Transcript 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 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
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
1. Previous trauma
2. Prior joint disease (JIA , RA , Gout , septic
arthritis , hemophilia )
3. Metabolic or endocrine disease ,
chondrocalcinosis , hemocromatosis ,
acromegally
Etiology and pathogenesis
4. Neuropathic joint : tabes dorsalis
5. Syringomyelia
6. Late avascular necrosis :SLE , Sickle cell
disease
7. Spondylo-epiphyseal dysplasia
8. 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
1. Remodeling of bone contour
2. Fibrillation and focal loss of hyaline cartilage
3. Marginal osteophyte
4. Subchondral sclerosis
5. Bone cysts
6. Secondary bursitis
7. Capsular thickening
8. Osteochondral body
9. Synovial hyperplasia
10.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
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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
Heberden’s nodules
Bouchard’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
women
• Posterior 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
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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