{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T18:09:16Z","timestamp":1769018956909,"version":"3.49.0"},"reference-count":31,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2009,2,4]],"date-time":"2009-02-04T00:00:00Z","timestamp":1233705600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Orthopaedic Research"],"published-print":{"date-parts":[[2009,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Primary cilia are found on nearly every mammalian cell, including osteocytes, fibroblasts, and chondrocytes. However, the functions of primary cilia have not been extensively studied in these cells, particularly chondrocytes. Interestingly, defects in the primary cilium result in skeletal defects such as polydactyly in Bardet\u2010Biedl syndrome (BBS), a ciliary disorder that also results in obesity, retinopathy, and cognitive impairments. Wild\u2010type mice and mutant mice of the ciliary proteins Bbs1, Bbs2, and Bbs6 were evaluated with respect to histological and biochemical differences in chondrocytes from articular cartilage and xiphoid processes. Using immunofluorescence microscopy, chondrocytic cilia were visualized from the load\u2010bearing joints and non\u2010load\u2010bearing xiphoid processes. Significant differences in ciliary morphology were not identified between mutant and wild\u2010type mice. However, after expanding chondrocytes in cell culture and implanting them in solid agarose matrix, it was seen that the fraction of ciliated cells in cultures from mutant mice was significantly lower than in the wild\u2010type cultures (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). In addition, in Safranin\u2010O\u2010stained whole joint sections, Bbs mutant mice had significantly lower articular joint thickness (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) and lower proteoglycan content saturation (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) than wild\u2010type mice. Moreover, there were statistically significant differences of cell distribution between Bbs mutant and wild\u2010type mice (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), indicating that mutant articular cartilage had changes consistent with early signs of osteoarthritis. These data indicate that Bbs genes and their functions in the chondrocytic primary cilium are important for normal articular cartilage maintenance. \u00a9 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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