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Modulation of OPG, RANK and RANKL by human chondrocytes and their implication during osteoarthritis
Rheumatology, 09/18/09

Tat SK et al. – Human chondrocytes express and produce OPG, RANK and RANKL. OA chondrocyte treatment with catabolic factors pointed towards an increased biological effect of OPG. Interestingly, OPG appears to be involved in OA progression by increasing two catabolic factors involved in cartilage pathophysiology.

Methods

Expression was determined using real-time PCR, production of RANK and RANKL by flow cytometry and that of OPG by ELISA
Modulation of these factors was determined upon treatment with IL-1?, TNF- and PGE2
The functional consequences were examined following treatment with soluble RANKL or OPG-Fc (OPG without the heparin-binding domain)

Results

OPG, RANK and RANKL were expressed and produced by human chondrocytes
Membranous RANK was produced only by an OA chondrocyte subpopulation (29%) localized throughout the cartilage
The OPG/RANKL ratio was significantly (P = 0.05) reduced on the OA chondrocytes, whereas the RANK/RANKL ratio was significantly (P < 0.03) increased
OPG and membranous RANKL levels were significantly enhanced by IL-1?, TNF- and PGE2, whereas membranous RANK was significantly increased only with IL-1?
Administration of soluble RANKL had no effect on the OA chondrocytes
However, addition of OPG-Fc significantly stimulated MMP-13 (P = 0.05) and protease-activated receptor-2 (PAR-2) (P < 0.04) production

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