degenerative joint disease Dr. TARIF AL-AKHRAS ORTHOPEADIC SURGEON KFMC

• Notice the smooth white Articular Cartilage in a knee

• Notice how the cartilage is no longer smooth and shiny… this is early degenerative joint disease 2

What is degenerative joint disease? Degenerative joint disease, also known as osteoarthritis is due to the loss of articular cartilage within the joints. The articular cartilage is the cushioning that is on the ends of long bones every diarthrodeal joint.

• Articular cartilage is a hayalin cartilage. • It is extremely strong, but very smooth • and flexable changes its shape under load and distributes compressive forces widely to the subarticular bone. • covered by a film of synovial fluid, it is more slippery than any man-made material, • offering very little frictional resistance to movement 4

• hayalin cartilage consists of living cells, chondrocytes, in rubbery matrix. • The matrix of hyaline cartilage appears glassy in the living state: hence, the name hyaline (Gr. hyalos, glass) • It has a high water content (60–80 per cent), most of which is exchangeable with the synovial fluid. • The matrix consisting of a proteoglycan and collagenous fibers , mainly type II. 5

• The proteoglycans exist mainly in the form of aggrecan, The main functions of aggrecan are to absorb changes in load and reduce deformation, while the collagen network deal with tensile forces. • During movement and loading fluid is squeezed out of the proteoglycan-rich cartilage and forms a thin ‘cushion’, then seeps back into the cartilage when loading ceases. 6

pathophysiology • The water content of healthy cartilage is finely balanced by compressive force driving water out & swelling pressure drawing water in. • Collagen fibres exert the compressive force, whereas the cartilage proteoglycans create osmotic pressure which tends to draw water in. However during onset of OA, the collagen matrix becomes more disorganized and there is a decrease in proteoglycan content within cartilage. The breakdown of collagen fibers results in a net increase in water content 7

• Inflammation Although OA is not primarily an inflammatory disease, shedding of fragments from the fibrillated articular cartilage, as well as release of enzyme from damaged cells, may give rise to a lowgrades ynovitis. • In the late stages, capsular fibrosis is and may account for joint stiffness. • Pain. The cause of pain is problematic; articular cartilage and synovium have no nerve supply but the capsule is sensitive to stretching and the bone is sensitive to changes in pressure. Pain, therefore , may be due to both capsular fibrosis and vascular congestion of the subarticular bone. 8

Aetiology • primary when there is no obvious factor. • Secondary when it follows a demonstrable abnormality •

OA

Primary OA

Secondary OA 9

Primary OA • More common than secondary OA • Cause –Unknown • Common-in elders where there is no previous pathology. • Its mainly due to wear and tear changes occuring in old ages mainly in weight bearing joints.

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Secondary OA • Due to a predisposing cause such as: 1.Injury to the joint 2.Previous infection 3.RA 4.CDH 5.Deformity 6.Obesity 7.hyperthyriodism 11

Clinical features • • • • • • • •

Pain the pain may ache, burning or sharp. Stiffness Muscle spasm Restricted movement Deformity Muscle weakness or wasting Joint enlargement and instability Crepitus 12

Clinical features Pain: • onset, duration of pain, aggravating and relieving factor, night pain. • location and radiation. • Hip pain rarely radiated below the knee • Differentiate hip pain from referred spinal pain

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Clinical features • Stiffness • It can be generalized or localized to particular joint. • Let the patients explain this in their own terms 14

Clinical features • Patrick’s ( Faber ) test (Figure of 4 test)

• Flexion, Abduction, • External Rotation of the hip • Painfull if in any pathology in the hip 15

• the most crucial element in musculoskeletal history is to differentiate between inflammatory and degenerative joint disease. • Each type of disease has classical distribution of the joint

OA

RA

Heberden’s nod

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• Degenerative disease in general the pain is active-related and improves by rest • Swelling due to degenerative disease is bony hard what the normal alignment in the knee? What the usual deformity in OA knee? 17

