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Pathological Features of Osteoarthritis


- Discussion:
    - osteoarthritis represents a gradual processes of destruction & regeneration;
    - early in dz, articular cartilage loses its glistening appearance;
    - later on surface layers flake off while deeper layers develop longitudinal fissures, process termed fibrillation;
    - cartilage becomes thin and sometimes denuded;
    - collagen fibre structure is altered and the number and quality of proteoglycan aggregates decreases
    - chondrocytes isolated from patients with OA produce 50-fold more PGE2 than chondrocytes from patients without OA;
    - prostaglandin-stimulated release of matrix metalloproteinases: may lead to cartilage degradation;
    - subchondral bone:
          - becomes thickened, sclerotic, & polished (eburnation);
          - subchondral bone displays thickened trabeculae and microfractures;
          - tidemark is disrupted by vessels from the subchondral layer;
    - cysts:
          - may be seen in subchondral bone;
          - cysts may arises from increases in intrasynovial pressure;
    - osteophytes:
          - spurlike bony outgrowths covered by hyaline cartilage, may develop at margins of joint & progressively enlarge;
          - small bits of cartilage-covered bone, known as joint mice, may actually break off into the joint;

- Histology:
    - see: articular cartilage
    - superficial zone demonstrates earliest changes;
    - there is a diminution of chondrocytes in superficial zones;
    - cartilage matrix loses its ability to stain for proteoglycans with alcian blue or safranin-O;
    - deeper chondrocytes demonstrate proliferation in clusters (brood capsules);
    - capillary buds penetrate the layer of calcified cartilage;
    - newly formed sements of cartilage push up from below;
    - tidemark:
          - demarcation between calcified and noncalcified cartilage;
          - becomes split & reduplicating tidemark;
    - synovium: becomes hypertrophied and thrown into villose folds;
          - may see infiltration with plasma cells, and lymphocytes;
          - syovial hypertrophy may be involved in producing joint pain by increased synovial fluid production and increased intra-articular pressure



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