Gong Aixiu, Liu Yining, Xu Fangrong, Chu Yiting, Wu Jun, Goltzman David, Miao Dengshun
Department of Stomatology, Children's Hospital of Nanjing Medical University Nanjing, PR China.
Research Center for Bone and Stem Cells, Department of Anatomy, Histology and Embryology, Nanjing Medical University Nanjing, PR China.
Am J Transl Res. 2022 May 15;14(5):3079-3091. eCollection 2022.
The goal of this study was to assess if endogenous 1,25(OH)D deficiency enhanced, whereas exogenous 1,25(OH)D supplementation alleviated alveolar bone loss and gingival inflammation induced by ligature-induced periodontitis.
A model of ligature-induced experimental periodontitis was generated in wild-type (WT) and Cyp27b1-knockout (KO) mice on a rescue diet (RD), and un-ligated genotype-matched littermates as control, or in WT mice on a normal diet (ND) with vehicle treatment or 1,25(OH)D treatment, and un-ligated WT littermates as control. Alveolar bone mass and turnover, T cell infiltration and inflammatory cytokines in gingival tissues were examined.
In WT mice, ligature-induced alveolar bone loss occurred by inhibiting alveolar bone formation. This was characterized by reduction of osteoblast numbers, alkaline phosphatase activity and type I collagen synthesis, as well as by augmentation of osteoclastic alveolar bone resorption and gingival inflammation, including increases of osteoclast numbers, inflammatory positive cells and up-regulation of mRNA expression levels of inflammatory cytokines. Alveolar bone destruction and gingival inflammation were more severe in diet-matched Cyp27b1-KO mice than in WT littermates on RD. Supplementation of exogenous 1,25(OH)D alleviated alveolar bone loss and gingival inflammation in ligated WT mice on ND, but those parameters did not reach levels observed in un-ligated WT ones.
Endogenous 1,25(OH)D deficiency enhanced, whereas exogenous 1,25(OH)D supplementation alleviated alveolar bone loss and gingival inflammation induced by ligature-induced periodontitis.
本研究旨在评估内源性1,25(OH)D缺乏是否会加重，而外源性补充1,25(OH)D是否能减轻结扎诱导的牙周炎所致的牙槽骨丧失和牙龈炎症。
在接受救援饮食（RD）的野生型（WT）和Cyp27b1基因敲除（KO）小鼠中建立结扎诱导的实验性牙周炎模型，以未结扎的同基因型 littermates 作为对照，或者在接受正常饮食（ND）的WT小鼠中进行载体处理或1,25(OH)D处理，并以未结扎的WT littermates作为对照。检测牙槽骨质量和周转率、牙龈组织中的T细胞浸润和炎性细胞因子。
在WT小鼠中，结扎诱导的牙槽骨丧失是通过抑制牙槽骨形成而发生的。其特征是成骨细胞数量减少、碱性磷酸酶活性和I型胶原合成降低，以及破骨细胞性牙槽骨吸收和牙龈炎症增加，包括破骨细胞数量增加、炎性阳性细胞增加以及炎性细胞因子mRNA表达水平上调。与接受RD的WT littermates相比，饮食匹配的Cyp27b1-KO小鼠的牙槽骨破坏和牙龈炎症更严重。外源性补充1,25(OH)D可减轻接受ND的结扎WT小鼠的牙槽骨丧失和牙龈炎症，但这些参数未达到未结扎WT小鼠中观察到的水平。
内源性1,25(OH)D缺乏会加重，而外源性补充1,25(OH)D可减轻结扎诱导的牙周炎所致的牙槽骨丧失和牙龈炎症。
