, Codsi MJ, Kwon YW, Derwin K, Ciccone J, Brems JJ. Porcine small intestine submucosa augmentation of surgical repair of chronic two-tendon rotator cuff tears. a randomized, controlled trial. J Bone Joint Surg Am 2006; 88:1238-1244 21. Malcarney HL, Bonar F, Murrell GA. Early inflammatory reaction after rotator cuff repair with a porcine small intestine submucosal implant: a report of 4 cases. Am J Sports Med 2005; 33:907-911 22. Zheng MH, Chen J, Kirilak Y, Willers C, Xu J, Wood D. Porcine small intestine submucosa (SIS) is not an acellular collagenous matrix and contains porcine DNA: possible implications in human implantation. J Biomed Mater Res B Appl Biomater 2005; 73:61-67 23. Gilbert TW, Freund JM, Badylak SF. Quantification of DNA in biologic scaffold materials. J Surg Res 2009; 152:135-139 24. Fini M, Torricelli P, Giavaresi G, Rotini R, Castagna A, Giardino R. In vitro study comparing two collageneous membranes in view of their clinical application for rotator cuff tendon regeneration. J Orthop Res 2007; 25:98-107 25. Barber FA, Herbert MA, Boothby. Ultimate tensile failure loads of a human dermal allograft rotator cuff augmentation. Arthroscopy 2008; 24:20-24 26. Adams JE, Zobitz ME, Reach JS Jr, An KN, Steinmann SP. Rotator cuff repair using an acellular dermal matrix graft: an in vivo study in a canine model. Arthroscopy 2006; 22:700-709 27. Ide J, Kikukawa K, Hirose J, Iyama K, Sakamoto H, Mizuta H. Reconstruction of large rotator-cuff tears with acellular dermal matrix grafts in rats. J Shoulder Elbow Surg 2009; 18:288-295 28. Burkhead W, Schiffern S, Krishnan S. Use of graft jacket as an augmentation for massive rotator cuff tears. SeminArthro 2007; 18:11-18 29. Dopirak R, Bond J, Snyder S. Arthroscopic total rotator cuff replacement with an acellular human dermal allograft matrix. Int J shoulder Surg 1:7-15 S22 Musculoskelet Surg 2011; 95:S13-S23 30. Bond JL, Dopirak RM, Higgins J, Burns J, Snyder SJ. Arthroscopic replacement of massive, irreparable rotator cuff tears using a GraftJacket allograft: technique and preliminary results. Arthroscopy 2008; 24:403-409 31. Wong I, Burns J, Snyder S. Arthroscopic GraftJacket repair of rotator cuff tears. J Shoulder Elbow Surg 2010; 19:104-109 32. Snyder SJ, Arnoczky SP, Bond JL, Dopirak R. Histologic evaluation of a biopsy specimen obtained 3 months after rotator cuff augmentation with GraftJacket matrix. Arthroscopy 2009; 25:329-333 33. Rotini R, Fini M, Giavaresi G, Marinelli A, Guerra E, AntonioliD, Castagna A, Giardino R. New perspectives in rotator cuff tendon regeneration: review of tissue engineered therapies. Chir Organi Mov 2008; 91:87-92 34. Bondioli E, Fini M, Veronesi F, Giavaresi G, Tschon M, Cenacchi G, Cerasoli S, Giardino R, Melandri D. Development and evaluation of a decellularized membrane from human dermis. J Tissue Eng Regen Med 2012; 8:325-36 35. Fini M, Bondioli E, Castagna A, Torricelli P, Giavaresi G, Rotini R, Marinelli A, Guerra E, Orlandi C, Carboni A, Aiti A, Benedettini E, Giardino R, Melandri D: Decellularized human dermis to treat massive rotator cufftears: in vitro evaluations. Connect Tissue Res 2012; 53:298-306 36. R. Rotini, A. Marinelli, E, Guerra, G. Bettelli, A. Castagna, M. Fini, E. Bondioli, M. Busacca. Human dermal matrix scaffold augmentation for large and massive rotator cuff repairs:  preliminary clinical and mri results at 1-year follow-up. Musculoskelet Surg 2011; 95:13-23

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Rational approach to the irreparable cuff tears from “functional” repair to muscle transfer Fabrizio Campi, Paolo Paladini, Carlo Buononato, Antonio Tartarone, Giovanni Merolla, Giuseppe Porcellini Shoulder and Elbow Unit - Cervesi Hospital - Cattolica, Rimini

Introduction The rotator cuff tears are very frequent diseases affecting 20.7% of the population, but few patients are symptomatic. Lesions are more frequent in elderly subjects (especially after 60 age), male, heavy workers and the dominant limb is most often affected 1. Rotator cuff tears are often the result of a chronic lesion, associated with myotendinous retraction, loss of elasticity, muscle fatty infiltration, superior subluxation of the humeral head and, ultimately, osteoarthritis. Acute trauma is a less frequent cause 2,3,4. A universally accepted definition of massive irreparable injury to the rotator cuff does not exist. Cofield and Rockwood et al. defined irreparable a massive tear (>5 cm) that cannot be repaired for size or retraction 3, 5. Gerber classificates as irreparable a tear that cannot be reduced without excessive tension with shoulder abducted to 60°, in a cuff with a massive lesion (> 5 cm or with two tendons completely broken) 6. The treatment of these lesions is extremely pleomorphic, ranging from conservative treatment to arthroscopic debridement with biceps tenotomy, partial suture, tendon transfer or reverse arthroplasty 4, 7, 8, 9, 10, 11, 12, 13, 14.

IRREPARABILITY CRITERIA There is no precise algorithm for the treatment of irreparable rotator cuff tears (RCTs). Surgical treatment should always be suggested in symptomatic patients, even if a complete repair is not possible 15, 16. However, there are clinical and imaging predictors:

Clinical criteria: in anterosuperior chronic tear with anterosuperior subluxation of the humeral head, head under the skin and pseudoparalytic arm flexion the tear cannot be repaired. In posterosuperior chronic tears the inability to flex the shoulder is a irreparability sign, it is often not associated with pain and in this lesions if the arm is abducted passively to about 90 degrees, the patient should not be able to maintain the arm in the abducted position. A true dropping sign indicates fatty infiltration of Goutallier 17 stage 2 and cannot be repaired. Imaging criteria: a simple anteroposterior X-Ray in neutral rotation may show a acromionhumeral gap less than 7 mm, indicative of a irreparable RCTs. The gold standards to assess tendon lesions and muscle fatty infiltration are the CT and, especially, the MRI 18. A grade 3 or greater indicates irreparable tear of the tendon involved. Finally, another important factor is the time elapsed between injury and observation because affect the tissue quality.

Criteria for functional demands: a RCT may not cause disability when the limb rests on the side. The problem arises when the patient tries to move the limb in space. So many patients, informed of the possible benefits and risks, with poor functional life activities decide to avoid surgery.

THE FUNCTIONAL REPAIR The glenohumeral joint is particularly unstable so rotator cuff represents an essential stabilizer, especially in the mid range of movement. There is a continuous balance between agonist and antagonist muscles (like between the infraspinatus / teres minor complex and subscapularis), because an important role of the entire cuff is to center the humeral head in the glenoid during deltoid contraction to give the right fulcrum. On the basis of these notions, Stephen Burkhart dictated five criteria which must have a functional rotator cuff 19: 1. Force couples must be intact in the coronal and transverse planes. 2. A stable-fulcrum kinematic pattern must exist. 3. The shoulder’s “suspension bridge” must be intact. 4. The tear must occur through a minimal surface area. 5. The tear must possess edge stability. Based on these insights, Burkhart developed the idea of “suspension bridge” in order to balance the force couple without repair the entire rotator cuff, thus providing an anatomically deficient but biomechanically intact shoulder. The surgical treatment of large or massive RCTs can be technically difficult, and the results are less reliable20,21,22,23. The size of the tendon tear and fatty infiltration of the muscles are strictly correlated to clinical outcomes. In particular, arthroscopic repair of large and massive RCTs can lead to excellent pain relief and improvement in the ability to perform daily life activities at short-term follow-up, despite the high rate of recurrent defects; however, at a minimum follow-up of 2 years, the clinical results seems to deteriorate. Although many RCTs and the majority of massive RCTs can be completely repaired to bone, a significant part of these cannot be sutured by these traditional techniques for the size of tendon tear and the tendon retraction. Numerous operative techniques have been described for the treatment of massive RCTs with severe retraction when anatomic repair is impossible, such as arthroscopic debridement and/or biceps tenotomy, tendon transfers and grafting, partial repair of the remaining rotator cuff ten-

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dons. Burkhart et al first introduced the concept of “functional repair” of the cuff to restore the force couple of the humeral head and to increase the acromion-humeral distance (AHD). In these arthroscopic procedures, complete cuff repair was not considered essential to restore the normal biomechanics. The technique allows the repair of the peripheral margins of the tear to restore the force couples, anterior and posterior, and the ‘‘suspension bridge’’ system of force transmission in the shoulder. Outcomes are obviously inferior than in complete rotator cuff repair but remain stable for AHD in medium-term follow-up. Previous authors have introduced the radiographic evaluation of the AHD as a standard exam before orthopaedic treatment. A decreased AHD is the most reliable radiographic finding for RCTs; an AHD of less than 6 mm has been considered proof of an RCT and narrowing of the AHD is strictly related to the size of the cuff tear. We wrote a study to evaluate clinical results and radiologic changes of AHD in patients treated with arthroscopic partial suture of irreparable tears of the supraspinatus tendon at long-term follow-up (5 years) 24, 25. Our initial hypothesis was that arthroscopic partial suture of the cuff leads to pain relief and functional improvement for patients with restoration of the AHD. In our case-series study, 153 consecutive patients with irreparable RCTs were arthroscopically treated with partial repair from January 2000 to March 2004. All patients had a symptomatic shoulder treated conservatively at least for 6 months, 51 with poor results. Of the patients, 72 (47%) had a posterior-superior lesion involving supraspinatus and infraspinatus tendons and 38 (25%) had an anterior- superior lesion involving supraspinatus and subscapularis tendons, whereas 43 (28%) had a global lesion involving infraspinatus, supraspinatus, and subscapularis tendons. We considered only patients affected by posterior-superior cuff lesion with grade I or II fatty degeneration of the infraspinatus and grade III or IV fatty degeneration of the supraspinatus (72 patients). None of these patients had a Hornblower sign, drop-arm sign, or pseudo-paralysis of the shoulder. The teres minor was intact in all cases. Exclusion criteria were: • Age older than 70 years • Fatty degeneration of the infraspinatus of grade III or IV • Fatty degeneration of supraspinatus of grade 0 or I • All subscapularis tears • Previous surgery • Nerve palsy • Cuff tear arthropathy (CTA) and arthritis of grade II or more following the Samilson-Prieto classification • Inflammatory arthropathy and diabetes or hypercholesterolemia This study indicates that, in cases of massive RCT with no subscapularis tear, long-term results of partial repair of the posterior cuff with covering of the infraspinatus footprint showed improved outcome scores. In addition, AHD increased minimally and was stable at final follow-up. These results were superior to those of a simple arthroscopic debridement in active patients. The target patient for partial

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Figure 1

repair of the cuff has good balancing of the cuff without signs of complete disruption of the posterior cuff, with no drop-arm or Hornblower sign, and with good function of the subscapularis.

PECTORALIS MINOR TRANSFER When an irreparable anterior-superior RCTs occours, a transfer of the pectoralis minor should be indicated to replace the function of the subscapularis tendon and to restore the anterior functional sling (Fig. 1). The subscapularis muscle is the largest and most powerful of the rotator cuff providing alone about 50% of the rotator cuff strength and it is important for the elevation of the limb. The rupture of the subscapularis tendon may also cause an imbalance on the forces couple acting on the shoulder, causing pain and disability. The lesions of the subscapularis tendon are uncommon, representing in agreement with the literature 5% of all lesions of the rotator cuff. Subscapularis injuries usually occur more frequently in association with other lesions of the rotator cuff, rarely are isolated 26. The reparability of rotator cuff lesion is influenced by tendon retraction, atrophy muscle and fatty infiltration. Lafosse classification has an important prognostic value too, some lesions allow an open or arthroscopic repair with good results that are maintained over time. In addition, the subscapularis tendon repair appears to reduce the stress on a supraspinatus tendon repaired, protecting it, in anterior superior rotator cuff lesions. The irreparable injury represents a difficult problem to treat, an option is represented by muscle transfer. One of the historical options was the transfer of the acromial portion of the trapezius. Recent experiences have shown that the transfer of the pectoralis major appears to be the most reliable option in the treatment of irreparable subscapularis lesions. The transfer of the pectoralis major and pectoralis minor muscles have been described for the first time by Wirth and Rockwood in 1997 27, in a study with 13 patients suffering for recurrent anterior dislocation of the shoulder associated with an irreparable subscapularis tear. Of the 13 cases, 7 were treated with pectoralis major transfer, 5 with pectoralis minor transfer and 1 of both. The result to 5 years

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toralis minor transfer would improve short-term functional outcomes in patients with lesions of the upper portion of the subscapularis tendon 30. The objectives of this study were therefore to explore the following: 1. The anatomic feasibility to use the pectoralis minor tendon as a graft to repair lesions of the upper portion of the subscapularis tendon, given the elongation that the muscle must withstand and the length of the neurovascular pedicle.

