Difference between revisions of "Joint Response to Injury"
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***Non-painful | ***Non-painful | ||
**Defects reaching subchondral bone | **Defects reaching subchondral bone | ||
| − | ***Filled with vascular fibroous tissue undergoing [[ | + | ***Filled with vascular fibroous tissue undergoing [[Disorders of Cell Growth - Pathology#Metaplasia|metaplasia]] into cartilage |
***Painful | ***Painful | ||
**Fibrillation - loss of proteoglycans -> condensation of collagen fibres -> fraying of surface | **Fibrillation - loss of proteoglycans -> condensation of collagen fibres -> fraying of surface | ||
Revision as of 20:04, 13 August 2009
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Causes of injury
- Trauma
- Instability
- Lubrication failure
- Infectious organisms
- Immune-mediated disease
Reaction to injury
- Articular cartilage has limited ability to regenerate
- Superficial defects are long standing
- Chondrocyte hyperplasia is ineffective at filling the defect
- Non-painful
- Defects reaching subchondral bone
- Filled with vascular fibroous tissue undergoing metaplasia into cartilage
- Painful
- Fibrillation - loss of proteoglycans -> condensation of collagen fibres -> fraying of surface
- Eburnation - loss of articular cartilage -> exposure of subchondral bone -> becomes dense and polished
- Superficial defects are long standing
- Synovial membranes respond by:
- Villous hypertrophy
- +/- synovitis
- Hyperplasia
- Villous hypertrophy