OCD pathogenesis and treatment

OCD – pathogenesis and treatment Dr. Lisa Fortier, DVM, PhD, Diplomate American College of Veterinary Surgeons Office C3-181 VMC, phone 253-3102, emai...
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OCD – pathogenesis and treatment Dr. Lisa Fortier, DVM, PhD, Diplomate American College of Veterinary Surgeons Office C3-181 VMC, phone 253-3102, email [email protected] Osteochondrosis is an orthopaedic disease that occurs commonly in horses. The term osteochondrosis is a general term for the disease that results from a disturbance in the process of endochondral ossification. Although the terms osteochondrosis, osteochondritis and osteochondritis dissecans are frequently used interchangeably, they each apply to distinct pathologic conditions. Osteochondrosis (OC) may be broadly defined as a failure in endochondral ossification, osteochondritis implies joint inflammation which occurs when the lesion reaches the joint surface, and osteochondritis dissecans (OCD) is usually reserved for those cases in which a dissecting flap of cartilage/bone is present (dissecans is from the Latin phrase “to separate”). Etiology The fundamental problem in OC/OCD is a focal failure of endochondral ossification leading to retention of growth cartilage. Endochondral ossification is the normal process by which cartilage is replaced by bone during development. It occurs in the metaphyseal growth plate (physis), the articular/epiphyseal cartilage complex, and in the cuboidal bones. Osteochondrosis can therefore occur in any of these locations. Endochondral ossification is initiated when blood vessels penetrate the diaphysis (nutrient artery) and epiphysis of the immature bone. The blood vessels terminate in cartilage canals within the growth cartilages and deliver osteoblasts which secrete osteoid to begin bone formation. There are strong experimental (pigs) and clinical data (pigs, horses) that suggest that disruption of the blood supply within cartilage canals supplying the hypertrophic zone of the growth cartilage, can cause OCD. The lack of blood supply precludes final maturation of growth cartilage into bone, and the retention of thickened growth cartilage. The epiphyseal/metaphyseal vessels might be occluded through trauma or repetitive microtrauma (think large, uncoordinated foal), or there might be a primary failure in some part of the complex signaling pathways that control the coordination of vascular patterning, growth, and mineralization during endochondral ossification. However, it is generally accepted that OC/OCD is multifactorial in nature and the detailed mechanisms of failed endochondral ossification remain unknown but under intense investigation in animals and human beings. Some of the proposed etiologies for OC/OCD are outlined below. Regardless of the cause, the end result is retention of growth cartilage which is weaker than the surrounding normal bone and cartilage tissues, rendering it susceptible to trauma with subsequent separation of the lesion from the parent bone. It is generally believed that OC/OCD is a multifactorial disease and several factors have been implicated in the pathogenesis of the disease. Genetics: There are few genetic studies on OCD in horses, but those performed by Grondahl and Disti groups suggest a substantial heritable component to the disease. The exact nature of the heritability has not been identified. Genetics and environment are difficult to separate and together probably impact the factors listed below. Growth rate: Rapid growth rate from 0-16 months has been linked to OCD of the distal intermediate ridge of the tibia in Standardbreds and to OCD of the lateral trochlear ridge of the femur in Warmbloods, but not to other OCD lesions. These results imply that growth rate is a contributing factor, but no specific lesions sites can be predicted based on breed or growth rate. Nutrition: There is no one mineral that, when administered, will prevent OCD, or vice versa will cause OCD when deficient. Excessively low copper, calcium or phosphorus will lead to several skeletal abnormalities and likely reflect a poor diet in general. Excessive zinc will lead to copper deficiency and increased incidence of OCD. Several studies have linked overfeeding (high-energy

