We sought to evaluate the effects of magnesium (Mg) intake deficiency on bone metabolism in rats with induced periodontal disease (PD). Holtzman rats were randomly divided into two groups: Control — animals fed a standard diet and test — animals fed a diet with 90% Mg deficiency. After 60 days on the diets, all animals received ligature on the lower left first molars to induce PD. Animals were euthanized after 30 days following ligature placement. Blood and urine were collected for determination of serum concentrations of Mg, calcium, osteocalcin (OCN), alkaline phosphatase and parathyroid hormone (PTH) by enzyme-linked immunosorbent assay, and the urinary concentration of deoxypyridinoline (DPD). Systemic bone mineral density (BMD), bone volume and architectural bone parameters were evaluated by micro-CT in L4 lumbar vertebrae and mandible. Tartrate-resistant acid phosphatase staining and immunohistochemical (IHC) analysis of inducible nitric oxide synthase (iNOS), Runt-related transcription factor 2 (RUNX2), CD86, CD80, proliferating cell nuclear antigen, vascular endothelial growth factor, OCN and osteopontin were investigated. Reverse-transcription polymerase chain reaction was employed to assess mRNA expression of receptor-activator of nuclear factor-kB ligand, osteoprotegerin (OPG) and interleukin (IL)-6. Mg deficiency was associated with higher concentrations of PTH and DPD, and significant decrease on both systemic and mandibular BMD, as well as greater severity of alveolar and trabecular bone loss. Significant increase in osteoclasts was observed in the test group with PD. IHC analysis showed significant increase in the expression of iNOS and decreased expression of OCN and RUNX2. Increased IL-6 mRNA and decreased OPG mRNA expressions were evidenced in the test group with PD. Mg deficiency caused systemic effects indicative of altered bone metabolism in the vertebrae and affected both immune and stromal cells, aggravating inflammatory bone resorption in the ligature-induced model of periodontitis.

我们试图评估镁（Mg）摄入不足对诱发牙周病（PD）大鼠骨骼代谢的影响。Holtzman大鼠随机分为两组：对照组-饲喂标准饮食的动物和受试动物-饲喂90％镁缺乏的饮食的动物。在节食60天后，所有动物的左下磨牙均接受结扎以诱导PD。结扎后30天将动物安乐死。收集血液和尿液，通过酶联免疫吸附测定法测定血清镁，钙，骨钙蛋白（OCN），碱性磷酸酶和甲状旁腺激素（PTH）的浓度，以及尿中脱氧吡啶啉（DPD）的浓度。通过微型CT评估L4腰椎和下颌骨的全身骨矿物质密度（BMD），骨量和建筑骨参数。研究了诱导型一氧化氮合酶（iNOS），矮子相关转录因子2（RUNX2），CD86，CD80，增殖细胞核抗原，血管内皮生长因子，OCN和骨桥蛋白的抗酒石酸酸性磷酸酶染色和免疫组化（IHC）分析。逆转录聚合酶链反应用于评估核因子-kB配体，骨保护素（OPG）和白介素（IL）-6受体激活剂的mRNA表达。镁缺乏与PTH和DPD浓度升高，全身和下颌骨BMD显着降低以及肺泡和小梁骨丢失的严重程度有关。在PD试验组中观察到破骨细胞显着增加。IHC分析显示iNOS的表达显着增加，而OCN和RUNX2的表达则下降。在PD组中，IL-6 mRNA的表达增加，OPG mRNA的表达减少。镁缺乏引起全身效应，表明椎骨中的骨代谢发生改变，并影响免疫细胞和基质细胞，在结扎性牙周炎模型中加剧了炎症性骨吸收。