ARTICULAR CARTILAGE by 8XlAP53

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									PATHOLOGY OF OSTEOARTHRITIS

F. ALHILLI
Department of Pathology, AGU
     ARTICULAR CARTILAGE
Avascular, alymphatic hyaline cartilage
Resist compressive forces by deforming
but recover on removal of load
Composed of
a. Chondrocytes
b. Intercellular matrix (Collagen,
   Proteoglycans, and Water)
Chondrocytes
 Synthesize matrix components (e.g. collagen
 and Proteoglycans)
 Synthesize enzymes (e.g. collagenase)
 Capable of phagocytosis
Collagen
 85-95% Type I Collagen
 Type V and IX also present
 Other proteins present include chondronectin,
 anchorin
 Arrangements of collagen fibers
Proteoglycans
 Link proteins, hyaluronic acid and
 glycosaminoglycans
 Bind large amount of water
           Osteoarthritris
Chronic progressive degenerative
destructive degradation of the articular
cartilage of weight bearing joints leading
to joint narrowing, subchondral bone
thickening and eventually
nonfunctioning painful joint
The disease is primarily not an
inflammatory lesion, but (reactive)
infiltration by lymphocytes and plasma
cells is present and minimal
AETIOLOGY and PATHOGENESIS OF
OSTEOARTHRITIS

 Primary Osteoarthritis
 Secondary Osteoarthritis
Primary Osteoarthritis
Degenerative articular cartilage disease of
  unknown aetiology
1. Increased unit load on the chondrocyte
2. Decreased resilience of articular
  cartilage
3. Increased stiffness of coarse cartilage
  and cancellous bone of the epiphysis
4. Biochemical abnormalities
5. Genetic influences
Early changes may be arrested or delayed
1. Metabolic alteration of chondrocytes
2. Alteration in the biochemistry of cartilaginous
  matrix (e.g. increased water contents and
  decreased concentration of proteoglycan)
3. Thickening of the subchondral bone plate thus
  preventing dissipation of compressive forces
  from the articular cartilage to underlying bone.
4. Chemical mediators (prostaglandins,
  Interleukin 1) suppress chondrocytes
  proteoglycan synthesis and metabolism.

 The mediators may not initiate the disease but
 help in progression of cartilage destruction
 Damage: Increased degradation of
 articular cartilage
 Repair Attempts: Focal replication of
 chondrocytes and increased synthesis
 of matrix.
 Failure of Repair: Due to continuing
 stress factors.

Early changes may be arrested or delayed
PATHOLOGY OF OSTEOARTHRITIS


Changes in Articular Cartilage
           Subchondral bone
           Synovial membrane
A. Articular Cartilage Changes
Early change is chondrocyte death and loss of
    proteoglycan of superficial zone of articular
    cartilage leading (in order) to:
1. Flaking i.e. tangential disruption of the smooth
    surface of the articular cartilage.
2. Proliferation and clustering of adjacent viable
    chondrocytes as attempt at healing to
    become territorial matrix.
3. Fibrillation i.e. vertical surface cracks
    gradually extending into the deeper zones
4. Abrasion and eventual exposure of underlying
    bone.
B. Bone Changes
1. Thickening of subchondral bone trabeculae in
    areas of cartilage loss leading to eburnation
2. Exposed marrow spaces plugged by synovial
    fluid and proliferating fibrocartilage leading
    to subchondral bone cyst formation.
3. Bone remodeling results in alteration of
    contour of joint surface (e.g. femoral head)
4. Outgrowth of proliferating cartilage at the
    lateral ends of the articular cartilage which
    undergo endochondral ossification forming
    lateral osteophytosis.
C. Synovial Changes

Villous hypertrophy
Villous fibrosis
Mild infiltration by lymphocytes and
occasional plasma cells
Abraded fragments of bone and cartilage
stimulate reactive synoviitis (detritus
synoviitis)
Early Osteoarthritis. Histology of a section through the articular surface showing
“fibrillation” and “fissuring”.
Osteoarthritis. Articular surfaces of the femoral condyles shows advanced
osteoarthritis. There are areas of complete cartilage loss with eburnated
subchondral bone.
RA vs OS

								
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