Читать книгу Biological Mechanisms of Tooth Movement - Группа авторов - Страница 74

The innervation of the dental pulp includes sensory nerve fibers, which may also subserve dentinal fluid dynamics and regulate pulpal blood flow, providing reflexes to preserve dental tissues and promote wound healing. The main neuropeptides associated with these functions include SP, CGRP, and NKA, which are abundant in the pulp and periodontium (Kim, 1990; Ohkubo et al., 1993). Release of these neuropeptides after stimulation of sensory nerve fibers induces vasodilatation and increases vascular permeability, a condition referred to as neurogenic inflammation (Fristad et al., 1997). It is concluded that the stimulation of sensitive teeth may induce pulpal changes such as induction of neurogenic inflammation and alteration of pulpal blood flow.

The morphology and distribution of CGRP and SP through immunoreactive nerves have been shown to change their pattern as a result of local pulp trauma, indicating their role in the inflammatory process in connection with tissue injury and repair. The expressions of SP, CGRP, and NKA in inflamed human dental pulp tissue are significantly higher compared with healthy pulp. In addition, it was observed that the expression of CGRP and/or SP increases in the dental pulp in response to orthodontic treatment in rats, cats, and humans (Parris et al., 1989; Kvinnsland and Kvinnsland, 1990; Norevall et al., 1998). Another report suggested that these neuropeptides might be involved in inflammation of the dental pulp at the time of OTM (Norevall et al., 1995). Previous immunohistochemical studies demonstrated that MMP‐1, 3, 8, 9, and tissue‐type plasminogen activator expressions were significantly higher in the inflamed pulps than in clinically healthy pulps. These mediators may play an important role in the pathogenesis of pulpal inflammation.

Yamaguchi et al. (2004) reported that SP and CGRP stimulated the production of IL‐1β, IL‐6, and TNF‐α in human dental pulp fibroblasts (HDPF) in vitro. Moreover, Kojima et al. (2006) reported that SP significantly stimulated the production of PGE₂ and RANKL by HDPF cells, and the increase of RANKL caused by SP stimulation in HDPF cells were partially mediated by PGE₂. Shimizu et al. (2013) demonstrated that the immunoreactivity for Th17, IL‐17, IL‐17R, IL‐6 and KC (IL‐8 related protein in rodents) in the atopic dermatitis group was found to be increased in the dental pulp tissue subjected to the orthodontic force on day 9. The atopic dermatitis patients increased the release of IL‐6 and IL‐8 from human dental pulp cells. Taken together, these findings and our results suggest that HDPF may be actively involved in the progress of inflammation in the pulp tissue during OTM.