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. Author manuscript; available in PMC: 2017 Nov 22.
Published in final edited form as: Osteoarthritis Cartilage. 2015 Dec 31;24(5):921–931. doi: 10.1016/j.joca.2015.12.009

Fig. 8.

Fig. 8

Schema for the effects of UAC on the BCP crystals formation in osteoarthritic cartilage. ①Abnormal mechanical force induced by UAC led the fragmentation of collagen fibers, making the Ca2+ binding site of the collagen fibers exposed. ② UAC stimulated cell death to produce matrix vesicles and apoptotic bodies to serve as mineral nucleation sites. ③UAC down-regulated the expression of inhibitors of mineralization accompanied with the up-regulation of TNAP and MMP13. ④The above changes contributed to the mineral deposition, especially BCP crystals. ⑤Mineral crystals served as a feed-forward signal to reduce production of matrix protein and enhanced the secretion of matrix degrading enzymes, thus further accelerating the cartilage degeneration.