Alveolar bone is a unique osseous tissue due to the proximity of dental plaque biofilms. Periodontal health and homeostasis are mediated by a balanced host immune response to these polymicrobial biofilms. Dysbiotic shifts within dental plaque biofilms can drive a proinflammatory immune response state in the periodontal epithelial and gingival connective tissues, which leads to paracrine signaling to subjacent bone cells. Sustained chronic periodontal inflammation disrupts “coupled” osteoclast‐osteoblast actions, which ultimately result in alveolar bone destruction. This chapter will provide an overview of alveolar bone physiology and will highlight why the oral microbiota is a critical regulator of alveolar bone remodeling. The ecology of dental plaque biofilms will be discussed in the context that periodontitis is a polymicrobial disruption of host homeostasis. The pathogenesis of periodontal bone loss will be explained from both a historical and current perspective, providing the opportunity to revisit the role of fibrosis in alveolar bone destruction. Periodontal immune cell interactions with bone cells will be reviewed based on our current understanding of osteoimmunological mechanisms influencing alveolar bone remodeling. Lastly, probiotic and prebiotic interventions in the oral microbiota will be evaluated as potential noninvasive therapies to support alveolar bone homeostasis and prevent periodontal bone loss.

中文翻译：

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维持牙周骨组织的稳态控制

由于牙菌斑生物膜的接近，牙槽骨是独特的骨组织。牙周健康和体内平衡是由对这些微生物生物膜的平衡宿主免疫反应介导的。牙菌斑生物膜内的不良生物转移可驱动牙周上皮和牙龈结缔组织中的促炎性免疫反应状态，从而导致旁分泌信号传导至下层骨细胞。持续的慢性牙周炎会破坏“耦合的”破骨细胞-成骨细胞的作用，最终导致牙槽骨破坏。本章将概述牙槽骨的生理状况，并强调为什么口腔微生物群是牙槽骨重塑的关键调节剂。牙菌斑生物膜的生态学将在牙周炎是宿主体内稳态的多微生物破坏的背景下进行讨论。牙周骨丢失的发病机理将从历史和当前角度进行解释，为重新探讨纤维化在牙槽骨破坏中的作用提供了机会。牙周免疫细胞与骨细胞的相互作用将根据我们目前对影响牙槽骨重塑的骨免疫学机制的理解来进行综述。最后，口腔微生物群中的益生菌和益生元干预措施将被评估为潜在的非侵入性疗法，可支持牙槽骨稳态并防止牙周骨丢失。提供机会重新探讨纤维化在牙槽骨破坏中的作用。牙周免疫细胞与骨细胞的相互作用将根据我们目前对影响牙槽骨重塑的骨免疫学机制的理解来进行综述。最后，口腔微生物群中的益生菌和益生元干预措施将被评估为潜在的非侵入性疗法，可支持牙槽骨稳态并防止牙周骨丢失。提供机会重新探讨纤维化在牙槽骨破坏中的作用。牙周免疫细胞与骨细胞的相互作用将根据我们目前对影响牙槽骨重塑的骨免疫学机制的理解来进行综述。最后，口腔微生物群中的益生菌和益生元干预措施将被评估为潜在的非侵入性疗法，可支持牙槽骨稳态并防止牙周骨丢失。