Current advances in orthodontic pain

Hu Long, Yan Wang, Fan Jian, Li-Na Liao, Xin Yang, Wen-Li Lai, Hu Long, Yan Wang, Fan Jian, Li-Na Liao, Xin Yang, Wen-Li Lai

Abstract

Orthodontic pain is an inflammatory pain that is initiated by orthodontic force-induced vascular occlusion followed by a cascade of inflammatory responses, including vascular changes, the recruitment of inflammatory and immune cells, and the release of neurogenic and pro-inflammatory mediators. Ultimately, endogenous analgesic mechanisms check the inflammatory response and the sensation of pain subsides. The orthodontic pain signal, once received by periodontal sensory endings, reaches the sensory cortex for pain perception through three-order neurons: the trigeminal neuron at the trigeminal ganglia, the trigeminal nucleus caudalis at the medulla oblongata and the ventroposterior nucleus at the thalamus. Many brain areas participate in the emotion, cognition and memory of orthodontic pain, including the insular cortex, amygdala, hippocampus, locus coeruleus and hypothalamus. A built-in analgesic neural pathway-periaqueductal grey and dorsal raphe-has an important role in alleviating orthodontic pain. Currently, several treatment modalities have been applied for the relief of orthodontic pain, including pharmacological, mechanical and behavioural approaches and low-level laser therapy. The effectiveness of nonsteroidal anti-inflammatory drugs for pain relief has been validated, but its effects on tooth movement are controversial. However, more studies are needed to verify the effectiveness of other modalities. Furthermore, gene therapy is a novel, viable and promising modality for alleviating orthodontic pain in the future.

Figures

Figure 1
Figure 1
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.
Figure 2
Figure 2
Pain transmission pathways for orthodontic pain.
Figure 3
Figure 3
Neural circuits of orthodontic pain.

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Source: PubMed

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