Figure 2

of follow-up was good in 10 patients and poor in 3 cases. In the work of Wirth and Rockwood the pectoralis minor was transferred with coracoacromial ligament, before disconnected from its acromial insertion, to compensate the poor length of tendon. Several authors have used the transfer of the pectoralis major for the treatment of irreparable lesions of the subscapularis. Jost et. al in 2003 28 reported the results of the transfer of the pectoralis major performed in 28 patients for a total of 30 shoulders treated with a mean follow-up of 32 months. The results showed an increase of the CS from 47% preoperatively to 70% postoperatively with statistically significant increases for pain, anterior elevation and strength in abduction. In addition the Constant score value, in patients whit an irreparable injury of the supraspinatus tendon, was minor compared to those with supraspinatus repairable lesions with value respectively of 49 % and 79%. The pre-operative lift-off test was positive in all 30 shoulders and continues to be positive in 23 postoperatively. Resch et al29 reported their experience in the treatment of irreparable lesions of the subscapularis using pectoralis major transfer with a modified surgical technique: passing the 2/3 upper tendon of the pectoralis major posted below the conjoined tendon to recreate the ubscapularis anatomy. Results showed a statistically significant improvement in terms of pain (mean 1.7 and 9.6, respectively, pre-and post-operative), with an improvement in functional score of 43 points (23 pre- post). Moreover, no nerve injury was reported as complication. We decided to investigate whether open pec-

Figure 3

2. The safety of the procedure in relation to the proximity of the brachial plexus and the musculocutaneous nerve. 3. The scope of this technique in improving the function of the (healthy) lower portion of the subscapularis tendon. After careful debridement of the subscapularis footprint and of the interval between the coracoid and the humeral head, the pectoralis minor tendon was detached from the coracoid with a bone fragment (Fig. 2) to foster the healing process and avoid muscle wasting. Two stay sutures placed over the osteotomy were used to drag the pectoralis minor tendon, which usually reaches the lesser tuberosity without excessive tension, under the coracoid. The pectoralis minor was then carefully released, the musculocutaneous nerve was identified and protected, and the tendon was finally sutured in areas 2 and 3 described by Arai et al 31, 32 (Fig. 3). Preoperative functional status was evaluated in relation to a number of outcome measures that included active ROM as part of the Constant score, total Constant score, Simple Shoulder Test (SST) score, liftoff test, and belly-press test. There were no cases of musculocutaneous nerve or brachial plexus injury or graft failure. Active forward flexion improved from 127° to 177°; external rotation with the arm on the side declined by 11°. The Simple Shoulder Test score improved by 5 points and the Constant score by 41 points, although the strength subscore did not rise significantly. This study showed that it is anatomically feasible to use the pectoralis minor tendon as a graft to treat upper subscapularis lesions; the procedure is safe for brachial plexus and musculocutaneous nerve injury; and pectoralis minor transfer can improve shoulder function and provide pain relief in patients with Lafosse grade III subscapularis tears, likely through a tenodesis effect, even in the the presence of irreparable supraspinatus tears.

LATISSIMUS DORSI TRANSFER Massive and irreparable postero-superior cuff tears actually represent a difficult problem for treatment. Combined latissimus dorsi transfer and teres major transfer were used by L’Episcopo in 1934 to regain external rotation in obstetric plexus paralysis 33. Gerber in 1988 34 was the first to use latissimus transfer to treat massive and irreparable posterosuperior cuff tears in active patients with pain, weakness or loss of overhead elevation, with an external rotation lag sign and with integrity of subscapularis tendon. In the original tecnique patient was in beach-chair position, through two incisions and the anchoring point of the tendon was there

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by the tip of great tuberosity. The results in patients undergone to latissimus dorsi tranfer show an improvement in the shoulder function, range of motion, strenght and pain relief. Subscapularis muscle insufficiency, advanced teres minor muscle atrophy and need for revision surgery were correlated with poor functional outcomes in some studies35, 36. A more complete discussion of the topic will be developed in another section of this text.

CONCLUSION To determine the best treatment for each individual, adequate radiologic images and a careful examination of an experienced shoulder surgeon are required. Treatment options and the results depend on many factors, not least the rehabilitation team. Despite all the previous options, massive irreparable rotator cuff tears are difficult to manage, treat effectively and with a limited goal.

REFERENCES 1. Iannotti JP. Full-thickness rotator cuff tears: factors affecting surgical outcome. J Am Acad Orthop Surg 1994; 2:87-95 2. Mellio AS, Savoie FH, Field LD. Massive rotator cuff tears: debridement versus repair. Orthop Clin North Am 1997; 28: 117 24 3. Rockwood CA Jr, Williams GR Jr, Burkhead WZ. Debridement of degenerative irreparable lesions of the rotator cuff. J Bone Joint Surg Am 1995; 77:857-66 4. Walch G, Edwards TB, Boulahia A, Nové-Josserand L, Neyton L, Szabo I. Arthroscopic tenotomy of the long head of the biceps in the treatment of rotator cuff tears: clinical and radiographic results of 307 cases. J Shoulder Elbow Surg. 2005; 14:238-46 5. Cofield RH.: Current concepts review: rotator cuff disease of the shoulder. J Bone Joint Surg Am 1985; 67:974-9 6. Gerber C, Fuchs B, Hodler J. The results of repair of massive tears of the rotator cuff. J Bone Joint Surg Am 2000; 82:505-15 7. Warner JJ. Management of massive irreparable rotator cuff tears: the role of tendon transfer. Instr Course Lect 2001; 50:63-71 8. Lo IK, Burkhart SS. Arthroscopic repair of massive, contracted, immobile rotator cuff tears using single and double interval slides: technique and preliminary results. Arthroscopy. 2004; 20:22-33 9. Liem D, Lengers N, Dedy N, Poetzl W, Steinbeck J, Marquardt B. Arthroscopic debridement of massive irreparable rotator cuff tears. Arthroscopy. 2008; 24:743-8 10. Klinger HM, Steckel H, Ernstberger T, Baums MH. Arthroscopic debridement of massive rotator cuff tears: negative prognostic factors. Arch Orthop Trauma Surg. 2005; 125:261-6 11. Klinger HM, Spahn G, Baums MH, Steckel H. Arthroscopic deb ridement of irreparable massive rotator cuff tears - a comparison of debridement alone and combined procedure with biceps tenotomy. Acta Chir Belg. 2005; 105:297-301 12. Boileau P, Baqué F, Valerio L, Ahrens P, Chuinard C, Trojani C. Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am. 2007; 89:747-57 13. Bond JL, Dopirak RM, Higgins J, Burns J, Snyder SJ. Arthroscopic replacement of massive, irreparable rotator cuff tears using a GraftJacket allograft: technique and preliminary results. Arthroscopy. 2008; 24:403-409. e1 14. Cordasco F, Bigliani L. Large and massive tears: technique of open repair. Orthop Clin North Am 1997; 28:179-93 15. Burkhart SS, Nottage WM, Ogilvie-Harris DJ, Kohn HS, Pachelli A.

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Partial repair of irreparable rotator cuff tears. Arthroscopy 1994; 10:363-70 16. Gartsman GM. Massive, irreparable tears of the rotator cuff. Results of operative debridement and subacromial decompression. J Bone Joint Surg Am. 1997; 79:715-21 17. Goutallier D, Postel JM, Bernageau J, Lavau L, Voisin MC. Fatty muscle degeneration in cuff ruptures. Pre- and post-operative evaluation by CT scan. Clin Orthop Relat Res 1994; 304:78-83 18. Fuchs B, Weishaupt D, Zanetti M, Hodler J, Gerber C. Fatty degeneration of the muscles of the rotator cuff: assessment by computed tomography versus magnetic resonance imaging. J Shoulder Elbow Surg 1999; 8:599-605 19. Burkhart SS, Athanasiou KA, Wirth MA Margin convergence: a method of reducing strain in massive rotator cuff tears. Arthroscopy. 1996; 12:335-8 20. Bigliani LU, Cordasco FA, McIlveen SJ. Operative repair of massive rotator cuff tears: long-term results. J Shoulder Elbow Surg 1992; 1:120-30 21. Cho NS, Yi JW, Rhee YG. Arthroscopic biceps augmentation for avoiding undue tension in repair of massive rotator cuff tears. Arthroscopy. 2009; 25:183-91 22. Duralde XA, Bair B.: Massive rotator cuff tears: the result of partial rotator cuff repair. J Shoulder Elbow Surg. 2005; 14:121-7 23. Rhee YG, Cho NS, Lim CT, Yi JW, Vishvanathan T. Bridging the gap in immobile massive rotator cuff tears: augmentation using the tenotomized biceps. Am J Sports Med. 2008; 36:1511-8 24. Porcellini G., Campi F., Castagna A., Paladini P. Functional partial cuff repair: five years follow-up. Shoulder Arthroscopy & Arthroplasty - Current Concepts Tome I. Editor: Pascal Boileau Nice Shoulder Course 2012 25. Porcellini G, Castagna A, Cesari E, Merolla G, Pellegrini A, Paladini P.: Partial repair of irreparable supraspinatus tendon tears: clinical and radiographic evaluations at long-term follow-up. J Shoulder Elbow Surg. 2011; 20:1170-7 26. Karas SE, Giachello TL.: Subscapularis transfer for reconstruction of massive tears of the rotator cuff. J Bone Joint Surg Am 1996; 78:239-45 27. Wirth MA, Rockwood CA Jr.: Operative treatment of irreparable rupture of the subscapularis. J Bone Joint Surg Am. 1997; 79:72231 28. Jost B, Puskas GJ, Lustenberger A, Gerber C. Outcome of pecto ralis major transfer for the treatment of irreparable subscapularis tears. J Bone Joint Surg Am. 2003; 85:1944-51 29. Resch H, Povacz P, Ritter E, Matschi W. Transfer of the pectoralis major muscle for the treatment of irreparable rupture of the subscapularis tendon. J Bone Joint Surg Am 2000; 82:372-82 30. Paladini P., Campi F., Merolla G., Pellegrini A., Porcellini G. Pectoralis minor tendon transfer for irreparable anterosuperior cuff tears. J. Shoulder Elbow Surg. 2013; 22:e1-5 31. Arai R, Sugaya H, Mochizuki T, Nimura A, Moriishi J, Akita K. Subscapularis tendon tear: an anatomic and clinical investigation. Arthroscopy. 2008; 24:997-1004 32. Arai R, Nimura A, Yamaguchi K, Yoshimura H, Sugaya H, Saji T, Matsuda S, Akita K. The anatomy of the coracohumeral ligament and its relation to the subscapularis muscle. J Shoulder Elbow Surg. 2014; S1058-2746 33. L’Episcopo JB Tendon transplantation in obstetrical paralysis. Am. J Surg 1934; 25:122-5 34. Gerber C, Vinh TS, Hertel R, Hess CW Latissimus dorsi transfer for the treatment of massive tears of the rotator cuff. A preliminary report. Clin Orthop Relat Res. 1988; (232):51-61 35. Gerber C, Maquieira G, Espinosa N. Latissimus dorsi transfer for the treatment of irreparable rotator cuff tears. J Bone Joint Surg Am 2006; 88:113-120 36. Habermeyer P, Magosch P, Rudolph T, Lichtenberg S, Liem D. Transfer of the tendon of latissimus dorsi for the treatment of massive tears of the rotator cuff: a new single-incision technique. J Bone Joint Surg Br 2006; 88:208-12

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Arthroscopically-assisted latissimus dorsi transfer Enrico Gervasi, Alessandro Spicuzza Ospedale Civile di Latisana, Udine

INTRODUCTION Epidemiology The majority of the rotator cuff tears can be repaired with surgery, either open or arthroscopically. Although relatively to the total amount the percentage of the irreparable lesions is low, these are frequently symptomatic, as much as to require a solution: surgical, rehabilitative, or both. The frequency of the rotator cuff lesions increases with age; this is due to biological laziness of the tendon, age-related, or due to toxic factors (e.g. smoke), or even to the damage consequent to mechanical stresses: local factors (subacromial impingement) or external ones (heavy working activities or strenuous sports). Acute post-traumatic onset of symptoms, mainly pain and loss of function, typically reveals the extension of a pre-existing injury, even if asymptomatic. The resultant functional disability is a true ataxia, with loss of spatial control of the hand in the most severe cases. Assuming that the percentage ratio between massive irreparable tears and the repairable ones does not vary with the age, the majority of lesions occur in the elderly population; its patients’ need is to reduce pain and improve the function for the daily-live activities. The goal for young people is often challenging, aiming to achieve power for re-start a stressful manual job. The heterogeneity among different needs and expectations gives rise to different treatment options, although the massive tears can be similar to each other.

History The surgery of the rotator cuff in the 80s enters a phase of evolution of orthopaedics, where immobilization, repeated infiltrations of corticosteroids (the same way as tonics), manipulation, give way to the scalpel. The surgeon is careful to repair the anatomical damage of the rotator cuff; only after he will shift the attention to restore the function rather than to repair the “hole in the tendon.” The “evidence based” medicine, the attention in the analysis of the results, checked by imaging, demonstrate the ineffectiveness of techniques of direct repair of the rotator cuff documenting the failures or the recurrences in many massive injuries, even when at the time of surgery the tendons appear firmly repaired to the bone. The role of Figure 1: position of the transposed latissimus dorsi tendon on the greater tuberosity

biology in the healing process is getting to be understood; the functional one of each motor unit throughout the kinetic chain is analysed. The goal of the surgery is aimed at restoring the function rather than to repair the injured tissues. The search for effective alternatives to direct repair leads to consider the muscle-tendon units transfer, used in the past to treat neurological injuries, obstetrical paralysis consequences of dystocic births. In these the external rotation is impaired, the fifth cervical root being more often the one involved. In this affection the internal rotators become predominant over the external rotators, resulting in the inability of the patient to bring the hand to the mouth or neck. The L’Episcopo surgical technique 1, that proposed balancing the postero-superior rotator cuff deficit, is forerunner of modern transpositions: it provides for the separation of both tendons, latissimus dorsi and teres major, off from the edge of the bicipital groove and their reinsertion to the diaphyseal cylinder, rotated in the opposite direction: from medial and posterior to lateral and anterior. At the end of the 80s Gerber remakes it 2, modifying and adapting it to the repair of the rotator cuff; in 2003 we translated it for use in endoscopy 3. Why does the arthroscopic choice? The arthroscope reaches any district, better than the scalpel and with less damage to the tissues being passed through. This principle led our group to conceive and establish arthroscopic techniques for “at distance” tendon transfers. The deltoid sparing thus obtained also guarantees a way out in case of failures, when the pathology rises towards a cuff

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tear arthropathy and the joint replacement with a reverse prosthesis becomes necessary. Finally we abandon the idea of using part of the transferred tendon to close the hole, fixing it to the residual medial cuff as proposed by other authors until then; we fix it, vice versa, to the most anterior part of the greater tuberosity in an autonomous way, thus acting as stabilizer of the humeral head, even passively Figure 1. In a similar way to the constraint of a reverse prosthesis, this favours the action of the deltoid; only partially the transposed latissimus dorsi acts as active external rotator.

