presents
Wheeless' Textbook of Orthopaedics
Tracking Pixel
Search Site by Word
My Account

Synovium





- See:
      - Pigmented Villonodular Synovitis
      - Friction and Lubrication
      - synovial fluid
      - Synovium of the Knee
      - Synovial Plica

- Discussion:
    - synovial membrane is innermost portion of capsular ligament of synovial joint;
    - synovial cavity may be continuous with bursae about the joint;
    - synovium is richly supplied with blood vessels, lymphatics, and nerves;
          - richness of blood capillaries and their proximity to inner surface account
                  for hemorrhage into joints that may follow minor injuries;
- Histology:
    - synovial membrane is comprised of a sheet of fibrous connective tissue;
    - synovial cells resemble fibroblasts;
    - it has no epithelial component;
    - two types of synovial cells have been described;
          - type A:
              - prominent surface ruffling w/ lysosomes & has smooth-walled vesicles;
              - resembles macrophages of the body;
          - type B:
              - secretory (fibroblast-like) cells w/ abundant rough endoplasmic reticulum;
              - this cell type seems likely to be the source of glycoprotein
                    and hyaluronic acid of synovial fluid;
- Regenerative Capacity:
    - synovial cells may transform into chondrocytes may occur at attachment
          site of the synovial membrane to periphery of articular cartilage;
    - synovial cells are capable of rapid and complete repair or regeneration;
- Innervation:
    - nerves entering the Synovium appear to be distributed primarily to
          blood vessels, probably as vasomotor and vasosensory nerves;
    - observation that the synovium is not very sensitive to pain suggests
          that relatively few of the nerve fibers are pain fibers;
- Response to Infection:
    - w/ challenged w/ an infectious inoculum, synovial membrane undergoes an
          acute inflammatory response w/ accumulation of PMN's & monocytes;
          - complement activation produces chemotactic factors and other mediators
                    of inflammation that enhance the inflammatory process;
    - if infection is not quelled, synovium will necrose w/ in 24 hrs, followed by
            necrosis of chondrocytes & failure of glycosaminoglycan production;
    - even if infection is quelled, PMN's will phagocyticize immune complexes,
            which secrete toxins that lead to death of the cells;
            - acute inflammatory respose along w/ cellular disintegration (w/ release of
                  lysosomal enzymes & proteases) will further injure chondrocytes;




Original Text by Clifford R. Wheeless, III, MD.