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Osteoarthritis (OA)
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Osteoarthritis Most common form of arthritis , which shows a strong association with aging and is a major cause of pain and disability in the elderly , characterized by both degeneration of articular cartilage and simultaneous proliferation of new bone
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Epidemiology There is steady rise in overall prevalence from age 30 , such that by 65 years 80 % of people have some radiographic evidence of OA , though only 25 – 30 % have associated symptoms Knee OA is more incidence than hip OA Inheritance is a major attributable factor especially hand and generalized OA , But also for hip and generalized OA , but also for hip and knee OA
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Epidemiology OA is more common in female except for hip joint where both genders are equally affected Trauma and occupation is very important factor as farming ( hip OA ) , mining (knee OA ) and professional foot ball ( knee OA ) The correlation between the presence of structural OA and pain and disability varies according to site , correlation is stronger at the hip than the knee and poor at most small joint sites
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Etiology and pathogenesis
Primary OA ( Idiopathic ) Secondary OA Previous trauma Prior joint disease (JIA , RA , Gout , septic arthritis , hemophilia ) Metabolic or endocrine disease , chondrocalcinosis , hemocromatosis , acromegally
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Etiology and pathogenesis
Neuropathic joint : tabes dorsalis Syringomyelia Late avascular necrosis :SLE , Sickle cell disease Spondylo-epiphyseal dysplasia Endemic OA
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Pathogenesis Cartilage changes in OA are highly characteristic Enzymatic degeneration of aggrecan and collagen by aggrecanase , collagenase and stromelysin Production of nests of chondrocytes ( metabolically active ) Turn over of aggrecan component is increased and eventually the concentration of aggrecan is decreased
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Pathogenesis The decrease of the size of the hydrophilic aggrecan molecules increases the water concentration and swelling pressure in the cartilage Fissuring of the cartilage surface ( fibrillation ) Development of deep vertical cleft , localized chondrocyte death and decrease in cartilage thickness These changes in OA cartilage encourage deposition of calcium pyrophosphate apatite crystals and formation of osteophyte
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Pathogenesis There is trabecular thickness in the subchondral bone , holes or cyst , often develop result from osteonecrosis due to increase intra osseous pressure Despite central and marginal new bone formation with severe cartilage loss there may be attrition of bone , such attrition may ablate the trabeculae and lead to smooth , shiny surface ( eburnation )
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Pathogenesis Hyperplasia of the synovium with formation of osteochondral bodies which reflect chondroid metaplasia Non specific type II fiber atrophy of the muscles overlying the joint
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Pathological changes in OA
Remodeling of bone contour Fibrillation and focal loss of hyaline cartilage Marginal osteophyte Subchondral sclerosis Bone cysts Secondary bursitis Capsular thickening Osteochondral body Synovial hyperplasia Secondary osteoplasia
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Clinical features Pain and functional restriction
Causes of pain : increase pressure in subchondral bone ( cause night pain ) , trabecular microfracture , capsular distension , low grade synovitis , bursitis , and enthesopathy The pain mainly related to movement and weight bearing , relieved by rest Morning stiffness <15 minutes
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Nodal generalized OA Polyarticular finger IPJ Heberden’s nodules
Bouchard’s nodules Marked female predominance Good functional outcome for hands Predisposition to OA at other joints especially knees Strong genetic predisposition Affect middle aged women (40-50 years ) Lateral deviation of the fingers reflecting focal cartilage loss Involvement of the first CMCJ resulting in thumb – base squaring
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Heberden’s nodules Bouchard’s nodules
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Knee OA Affect patello – femoral and medial tibio – femoral compartment of the knee Trauma is important risk factor Mostly bilateral and symmetrical especially in women Posterior knee pain suggest complicating popliteal cyst
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Local examination Local examination revealed :
jerky asymmetric , antalgic gait Varus or less commonly valgus or fixed flexion deformity Weakness and wasting of the quadriceps Restricted flexion / extension with coarse crepitus bony swelling around the joint line
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Hip OA Superior pole OA :usual pattern in man and most OA that is secondary to structural abnormality Unilateral Often progresses with superolateral migration of the femoral head Has poor prognosis Less common : central (medial ) OA.
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Hip OA Central cartilage loss Confined to women Bilateral
May associated with nodal generalized OA Uncommonly progresses either axial femoral migration Better prognosis
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Signs and symptoms Correlation between symptoms and radiographic changes Hip pain in the anterior groin , radiate to the buttock , anterolateral thigh , knee joint or shin Lateral hip pain due to trochanteric bursitis Antalgic gait Weakness and wasting of quadriceps and gluteal muscles
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Signs and symptoms Pain and restrictions of internal rotation with hip flexed , which occur early Anterior groin tenderness just lateral to the femoral pulse Fixed flexion , external rotation deformity of the hip Ipsilateral leg shortening
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Investigations Normal full blood count , ESR , CRP
Synovial fluid is viscous with low turbidity and CPPD crystals may be identified in 50 % of patients Plain radiographs shows focal narrowing of joint space , marginal osteophyte , subchondral sclerosis , cysts , osteochondral ( loose bodies ) and deformity Tests to exclude secondary causes , as serum growth hormone , skull radiograph for acromegally , urine homogentistic acid for ochronosis
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Patello-femoral J. OA
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Osteophytes of knee J.
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Osteophytes of the shoulder J.
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OA of MCP J. – bony cyst
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OA of MCP J.
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Bony cyst –OA
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Bony cyst –OA
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OA – hip J.
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OA – hip J.
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OA – hip J.- bony cyst
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Advanced OA – knee J.
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Advanced OA – knee J.
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MTP J OA
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OA – cervical spine
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OA – cervical spine
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OA – lumbar spine
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Advanced OA – lumbar spine
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