Cooper Paul R, Holder Michelle J, Smith Anthony J
Oral Biology, School of Dentistry, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Oral Biology, School of Dentistry, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
J Endod. 2014 Apr;40(4 Suppl):S46-51. doi: 10.1016/j.joen.2014.01.021.
Dental tissue infection and disease result in acute and chronic activation of the innate immune response, which is mediated by molecular and cellular signaling. Different cell types within the dentin-pulp complex are able to detect invading bacteria at all stages of the infection. Indeed, at relatively early disease stages, odontoblasts will respond to bacterial components, and as the disease progresses, core pulpal cells including fibroblasts, stems cells, endothelial cells, and immune cells will become involved. Pattern recognition receptors, such as Toll-like receptors expressed on these cell types, are responsible for detecting bacterial components, and their ligand binding leads to the activation of the nuclear factor-kappa B and p38 mitogen-activated protein (MAP) kinase intracellular signaling cascades. Subsequent nuclear translocation of the transcription factor subunits from these pathways will lead to proinflammatory mediator expression, including increases in cytokines and chemokines, which trigger host cellular defense mechanisms. The complex molecular signaling will result in the recruitment of immune system cells targeted at combating the invading microbes; however, the trafficking and antibacterial activity of these cells can lead to collateral tissue damage. Recent evidence suggests that if inflammation is resolved relatively low levels of proinflammatory mediators may promote tissue repair, whereas if chronic inflammation ensues repair mechanisms become inhibited. Thus, the effects of mediators are temporal context dependent. Although containment and removal of the infection are keys to enable dental tissue repair, it is feasible that the development of anti-inflammatory and immunomodulatory approaches, based on molecular, epigenetic, and photobiomodulatory technologies, may also be beneficial for future endodontic treatments.
牙齿组织感染和疾病会导致先天性免疫反应的急性和慢性激活，这是由分子和细胞信号传导介导的。牙本质 - 牙髓复合体中的不同细胞类型能够在感染的各个阶段检测入侵的细菌。实际上，在疾病相对早期阶段，成牙本质细胞会对细菌成分作出反应，随着疾病进展，包括成纤维细胞、干细胞、内皮细胞和免疫细胞在内的牙髓核心细胞将被累及。模式识别受体，如这些细胞类型上表达的Toll样受体，负责检测细菌成分，其配体结合会导致核因子 - κB和p38丝裂原活化蛋白（MAP）激酶细胞内信号级联反应的激活。这些信号通路中转录因子亚基随后的核转位将导致促炎介质的表达，包括细胞因子和趋化因子的增加，从而触发宿主细胞防御机制。复杂的分子信号传导将导致针对对抗入侵微生物的免疫系统细胞的募集；然而，这些细胞的运输和抗菌活性可能导致附带的组织损伤。最近的证据表明，如果炎症得到缓解，相对低水平的促炎介质可能促进组织修复，而如果发生慢性炎症，修复机制就会受到抑制。因此，介质的作用取决于时间背景。虽然控制和清除感染是实现牙齿组织修复的关键，但基于分子、表观遗传和光生物调节技术开发抗炎和免疫调节方法也可能对未来的牙髓治疗有益。
