Periodontol 2000. 2018 Feb;76(1):97-108. doi: 10.1111/prd.12160. Epub 2017 Nov 30.
The signaling network involved in the pathogenesis of periodontal disease is not yet fully understood. This review aims to describe possible mechanisms through which the bacterial modulators may be linked directly or indirectly to the process of alveolar bone loss in periodontitis. From the late 1970s to present, new paradigm shifts have been developed regarding our understanding of pathological bone remodeling in periodontal disease. Upcoming evidence suggests that in periodontal disease the local immune response is exacerbated and involves the existence of signaling pathways that have been shown to modulate bone-cell function leading to alveolar bone loss. Those complex signaling pathways have been observed not only between bacteria but also between bacteria and the gingival surface of the host. More specifically, it has been shown that bacteria, through their secretion molecules, may interact indirectly and directly with immune-type cells of the host, resulting in the production of osteolytic agents that enhance bone resorption. Further research is required to provide a clear understanding of the role of these molecules in the pathogenesis of periodontal disease, and the availability of new technologies, such as next-generation sequencing and metagenomic analysis, may be useful tools in achieving this.
牙周病发病机制中涉及的信号转导网络尚未完全阐明。本综述旨在描述细菌调节剂可能通过直接或间接途径与牙周炎牙槽骨丧失过程相关的可能机制。自 20 世纪 70 年代末至今，人们对牙周病病理性骨重塑的理解发生了新的转变。新出现的证据表明，在牙周病中，局部免疫反应加剧，并涉及信号通路的存在，这些信号通路已被证明可调节骨细胞功能，导致牙槽骨丧失。这些复杂的信号通路不仅存在于细菌之间，也存在于细菌与宿主牙龈表面之间。更具体地说，已经表明细菌通过其分泌分子可能与宿主的免疫细胞间接和直接相互作用，导致产生增强骨吸收的溶骨剂。需要进一步的研究来更清楚地了解这些分子在牙周病发病机制中的作用，而新技术的出现，如下一代测序和宏基因组分析，可能是实现这一目标的有用工具。