METHODS Patient selection The ideal candidate for surgery is the patient with massive, irreparable, rupture of the rotator cuff with a limitation of the function of the upper limb incompatible with the dailylive activities. If local anaesthetic injected into the subacromial space act as painkiller regaining function, then a different, limited procedure as the biceps tenotomy and the smooth contouring of the greater tuberosity can be considered. It could be defined that the muscle-tendon transfer is therefore recommended when is impossible or inadequate by direct repair to recover the function, lost and functionally essential, of the native rotator cuff. The function that has to be resuscitated depends on topography of the cuff lesion. The brain is set by function rather than by activity of individual muscles. The transposed tendon is not affected by regressive phenomena (degeneration), as conversely happens to the cuff tendons working in the subacromial space. The success of the “tendon-transfer surgery” is less influenced by the typical “lazy biology” of the torn cuff. The age also is not crucial in the decision-making: other factors as important as tendon vitality should be considered: patient activity, his involvement in recreational sports (if any), the expectations. Furthermore is important the patient’s intellectual capacity to understand objectives and limits of the rehabilitation program, in order to take part to one, lasting several months. It is based on reprogramming the neuro-motor skills, with stimulation of the transposed unit. At the early rehabilitation phase is used the mechanical improvement given by the tenodesis effect of the transfer. However patients “over 70” must be carefully drafted to a complex surgery also in terms of rehabilitation, since the implantation of a reverse prosthesis is a viable alternative, which requires a simpler and shorter rehabilitation program. The choice between the two procedures beyond the boundary of the age of 70 years, when the prosthesis is rarely indicated, is played on other factors: integrity of cartilage, biological age (transfer indicated in youths), subscapularis integrity or reparability. The damage of articular surfaces orient toward the prosthesis. Coexisting lesions of the subscapularis and previous surgeries can lead to significant improvement despite the final outcome is less satisfactory compared to the average. Some patients have a large size or massive cuff lesion functionally compensated. If at medical examination their concern is pain, whilst the function is preserved, the long head of biceps tenotomy

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can be a viable solution, even palliative. In this case the transfer is rarely the procedure of choice, because it lacks the pre-requisite of loss of the essential function. These shoulders have a relatively stable humeral epiphysis. The contact surface between humerus and the acromion is the fulcrum acted by the deltoid to elevate the limb. The radiographic examination performed in patients with massive rupture of the rotator cuff shows different patterns of images: by the cranial migration of the humeral head with minimal signs of bone adaptation to others in which the acromion and its anterior osteophyte, large, gets to contact the humeral head, thus limiting either the humeral migration and the loss of relation between its centre of rotation and the centre of the glenoid. The intact acromial arc opposes to the cranial migration of the humeral head; thus, preventing the excessive shortening of the deltoid muscle fibres, the linear movement produced by the contraction shifts in a rotational one. The described effect is greater the more congruent are the surfaces of the neo acromialhumeral articulation, modified by taking an acetabular pattern. Even the remaining rotator cuff takes advantage of it, not depriving muscle strength to the rotations, which would be spent, vice versa, by the humeral head centring action. This explains how the acromiplasty sometimes leads to a functionally catastrophic result: the shoulder with weakness in elevation becomes pseudo paretic following the surgery. The transformation towards the neocotyloid appearance is given from wear by friction of the bone surfaces, related to their mutual movement. Patients with valid movement and massive cuff tear can be expected to show at radiographic examination that “compensatory” aspect of centred glenoid wear, rather then off centre, light of the movement itself. Individuals with acute onset of severe deficit are often the ones affected by traumatic extension of an existing lesion; it happens in the absence of gradual adaptation, thus the bone surfaces are anatomically regular. According to some authors, the reduction of the humeral-acromial space and cranial migration of the humeral head is a contraindication to tendon transfer; they report that it cannot contribute in any way to the distal re-centering of the humeral head. Surgery is contraindicated when the humeral-acromial contact determines bone changes, humeral, of the glenoid (cotyloid aspect) Figure 2 or acromialis. The rounding of the greater tuberosity after all is acceptable. The impossibility to repair the subscapularis tendon gets the latissimus dorsi transfer ineffective. This rule has anecdotal exceptions, whose biomechanical justification (why sometimes the transposed tendon is still effective) is not yet clear. The combined transfer, anterior and posterior, is definitively rare in the literature and the reported results are unsatisfactory. It requires the about impossible reorganization of a motor engram reprogramming either, the external and internal rotation. The transfer is not suitable for patients who need to recover the function of the limb for a repetitive manual work: because the force is only partially restored, is exhaustible, has no resistance to fatigue or to cyclic loading. The weight of the limb itself, when significant, adversely affects prognosis. I give the patient the example of those who suffer a serious heart attack: the recovery, even when good, is never

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Figure 2: cotyloid aspect of the gleno-acromial arch

complete and the considerable effort must be avoided. The goals of surgery, limitations, as well as the possible complications should be discussed during the visit with the patient.

Choosing the graft Several solutions have been suggested to treat chronic rotator cuff deficiency: debridement4, partial rotator cuff repair5, subscapularis tendon transfer6, transfer of the subscapularis and teres minor7, transfer of the long head of triceps8, teres major transfer9,10, interposition of a biceps tendon autograft11, freeze-dried rotator cuff allograft12, and use of synthetic grafts13. The muscle-tendon unit candidate to be transferred (substitute) must replicate the lost function. The suitability depends on the amounts of certain qualities: strength (size and the plane on which lies the vector), the excursion, and synergy, present when substitute and replacing are naturally agonists for the function to be vicariate. Besides these is specially relevant the accessibility, which makes possible withdrawing and transferring the graft with the lowest damage to healthy structures to pass through and with the lowest risk of damage to vessels and nerves. By the term “consistent” we mean the structure that has characteristics suitable to the specific transposition. The study of Herzberg shows an analysis essential for the choice of the graft, the one among various transplants in use today, ideal for to take place of specific functions of the torn cuff. The bias is that this study is based on preparations obtained from cadavers. Possible substitutes are

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categorized into three series: thoraco-scapular, thoracohumeral and scapular-humeral. Of each muscle are analysed the following characteristics: the length at rest, the potential range of elongation in cm. and the relative basal tension, related to a ratio of its sectional area and that of the whole group of muscles acting on the shoulder. The relative basal tension and the excursion of the units to be replaced are compared with those of the transfer, to estimate its suitability to the new work. The analysis considers, however, the action on just two planes: the sagittal section, for the measurement of the cross-sectional size of the muscle belly, and the coronal one, for to assess length and elongation. The third plane of the space, where the vector of force lies on, is not considered. Some of the energy produced by the graft is in fact is dissipated by spready forces, inconsistent with those to be replaced. From this study it appears that the problem lies in the strength rather than in the intended stretchability of the graft. Let us now consider the latissimus dorsi, isolated or combined with the teres major pro posterior cuff. The latissimus dorsi isolated lacks basal relative tension, recoverable with the simultaneous transfer of the teres major. Our choice, of transposing the latissimus dorsi isolated, is given by the limited elongation capacity of the teres major. If the teres major is transferred as a unit along with the non-autonomous latissimus dorsi, the teres restrains the possibility that the latissimus reaches the very anterior area of the greater tuberosity, wrapping itself on this as on a flywheel. The volume of both muscle bellies, moreover, would be likely to compete for space with the circumflex nerve, putting it at risk of a canalicular disease. In conclusion, the latissimus dorsi isolated seems at the moment the more “consistent” transfer for massive “irreparable” postero-superior cuff tears.

The transfer of the latissimus dorsi assisted by endoscopy Patients eligible for transfer of the latissimus dorsi are those set by the posterior cuff deficiency. When associated the lesion extends to the subscapularis and has to be repaired. Absolute contraindications to transfer are: humeral-scapular evolved arthropathy, the chronic dehiscence and irreparability of the deltoid, the axillary nerve palsys. The preoperative diagnostic imaging includes a series of radiographic projections: AP “normalized”, “outlet” of Lamy and axillary view. Examination reveals, if any, signs of arthropathy (glenohumeral space reduced) and acetabular transformation of the acromial arch, with changes of the upper glenoid profile. Those factors make this surgery contraindicated. Magnetic resonance imaging is routinely performed: it evaluates the tendon defect on coronal and axial planes; the sagittal plane allows to get the occupation index of the scapular fossa (Zanetti) and the degree of fatty infiltration (Thomazeau) Figure 3, expression of the trophism of the muscle and of the eventual irreversibility of the changes. When planning is important to know whether you should repair the subscapularis: that because the setup of the operating room is then set by placing the patient in the “ modified beach chair “ rather than in lateral decubitus position , as a rule. The physical examination assesses the

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integrity of the deltoid and the presence of rigidity, this relatively frequent in patients who come to the transfer as revision of a previous surgery or in trauma cases. The expected results in revisions are less favourable. The stiffness, even inconspicuous, prejudices the possibility of humeral re-centring with respect to the glenoid and then the functional effectiveness of the transfer.

Postoperative treatment The postoperative protection of the transfer follows the general rules of the surgery for massive rotator cuff injuries. Before surgery and in preparation to it, patients are instructed to perform analytic exercises for the various muscles. After the surgery, because of pain (however slight) and awe to use anatomical elements involved in the surgical trauma, learning would be very difficult. During the first period the active movement is under strict control. The adoption of a mini-sling in 15° of external rotation or an abduction pillow is continued for 6 weeks. Meanwhile patients are allowed for few pendulum exercises to limit adhesions between teres minor and deltoid. Elbow flexion and hand exercises are encouraged, as well as those for the scapulothoracic articulation, trunk and lower limbs. The maintenance of kinetic chains of joints not involved by the surgery promotes functional recovery. The rehabilitation in water (hot pool) is useful since the sixth week and throughout the period of functional recovery. The exercises are performed with both limbs to use the “mirror” effect, favouring the trophism and the recovery of motor engram. In the rehabilitation program the limb lifting against gravity is carried out gradually. The patient starts the exercises lying on the unoperated side, the back tilted 30 degrees backward, in order to place the glenoid parallel to the ground and thereby reducing shear forces acting on the humeral head. The elbow maintained is flexed at first, reducing the lever arm. The gradual erection of the trunk gets ready to perform exercises in a full upright position. Rehabilitation takes many examples from

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Figure 3: oblique sagittal MR view shows fatty degeneration of posterior superior rotator cuff (a: supraspinatus muscle, b: infraspinatus muscle, c: teres minor muscle)

the actions of everyday life to motivate the patient. Functional recovery takes place ranging from a few months to a year after surgery. The transposed latissimus dorsi gets ability to work actively, as shown in the transpositions carried out for obstetric paralysis, in which it is moved around the diaphyseal cylinder.

RESULTS Results and complications We evaluated a first cohort of 25 patients who underwent to latissimus dorsi transposition assisted by endoscopy, performed by the senior author, with at least three years of follow up (data being published). In this series there were no major complications, as conversely recorded in a more recent one (two neurological involving the circumflex nerve: one primary, one subsequent to infection and Figure 4: Humeral head re-centered. a) preoperative X-ray b) postoperative X-ray

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debridement). The infection occurred in one patient affected by acne. Few patients developed blood or serous effusion in the area subject to release of the latissimus dorsi muscle. Superficial tissues for a first time after the release do not adhere to the muscle, thus leading to “third space” progress. Our attention to coagulate the vessels crossing distally from muscle to subcutaneous made ​​negligible this complication. When it occurs, the drainage through a skin incision in the most distal part of the collected fluids solves the problem. As already reported in the literature for the revision of previous failed cuff surgery gets less favourable results, especially after large acromioplasty. The integrity of the subscapularis is crucial although some patients with a tear found to be irreparable at the time of surgery equally benefit from the procedure. The weight of the limb seems to play as disadvantage. The postoperative centring of the humeral head over the glenoid, even if partial, is favourable to functional recovery. Postoperative radiographic study quantifies it Figure 4. The comparative long term rx studies show the reduction of the space humerus-acromial over time and the progression of arthritic changes14. These also show an impression on the tuberosity, as it would be carved by the action of the transposed tendon. The humeral centring is greatly favoured by the capsuloligamentous release we currently perform extensively. Gain about the external rotation strength is moderate. In conclusion we consider the technique of latissimus dorsi transfer assisted by arthroscopy as the procedure of choice for the irreparable posterior superior rotator cuff tears functionally disabling. The basal tension of the latissimus dorsi is insufficient to replicate the whole force of the postero-superior cuff; the position we choose for the fixation improves elevation more than external rotation. The combined transfer with that of the teres major as a single not separated unit, limits the graft possibility of sliding and crowds the passage from the armpit to the subacromial space. It increases the risk of compression of the circumflex nerve or need for fixing the graft at back site with respect to the desired point.