• Inflammatory joint disease is characterised by presence of symptoms after period of immobility. Morning stiffness • Joint swelling (synovitis) is boggy in nature. • The joint is warm with overlying erythema. • There is often pain in the extremes of movement. • Extra-articular manifestation: eye, skin, nail, respiratory and bowel symptoms 18

HOW IS OSTEOARTHRITIS DIAGNOSED? • Most often OA detect based on the typical symptoms (described earlier) and the physical exam. • BLOOD TEST . No blood test is diagnostic for OA, their value is in ruling out other types of arthritis. • X RAY the main diagnostic modality and it used for classification .

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XRAY FINDING IN OA

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XRAY FINDING IN OA • • • • •

Joint Space Narrowing Osteophytes Subchondral Sclerosis Subchondral Cyst Subluxation

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Radiographic Classification • Stage 1 • Stage 2 • Stage 3

• Bony spur only • Narrowing of joint. Space , less than half of the normal joint. space • Narrowing of joint. Space , more than half of the normal joint. Space

• Stage 4

• Obliteration of joint. space

• Stage 5

• Subluxation or sec. lateral arthrodsis 23

Treatment Principles • Education • Physiotherapy – Exercise program – Pain relief modalities

• Aids and appliances • Medical Treatment • Surgical Treatment 24

Education • Nonsystemic nature of disease • Prevent overloading of joint. Obesity!! • Appropriate use of treatment modalities – Importance of exercise program – Aids, apliances, braces – Medial treatments – Surgical treatments

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Exercise • Will not ‘wear the joint out’ • Important for cartilage nutrition • Some evidence that lack of exercise leads to progression of OA • Encourage full range low impact movements eg swimming, cycling • Avoid – – – –

Prolonged loading Activities that cause pain Contact sports High impact sports eg running 26

Aids and appliances • Braces / splints • Special shoes/insoles • Use of a cane, stick or other walking aid It reduce the loading, and the effect on symptoms and give confidence with walking.

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Medical Treatment • Simple analgesics: paracetamol, low dose ibuprofen • NSAID’s/Coxibs PRN regular • Intra-articular corticosteroids (only in end stage) • Topical treatment eg NSAID creams • ‘Chondroprotective agents’ ??? • Intra-articular hayaloronic acid injection 28

viscosupplementation • In this procedure, hyaluronic acid is injected into the knee joint. Hyaluronic acid is a naturally substance found in the synovial fluid. It acts as a lubricant to enable bones to move smoothly over each other and as a shock absorber for joint loads. • Effects may last for several months. • It may be effective in relieving the symptoms, but has never been shown to reverse the arthritic process or re-grow cartilage. 29

Surgical intervention for OA • • • • •

JOINT DEBRIDEMENT BONY DECOMPRSSION OSTEOTOMY ARTHROPLASTY Arthrodesis

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OSTEOTOMY

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ARTHROPLASTY

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Arthrodesis • Arthrodesis of large joints hip & knee has fallen out of favour as a primary procedure, and now are only used as procedures of last-resort in some failed arthroplasties. • Still benefit in the foot and spine 33

LIVING WITH OSTEOARTHRITIS • There is no cure for OA, but you can manage how it affects your lifestyle. Some tips include: • Properly position and support your neck and back while sitting or sleeping. • Adjust furniture, such as raising a chair or toilet seat. • Avoid repeated motions of the joint, especially frequent bending. • Lose weight if you are overweight or obese, which can reduce pain and slow progression of OA. • Exercise each day. • Use arthritis support devices that will help you do daily activities. 34

POINTS TO REMEMBER • OA is the most common form of arthritis and can occur together with other types of arthritis. • The goal of treatment in OA is to reduce pain and improve function. • Exercise is an important part of OA treatment because it can decrease joint pain and improve function. • At present, there is no treatment that can reverse the damage of OA in the joints. Researchers are trying to find ways to slow or reverse this joint damage. 35