Fetal chondrogenesis as a means of deciphering adult chondrocyte behaviorA very important and interesting aspect of cell behavior in the adult organism is the recapitulation of molecular mechanisms that occurred during fetal development.19 This phenomenon is also true for osteoarthritic chondrocytes (Figure 2).19 In fact, many of the biological changes that occur in diseased cells mimic a differentiation pattern characteristic of fetal skeletogenesis. This not only includes changes in cellular phenotypes, and in anabolic and catabolic events, but also other basic mechanisms such as matrix calcification, apoptosis, and proliferation. Such a comparison may seem attractive for explaining cellular behavior and disease pathways in the adult, but uncoordinated degenerative events should not be mistaken for tightly regulated developmental processes. Both scenarios may involve similar molecular and regulatory events, but how these events affect matrix composition and function may be totally different. For example, expression of the alter-natively-spliced type IIA collagen isoform has been identified in cells from the middle zones of degenerating cartilage.20 This collagen isoform is also a marker of chondroprogenitor cells, but it is not known if it functions similarly in OA cartilage and during the early development of cartilage tissue.