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REFERENCES 1 L’Episcopo JB. Tendon transplantation in obstetrical paralysis. Am J Surg. 1934; 25:122–125 2 Gerber C, Vinh TS, Hertel R, Hess CW Latissimus dorsi transfer for the treatment of massive tears of the rotator cuff. A preliminary report Clin Orthop Relat Res 1988; 232:51–61 3 Gervasi E, Causero A, Parodi PC et al Arthroscopic latissimus dorsi transfer, Arthroscopy 2007; 23:1243.e1-4 4 Rockwood CA Jr, Williams GR Jr, Burkhead WZ Jr. Debridement of degenerative, irreparable lesions of the rotator cuff. J Bone Joint Surg Am 1995; 77:857-66 5 Duralde XA, Bair B. Massive rotator cuff tears: the result of partial rotator cuff repair. J Shoulder Elbow Surg 2005; 14:121-7 6 Cofield RH. Subscapular muscle transposition for repair of chronic rotator cuff tears. Surg Gynecol Obstet 1982; 154:66772 7 Neviaser JS. Ruptures of the rotator cuff of the shoulder. New concepts in the diagnosis and operative treatment of chronic ruptures. Arch Surg 1971; 102:483-5 8 Malkani AL, Sundine MJ, Tillett ED, Baker DL, Rogers RA, Morton TA. Transfer of the long head of the triceps tendon for irreparable rotator cuff tears. Clin Orthop Relat Res 2004; 428:228-36 9 Wang AA, Strauch RJ, Flatow EL, Bigliani LU, Rosenwasser MP. The teres major muscle: an anatomic study of its use as a tendon transfer. J Shoulder Elbow Surg 1999; 8:334-8 10 Celli L, Rovesta C, Marongiu M et al Transplantation of teres major muscle for infraspinatus muscle in irreparable rotator cuff tears, J Shoulder Elbow Surg 1998; 7:485-490 11 Neviaser JS. Ruptures of the rotator cuff of the shoulder. New concepts in the diagnosis and operative treatment of chronic ruptures. Arch Surg 1971; 102:483-5 12 Neviaser JS, Neviaser RJ, Neviaser TJ. The repair of chronic massive ruptures of the rotator cuff of the shoulder by use of a freeze- dried rotator cuff. J Bone Joint Surg Am 1978; 60:681-4 13 Ozaki J, Fujimoto S, Masuhara K, Tamai S, Yoshimoto S. Reconstruction of chronic massive rotator cuff tears with synthetic materials. Clin Orthop Relat Res 1986; 202:173-83 14 Hamada K, Fukuda H, Mikasa M, Kobayashi Y Roentgenographic findings in massive rotator cuff tears. A long-term observation, Clin Orthop Relat Res 1990; 254: 92-6

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The rotator cuff irreparable tears: latissimus round muscle transfer Ferdinando Odella, Simona Odella* Istituto Clinico San Siro, Milano * Ortopedia Traumatologica per la Chirurgia della Mano, Istituto Ortopedico G. Pini, Milano

INTRODUCTION

ABSTRACT

The factors that affect the type of treatment of lesions of the rotator cuff are the patient’s age the functional requirements, the painful symptoms and the type of lesion. The repairability of the lesion depends on three main elements:

The transfer of the tendon of the muscle large round is one of the surgical solutions used in the treatment of the massive irreparable supero-posterior rotator cuff tears. The purpose of this retrospective study is to report the long-term validity of the results with the change in the treatment characterized by suturing the tendon of the subscapularis tendon also transferred intact as well as the greater tuberosity.

• the extension of the lesion, we distinguish partialthickness tendon injuries (bursal, intratendinous, joints) and those with full-thickness which we believe should not be evaluated on the basis of cm but in view of the number of tendons involved, we define a lesion as massive if affecting two or more tendons, you must also consider the location of the lesion which, according to Patte1 can be higher, superior- posterior, superior- anterior or massive; • retraction of the tendon which we evaluate the entity in three grades: Grade 1: slight retraction, occurs only in small tears; Grade 2: Average tendon retraction, (figure 1) the tendon still partially covers the head of the humerus and the retraction is at the level of the acromioclavicular joint; Grade 3: severe tendon retraction, the humeral head is uncovered and the tendon is retracted to the glenoid; but the most important element is • fixity or elasticity of this retraction, we recognize three stages Stage 1 : The cuff injury is recent, the tendons are still healthy and mobile, the muscle retains its function and the joint is stable; Stage 2 : the injury occurred more than six weeks, the tendons are hypomobile but recoverable in anatomical site in spite of being already an initial degeneration of the tendon and muscle, the joint has a dynamic instability; Stage 3: the lesion is deep-rooted, the retraction of the tendon is fixed, the muscle and tendon tissue is gone to meet fatty infiltration, the glenohumeral joint is unstable, in this case it is not possible to make a direct repair but you must perform a muscle transposition. The quality of the tendon tissue and of the muscle belly depends on the fatty infiltration, Goutallier 2 in 1996, identifies five stages according to the relationship between the

degenerated muscle volume and the volume of healthy muscle. Because there is a good result functional muscle degeneration must not be higher than the second stage (Figure 2). Ide3 in agreement with Romeo4 considers that the extension of the lesion, if it exceeds 5 cm, results in clinically unsatisfactory results, in fact, in our opinion is not the extent of the lesion but its fixity the element that determines the repairability of the lesion while the functional outcome depends on the quality of the tendon tissue and of the residue muscle trophism. Fuchs5 observed that, in the cuff repaired that had a muscular atrophy of tendons involved in the lesion, this condition does not regress, but in case of rupture of the tendon of the supraspinatus atrophy is stable if the injury heals in case of involvement of the subscapular tendon, although healed after repair, not just the atrophy does not regress but increases also the fatty infiltration of the infraspinatus tendon that was not involved in the lesion. The authors do not exclude the possibility of suffering neurological due to technique of repair.

Figure 1: immagine RMN che evidenzia retrazione del tendine che parzialmente ancora ricopre la testa omerale

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Figure 2: immagine RMN che evidenzia degenerazione grassosa di 2 grado secondo Gouttalier

Object of our study are the lesions that can not be repaired, the massive tears with severe fatty infiltration of the muscle bellies, in these cases, in patients older than 70 years, you can perform muscle transfers: if the lesion is posterior superior is necessary that the front wall, represented mainly by the subscapularis is intact to have a good focus during the elevation of the limb. If possible it may be useful to anchor the tendon transferred to the tendon of the subscapularis muscle; if the lesion is superior anterior we are used to transpose the anterior tendon of the pectoralis major muscle.

MATERIALS AND METHODS From 1998 to 2012 142 patients underwent surgical treatment (transfer of large round muscle in superior- posterior rupture massive irreparable rotator cuff). The median age was 67.8 years in the female population, 71.4 years in male population. Males constitute 60 % of the population. At mean follow-up of 7 years, the constant total score is equal to 66, the front elevation 158 degrees external rotation in adduction 41 degrees, 66 degrees external rotation in abduction, and the strength of 2.4 according to the cs. Patients who have undergone surgical treatment of great Figure 3a, b: quadro RMN lesione massiva della cuffia dei rotatori, si osserva retrazione tendinea alla glena e degenerazione grassosa di 3 gradi secondo Gouttalier

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round transfer had an irreparable rupture of the rotator cuff tendon of the superior- posterior with subscapularis intact; were excluded unmotivated patients with moderate pain and age over 75 years, in addition to patients with glenohumeral osteoarthritis, retractile capsulitis, or neurological problems. Surgical treatment was performed in the open surgery with two skin incisions, postoperative treatment provided by a sling immobilization for 40 days at 45 degrees of abduction, followed by a re-education for 6 months. The transfer of the latissimus round requires as a necessary condition for the integrity of the tendon of the subscapularis muscle. We recently rechecked the 10 patients in our series and subjected to evaluation as well as clinical, electromyographic and all patients were satisfied with regard to pain and function even if the recovery of strength was not equal to the contralateral limb, and in eight of the ten patients examined, we observed electromyographic activation of the muscle passed during external rotation with limb adduct the hip (Figg. 3-5).

DISCUSSION For massive lesions according to Patte and Elman we intend lesions involving two or more tendons. To choose a proper treatment we must consider several important parameters, such as: type of injury, age and activity of the patient and the patient’s motivation. To evaluate the type of lesion should consider the following elements: the location, the extension and the form, the retraction of musculotendinous and quality of the muscle tissue. A retraction of the tendon to the glenoid make it very difficult if not impossible to complete repair of the lesion, also a muscle fatty degeneration (visible by NMR) of 3° - 4° degree by Goutallier is a negative prognostic factor. Therefore, in these conditions a massive lesion can be considered as irreparable. Different types of treatment for massive lesions have been described: the conservative treatment, the simple open or arthroscopic debridement (5. 6), generally associated to an acromioplasty; partial repairs; tendon allograft and synthetic, and the muscle transfers. Many patients with chronic massive lesions can be treated conservatively with success through modification of activities, NSAIDs, physiotherapy and infiltration of corticosteroids in the sub acromial space. Bokor et al6 have noted an improvement between 50 % and 85 % of patients treated conservatively. Many studies on the other hand showed a negative correlation between the number of preoperative infiltration of corticosteroids and the results obtained after repair of tendon injury. Rockwood in a 1984 study reported satisfactory results in the treatment of full-thickness lesions with debridement and subacromial decompression in the open air7. Always Rokwood in 19958 demonstrated that the simple debridement and acromioplasty in massive lesions irreparable gave satisfactory results, but at a distance of time, follow up > 5 years, tended to deteriorate. Several authors have obtained similar results using a similar technique but al-

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Figure 4a, b: riscontro intraoperatorio della lesione massiva della cuffia dei rotatori, la testa è scoperta il tendone retratto, sutura del tendine trasposto

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ways without arthroscopic repair of the lesion5. In contrast to other authors have described unsatisfactory results in the long term with the only decompression and debridement9-12. A study of Melillo et all, 199713 showed that in a group of 52 patients, 27 treated by repair of tendon injury and 25 with debridement and decompression, only 8% of patients treated with the latter procedure was satisfied, compared to 87 % of patients who underwent cuff repair. This type of treatment can be taken into consideration for elderly patients with few requirements, in which the test Neer with subacromial injection of anesthetic is able to resolve the pain with improved function. You can also perform the resection and tenodesis of the long head of the biceps, thereby eliminating the biological causes of pain (inflammatory synovial tendon reaction) and the mechanical action of the medial displacement of the clb against the tendon of the subscapularis (Burkart 1996)10. To achieve good results in the treatment of massive injuries, tendon repair should be respected by prognostic factors set out above. In a study conducted by Wolf et all. in 2000 14, we wanted to demonstrate just that the quality of the results is directly proportional to the respect of preoperative prognostic factors. To this were included in the study patients with a tendon degeneration not exceeding at stage 2 of Goutallier, absence of pseudoparalysis, absence of anterior-superior subluxation of the humeral head. The results were positive, with a mean postoperative Constant score of 85.5. The results obtained by different authors who have not taken account of prognostic factors have not been up to expectations . Lately in elderly patients with irreparable lesions with involvement of the subscapularis and cuff tear arthropathy space is treated with reverse prosthesis. While, in irreparable injury posterior superior muscle transfers represent a

B

true palliative treatment, as they use muscles of the shoulder joint in order to recover the functions of stability and movement of his cuff muscles degenerate irreversibly. The indication to muscle transfers occurs in the presence of massive lesions or relapsed chronic pain in patients with active and severe functional deficit highly motivated to functional recovery. By contrast, in the presence of joint stiffness, severe bone and joint abnormalities of the glenohumeral joint, insufficiency of the deltoid muscle and nerve damage, muscle transfers are contraindicated. Transfers muscle can be divided into local and regional. The first uses the remaining tendon tissue by rotating to cover the head using subscapularis. (Cofield 1982)15 or the small round (Paavolainen 1988)16. With this type of treatment, there is the risk of clinical worsening (loss of elevation of the limb) if the tendon insertion in the new location does not heal. Debeyre, Patte, Goutallier 17 suggest a muscle-tendon advancement of the elements of the rotator cuff. The reinsertion of tendon after lateral movements of the muscle bellies of the supra and infraspinatus, creates a technique that restores the ‘ anatomy as close to normal as possible. The results of this method are questionable and there are conflicting opinions in the literature. Patte 1 reported good results in 41% of patients, 11 % Walch (1992)18 and Patte Goutallier 17 36%. The best results are obtained when the humeral head is centered with moderate muscle degeneration. Experimental studies on cadavers carried out by Warner and Gerber (1992)19 show that this technique allows a limited traverse and risk to damage the neuro-muscular structures. Combes and Mansat 20 think that this treatment is illogical because it uses muscles retracted and not working. We agree, in fact the fibrous structure - muscle, in the case

Figure 5a, b: clinica pre e post operatoria

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of chronic injury, is retracted and little expandable and the possible muscle fatty degeneration makes this technique useless. In the case in which the trophism is good it is supposed that the lesion is recent and the mobilization of the muscletendon is possible with a capsular release. The regional transfers can use a deltoid flap (AugereauApoil 198521, Takagishi 22, Vandenbussche (2004)23, the trapezius (Mikasa)24, the muscle angle of the scapula (Celli 1986) pro supraspinatus. The big round (Combes - Mansat 1993)20 and the latissimus dorsi (Gerber 1987) 25,27 can be used to vicariare the infraspinatus. The pectoralis can be used in the rare, but serious degeneration of the subscapularis (Chaffaï - Mansat 1988)26.

DISCUSSION The rupture of the rotator cuff is a common disease in the aging population, repair techniques and the means available are varied but relapses are equally present. Factors that should be considered to address the repair of the rotator cuff of the shoulder, such as age, pain, patient motivation, muscle trophism, the status of the long head of the biceps, make it difficult to systematize this disease. Not all broken rotator cuff must be treated surgically. MRI has allowed us to assess not only the size of the lesion but also the trophic muscle, which together with the pain and the functional needs of the patient allows us to give an indication to the appropriate treatment for the individual patient. Mc Laughlin 28 in 1944 describes a technique in repair of tendon injuries of the shoulder by means of sutures transosse tendon to the greater tuberosity, several authors subsequently studied various fixation techniques to achieve a better seal to the bone, but the method of McLaughlin and subacromial decompression is still the most widely adopted with excellent or satisfactory in 80% of cases according to Cofield 29.