diets) to increased incidence of OCD. The diet of the neonate is clearly important, but the diet of the mare should be analyzed as well to ensure that a balanced, non energy-excessive diet is administered during gestation and lactation. Gender: OCD appears to be more common in males than in females, but the reports are inconsistent. Exercise: Again, conflicting reports. Moderate exercise is not a major factor in the development of OCD lesions. Excessive exercise should be considered as trauma/biomechanical forces. Trauma and biomechanical forces: It is generally believed that trauma can convert an OC into an OCD, but the effects of trauma on the development of OC/OCD are less well established. The theory of repetitive microtrauma insulting the relatively fragile metaphyseal/epiphyseal blood supply and halting endochondral ossification is an attractive and popular theory. Whether the trauma results in increased negative signals for progression of endochondral ossification or decreased positive signals is not known but is under intense investigation. OCD of the articular epiphyseal growth cartilage In synovial joints, OCD presents as symptomatic lesions that cause pain, recurrent synovitis (effusion), altered joint mechanics, and possible pain from interference in joint mobility by loose bodies (aka joint mice). OCD is a probable precursor of osteoarthritis because of altered joint mechanics and recurrent synovitis. Therefore, early recognition and surgical treatment may prevent long-term sequelae such as osteoarthritis. Synovitis and lameness are typical presenting signs and horses are typically more lame after flexion of the affected joint. The synovitis may be quite marked in cases where the OCD fragment has broken free from the parent bone. However, joint effusion in the absence of lameness is not uncommon. The effusion may increase following work, and diminish with 24-48 hours of stall rest or administration of NSAIDs. Clinical signs of lameness and synovitis can be triggered by mechanical or traumatic forces. This is an important point of discussion with many owners/breeders who would much rather believe that their horse has a traumatic fracture rather than a potentially heritable OCD lesion. Radiographic examination will reveal the extent of the lesion in depth and length, the presence of any loose bodies, and, in chronic or severe cases, possible signs of osteoarthritis. Radiographs will provide a starting point for discussions with the client concerning the patient’s prognosis. The prognosis may need to be adjusted following surgical exploration. Always be sure to radiograph the opposite, apparently normal joint and be sure to palpate all joints for synovitis. In humans, MRI is the most commonly used diagnostic imaging method. With the advent and increasing availability of standing MRI units for horses, this technique may gain popularity in horses as well. OC of the metaphyseal physis Thickened cartilage has been found in the growth plates of foals in association with radiographic and clinical signs of the condition known as physitis (aka epiphysitis). This condition occurs most frequently in the distal radius growth plate. Physitis occurs most frequently in large, fast growing foals and may be associated with angular limb deformities. In general, the relationship between OC and physitis is not well established. Foals with physitis are variably lame and present with visibly enlarged growth plates that are sensitive to palpation. Radiographs reveal wide, irregular growth plates with metaphyseal flaring. The disease is self limiting and rarely requires treatment. Short-term NSAID administration may be necessary for patient comfort. Joints affected The larger diarthrodial joints such as the scapulohumeral, femoropatellar, tarsocrural and metacarpophalangeal joints are more commonly affected than the smaller joints. Although a single joint

may be involved, bilaterally symmetric lesions are common and therefore bilateral radiographs should always be obtained, even in the absence of effusion or lameness in the presumably unaffected joint. Multiple joints may also be involved in one animal. There is an apparent site-predilection due to breed and the most frequently observed OCD lesions will vary from practice to practice. However, the femoropatellar joint (lateral trochlear ridge of the femur), tarsocrural joint (distal intermediate ridge of the tibia (aka DIRT lesion), medial malleolus of the tibia, lateral and medial trochlear ridges of the talus), metacarpo/metatarsophalangeal joints (mid-sagittal ridge of MCIII/MTIII, and plantar/palmar aspect of P1), and the scapulohumeral joint (glenoid fossa and humeral head) are the most commonly affected sites. OC/OCD of the hip, elbow, and cervical vertebral joints (wobbler) also occurs. Lesions that are (probably) not OC/OCD Although still somewhat controversial, the terms OC/OCD are probably inappropriately applied to cystic lesions of the medial femoral condyle and to osteochondral lesions of the proximal, plantar/palmar aspect of the first phalanx. Both of these osteochondral abnormalities are now considered by many to be traumatic in origin. Cystic lesions of the medial femoral condyle are most common in horses with an upright or straight conformation of their hind limbs. This results in increased contact during weight bearing between the medial femoral condyle and the proximal tibia, which results in repetitive microtrauma to the cartilage and subchondral bone of the medial femoral condyle. Cystic lesions can be experimentally created by surgically cutting the cartilage on the medial femoral condyle, supporting the theory of trauma as the initiating factor. Osteochondral lesions of the proximal, plantar/palmar aspect of the first phalanx are thought to be avulsion fractures. These fragments occur precisely where the short distal sesamoidean ligament inserts on the proximal/plantar aspect of P1. Arguments against this theory are based on the observation that these lesions occur with greater frequency in Standardbred horses than in any other breed. Treatment of OCD flap lesions The treatment of choice for most OCD lesions is arthroscopic surgical removal and subchondral bone curettage. In select cases where the OCD lesion has not detached from the parent bone, pinning (absorbable, not stainless steel pins) of the OCD back onto the parent bone may be considered. The primary advantage of pinning is restoration of normal anatomy. In very young horses, OCD lesions have been reported to heal, most commonly for lesions of the lateral trochlear ridge of the femur. However, these same lesions have also been observed to progress in horses. Frequent radiographic monitoring will allow the surgeon to determine the healing/progression of OCD lesions and make recommendations for surgical intervention before the onset of osteoarthritis. In young horses with OCD lesions, if clinical signs such as synovitis and/or lameness are present, it is a good indication that surgical intervention is warranted. Extreme care should be taken when operating OCD lesions on young horses as it can be difficult to distinguish OCD from normal young cartilage and it is not uncommon for inexperienced surgeons to remove excessive normal cartilage. Treatment of cystic lesions For horses with cystic lesions of the medial femoral condyle, intra-articular steroids are commonly used as a first-line treatment. There is insufficient data to generate a clear recommendation on case selection or whether the steroids are best administered using ultrasound vs arthroscopic guidance. There are also no data directly comparing outcome of steroid injection vs simple surgical debridement. Improved methods for bone/cartilage regeneration may be particularly important in older horses with SBC. A study by Smith et al of 85 horses undergoing arthroscopic surgery for debridement of medial femoral condyle SBC

