- 著者
- Tatsuro Suzuki Masahiro Kondo Ikuko Shibuta Hidekazu Nagashima Naoyuki Sugano Shuichi Sato Koichi Iwata
- 出版者
- Nihon University School of Dentistry
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- vol.60, no.4, pp.500-506, 2018 (Released:2018-12-27)
- 参考文献数
- 25
- 被引用文献数
- 1
The inferior alveolar nerve (IAN) comprises several types of sensory fibers. To clarify whether each type of primary afferent is regenerated comparably after injury, we developed a model of complete IAN transection (IANX) in mice. A retrograde tracer, fluoro-gold, injected into the mental skin was transferred to the cell bodies of a subset of isolectin B4 (IB4)-binding (non-peptidergic C) or CGRP-positive (peptidergic C) neurons at 2 weeks post-axotomy, indicating that the injured C afferents had regenerated anatomically. IANX led to a decrease of IB4-binding and CGRP immunoreactivity (IR) in the trigeminal ganglion (TG) and within the trigeminal spinal subnucleus caudalis (Vc) (i.e. terminals of the central branch of TG neurons). Two weeks after IANX, the reduction in IB4-binding activity and CGRP expression in the TG recovered to the control level; however, IB4-binding within the Vc did not, suggesting that central branch non-peptidergic neurons remained impaired. Two weeks after IANX, pinching or heat stimulus-induced extracellular signal-regulated kinase phosphorylation (pERK) was restored to the control level, but in the case of pinch stimulation the distribution pattern of pERK-IR cells was altered in the Vc. Taken together, our results support the possibility that peptidergic neurons regenerate more efficiently than non-peptidergic neurons after trigeminal nerve injury.
- 著者
- Hidekazu Nagashima Masamichi Shinoda Kuniya Honda Noriaki Kamio Akira Hasuike Naoyuki Sugano Yoshinori Arai Shuichi Sato Koichi Iwata
- 出版者
- 日本大学歯学部
- 雑誌
- Journal of Oral Science (ISSN:13434934)
- 巻号頁・発行日
- pp.16-0830, (Released:2017-10-31)
- 参考文献数
- 45
- 被引用文献数
- 13
Periodontitis caused by bacterial infection gradually progresses accompanied by periodontal tissue destruction. As a result, teeth lose their supporting structures, and this leads to tooth exfoliation. CXC-chemokine receptor 4 (CXCR4) is known to be expressed in lymphocytes, fibroblasts and osteoclasts in periodontal tissues, suggesting that periodontal CXCR4 signaling contributes to alveolar bone resorption in the milieu of periodontitis. However, the role of CXCR4 signaling in the pathogenesis of periodontitis has remained unknown. We established a mouse model of periodontitis by inoculation of Porphyromonas gingivalis (P.g.) into a silk ligature placed around the maxillary molar. Although there was no significant difference in the mechanical sensitivity in the periodontal tissue between P.g. treatment and sham treatment during the experimental period, mechanical allodynia in the periodontal tissue was induced after gingival injection of complete Freund’s adjuvant compared with that resulting from sham and P.g. treatment alone. Moreover, CXCR4 neutralization in the periodontal tissue following P.g. treatment enhanced periodontal inflammatory cell infiltration and depressed alveolar bone resorption. These findings suggest that periodontal CXCR4 signaling in several cell types in P.g.-induced periodontal inflammation depresses alveolar bone resorption in periodontitis. CXCR4 signaling might be a target for therapeutic intervention to prevent alveolar bone resorption in periodontitis.