- 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
- reference: