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Inflammatory mediators in OTM

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The transduction of mechanical forces to the cells triggers a biological response that has been described as an aseptic inflammation because it is mediated by a variety of inflammatory cytokines and does not represent a pathological condition. In contrast to chronic inflammatory responses, in which persistent stimuli sustain a long‐lasting inflammatory response and result in tissue damage, the expression of inflammatory mediators after orthodontic force application is transitory and essential for orthodontic movement, as anti‐inflammatory drugs are capable of blocking tooth movement. The concept of aseptic inflammation was recently strengthened by discovery of the DAMPs system, where endogenous molecules are able to trigger inflammatory response by cellular stress or damage through the binding of toll‐like receptors (TLRs) and nod‐like receptors (NLRs) (Chen and Nunez, 2010). This tissue response initially involves vascular changes, followed by the synthesis of prostaglandins, cytokines, and growth factors. Finally, such mediators are believed to activate tissue remodeling, characterized by selective bone resorption or deposition in compression and tension regions of the PDL, respectively (Garlet et al., 2007). Various inflammatory mediators, identified to date, associated with OTM, are summarized in Table 4.2.

Table 4.2 Inflammatory factors from PDL in response to OTM.

In vitro studies (stimulated by mechanical stress) In vivo studies
Prostaglandin E2 (PGE2) Prostaglandin E2 (PGE2)
cAMP cAMP, cGMP
IL‐1β IL‐1α
IL‐6 IL‐6
TNF‐α
RANKL RANKL
MMP‐1, 2 MMP‐1, 2, 3, 8, 9, and 13
CGRP and SP
Biological Mechanisms of Tooth Movement

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