documented that horses 3 years of age, only 35% returned to soundness. In addition to age, lesion size and breed appear to influence outcome. In one study, Quarter Horses had only a 35% return to function and in another study of Thoroughbred horses, only 30% of those with >15 mm loss of articular surface raced following simple surgical debridement. Given the modest-to-poor results obtained with surgical debridement in some breeds and in those cases with large cyst openings, other treatment options have been explored. Several substances have been used in an attempt to enhance bone and cartilage repair. These include combinations of chondrocyte and growth factor grafts, autogenous cancellous bone graft with or without composites of calcium sulfate or calcium phosphate. While the majority of cases of SBC involve the femoral condyle, similar treatment issues and treatment aims exist for subchondral cysts of the distal metacarpus, glenoid cavity of the shoulder, proximal tibia, and other locations. Prognosis The prognosis for athletic function and resolution of synovitis depends on the site and extent of the OCD lesion. The percentages listed are approximate figures based on the clinical caseload at the Cornell University Hospital for Animals. uFor OCD of the lateral or medial trochlear ridge of the talus, or the lateral trochlear ridge of the femur, the prognosis is good when the lesion occurs distally (>70% achieve soundness) but only fair (6070%) when occurring up high on the trochlea. Severe lesions of the lateral trochlear ridge of the femur can lead to lateral patellar luxation. Part of the physical examination of all foals with OCD of the femoral lateral trochlear ridge should include assessment of patellar stability by manually attempting to luxate it laterally. If the patella luxates pre-operatively, the prognosis for soundness is very poor (0-5% chance of athletic soundness). If it doesn’t luxate, but radiographs suggest that the OCD lesion is over ½ the length of the lateral trochlear ridge, the prognosis is still poor (25%). uIn contrast, distal lesions of the sagittal ridge of MCIII carry a fair-poor prognosis while proximal lesions carry a good prognosis. OCD of the sagittal ridge can occur in all four fetlocks in the same animal so be sure to radiograph all four joints. uOCD of the distal intermediate ridge of the tibia carries a good prognosis. uOCD of the shoulder typically has a fair prognosis with approximately 50% achieving soundness. The prognosis decreases for those animals with both the humeral head and glenoid affected. uHorses with medial femoral condyle cystic lesions have a fair-good (50-70%) chance of returning to soundness. Horses with palmar/plantar proximal P1 lesions typically have a good prognosis for soundness. In all instances, chronic OCD lesions warrant a decreased prognosis for future soundness due to the perpetual synovitis which leads to cartilage degradation and eventually to arthritis. Therefore, early diagnosis and prompt surgical removal of OCD lesions will offer the best overall prognosis for your patients. Selected References 1) Diagnostic and Surgical Arthroscopy in the Horse, 3rd Edition. CW McIlwraith, I Wright, AJ Nixon, KJ Boening Eds. Mosby, Ltd. 2006. 2) Fortier LA, Nixon AJ. New surgical treatments for osteochondritis dissecans and subchondral bone cysts. Vet Clin North Am Equine Pract. 2005;21:673-690. 3) Wallis TW, Goodrich LR, McIlwraith CW, et al. Arthroscopic injection of corticosteroids into the fibrous tissue of subchondral cystic lesions of the medial femoral condyle in horses: a retrospective study

of 52 cases (2001-2006). Equine Vet J. 2008 Jul;40(5):461-7. 4) Smith MA, Walmsley JP, Phillips TJ et al. Effect of age at presentation on outcome following arthroscopic debridement of subchondral cystic lesions of the medial femoral condyle: 85 horses (1993-2003). Equine Vet J 2005 March;37(2):175-80. 5) Sandler EA, Bramlage LR, Embertson RM, Ruggles AJ, Frisbie DD. Correlation of lesion size with racing performance in thoroughbreds after arthroscopic surgical treatment of subchondral cystic lesions of the medial femoral condyle. Proc Am Ass equine Pract 2002;48:255-6. 6) Nixon AJ, Fortier LA, Goodrich LR, Ducharme NG. Arthroscopic reattachment of osteochondritis dissecans lesions using resorbable polydioxanone pins. Equine Vet J 2004 July;36(5):376-83. 7) Dabareiner RM, Sullins KE, White NA. Progression of femoropatellar osteochondrosis in nine young horses. Clinical, radiographic and arthroscopic findings. Vet Surg 1993 November;22(6):515-23.