Department of Otolaryngology-Head & Neck Surgery, School of Medicine, Indiana University, Indianapolis, Indiana, USA.
Indiana Center for Musculoskeletal Health, School of Medicine, Indiana University, Indianapolis, Indiana, USA.
J Periodontol. 2023 Feb;94(2):277-289. doi: 10.1002/JPER.22-0192. Epub 2023 Jan 19.
Type 1 diabetes mellitus (T1DM) and periodontitis have long been thought to be biologically connected. Indeed, T1DM is a risk factor for periodontal disease. With the population of diabetic individuals growing, it is more important than ever to understand the negative consequences of diabetes on the periodontium and the mechanisms. The aim of this study was to find out the early effects of T1DM on the periodontium without any experimentally induced periodontitis.
We established the streptozotocin (STZ)-induced diabetic mouse model and examined the periodontium 8 weeks later by histology, molecular and cellular assays. Microcomputed tomographic (𝜇CT) imaging and in vivo fluorochrome labeling were also used to quantify bone volume and mineral apposition rates (MAR).
The histologic appearance of epithelium tissue, connective tissue, and periodontal ligament in the diabetic condition was comparable with that of control mice. However, immune cell infiltration in the gingiva was dramatically elevated in the diabetic mice, which was accompanied by unmineralized connective tissue degeneration. Bone resorption activity was significantly increased in the diabetic mice, and quantitative 𝜇CT demonstrated the bone volume, the ratio of bone volume over tissue volume, and cemento-enamel junction to alveolar bone crest (CEJ-ABC) in the diabetic condition were equivalent to those in the control group. In vivo fluorochrome labeling revealed increased MAR and bone remodeling in the diabetic mice. Further investigation found the diabetic mice had more osteoprogenitors recruited to the periodontium, allowing more bone formation to balance the enhanced bone resorption.
STZ-induced T1DM mice, at an early stage, have elevated gingival inflammation and soft tissue degeneration and increased bone resorption; but still the alveolar bone was preserved by recruiting more osteoprogenitor cells and increasing the rate of bone formation. We conclude that inflammation and periodontitis precede alveolar bone deterioration in diabetes.
1 型糖尿病(T1DM)和牙周炎长期以来一直被认为具有生物学联系。事实上,T1DM 是牙周病的一个危险因素。随着糖尿病患者人数的增加,了解糖尿病对牙周组织的负面影响及其机制变得比以往任何时候都更加重要。本研究旨在在没有任何实验性诱导牙周炎的情况下,研究 T1DM 对牙周组织的早期影响。
我们建立了链脲佐菌素(STZ)诱导的糖尿病小鼠模型,并在 8 周后通过组织学、分子和细胞检测来检查牙周组织。还使用微计算机断层扫描(μCT)成像和体内荧光标记来定量骨体积和矿化沉积率(MAR)。
糖尿病状态下上皮组织、结缔组织和牙周韧带的组织学外观与对照小鼠相似。然而,糖尿病小鼠牙龈中的免疫细胞浸润显著增加,同时伴有未矿化的结缔组织退化。糖尿病小鼠的骨吸收活性显著增加,定量 μCT 显示糖尿病小鼠的骨体积、骨体积与组织体积比以及釉牙骨质界到牙槽骨嵴(CEJ-ABC)与对照组相当。体内荧光标记显示糖尿病小鼠的 MAR 和骨重塑增加。进一步的研究发现,糖尿病小鼠有更多的成骨前体细胞募集到牙周组织,从而使更多的骨形成来平衡增强的骨吸收。
STZ 诱导的 T1DM 小鼠在早期阶段表现出牙龈炎症和软组织退化增加以及骨吸收增加;但通过募集更多的成骨前体细胞和增加骨形成率,仍然保留了牙槽骨。我们得出结论,炎症和牙周炎先于糖尿病中的牙槽骨恶化。