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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

DNA Methylation in Osteoarthritis

Analysis of genetics and DNA methylation in osteoarthritis: What have we learnt about the disease?

Is It Time for Epigenetics in Osteoarthritis?

Epigenetic Mechanisms in Osteoarthritis

Angiogenesis in two animal models of osteoarthritis

Angiogenesis and nerve growth factor at the osteochondral junction in rheumatoid arthritis and osteoarthritis.

The coexistence and characteristics of osteoarthritis and osteoporosis.

The incidence of fabellae in osteoarthrosis of the knee.

Intraarticular corticosteroids in treatment of osteoarthritis.

Does osteoarthrosis depend on growth of the mineralized layer of cartilage

Gait analysis study on patients with varus osteoarthrosis of the knee.

Tibial torsion in patients with medial-type osteoarthrotic knees.