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. 2016 Jun 24;8(2):67–75. doi: 10.1038/ijos.2016.24

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Copyright © 2016 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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The mechanisms underlying orthodontic pain. The dental root (left) moves in the direction of force towards the alveolar bone (right) with the periodontium between them. Upon vascular compression and local ischaemia, periodontal cells, mainly fibroblasts, undergo anaerobic respiration and cause local acidosis. The proton ion (H⁺) binds to ASIC3 receptors on sensory endings to generate pain. As local ischaemia progresses, mast cells and fibroblasts release various chemotaxins to recruit leucocytes, for example, neutrophils and monocytes. These leucocytes release abundant inflammatory mediators (for example, bradykinin and prostaglandin) and cytokines (for example, IL-1 and TNF). Bradykinin and prostaglandin bind to sensory endings to generate painful sensations. The released cytokines amplify local inflammation and stimulate monocyte-derived macrophages to participate in alveolar bone remodelling. Moreover, via anterograde transportation, sensory endings release various neurogenic mediators (for example, CGRP and SP) to dilate local blood vessels and enhance local inflammation, amplifying local painful sensation and alveolar remodelling. CGRP, calcitonin gene-related peptide; IL, interleukin; SP, substance P; TNF, tumour necrosis factor.