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4 CGRP (Krishnan and Davidovitch, 2009; Masella and Meister, 2006; Meikle, 2006). Together, the result is the modulation of the RANK-RANKL-Osteoprotegrin (OPG) pathway such that in an area of compression, bone is resorbed and in the area of tension bone is deposited (Krishnan and Davidovitch, 2009; Masella and Meister, 2006; Meikle, 2006). The extent of bone remodelling is limited by the compartmentalization and the creation of a local vascular environment involved in the differential expression of RANK/RANKL/OPG and other cytokines around a tooth during orthodontic force application. This is referred to as the “Basic Multicellular Unit” around an orthodontically moving tooth (Eriksen, 2010; Boyce and Xing, 2008). Despite the histological similarity to inflammation, changes in the PDL during OTM have been described as undergoing aseptic inflammation (Ren and Vissink, 2008) or a “form of normal physiological turnover combined with foci of tissue repair, particularly at the compression sites where hyalinized tissue and adjacent bone and cementum are being remodelled” (Meikle, 2006). Since phototherapy has been shown to produce inflammatory and connective tissue metabolic changes (described below), these aceptic inflammatory processes are a potential site for phototherapy mediated changes in the rate of OTM. 1.3 Orthodontic Tooth Movement: Rate and Methods to Increase the Rate It is widely accepted that the rate of OTM varies from individual to individual. However, clinical experience combined with scientific evidence points towards an average rate of OTM of 1mm per month (Barlow and Kula, 2008). As an alternative to surgically derived regional accelerations of OTM (Wilcko et al., 2010), several studies have attempted to expedite orthodontic treatment by increasing the velocity of OTM via pharmacological andPDF Image | Effect of LED Phototherapy on the Rate of Orthodontic Tooth Movement
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