REFERENCES 1. Patte D Classification of rotator cuff lesions. Clin Orthop Rel Res 1990; 254:81-6 2. Goutallier D, Postel JM, Boudon R et al. A study of the neurologic risk in tendino-muscular advancement of supra-spinatus and infra-spinatus in the repair of large rotator cuff rupture. Rev Chir Orthop Reparatrice Appar Mot. 1996; 82:299-305 3. Ide J, Maeda S, Katsumasa T. A comparison of arthroscopic and open rotator cuff repair. Arthroscopy 2005; 21:1090-1098 4. Romeo AA, Hang DW, Bach BR, Shott S. Repair of full thikness rotator cuff tears. Clin Orthop 1999; 367: 243-255 5. Fuchs B, Gilbart MK, Hodler J, Gerber C. Clinical and structural results of open repair of an isolated one tenson tear of the rotator cuff J Bone Joint Surg 2006; 88:309-316 6. Bokor DJ, Hawkins RJ, Huckell GH et al. Results of nonoperative management of full-thickness tears of the rotator cuff. Clin Orthop Rel Res1993; 294:103-110 7. Szalay EA, Rockwood CA. Injuries of the shoulder and arm. Emerg Med Clin North Am. 1984; 2:279-294

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8. Rockwood CA, Williams GR, Burkhead WZ. Débridement of degenerative, irreparable lesions of the rotator cuff. J Bone Joint Surg 1995; 77:857-866 9. Baleani M, Schrader S, Veronesi CA et al. Surgical repair of the rotator cuff: a biomechanical evaluation of different tendon grasping and bone suture fixation techniques. Clin Biomech 2003; 18:721-729 10. Burkhart SS, Athanasiou KA, Wirth MA Margin convergence: a method of reducing strain in massive rotator cuff tears. Arthroscopy 1996; 12:335-338 11. Accousti KJ, Flatow EL, Technical pearls on how to maximize healing of the rotator cuff. Instr Course Lect 2007; 56:3-12 12. Baring T., Emery R, Reilly P Management of rotator cuff disease: specific treatment for specific disorders. Best Practice and Research. Clin Rheumatol 2007; 21: 279-294 13. Melillo AS, Savoie FH, Field LD. Massive rotator cuff tears: debridement versus repair. Orthop Clin North Am 1997; 28:117-124 14. Wolf BR, Bries AD, Nepola JV Greater tuberosity osteotomy and teres minor transfer for irreparable superior rotator cuff tears. Iowa Orthop J 2007; 27:65-70 15. Cofield RH. Subscapular muscle transposition for repair of chronic rotator cuff tears. Surg Gynecol Obstet 1982; 154:667-672 16. Björkenheim JM, Paavolainen P, Ahovuo J, Slätis P Surgical repair of the rotator cuff and surrounding tissues. Factors influencing the results. Clin Orthop Rel Res 1988; 236:148-53 17. Patte D, Goutallier D, Debeyre J Ruptures of the rotator cuff. Results and perspectives of the retrostructure. Orthopade 1981; 10:206-215 18. Walch G, Maréchal E, Maupas J, Liotard JP Surgical treatment of rotator cuff rupture. Prognostic factors. Rev Chir Orthop Reparatrice Appar Mot 1992;78:379-388 19. Warner JP, Krushell RJ, Masquelet A, Gerber C Anatomy and relationships of the suprascapular nerve: anatomical constraints to mobilization of the supraspinatus and infraspinatus muscles in the management of massive rotator-cuff tears. J Bone Joint Surg 1992; 74:36-45 20. Bonnevialle P, Savorit L, Combes JM et al. Value of intramedullary locked nailing in distal fractures of the tibia. Rev Chir Orthop Reparatrice Appar Mot 1996; 82:428-436 21. Apoil A, Augereau B Deltoid flap repair of large losses of substance of the shoulder rotator cuff. Chirurgie 1985; 111:287290 22. Takagishi K, Kaibara N, Hotokebuchi T et al. Serum transfer of collagen arthritis in congenitally athymic nude rats. J Immunol 1985; 134:3864-3867 23. Vandenbussche E, Bensaïda M, Mutschler C et al. Massive tears of the rotator cuff treated with a deltoid flap. Int Orthop 2004; 28:226-230 24. Hamada K., Fukuda H., Mikasa M., Kobayashi Y.Roentgenographic findings in massive rotator cuff tears. A long-term observation. Clin Orthop Rel Res 1990; 254:92-96 25. Gerber C, Ganz R, Vinh TS Glenoplasty for recurrent posterior shoulder instability. An anatomic reappraisal. Clin Orthop Rel Res1987; 216:70-79 26. Chaffaï MA, Mansat M Anatomic basis for the construction of a musculotendinous flap derived from the pectoralis major muscle. Surg Radiol Anat 1988; 10:273-282 27. Jost B, Zumstein M, Pfirrman CWA, Gerber C. Long term out come after structural failure of rotator cuff repairs. J Bone J Joint Surg 2006; 88:472-479 28. McLaughlin, HL, Lesion of the muscolotendinous cuff of the shoulder. The exposure and treatment of tears with retraction. J Bone Joint Surg 1944; 26:31-51 29. Cofield HR, Parvizi J, Hoffmeyer PJ et al. Surgical repair of chronic rotator cuff tears. J Bone Joint Surg 2001; 83:71-77

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Reverse shoulder arthroplasty with and without tendon transfer for arthropathy with massive rotator cuff tear: personal experience and critical analysis of the literature Nicola Ivaldo, Giovanni Caione, Mario Rossoni, Tony Mangano* GSL - Gruppo Sanitario Ligure, Ospedale S.M. di Misericordia, Albenga *Clinica Ortopedica e Traumatologica, IRCCS S. Martino - IST, Genova

Indications and rationale for reverse shoulder arthroplasty in CTA The first cases of glenohumeral arthritis occurring with tears of the rotator cuff were described by Adams and Smith in the 1850s1. In 1983 Neer defined this condition “cuff tear arthropathy” and described it as a massive rotator cuff tear with superior humeral migration and diminished acromionhumeral distance, erosion of the great tuberosity (“femoralization”) and other arthritic changes in the glenohumeral joint2. Goal of the reconstructive surgery should be to repair the rotator cuff, restoring a balanced shoulder in which the rotator cuff tendons keep the humeral head within the center of the glenoid during arm elevation, allowing motion while maintaining joint stability. Unfortunately, in severe massive RCT tendons retraction often makes repair impossible. Sometimes, despite a moderate retraction and technically possible repair, tendons degeneration makes the repair biomechanically useless. If the anterosuperior or posterosuperior cuff is compromised, dynamic and/or static superior humeral subluxation may occur, and this ultimately lead to an unbalanced shoulder, with decreased acromionhumeral distance and function impairment. In this condition indeed, when deltoid muscle fibers contract the humeral head will migrate superiorly, instead of allowing arm elevation, leading to painful acromial erosions and glenohumeral arthritis. If a balanced shoulder cannot be restored through a standard RC repair, alternative treatment options should be considered in order to improve symptoms3,4. However, when pseudoparalysis develops, RTSA may be the sole treatment option able in restoring the glenohumeral joint function, recreating a stable joint fulcrum on which the deltoid can lever and raise the arm5. Patients must be made aware, however, that full range of motion may not be obtained, with good anterior elevation and abduction recovery, but limited and not predictable gain in internal and external rotation. Despite shoulder motion may be improved compared with preoperative levels, it may not be completely restored.

Alternative treatment solutions and RTSA: where is it the boundary? A potential error is to implant an RTSA in a patient with a painful massive irreparable RCT with good function and without arthritis. If the patient has nearly normal active elevation, then the shoulder is still balanced and the RTSA would be an overtreatment. Nonoperative modali-

INTRODUCTION Prof. Grammont’s reverse total shoulder arthroplasty (RTSA) reliably reduces pain and improves shoulder function by increasing active abduction and forward elevation in patients with massive rotator cuff tears (RCT) and cuff tear arthropathy (CTA). Several works have been published in the last years, mirroring the increasing interest this kind of prosthesis received after FDA approval in 2003. Since that year, popularity of RTSA grew up among the initially skeptic surgeons in USA and furtherly increased in Europe and other countries as well. We can actually identify more than 400 works, when looking for shoulder reverse arthroplasty in the PubMed engine, most of which are reviews of the literature. We aimed at focusing our work mainly on the controversial aspects about RTSA. Sharing our own 13 years experience, we tried and carry out a fruible critical reading of the available literature, and some practical advices too, for surgeons approaching this fascinating surgery. ties should be considered first, as subacromial steroid injections coupled with stretching exercices and, after pain resolution, strenghtening excercices. In refractory cases, the arthroscopic joint débridement is indicated and, if the biceps is still in place, biceps (LHB) tenotomy3,4. Despite good results are published, several factors may lead to a negative outcome after débridement with or without LHB tenotomy: preoperative superior migration of the humeral head, presence of a subscapularis tear, presence of glenohumeral arthritis and decreased range of motion6,7. We did not find research works specifically addressed at simple débridement in presence of a spontaneously ruptured biceps tendon. Klinger et al. compared the outcome of simple débridement with and without LHB tenotomy, and reported similar results8. After considering the safety of the procedure and the low risk of (solely) cosmetic damage, we actually proceed with tenotomy in our practice. Sometimes, patients show a complete active elevation but are unable to lift even low weights. In this situation, we always suggest an initial physiotherapic approach but, in case of failure, an RTSA could be considered for functional recovery, even if pain is not prominent9.

RTSA in umbalanced massive cuff tears without arthritis In the recent past, surgeons were reluctant to implant RTSA in case of pseudoparalysis without clear degenerative arthropathy. Actually, several works report about this

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subgroup of patients10. In particular Hyun et al. warned about possible errors in indication, when a cause for functional impairment different from the RC tear is underestimated (e.g. neurological lesion), and in case the functional recovery possibilities are overestimated, in patients with preoperative preserved active forward elevation greater than 90°. Both of these conditions are unlikely to benefit from RTSA11.

What can we do when medical therapies and conservative surgery fail? The role of the latissimus dorsi (LD) transfer in massive RCT has been extensively cleared by Gerber, who also identified limits for this procedure. In particular, a not reparable subscapularis tear and a Goutallier grade II or more fatty degeneration of the teres minor represent independent negative prognostic factors. On the other hand, we should consider that when these muscles are not compromised, most of shoulders show an acceptable function, which excludes them from substitution with RTSA. Weening and Willems reported about 16 patients treated with LD transfer, where they found a 26° mean recovery in active elevation (from 79° to 105°) and did not observed the humeral head recentering in most of cases. Mean functional results in this series are worse than those obtained with RTSA in similar cases12-14. In our practice, we gradually limited the isolated LD transfer, considering the correct indication still unclear. We reserve the combined transfer of LD and teres major (TM) to patients in which, due to massive posterosuperior RCT and teres minor impairment, preserved active elevation and abolished external rotation are shown. Furthermore, we use the same transfer procedure in association with RTSA in cases of combined forward elevation and external rotation deficits. Recently, Savarese and Romeo reported a technical note about using a biodegradable subacromial spacer able in re-centering the humeral head at the glenoid. This device could represent a possible new and original solution, and we wait for clinical results15. Table 1

Study

Mean FU (months)

Revision rate

Function Scores

Sirveaux et al.20

44.5

4%

67 (Constant-Murley)

Werner et al.23

38

18%

72% (Relative Constant-Murley)

Frankle et al.19

33

13%

68.2 (ASES)

Favard et al.18

91

5%

61 (Constant-Murley)

Nolan et al.24

24

0%

62 (Constant-Murley), 76 (ASES)

Functional results and revision rate in published series of RTSA for massive RCT with or without glenohumeral arthritis.

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RTSA for young patients Despite not frequently, it is possible to find out a massive RCT with severe function impairment in patients aging the V or VI decade of life. Most of works state RTSA should be reserved for patients aged 70 years or more, because of the risk of components wear. Our personal choice is to consider the possibility of a RTSA implantation together with younger patients, clearly presenting them the eventual doubts concerning components wear due to strenuous activities, and the need for frequent radiographic followup evaluations. It is not unfrequent that after extensive explanations these patients accept the proposed solution. Two recently published works seem to support this behaviour. Sershon et al.16 report a short term success rate of 75% in a series of patients, most of which treated for post-traumatic arthropathy or revision surgery, indication subgroups known to have a worse prognosis than CTA and massive RCT. Neukom et al. describe good results in the long term follow-up, despite evidencing an high complication rate17. Of note, most of the complications described have been treated successfully without compromise to clinical outcome.

Results of RTSA in Cuff Tear Arthropathy and Massive Rotator Cuff Tears Favard et al.18 recently published the largest series (464 patients with a 7.5 years mean follow-up) of RTSA implanted for CTA. Reported mean active anterior elevation (AAE) improved from 69.3° to 128.6°, active external rotation (AER) with the abducted arm improved from 23.5° to 42.1°, while AER with the arm at the side showed little improvement, from 4.9° to 10.6°. Survivorship free of revision was 89% at 10 years with a marked break occurring at 2 and 9 years. Survivorship to a Constant-Murley score of less than 30 points was 72% at 10 years, with a marked break observed at 8 years. They observed progressive radiographic changes after 5 years and increasing frequency of large notches with long-term follow-up. Of note, most of the surgeons were at the beginning of their experience with RTSA, then data could suffer from the learning curve. Frankle et al.19 reported results of sixty patients with a rotator cuff deficiency and glenohumeral arthritis, with a mean follow-up of 33 months. The mean total score on the American Shoulder and Elbow Surgeons score improved from 34.3 to 68.2. The score for function on the visual analog scale (VAS) improved from 2.7 to 6, and the VAS score for pain improved from 6.3 to 2.2. AAE increased from 55° to 105.1°, and 41 of the sixty patients (67.2%) rated the outcome as good or excellent. Sirveaux et al.20 reviewed 80 shoulders with a mean follow-up of 44 months. Three implants had failed and had been revised. Mean Constant-Murley score increased from 22.6 points pre-operatively to 65.6 points at review. In 96% of these shoulders there was no or only minimal pain. Mean AAE increased from 73° to 138° (table 1). Studying a series of patients treated with RTSA, Wall et al. demonstrated that patients with primary CTA or massive RCT had better clinical outcomes than other diagnosis21.

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Figure 1. a) High degree scapular notching at 8 years follow-up. b) Delta III RTSA with upwards directed inferior screw: no sign of notching at 7 years follow-up.

The same conclusion can be found in a precedent work from Boileau et al.22 Furthermore, comparing results on two series of patients treated for primary or revision surgery, Werner et al. stated that patients in the two groups showed similar amounts of improvement. However, this observation should be taken with caution, because authors included in the “primary surgery” group also previously operated post-traumatic cases, probably biasing final results. In our experience, cases with sequelae from previous reduction and synthesis surgeries are more consistently comparable to revisions, with respect to technical difficulties and outcome results23.

