By Trapman P.
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Additional info for A branching model for the spread of infectious animal diseases in varying environments
Leptin levels are increased in OA cartilage , and injections of leptin into the joints of normal rats can mimic osteoarthritic features . Indeed, leptin increases by ∼40% alkaline phosphatase activity, osteocalcin release, the production of collagen I 1 chains, insulin-like growth factor-1 (IGF-1), and TGF-ß1 levels in normal human osteoblasts ; all these parameters are increased over normal levels in OA subchondral osteoblasts [100,102,149]. Leptin is also associated with inflammatory states [33,63,152] and stimulates prostaglandin E2 (PGE2 )  and leukotriene (LT) production .
A report by Bettica et al  has clearly shown that bone resorption is increased in patients with progressive knee OA. These changes are associated with an increase in the number and size of the remodeling units . Moreover, in experimental dog OA, osteoblasts isolated from subchondral bone have been shown to overproduce biochemical factors that favor osteoblast maturation and activation and the resorption of the bone matrix [128,179]. Subchondral bone remodeling and resorption in dog OA can be reduced by a nonsteroidal antiinflammatory drug (NSAID) that inhibits cyclooxygenase activity .
Clusters of chondrocytes in OA cartilage express collagens type I and III, which are either absent or occur very sparingly in normal articular cartilage [2,3,171, 183,242]. OA chondrocytes also express type IIA collagen, a marker of prechondrocyte phenotype. This expression is enhanced by transforming growth factor- 1 (TGF- 1). Bone morphogenetic protein-2 (BMP-2), on the other hand, favors the expression of type IIB collagen isoform, a normal component of articular cartilage . It is therefore evident that high synthetic activity notwithstanding, dedifferentiated chondrocytes do not express cartilagespecific anabolic genes such as aggrecan or type II collagen.