Osteoarthritis OA

Osteoarthritis(OA)

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

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 OAInheritance is a major attributable factor especially hand and generalized OA , But also for hip and generalized OA , but also for hip and knee OA

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

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

Etiology and pathogenesis

Neuropathic joint : tabes dorsalis Syringomyelia Late avascular necrosis :SLE , Sickle cell disease Spondylo-epiphyseal dysplasia Endemic OA

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


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

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 )

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

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

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

Nodal generalized OA

Polyarticular finger IPJHeberden’s nodulesBouchard’s nodulesMarked female predominanceGood functional outcome for handsPredisposition to OA at other joints especially knees Strong genetic predispositionAffect middle aged women (40-50 years )Lateral deviation of the fingers reflecting focal cartilage lossInvolvement of the first CMCJ resulting in thumb – base squaring

Heberden’s nodulesBouchard’s nodules

Knee OA
Affect patello – femoral and medial tibio – femoral compartment of the knee Trauma is important risk factor Mostly bilateral and symmetrical especially in womenPosterior knee pain suggest complicating popliteal cyst

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

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.

Hip OA

Central cartilage loss Confined to women Bilateral May associated with nodal generalized OA Uncommonly progresses either axial femoral migration Better prognosis

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

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

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


Patello-femoral J. OA

Osteophytes of knee J.

Osteophytes of the shoulder J.

OA of MCP J. – bony cyst

OA of MCP J.

Bony cyst –OA

Bony cyst –OA

OA – hip J.

OA – hip J.


OA – hip J.- bony cyst

Advanced OA – knee J.

Advanced OA – knee J.

MTP J OA

OA – cervical spine

OA – cervical spine

OA – lumbar spine

Advanced OA – lumbar spine