Radiological results: focus on scapular notching RTSA ������������������������������������������������������ is associated with higher complication rates than anatomic shoulder arthroplasties. Most common complications include baseplate failure, instability, infection, nerve lesion, surgical site haematoma and scapular fracture. Despite a systematic treating is out of the purpose of this work (for review, see ref. 25) we agree with other authors in that we have only very limited series relating to RTSA in specific indications and we need to know how likely each complication is in a specific patient and not in completely different circumstances. Behind this consideration, we would tribute particular attention to the almost constantly reported radiographic complication of scapular notching. Infraglenoidal scapular notching in RTSA is a frequent finding related to mechanical impingement by the medial rim of the humeral cup against the scapular neck in adduction and internal-external rotation (Fig. 1a). This complication typically occurs within the first few months after RTSA24 and the reported incidence ranges from 44% to 96%. The influence of infraglenoidal scapular notching on clinical outcome has not been fully delineated yet and is still controversial in the current literature. Sirveaux20 showed a negative effect of scapular notching on the Constant-Murley score. On the contrary, Lévigne et al.26 do not report a correlation of scapular notching with clinical findings. Recent series with longer follow-up have demonstrated notching can be progressive and associated with reduced shoulder ROM,

strength, decreased subjective shoulder scores and relative Constant-Murley score, and increased polyethylene wear and potential for implant loosening27. Most of high-grade scapular notching cases is found between patients with longer follow-up18,27. This could reflect not only the progression of notching itself, but also technical changes that took place in the years, with actual trend towards a lowered and tilted positioning of the glenoid metal back. Whatever its final involvement be in implant stability and survival, attention should be paid, in our opinion, in order to minimize the occurrence of scapular notching. An inferior tilt of the metal back (10-15°) is auspicated. Just a little trick: the inferior screw fixating the metal back should be parallel to the central peg, and not inferiorly directed (Fig. 1b). When correctly placing the metal back in the lower part of the glenoid, this will avoid the inferior screw to pierce the cortical bone and, in case of notching, the polyethylene liner to take contact with the screw itself (with foreseeable consequences in terms of components wear). At this moment, it is not clearly defined how much the incidence of notching could be limited by using an inverted tribology (i.e. glenosphere in PE, metallic liner), while it is bona fide accepted that major diameter glenosphere could carry some advantages. Furthermore, some authors recently demonstrated good results in terms of limited notching incidence by using a glenosphere with eccentric design28.

RTSA combined with muscle transfer for combined pseudoparalysis Some patients show a combined deficit of active anterior elevation (AAE) and external rotation (AER), also referred to as combined pseudoparalysis. This condition generally relates to a massive posterosuperior tear of the rotator cuff, involving a ruptured or, more frequently, ipotrophic teres minor, with Goutallier grade III-IV fatty degeneration and positive hornblower’s and dropping signs. Both a massive RCT and CTA could underlie this pathology, and patient’s quality of life is often blunted. Activities of daily living such as eating, holding a phone or combing hair become difficult or impossible, since the patient cannot control the spatial positioning of his upper limb while raising an object with the hand30,31.

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Figure 2. a) Missing postoperative AER recovery after RTSA in a patient devoid of a functional teres minor muscle. b) T1-weighted MRI cut showing severe fatty degeneration of the posterior muscle of the rotator cuff (teres minor is highlighted).

RTSA allows the restoration of active overhead elevation in patients with a massive rotator cuff tear and pseudoparalysis of elevation. However, it does not restore active external rotation, the lack of which can substantially compromise the functional outcome. The teres minor muscle contributes to AER, and its deficiency may impair the clinical outcome after RTSA (Fig. 2). Simovitch et al.32 published results of 42 RTSA and correlated results to teres minor integrity and fatty degeneration. Shoulders with stage 0, I or II fatty infiltration of the teres minor muscle (group 1) had a significantly better ConstantMurley score and subjective shoulder value, than shoulders with stage III or IV (group 2). Group 1 had a net gain of 9° of external rotation with the arm at the side compared with an average loss of 7° in group 2. Authors therefore concluded that teres minor stage III or IV fatty infiltration compromises the clinical outcome of RTSA for massive RCT. Although AER deficit can be treated with a tendon transfer surgery, this technique alone may be inadequate to power external rotation and elevation with such global dysfunction, and is contraindicated when arthritic changes are present32-36. In our early experience with RTSA (without tendon transfer) we observed some patients functionally disabled after surgery. This was probably due to the absence of external rotator cuff muscles (infraspinatus and teres minor) with consequent no counterbalance for the strong functional internal rotators (pectoralis major, latissimus dorsi, teres major and subscapularis). Several surgeons, and we too, tried and find a solution by mean of a tendon transfer combined with the RTSA procedure. Gerber chose a double approach solution with transfer of the latissimus dorsi (LD) alone37. On the contrary, Boileau chose a combined transfer of LD and teres major (TM) by mean of a single deltopectoral approach, inspired by the old technique Merle D’Aubigné used for the treatment of obstetric paralysis (also referred to as modified L’Episcopo)38. And this was our first orientation. With this technique we obtained good results in recovering AER, with a significant loose in active internal rotation (AIR). Therefore, we hypothesized a single LD transfer where the tendon was passed through a split TM, by mean of a deltopectoral approach, but results were unsatisfactory again due to great variability.

Because of this, we finally came back and aligned with Boileau’s idea, accepting the residual AIR deficit39. Candidates for the combined procedure (RTSA & tendon transfer) are those patients showing severe active anterior elevation deficit with impossibility in keeping shoulder external rotation with the arm adducted, independently from the X-ray status of the joint. In most of these patients, the hornblower’s sign can’t be evidenced because of pain, limited elevation or joint stiffness, and the quantitative evaluation of ER with 90° arm abduction is sometimes not possible. This parameter would be of great interest when looking for functional results after transfer surgery but, because of the aforementioned reasons, few published series reported it37,38. In our practice, we evaluate the preoperative AER at maximum abduction, with the examinator sustaining the patient’s elbow. In the postoperative follow up visit the same evaluation is taken, at the same degrees of abduction, in order to obtain comparable measures. The indication for a combined procedure should be corroborated by imaging studies like CT or MRI, with axial and oblique-sagittal cuts directed to teres minor evaluation. In some cases, the indication is considered in the operative setting, after direct evaluation of the low quality of the teres minor and the high quality of muscles to be transferred. This is not an obvious find, because LD and TM could be damaged by rheumatoid pathologies, steroid therapies and previous surgeries as well, particularly at their humeral insertion. Some advantages are foreseeable, in such cases, for the single approach procedure with respect to Gerber’s technique, in which the preparation of the LD tendon precedes the prosthesis implantation and takes place through a different access.

RTSA with LD/TM transfer through deltopectoral approach: surgical technique With the patient in a beach-chair position, we use a classical deltopectoral approach, with distal extension to pectoralis major humeral insertion. This is cut 1,5 cm from the lateral margin of the biceps groove, allowing final reinsertion. Both the anterior axillary vessels and the axil-

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Figure 3. a) LD/TM tendon transfer showed in a cadaver specimen before reinsertion. b) Transferred LD and TM tendons after insertion at the teres minor insertion site.

lary nerve should be identified at the inferior border of the subscapularis. In these patients the subscapularis tendon is generally conserved, and it should be accurately detached form the lesser tuberosity and tagged40. The LHB is identified in its groove and it is cut or tenodesed, and the intra-articular portion resected. The humeral head is dislocated anteriorly allowing the RTSA to follow a standard technique. Medial reflection of the pectoralis major then exposes the combined insertions of the LD/TM. With the arm in internal rotation, these tendons are detached from the humerus. Heavy, nonabsorbable sutures are placed in the free ends of the combined tendons in a baseball stitch fashion. Both tendons are released to gain length, with attention in avoiding damage to the neurovascular pedicles. Adhesions are released with bluntly dissection when it is pushed medially, and always with the arm in adduction and flexion to relax the brachial plexus. Dissection should not venture beyond 6 cm medial to the tendon insertions, as anatomic studies identified the neurovascular pedicles of LD and TM at a minimum distance of 7.4 cm proximal to the humeral insertions41. When sufficient length is obtained (approximately 3–5 cm), the humerus is dislocated anteriorly and the tendons are transferred around its posterolateral aspect. The transferred tendons are fixed at the level of teres minor insertion, using transosseous sutures (Fig. 3). The sutures are placed before implantation and cementation of the definitive humeral prosthesis, reinforcing the construct by passing them around the prosthetic neck. When the tendon transfer is completed the prosthesis is reduced, and the subscapularis tendon reattached to the

lesser tuberosity with transosseous sutures passed through the bone at the bicipital groove level (also placed before cementation of the final implant). The pectoralis major is repaired then, and the wound closed under suction drainage. After surgery, the arm is placed in a sling in slight abduction and neutral rotation that is maintained for five weeks.

Results and discussion Boileau reported on seventeen consecutive patients who underwent the modified L’Episcopo procedure through a single deltopectoral approach and were followed for at least 12 months. Mean AAE increased from 74° preoperatively to 149° postoperatively, and AER increased from -21° to 13°42. In our experience, we followed 17 patients for an average of 30 months, basically managed with the same procedure proposed by Boileau. We prefer to call it Merle D’Aubigné procedure since he described in 1947 LD/TMtransfer through a single deltopectoral approach, suturing the transferred muscles on the pectoralis major stump, for treatment of birth brachial plexus palsy43. Our results were presented in Lyon Secec Meeting on September 2011 but are unpublished so far. In our series mean Constant-Murley score improved of 31 points (from 34 to 65), SSV 45% (from 29% to 74%), mean AER with the arm at the side improved 17° (from -12° to +5°). We also evaluated external rotation in ab-

Table 2

Sirveaux et al.20

Boileau et al.29

Werner et al.23

Simovitch et al.27

Nolan et al.24

Lévigne et al.26

Wall et al.21

Mizuno et al.28

80

45

58

77

71

337

152

47

Follow-up (months)

44,5

40

38

44

24

47

40

30.4

Notching

64 % 36 % 74 % 26 %

68 % 32 % 82 % 18 %

96 % 4 % 54 % 46 %

44 % 56 % 59 % 41 %

49 % 51 % 76 % 24 %

62 % 38 % 66 % 34 %

51 % 49 % 63 % 37 %

40 % 60 % 95 % 5 %

N of prosthesis

No notching Grades 1 & 2 Grades 3 & 4

Incidence of scapular notching in the main published series is summarized.

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duction, with the aforementioned technique, and gain was 32° (from 8° to 40°). Functional external rotation gain was excellent: 4.1 points (from 3.5 to 7.6), reflecting improvement of both elevation and external rotation. Patients were able to use the arm over the head level postoperatively, while they used it at the level of the sternum in the preoperative setting. Internal rotation significantly worsened: from a preoperative level of L1-L2 to buttock at follow-up. This worsening reflects what we call the “short blanket effect“: we explain to our patients that the price to pay to improve external rotation is to loose the opposite movement. This should be clearly discussed with the patient when the indication is given, taking into account internal rotation in the opposite limb: in presence of a bilateral deficit of internal rotation, to avoid a serious handicap in activities that involve such a movement (e.g. hygiene care), we believe the transfer procedure inadvisable. Boughebri et al.44 published results about 14 patients managed with the combined procedure through single deltopectoral approach. At an average 33.2 months follow-up, mean AAE and AER with the arm at the side improved significantly, from 64° to 126°, and from -9° to 27° (gain 36°) respectively. In their series, contrary to all the published ones and ours too, authors did not evidence a worsening of active internal rotation. Ortmaier et al.45 reported on 13 patients treated with RTSA in combination with latissimus dorsi transfer with a modified technique, harvesting the LD with a small piece of bone. At a mean 6 years follow-up, mean AAE improved from 55° to 138° and mean AER improved from -16° to 21° (gain 37°). They conclude that the modified technique leads to good tendon integrity, low rupture rates and good clinical outcome. Recently, Puskas et al.46 published results about 32 cases followed up for an average of 53 months after RTSA with LD transfer through a double approach technique. The age-related mean Constant-Murley score significantly increased from a preoperative value of 45% to 89%. The mean SSV increased from 33% to 75%. AER significantly improved from a mean of 4° to 27° (gain 23°). A preoperative external rotation lag sign could be corrected in 25 of the 32 shoulders. In their series, authors described a worsening of AIR, despite at a lower extent with respect to the AIR loss Boileau and we observed.

Conclusions Reverse total shoulder arthroplasty represents a useful solution in case of cuff tear arthropathy or massive rotator cauff tear with function impairment. Due to its inherent design, this kind of implant is able in recovering active anterior elevation at the overhead level in most of patients, despite lower results could be expected for active external and internal rotation. In presence of severe loss of active elevation and external rotation, combined latissimus dorsi transfer and reverse total shoulder arthroplasty can restore both AAE and AER. In our experience, the overall functional improvement in these patients is excellent: AER with the arm at the side improves of relatively few degrees, but AER in abduction

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improves of more than 30 degrees. Active internal rotation clearly worsen and it requires a thoughtful and eclectic behavior in presence of bilateral disease, for consequences inherent the activities of daily living. In some patients, tendons that should be transposed show a poor tissue quality due to prolonged corticosteroid therapy or iatrogenic lesions. In these cases, the decision about executing the transfer procedure should be considered in the operative setting, according to directly verified tendon quality. Surgery through a single deltopectoral approach is easier and faster compared to the dual access technique. Furthermore, according to our experience, it is also burdened by a lower complication rate. In our practice, we observed some cases in which RTSA without muscle transfer in patients completely devoid of the posterior cuff finally resulted in a sensible recovery of AER. The role the posterior deltoid muscle could lead in these situations and, more generally, in recovering AER has not been clearly defined yet. Finally, when considering indication for adding a tendon transfer, surgeons must keep in mind that most of expert authors indicate it in no more than 10-15% of their patients requiring RTSA for cuff tear arthropathy or massive rotator cuff tear.

