OSTEOARTHRITIS Definition: Chronic joint disease characterized by progressive deterioration of a joint in which localized loss of cartilage occurs in association with §  Subchondral sclerosis §  cyst formation §  osteophytosis §  capsular and synovial thickening. It is a dynamic condition, characterized by both reparative and degradative processes of the joint cartilage and bone. Classification Primary - No obvious cause found for the changes. Secondary - This is as a result of increased stress, weakened cartilage or abnormal support of cartilage e.g. avascular necrosis 1.Genetic or developmental §  Congenital hip dislocation §  Slipped upper femoral epiphysis §  Chondrodysplasia §  Perthe's disease §  Genu valgum or varum §  Haemophilia 2.Metabolic §  Calcium pyrophosphate dehydrate Arthropathy §  Alkaptonuria §  Hyperuricaemia §  Gaucher's disease 3.Endocrine §  Hypo/Hyperthyroidism §  Acromegaly §  Diabetes mellitus 4. Inflammatory Disorders §  Rheumatoid Arthritis §  Ankylosing spondylitis §  Psoriatic arthritis §  Septic arthritis 5.Trauma §  Fracture (particularly osteochondral fractures) §  Joint instability (e.g. cruciate ligament injury, joint hypermobility syndromes) §  Post meniscectomy §  Osteochondritis dissecans §  Neuropathic joints (Charcot joints) §  Mechanical causes including leg length discrepancy, instability, repetitive (occupational) injuries Age:  Usually old people are affected, but in situations where there are predisposing factors, even younger people are affected. Sex Until middle age, osteoarthritis occurs with the same frequency in men and women, but after the age of  50 symptomatic osteoarthritis is more common in women, and this difference in prevalence widens with increasing age. Most affected joints: Weight bearing joints especially Hips, Knees and Spine.  However any joint can develop OA such as is seen in ankles, elbows, wrists, hallux rigidus, etc. In the hip some changes such as protrucio acetabulare may accompany the osteoarthritic changes necessitating early action. Clinical features: History i) Pain -pain on motion and later also at rest ii) Stiffness morning stiffness that lasts less than 30 minutes stiffness after periods of inactivity during the day, or so-called gelling iii) Swelling + Heberden’s nodes at the distal inetrphalangeal joints and bouchard  nodules in the proximal interphalangeal joints iv) Deformity of the joints. In the hands tends to have a radial deviation deformation ( RA-ulnar deviation.) v) Loss of function. On Examination:  1)  Limited movement with crepitus- -due to incongruity of joint surfaces, muscle or capsular contracture, or mechanical block from osteophytes or loose bodies  2)  Tenderness on active/ passive motion and crepitus, a crackling sound or sensation as the joint is moved, are common findings. 3. Usually absence of signs of acute inflammation, effusion if present is minimal. 4)  Joint enlargement may result from proliferative synovitis, an increase in synovial fluid, or osteophyte formation. 5)   Deformity-genu varus or genu valgus may be observed in the knee involvement. Heberden's nodes are characterized by bony enlargement of the dorsolateral and dorsomedial aspects of the distal interphalangeal joints of the fingers. Flexor and lateral deviation of the distal phalanx are common. Similar nodes at the proximal interphalangeal joints are known as Bouchard's nodes. Investigations: 1.X rays:  Plain xrays are diagnostic in most cases, seen are:- The Kellgren Grading System uses the following 4 radiographic features: a)Joint space narrowing b) Osteophytes c) Subchondral sclerosis d) Subchondral cysts e) subluxation of joint in severe cases 2) Haemogram Usually contributes little to diagnosis.  3)↑ CRP 4)Radionuclide scanning (99mTc) - shows increased activity during the bone phase in the subchondral regions of the affected joints. This is due to increased vascularity & new bone formation.  Differential diagnosis: 1)  Chronic infections. 2)  ANFH 3)  Rheumatoid arthritis 4)  Psoriatic Arthritis. 5)  Gout and pseudogout 6)  Diffuse idiopathic skeletal hyperostosis 7) Patellofemoral Syndrome 8) Prepatellar Bursitis Management of Osteoarthritis:                 1)  History                 2)  Examination                 3) Investigations                 4)  Treatment

