Growth factors are obvious tools to enhance cartilage repair. Understanding
of reactivities in normal and arthritic cartilage and potential side effec
ts on other compartments in the joint will help to identify possibilities a
nd limitations. Growth factor responses have been evaluated in normal and d
iseased murine knees. The main cartilage anabolic factor, insulinlike growt
h factor-1, shows great safety, but has little contribution in diseased car
tilage because of insulinlike growth factor nonresponsiveness of arthritic
chondrocytes. Transforming growth factor-beta can overrule interleukin-1 ca
tabolic effects and can enhance cartilage repair in arthritic tissue, unlik
e bone morphogenetic protein-2 that only is capable of enhancing chondrocyt
e proteoglycan synthesis in the absence of interleukin-1. Transforming grow
th factor-beta and bone morphogenetic protein-2 induce chondrophyte formati
on at the margins of the joint. Studies with scavenging transforming growth
factor beta soluble receptor identified endogenous transforming growth fac
tor-beta involvement in spontaneous cartilage repair and chondrophyte and s
ubsequent osteophyte formation in arthritic conditions. Osteophyte inductio
n may hamper intraarticular transforming growth factor-beta application in
the joint and warrants targeted growth factor application to cartilage lesi
on sites only.