Division of Periodontology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8514, Japan.
Center for Advanced Oral Science, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8514, Japan.
Int J Mol Sci. 2022 May 16;23(10):5540. doi: 10.3390/ijms23105540.
Periodontitis is one of the most common oral diseases resulting in gingival inflammation and tooth loss. Growing evidence indicates that it results from dysbiosis of the oral microbiome, which interferes with the host immune system, leading to bone destruction. Immune cells activate periodontal ligament cells to express the receptor activator of nuclear factor kappa-B (NF-κB) ligand (RANKL) and promote osteoclast activity. Osteocytes have active roles in periodontitis progression in the bone matrix. Local proteins are involved in bone regeneration through functional immunological plasticity. Here, we discuss the current knowledge of cellular and molecular mechanisms in periodontitis, the roles of local proteins, and promising synthetic compounds generating a periodontal regeneration effect. It is anticipated that this may lead to a better perception of periodontitis pathophysiology.
牙周炎是导致牙龈炎症和牙齿脱落的最常见口腔疾病之一。越来越多的证据表明,它是由口腔微生物组的失调引起的,这种失调会干扰宿主的免疫系统,导致骨破坏。免疫细胞激活牙周韧带细胞表达核因子 κB 受体激活剂配体(RANKL),并促进破骨细胞的活性。成骨细胞在骨基质中的牙周炎进展中发挥积极作用。局部蛋白通过功能免疫可塑性参与骨再生。在这里,我们讨论了牙周炎中细胞和分子机制的最新知识、局部蛋白的作用以及有前景的合成化合物产生牙周再生效果。预计这可能会导致更好地理解牙周炎的病理生理学。