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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: J Bone Miner Res. 2012 May;27(5):1080–1092. doi: 10.1002/jbmr.1552

Fig 7. Overexpression of OSX in cementoblasts inhibited cell proliferation, induced the formation of mineralized nodules and stimulated differentiation.

Fig 7

a. The MTT assay shows a significant inhibition of cementoblast proliferation at days 3 and 5 after transient transfection with PEX3-Osterix plasmids; b. Representative photo images of Alizarin red assay reveals acceleration of mineralization after OSX transfection; c. Overexpression of OSX significantly increases expressions of BSP, OCN, and ALP, differentiation markers for cementoblast. Levels of different differentiation markers were normalized with those of the loading control GAPDH in three independent experiments. *, p <0.05; d. working hypothesis: OSX is initially expressed at low levels during cementogenesis in dental follicle cells, which increases as cellular cementum formation is being initiated. OSX controls cellular cementum formation by inhibiting proliferation of cells in the local region (PDL and follicle cells), while accelerating differentiation of follicle and PDL cells toward a cementoblast (Cb)/cementocyte (CMC) phenotype. Similar to dentinogenesis, but in contrast to osteogenesis, there appears to be a lack of remodeling in cementum. PDL, periodontal ligament; DF, dental follicle; DP, dental papilla; HERS, Hertwig’s epithelial root sheath cells.