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The procedure resulted in retardation of the progression of destruction of the degenerative cartilage.
1– 6 The correlation between inflammation and joint destruction has been recently even further accentuated by the observation that progression of damage occurs mostly in joints which are swollen and that joint swelling may contribute more strongly to progression of destruction than the acute phase response.
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Even with low disease activity, damage progresses and only sustained remission is capable of abrogating progression of joint destruction [ 3].
Progression of joint destruction in rheumatoid arthritis (RA) is partly heritably; 45 to 58% of the variance in joint destruction is estimated to be explained by genetic factors.
One of the critical challenges in developing structure-modifying therapies for arthritis, especially osteoarthritis (OA), is measuring changes in progression of joint destruction.
It doesn't matter because it is becoming obvious that there are people from all nationalities, religions, and cultural backgrounds who are determined to resist the progression of imminent destruction.
Moreover, IL-10 has been described to stimulate PG synthesis and to reverse cartilage degradation induced by activated mononuclear cells [14] and it negatively correlated with progression of joint destruction in RA [36], showing the important anti-inflammatory function of IL-10 in human RA.
Anti-TNF therapy also prevents radiological progression of joint destruction [ 8- 10].
One SNP, OPG-rs14085305, was observed to significantly associate with progression of joint destruction in RA.
Low serum OPG/RANKL ratio's have been associated with progression of joint destruction [ 12].
High level of Fn in the synovial fluid was positively correlated with the progression of joint destruction [ 15, 16].
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