References 1. Smith JG. Pathologic appearance of seven cases of injury of the shoulder joint with remarks. London Medical Gazette. 1834; 14: 280 2. Neer CS 2nd, Craig EV, Fukuda H. Cuff-tear arthropathy. J Bone Joint Surg Am. 1983; 65: 1232-44 3. Boileau P, Baque F, Valerio L, Ahrens P, Chuinard C, Trojani C. Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am. 2007; 89: 747-57 4. Walch G, Edwards TB, Boulahia A, Nove-Josserand L, Neyton L, Szabo I. Arthroscopic tenotomy of the long head of the biceps in the treatment of rotator cuff tears: clinical and radiographic results of 307 cases. J Shoulder Elbow Surg. 2005; 14: 238-46 5. Grammont PM, Baulot E. Delta shoulder prosthesis for rotator cuff rupture. Orthopedics. 1993; 16: 65-8 6. Klinger HM, Steckel H, Ernstberger T, Baums MH. Arthroscopic debridement of massive rotator cuff tears: negative prognostic factors. Arch Orthop Trauma Surg. 2005 May; 125 7. Liem D, Lengers N, Dedy N, Poetzl W, Steinbeck J, Marquardt B. Arthroscopic debridement of massive irreparable rotator cuff tears. Arthroscopy. 2008; 24(7): 743-8 8. Klinger HM, Spahn G, Baums MH, Steckel H. Arthroscopic debridement of irreparable massive rotator cuff tears - a comparison of debridement alone and combined procedure with biceps tenotomy. Acta Chir Belg. 2005; 105(3): 297-301 9. Drake GN, O’Connor DP, Edwards TB. Indications for reverse total shoulder arthroplasty in rotator cuff disease. Clin Orthop Relat Res. 2010; 468(6): 1526-33 10. Harreld KL, Puskas BL, Frankle MA. Massive rotator cuff tears without arthropathy: when to consider reverse shoulder arthroplasty. Instr Course Lect. 2012; 61: 143-56 11. Hyun YS, Huri G, Garbis NG, McFarland EG. ���������������� Uncommon indications for reverse total shoulder arthroplasty. Clin Orthop Surg. 2013; 5(4): 243-55 12. Gerber C. Latissimus dorsi transfer for the treatment of irrepa-

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rable tears of the rotator cuff. Clin Orthop Relat Res. 1992; 275: 152-60 13. Costouros JG, Espinosa N, Schmid MR, Gerber C. Teres minor integrity predicts outcome of latissimus dorsi tendon transfer for irreparable rotator cuff tears. J Shoulder Elbow Surg. 2007; 16(6): 727-34 14. Weening AA, Willems WJ. Latissimus dorsi transfer for treatment of irreparable rotator cuff tears. Int Orthop. 2010; 34(8): 1239-44 15. Savarese E. and Romeo R. New solution for massive, irreparable rotator cuff tears: the subacromial “Biodegradable Spacer”. ��� Arthrosc Tech. 2012; 1(1): e69-e74 16. Sershon RA, Van Thiel GS, Lin EC, McGill KC, Cole BJ, Verma NN, Romeo AA, Nicholson GP. Clinical outcomes of reverse total shoulder arthroplasty in patients aged younger than 60 years. J Shoulder Elbow Surg. 2014; 23: 395-400 17. Ek ET, Neukom L, Catanzaro S, Gerber CJ. Reverse total shoulder arthroplasty for massive irreparable rotator cuff tears in patients younger than 65 years old: results after five to fifteen years. J Shoulder Elbow Surg. 2013; 22(9): 1199-208 18. Favard L, Levigne C, Nerot C, Gerber C, De Wilde L, Molé D. Reverse prostheses in arthropathies with cuff tear: are survivorship and function maintained over time? Clin Orthop Relat Res. 2011; 469(9): 2469-75 19. Frankle M, Siegal S, Pupello D, Saleem A, Mighell M, Vasey M. The reverse shoulder prosthesis for glenohumeral arthritis associated with severe rotator cuff deficiency: a minimum two-year follow-up study of sixty patients. J Bone Joint Surg Am. 2005; 87: 1697-705 20. Sirveaux F, Favard L, Oudet D, Huguet D, Walch G, Molé D. Grammont inverted total shoulder arthroplasty in the treatment of glenohumeral osteoarthritis with massive rupture of the cuff: results of a multicentre study of 80 shoulders. J Bone Joint Surg Br. 2004; 86: 388-95 21. Wall B, Nove-Josserand L, O’Connor DP, Edwards TB, Walch G. Reverse total shoulder arthroplasty: a review of results according to etiology. J Bone Joint Surg Am. 2007; 89: 1476-85 22. Boileau P, Watkinson D, Hatzidakis AM, Hovorka I. Neer Award 2005: The Grammont reverse shoulder prosthesis: results in cuff tear arthritis, fracture sequelae, and revision arthroplasty. J Shoulder Elbow Surg. 2006; 15: 527-40 23. Werner CM, Steinmann PA, Gilbart M, Gerber C. Treatment of painful pseudoparesis due to irreparable rotator cuff dysfunction with the Delta III reverse-ball-and-socket total shoulder prosthesis. J Bone Joint Surg Am. 2005; 87: 1476-86 24. Nolan BM, Ankerson E, Wiater JM. Reverse total shoulder arthroplasty improves function in cuff tear arthropathy. Clin Orthop Rel Res. 2011; 469(9): 2476-82 25. Farshad M, Gerber C. Reverse total shoulder arthroplasty from the most to the least common complication. Int Orthop. 2010; 34(8): 1075-82 26. Lévigne C, Boileau P, Favard L et al. Scapular notching in reverse shoulder arthroplasty In: Walch G, Boileau P, Molé D, Favard L, Lévigne C, Sirveaux F: Reverse shoulder arthroplasty: Clinical results, Complications, Revisions. Ed. Sauramps Médical, Montpellier, France 2006, pp. 353-72 27. Simovitch RW, Zumstein MA, Lohri E, Helmy N, Gerber C. Predictors of scapular notching in patients managed with the Delta III reverse total shoulder replacement. J Bone Joint Surg Am. 2007; 89: 588-600 28. Mizuno N, Denard PJ, Raiss P, Walch G. The clinical and radiographical results of reverse total shoulder arthroplasty with eccentric glenosphere. Int Orthop. 2012; 36(8): 1647-53 29. Boileau P, Watkinson D, Hatzidakis AM, Balg F. Grammont reverse prosthesis: design, rationale and biomechanics. J Shoulder Elbow Surg. 2005; 14: 147S–51S

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30. Goutallier D, Postel JM, Bernageau J, Lavau L, Voisin MC. Fatty muscle degeneration in cuff ruptures. Clin Orthop Relat Res. 1994; 304: 78-83 31. Walch G, Boulahia A, Calderone S, Robinson AH. The ‘dropping’ and ‘hornblower’s’ signs in evaluation of rotator-cuff tears. J Bone Joint Surg Br. 1998; 80: 624-8 32. Simovitch RW, Helmy N, Zumstein MA, Gerber C. Impact of fatty infiltration of the teres minor muscle on the outcome of reverse total shoulder arthroplasty. J Bone Joint Surg Am. 2007; 89: 934-9 33. Covey DC, Riordan DC, Milstead ME, Albright JA. Modification of the l’Episcopo procedure for brachial plexus birth palsy. J Bone Joint Surg Br. 1992; 74: 897-901 34. Edwards TB, Baghian S, Faust D, Willis RB. Results of latissimus dorsi and teres major transfer to the rotator cuff in the treatment of Erb’s palsy. J Pediatr Orthop. 2000; 20: 375-9 35. Freund RK, Terzis JK, Jordan L, Taylor G. Modified latissimus dorsi and teres major transfer for external rotation deficit of the shoulder. Orthopedics. 1986; 9: 505-6 36. Gerber C, Maqueira G, Espinoza N. Latissimus dorsi transfer for the irreparable rotator cuff tears. J Bone Joint Surg Am. 2006; 88: 113-20 37. Gerber C, Pennington SD, Lingenfelter EJ, Sukthankar A. Reverse Delta-III total shoulder replacement combined with latissimus dorsi transfer. A preliminary report. J Bone Joint Surg Am. 2007; 89: 940-7 38. Boileau P, Chuinard C, Roussanne Y, Bicknell RT, Rochet N, Trojani C. Reverse shoulder arthroplasty combined with a modified latissimus dorsi and teres major tendon transfer for shoulder pseudoparalysis associated with dropping arm. Clin Orthop Relat Res. 2008; 466: 584-93 39. Ivaldo N, Rossoni M, Caione G, Franzi P. Latissimus dorsi transfer associated to Grammont reversed shoulder prosthesis: results at 22 months of follow up. Minerva Ortop Traumatol. 2006; 57: 329-36 40. Boileau P, Chuinard C, Roussanne Y, Neyton L, Trojani C. Modified latissimus dorsi and teres major transfer through a single deltopectoral approach for external rotation deficit of the shoulder: as an isolated procedure or with a reverse arthroplasty. J Shoulder Elbow Surg. 2007; 16: 671-82 41. Bartlet SP, May JW, Yarenchuk MJ. The latissimus dorsi muscle: a fresh cadaver study of the primary neurovascular pedicle. Plast Reconstr Surg. 1981; 67: 631-6 42. Boileau P, Rumian AP, Zumstein MA. Reversed shoulder arthroplasty with modified L’Episcopo for combined loss of active elevation and external rotation. J Shoulder Elbow Surg. 2010; 19: 20-30 43. Merle D’Aubigné R. Paralysie obstétricale du plexus brachial traitée par transposition des tendons du grand rond et du grand dorsal. Mémoire Académie de Chirurgie 1947; 73: 561 44. Boughebri O, Kilinc A, Valenti P. Reverse shoulder arthroplasty combined with a latissimus dorsi and teres major transfer for a deficit of both active elevation and external rotation. Results of 15 cases with a minimum of 2-year follow-up. Orthop Traumatol Surg Res. 2013; 99: 131-7 45. Ortmaier R, Resch H, Hitzl W, Mayer M, Blocher M, Vasvary I, Mattiassich G, Stundner O, Tauber M. Reverse shoulder arthroplasty combined with latissimus dorsi transfer using the bonechip technique. Int Orthop. 2014; 38:553-559 46. Puskas GJ, Catanzaro S, Gerber C. Clinical outcome of reverse total shoulder arthroplasty combined with latissimus dorsi transfer for the treatment of chronic combined pseudoparesis of elevation and external rotation of the shoulder. J Shoulder Elbow Surg. 2014; 23: 49-57

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Shoulder arthroplasty’s rehabilitation Rossella Costantino, Lorenzo Panella, Elisa Prisco U.O.C. Medicina fisica e riabilitazione, Istituto Ortopedico G. Pini, Milano

Introduction The shoulder joint is often subject to different kinds of traumatic events or various degenerative diseases which may become disabling in course of time. The most common reasons that cause imbalances in the shoulder are injuries to the soft tissues (rotator cuff), osteoarthritis, arthritis, avascular necrosis and fracture of the proximal humerus. For the rehabilitation therapist is necessary to know the pathology of disease accurately, the choices and the modus operandi of the surgeon who performed the prosthesis surgery, in order to draw up a careful rehabilitation program that bears the patient’s peculiarities in mind. The rehabilitation program is applied following a temporal sequence. This allows the tissues healing, the joint mobilization and, finally, the strengthening muscle and the functional recovery1. Mobility, strength and stability are the three functional elements of the shoulder that can be compromised by an acute or chronic injury and they must be restored. The physiotherapist has to inform the patient about the possibility to run into functional limitations and must instruct him the strategies to be able to carry out everyday activities using better the potentialities of the “new” articulation2. However, we must always remember that while the therapist evaluation parameters can and must be others as well, for the patient one of the main valutation measures of the operation and of rehabilitation success will be the disappearance of pain3.

Rehabilitation treatment Rehabilitation begins immediately after surgery. The rehabilitation program has the following purposes (Brotzman SB, Wilk KE)1: passive amplitudes recovery; active motion recovery; muscular strengthening and returning to normal activities of daily living. This protocol takes long time and a few months pass between the first passive movements and the complete recovery of motion and strength. The phases of rehabilitation following a logical sequence that must be respected carefully. The time that is dedicated to each stage in order to move to the next one is not constant, but extremely variable from one patient to another. It also depends on the goals he intends to reach, his overall physical conditions which are often related to age and status of the periarticular structures before the surgery. For this reason it is not possible to determine fixed deadlines between one phase and the other of the rehabilitation program, but only general indicative lines on the timing which is normally required to reach a certain goal. Therefore, through exercise, the rehabilitator must assign

to the patient some tasks, which must have as purpose the specific activation request to local strategies compromised and not to the attainment of the final result or to the muscle strengthening. Thus it must be activated the capacity deriving from the ability to connect central and peripheral mechanisms in a variable dynamic way. The exercises, that are gradually included, before passive then active assisted and active lastly, do not replace each other, but they are added to those already acquired previously. In the end they allow an overall recovery of motility (clearly dictated by individual variables). Generally a series of rehabilitation programs are applied because of the compliance with the various biological phases of traumatized tissues repair by careful exercises of passive, segmental and global motility, isotonic exercises in a particular joint range and isometric exercises. It also provides a strengthening of the insufficient musculature through exercises in a closed kinetic chain, exercises against increasing resistance, isokinetic and proprioceptive exercises. The passive mobilization is the first physiotherapic operation implemented in all types of shoulder pathology. It is performed by the therapist, but also through practices of gravitational and self-assisted mobility. Traditional exercises are usually preferred. Permforming them you must check that the mobilization takes place in the scapular plane. Actually, the exercises executed on this level guarantee a correct biomechanical alignment. The first few weeks of treatment are usually set up with caution because of the pain4. In this first phase, the scar treatment is important to encourage the flow of the underlying tissues and to soothe the pain of the pulled cutis. Generally, at the beginning of the session, we prefer to start with the treatment of relaxation of the trapezius and paravertebral through cervical pompages and the help of deep breathing5. It continues with a cautious passive motility of the elbow to retrieve the extension, also using postures of relaxation in extension. The patient is educated on the movements he has to avoid when he practices them at home because they might endanger the stability of the prosthesis and self-mobilization exercises of hand, wrist and elbow6. Through the exercises defined commuters, proposed by Codman, we try to get mobilization by the force of gravity, making a pendulum movement to be performed first in the frontal, then sagittal and finally, in a circular, clockwise and counterclockwise way. After the first stage of passive exercises, we will switch to an active phase, in which we distinguish an initial segmental treatment following by another defined global. The first step is dedicated to the recovery of motility, maintaining, initially, a free range from pain, using the scapular plane

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and having the foresight to support the arm and then extend more and more the motility range. The initial movements, which are performed in the supine position trying to avoid as much as possible any compensations, are aimed at the recovery of flexion and extension . In addition, you can begin the passive motility of the shoulder blade sliding it slowly on the chest wall, in the directions physiological scapulars, trying to restrict acromion movements in the lateral decubitus position on the healthy side. Afterwards abduction and adduction movements will be introduced always in a supine position. At a later time, you can devote to the strengthening of the individual muscles. Currently, for the shoulder pathology, strengthening exercises aimed at the individual muscle are suggested, performing them either against the resistance offered by the therapist, or against the resistance made by the patient himself or with his help. Beside exercises which require the voluntary contraction of individual muscles, defined segmental, at a later stage of treatment, the use of global type exercises in which the activation of a large number of muscles is requested is raccomanded. In later stages, rotational movements, both internal and external, are added. When you plan the exercises you will need: to identify the function which is involved in the ability of the shoulder to participate in organizational processes (for instance, function of indication, tracking, achievement, pressure and boost, etc.); to identify which contribution the shoulder gives to the retrieval object function; to identify through which ways the shoulder is able to cope with the need to allow the relationships among the various body segments in relation to different functions. The exercise must be a cognitive problem to be solved by the selection and splitting of some body segments and, therefore, it will be based on the development and testing of perceptual hypotheses aimed at solving the problem.

