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This study was undertaken to investigate the role and mechanisms of FGF receptor 3 (FGFR\u20103) in the pathogenesis of osteoarthritis (OA) caused by surgery and aging in mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      FGFR\u20103 was conditionally deleted or activated in articular chondrocytes in adult mice subjected to surgical destabilization of the medial meniscus (DMM). A mouse model of human achondroplasia was also used to assess the role of FGFR\u20103 in age\u2010associated spontaneous OA. Knee joint cartilage was histologically evaluated and scored using the Osteoarthritis Research Society International system. The expression of genes associated with articular cartilage maintenance was quantitatively evaluated in hip cartilage explants. The effect of inhibiting Indian hedgehog (IHH) signaling in\n                      <jats:italic>Fgfr3<\/jats:italic>\n                      \u2010deficient explants was analyzed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Conditional\n                      <jats:italic>Fgfr3<\/jats:italic>\n                      deletion in mice aggravated DMM\u2010induced cartilage degeneration. Matrix metalloproteinase 13 and type X collagen levels were up\u2010regulated, while type II collagen levels were down\u2010regulated, in the articular cartilage of these mice. Conversely, FGFR\u20103 activation attenuated cartilage degeneration induced by DMM surgery and age. IHH signaling and runt\u2010related transcription factor 2 levels in mouse articular chondrocytes were up\u2010regulated in the absence of\n                      <jats:italic>Fgfr3<\/jats:italic>\n                      , while inhibition of IHH signaling suppressed the increases in the expression of\n                      <jats:italic>Runx2<\/jats:italic>\n                      ,\n                      <jats:italic>Mmp13<\/jats:italic>\n                      , and other factors in\n                      <jats:italic>Fgfr3<\/jats:italic>\n                      \u2010deficient mouse cartilage explants.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings indicate that FGFR\u20103 delays OA progression in mouse knee joints at least in part via down\u2010regulation of IHH signaling in articular chondrocytes.<\/jats:p>\n                  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