NB Anybody living long enough is likely to get OA of one joint or another.  In some situations presence of osteophytes although indicative of OA change is not necessarily a disease requiring treatment e.g. OA in Spine. Predisposing factors 1.        Age 2.        Genetic 3.        Hormonal 4.        Local mechanical stresses 5.        Pre-existing joint disease. 6.        Trauma Cause of Osteoarthritis  Disparity between stresses applied to articular cartilage and the ability of the cartilage to stand the stress. 1)Stress   Load per unit urea.  i.e .Load/Area =   Stress So disparity can occur as a result of increased load or decreased area. Both factors common in Osteoarthritis of the knee, and probably spine. 2. Weak Cartilage: Due to age. Knee joint with Osteoarthritis 3. Abnormal Subchondral Support:  Examples in ANFH. Pathogenesis: -This is thought to be as a result of intrinsic disturbances in the metabolism of cartilage which leads to increase in water content of the cartilage & easier extractability of the matrix proteoglycans which leads to chondrocyte damage & cartilage deformation. -Pathological changes occur in the articular cartilage of synovial joints, synovial fluid, as well as in the underlying (subchondral) bone and overlying joint capsule. -The affected cartilage initially develops small tears known as fibrillations, then larger tears, and eventually it fragments off into joints. -Chondrocytes replicate in an attempt to keep up with the cartilage loss; but are unable to, and the underlying bone is left denuded.  -Bone along the periphery of the joint replicates to form osteophytes, while the subchondral bone along the mid portion of the joint becomes sclerotic, and areas within it eventually may undergo cystic degeneration. -Complex chemical changes leading to: ·         Water content of cartilage increases. ·         Loss of matrix proteoglycans. ·         Cartilage softens. ·         Chondrocytes are damaged. ·         Collagen network damaged. -With loss of cartilage integrity the stress normally borne by cartilage is passed over to bone.  This it cannot stand. Bone crumbles, cysts form in the subchondral bone. -The osteoarthritic joint is characterized by decreased concentration of hyaluronic acid because of reduced production by synoviocytes and increased water content as a result of inflammation Pathology of Osteoarthritis: 1)       Progressive cartilage destruction 2)       Subarticular cysts formation. 3)       Sclerosis of surrounding bone. 4)       Osteophyte formation. 5)        Capsular fibrosis. Treatment: Early: 1)Relief of pain NSAIDS These play major role. Problems: How long should they be given, Dyspepsia Affordability 2)   Increase movement -physiotherapy and several short periods of walking, interspersed with rest periods, are preferable to sustained walking for the patient with osteoarthritis of the hip or the knee. Strenuous exercises and stair climbing should be avoided whenever possible. 3)   Reduce load - Use of walking aids -Wedged insoles that change the angle of the legs - Shock-absorbing footwear that reduces impact - Heel lift if one leg is shorter than the other. -Weight reduction in obese patients 4)   Correction of predisposing factors if possible. Specific exercise programs designed to preserve or to improve the range of motion and to strengthen periarticular muscles frequently result in significant pain relief and improvement in such parameters as strength, endurance, speed, and joint stability. Late  1)  Analgesics and NSAIDs 2)  Physiotherapy Surgical interventions 1.Arthroscopic lavage - Using a saline lavage to wash out the joint 2.Joint realignment (realignment osteotomy) 3.Joint fusion (arthrodesis) - Surgically fusing the joint to eliminate motion 4Joint replacement (arthroplasty NB.Charcot Joints Neuropathic arthropathy 2° to loss of sensation associated with certain chronic disorders. The joint disease is usually progressive, with insidious swelling and instability of a single joint. Although said to be painless, Charcot's joints may be painful, but not in proportion to the joint destruction. Causes (affected joint); ·         Peripheral neuropathy ·         Diabetes (tarsal and metatarsal, ankle) ·         Tertiary syphilis ·         Leprosy ·         Tabes dorsalis (the vertebrae, hips, knees, & ankles) ·         Syringomyelia (Shoulder or elbow) ·         Myelomeningocele ·         Amyloid neropathy ·         Subacute combined degeneration of the spinal cord