Proprioceptive exercises Starting from this premise, we propose a initial group of exercises directed specifically to enable local strategies which affect the relationship among the sternum, clavicle and scapula in order to ask the patient the building of a correct relationships. The patient suffering from shoulder disorders, hardly presents a perfect symmetry of body towards the midline. Problems posed by this situation can be controlled through the application of touch operations, evoked through the request for the recognition of sponges of different texture in a sitting position2. The exercise proposed to recognize contact-pressure information, through the use of sponges of different consistency. Therapists place these sponges significantly, in correspondence of the scapula, in the direction of the movement of the rear position of the track, in correspondence of the clavicle, in relation to the direction of elevation movement of shoulder and in correspondence of the front part of the track for anteposition movements. With this type of information you are able to reconstruct more accurate reports of fragmentation among different joints, through proper use of muscle systems. In this way an evolution of the scapula motility occurs. From an initial

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static breakaway, i.e. to not relations with the trunk, it starts to build more meaningful relationships, also of dynamic type, which enable the movements for the proper maintenance of the correct position of upper limb. From this first step an improvement in pain symptoms may also derives. Its genesis is to be found both in the antalgic contracture, and in a sort of deafferentation, but also in a reduced ability to perceive correctly the somesthetic information. In the third group of exercises the requests made to the patient are designed to require the activation of spatial operations, characterized by a broader hike and more attention is given to the mobility of the glenohumeral joint, whose movements and informative activities are interested in solution of spatial type tasks. In this group of exercises, the preference is given to the pursuit and achievement of trajectories, among which you should preferred circular paths as there are substantial evidences which support some hypothesis that the upper limb movements occur within strategies related to movements with conical apex at the level of the glenoid and they allow full activation of all muscle components of the joint. The solution of the problem posed by this exercise to the patient requires the construction of a correct rotational orientation of the humeral head with the glenoid; the exercise evolution allows the hand the reacquisition of freedom to move properly in a broader space.

Idrokinesitherapy For nearly a century, both in orthopedics and traumatology, and in neurological field, we tried to use water as a rehabilitative means exploiting its inherent characteristics. For the last thirty years, however, this branch of rehabilitative medicine has taken on its own identity. It has been the subject of scientific studies and critical evaluation in order to define precise clinical indications and protocols to be followed in every single diseases. Rehabilitation in water can be active and passive, instrumental or it can be consisted on physical exercises performed in water, not necessarily of swimming type. In any case, we use the water capacities, from the principles of hydrodynamics to the ludic effect7. Inherent properties of water play an important role in the therapeutic targets, and they can be amplified through appropriate techniques enriching the therapeutic possibilities. It also important to point as the motor activity, carried out in water, offers the possibility of a recovery of “schemes and images” motility which, although partially summoned after the trauma or disease are been “lost”, forgotten, because they have been exercised no more. Moreover, the use of water can lead significant changes to the components of motor deficit hindering functional recovery and finally it integrates itself with the other rehabilitative strategies. Therefore, the intervention must seek the best conditions for the patient to move in everyday life, through a process of adaptation to a situation of dipping, or confronting the physical properties of water and the constraints that follow. In other words, he can use the facilities and difficulties, that exercising in the water offers, for progressively recover the best motor conditions on earth. Rehabilitation in water is a strong tool for a rehabilitation treat-

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ment because the practice of this activity takes as the meaning of a complement to the rehabilitation program implemented in the gym and it agrees with the therapeutic goals. There are many parameters that should be taken into consideration for a good personalization of a therapeutic program. Everything can undergo same changes, from the time of application to the number of sessions, its approach may change and, not least, the patient’s intrinsic aquatic ability affects the treatment. In conclusion, the progress of stages and phases of the patient should illuminate the rehabilitation process. Some objectives are often longer than expected, but in the other side, other objectives amaze for the simplicity and speed in their implementation7. Thanks to the properties of water it is possible to earn both objectively a wider and fluid range of motility and give the possibility of muscular strengthening, and subjectively it gives a positive psychological feedback to patients. It will be illustrated below rehabilitation programs for two common situations, in which greatly vary rehabilitation time and manners2: 1. Shoulder prosthesis with anatomic rotator cuff valid; 2. Reverse shoulder replacement with rotator cuff invalid.

1. Shoulder prosthesis with anatomic rotator cuff valid Phase - I ( 1st -5th week) 1st week: after the surgery is packaged in a brace abduction of 10 °, to be maintained for 15-20 days. We Use removable brace, to allow personal hygiene and mobilization of the elbow of the hand. 2nd-3rd week: the brace is removed to perform physical therapy. It is possible passive mobilization of the shoulder, without reaching painful amplitudes. It is permitted up to 90° flexion and 45° abduction. Passive mechanical immobilizers (CPM) appear useful at this stage, with a programming of the arc allowable movements type. The patient should perform independently the commuters Codman exercises and the passive motility in flexion with the help of the other arm. 4th Week: the use of the brace is limited at night and a few hours a day. 5th week: patient leaves the brace and the assisted exercises in flexion-extension and abduction are allowed. The patient can begin rehabilitation in water. Phase II (6th -12th week) 6th week: we switch to active physiotherapy in flexion-extension and larger movement arc. Rotation are begun. Some stretching movements are useful to counteract the tendency of the capsule to stiffen, especially in his back. When patient has reached a good range of motility, we start with muscular strengthening. In the end of the period, patient starts the receptive exercises for restoring efficiency and speed in automatic gestures. Phase III (13th -16th week) 13th week: we continue with the muscular strengthening and training of perception; the other muscular chains are involved in a more intensive way, in order to re- inscribe the shoulder in its natural context of “pivot” between the creative gestures of upper arts and the task of supporting his own lower limbs2,8.

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2. Reverse shoulder replacement with rotator cuff invalid The rehabilitation of the reverse prosthesis requires from the rehabilitator the knowledge of the peculiarities of the plant. In addition, as this is often used in absence of the rotator cuff, it is important to know the conditions of the pre-operative group of the deltoid muscle, even if the validity of deltoid typically has already been established by the surgeon in pre-operative phase, because this is essential for the prosthesis function. Generally, the plant input allows the recovery of the abduction bending within acceptable limits for a discreet personal autonomy, as these movements are simplified by the positioning of the center of rotation in a lower and laterally way with respect to the norm. The achievement of an active elevation between 100-150 ° is a frequent result. Rotations are limited, but still possible, due to the preservation of the front cuff (subscapularis) and rear (small round and remaining portion of the infraspinatus)9. The reverse prosthesis often represents the final attempt to rescue a situation that is already compromised. Therefore, the main objectives of rehabilitation should be the pain reduction for the patient and a decent autonomy. An exaggerated quest for an unlikely extension of the joint range may expose the patient to risks that are not relatable to the hypothetical advantages. This kind of prosthesis allows a rehabilitation more or less earlier than the endo and arthroplasty in sliding2 . Phase - I ( 1th -3th week) 1st week: after surgery, the shoulder is immobilized with a brace in slight abduction and neutral rotation for 15-20 days; elbow and hand are free and must be mobilized early. 2nd week: if the absence of the headset is complete and it has not been made any reconstruction of the subscapularis, after about seven days, the limb can be temporarily released from the brace and mobilized passively in flexion and abduction, from 45° to 60°, taking care to respect the limits obtained by intraoperative measurements. Commuters exercises can be carried on for a few minutes, several times a day. 3rd week: you can begin the assisted mobilization. At the same time, you can start a rehabilitation cycle in pool. Phase II (4th - 5th week) 4th week : we allow the use of discontinuous brace, which is left at night for a few hours. Then, we begin the kinesitherapy. 5th week: the brace is removed. We seek the muscular compensation, if the amplitude of joint allows it. We will assist the patient in the realization of possible movements, inserting them in the functional diagrams, and most common and useful for him. Measures in the rehabilitation of shoulder replacement in fracture. Functional recovery after shoulder replacement surgery in fracture is more delicate than prosthetic interventions performed with other indications such as osteoarthritis and rheumatoid arthritis. This functional recovery is based on the opposite need to mobilize early the patient to avoid the formation of adhesions that can limit the range of joint motility and to protect the tuberosity osteosutured carefully by the surgeon. This seemingly irreconcilable requirement finds its manifes-

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tation identifying the type of patient to be treated and dedicating a physiotherapist for each patient in the early stages of immobilization of replaced joint . The identification of the patient is based, first, on the “report” provided by the surgeon who will indicate with “good”, “satisfactory” or “poor “ the mechanical quality of tuberosity osteosuture; on the other hand, it will be based on the study of the patient performed by the physiatrist . Physiatrists must investigate the following parameters for each patient candidated for a rehabilitation of prosthesis on fracture: the resilience of motor pattern; the ability to follow directions provided by the therapist in the delicate phase of passive mobilization; the quality of bone, muscle and tendon tissues; personal response to pain, possibly basing on a carefulness collection of the history of previous works carried out by the patient; personal motivations for a maximum recovery. At this point, we identify two kinds of patients to who will be devoted as many types of customized rehabilitation programs, always aiming to minimize the immobilization time10.

1) The normal rehabilitation program. It is dedicated to patients whose osteosuture quality was judged sufficient, and in which there is inability to perform a true passive mobilization. The patient protection will be total for 16-18 days. Then, we will begin with an elevation passive which should get to 90° after 25-30 days. Rotations will be protected for about four weeks, and then gradually increase the range of motility in a selective manner, while we enhance the elevation. 2) Deleyed rehabilitation program. It is dedicated to patients whose osteosuture quality was judged poor and in who there is a poor tolerability to pain, resulting an inability to perform a true passive mobilization. It is recommended maximum protection for four weeks. Passive elevation recovery begins after four weeks, expecting to reach 90° in a few weeks. Rotation recovery starts after about 50-60 days from the surgery with extreme caution. In this category of patients, introducing hydrokinetic may be useful after four weeks post-surgery in order to reduce joint stiffness that always accompanies long periods of immobilization.

Conclusions The results obtained after surgery of the shoulder prosthesis are closely related to a careful study of pre-operative of patient for a correct direction, the proper positioning of prosthesis and a personalized program of functional rehabilitation. Actually, it is noted as the rehabilitation program will vary, sometimes considerably, depending on the disease and the type of surgery performed1. Therefore, it is necessary for the rehabilitation therapist a deep understanding of the disease pathology and the surgical technique used, in order to make a precise and timely rehabilitation daily program, taking care the peculiarities of

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the patient, and that lasts up to several months after intervention. However, in literature, the results obtained appear to be the best in terms of articulation, functionality and disappearance of pain in those patients who have had the opportunity to access treatments hydrokinetic in the course of rehabilitation. In fact, hydrokinetic becomes essential in the shoulder treatment because: the articulation gradually returns without stressing the articular heads; it allows the execution of movements ever wider, respecting the recovery times; it allows to perform exercises in a tridimensional space and to change positions easily and without effort; it limits pain, reduces recovery times and forces to postural symmetry, reducing fees11. In addition, results improve significantly in those patients who, despite having completed the cycle of re-education, performed regularly recalls with a rehabilitation therapist or independently. In fact, these calls allow to avoid complications and, above all, to preserve over time the results obtained in the months following the intervention. In conclusion, we feel in any case to support the importance of a rehabilitation program also taken up to several months after surgery, focusing on respect for the physiological time of tissue healing, a careful and conscious articulation motility, and finally, a muscular strengthening and functional recovery which uses the physical characteristics of the aquatic environment as a rehabilitation setting preferred in diseases of the upper track.

REFERENCES 1. Brotzman SB, Wilk KE La riabilitazione in ortopedia. II ed., Excerpta Medica, Milano 2004 2. Valobra GN, Gatto R, Monticone M Medicina fisica e riabilitazione. Utet 2008: cap. 55-56-108-112 3. Di Domenica F, Galletti R, Leo R Riabilitazione dopo intervento di osteosintesi o protesi di spalla in frattura. Arch Ortop e Reumatol 2011; 122: 31-3 4. Marinko LN, Chacko JM, Dalton D, Chacko CC The effectiveness of therapeutic exercise for painful shoulder conditions: a metaanalysis. J Shoulder Elbow Surg 2011; 20(8): 1351-9 5. Gleyze P, Flurin PH, Laprelle E, et al. ���������������������������� Pain management in the rehabilitation of stiff shoulder: prospective multicenter comparative study of 193 cases. OTSR 2011; 97: S195-203 6. Gleyze P, Georges T, Flurin PH, et al. Comparison and critical evaluation of rehabilitation and home-based exercises for treating shoulder stiffness: prospective, multicenter study with 148 cases. Orthopaedics & traumatologi, surgery and research: OTSR 2011; 97: S182-94 7. Becker BE Aquatic Therapy: Scientific Foundations and Clinical Rehabilitation Applications. Bruce American Academy of Physical Medicine and Rehabilitation. PM&R 2009; 1:859-872 8. Seitz WH, Michaud EJ Rehabilitation after shoulder replacement: be all you can be! Semin Arthr 2012; 23: 106-113 9. Marrero L, Garcia G, Pacheco I Early outcomes of reverse total shoulder arthroplasty. Boletín de la Asociación Médica de Puerto Rico 2009; 101:34-7 10. Inglese F, Creta D, Biondi M Fratture dell’estremo prossimale dell’omero e protesi di spalla: trattamento riabilitativo. Lo Scalpello 2009; 23:70-4 11. Castillo-Lozano R, Cuesta-Vargas A, Gabel CP Analysis of arm elevation muscle activity through different movement planes and speeds during in-water and dry-land exercise. J Shoulder Elbow Surg 2013; 23:159-65

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