Figure 6

Model for a role of ultra-short telomeres in OA. In theory, two models for involvement of telomere shortening in OA can be considered: (i) gradual linear shortening resulting from replication for chondrocyte renewal (mainly reflected by decreased mean telomere length); and (ii) extensive shortening induced by stress factors such as oxidative damage and believed to be a key trigger of senescence (mainly reflected by the number of ultra-short telomeres). The present observations taken together with literature data strongly suggest that the latter process prevails over the former (see text). OA-induced damage is likely to cause in turn more production of oxygen radicals and cell replication, as shown by the feedback loop on the left. OA, osteoarthritis.