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Activation of inflammation, apoptosis, and cell cycles of PDL in OTM

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Funakoshi et al. (2013) reported increased numbers of TUNEL‐ and caspase 8‐positive PDL cells at day 5 after the application of an orthodontic force in rat OTM experiments. They also reported that application of a compressive force to human PDL cells induced G1 arrest and caspase 8 protein production in human PDL cells. McCulloch et al. (1989) and Kobayashi et al. (1999) reported that cell death by apoptosis occurred following cell proliferation in response to mechanical stress. Mabuchi et al. (2002) reported that the ratios of cell proliferation and cell death were closely related to the regeneration and reconstruction of PDL in response to orthodontic force. Therefore, the rate of tooth movement may be involved in the ratios of cell proliferation and cell death of PDL cells. Furthermore, TNF‐α plays a significant role in the control of proliferation, differentiation, and apoptosis. TNF‐α has been shown to trigger apoptosis in osteoblast and PDL cells. Sugimori et al. (2018) concluded that micro‐osteoperforations may accelerate tooth movement through activation of cell proliferation and apoptosis of PDL cells.

These present and previous findings suggest that activation of inflammation, apoptosis, and cell cycles of PDL may potentially increase the rate of tooth movement.

Biological Mechanisms of Tooth Movement

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