Type 1 diabetes mellitus leads to gingivitis and an early compensatory increase in bone remodeling.
Type 1 diabetes mellitus leads to gingivitis and an early compensatory increase in bone remodeling.
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1型糖尿病会引发牙龈炎，以及早期骨骼重塑的代偿性增加。
DOI：
10.1002/jper.22-0192
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发表时间：
2023-02
影响因子：
4.3
通讯作者：
Turkkahraman, Hakan
中科院分区：
文献类型：
--
作者：
Yuan, Xue;Amin, Vedanshi;Zhu, Tianli;Kittaka, Mizuho;Ueki, Yasuyoshi;Bellido, Teresita M.;Turkkahraman, Hakan
长期以来，I型糖尿病(T1 DM)和牙周炎一直被认为是生物学上的联系。的确，T1 DM是牙周病的危险因素。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比以往任何时候都更加重要。本研究的目的是在没有任何实验性牙周炎的情况下，了解T1 DM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，8周后对牙周组织进行组织学、分子和细胞检测。采用显微计算机断层扫描(μCT)和体内荧光标记技术定量测定骨体积和矿物质沉积率(MAR)。糖尿病组小鼠上皮组织、结缔组织和牙周韧带的组织学形态与对照组相当。然而，糖尿病小鼠牙龈中的免疫细胞浸润显著增加，并伴有未矿化的结缔组织变性。糖尿病组小鼠骨吸收活性明显增强，定量μCT显示糖尿病组小鼠的骨体积、骨/组织体积比、牙骨质-釉质结合部与牙槽骨冠的比值与对照组相当。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骨祖细胞被招募到牙周组织，允许更多的骨形成，以平衡增强的骨吸收。STZ诱导的T1 DM小鼠早期牙龈炎症和软组织变性加重，骨吸收增加，但牙槽骨仍通过招募更多的骨祖细胞和增加骨形成率而得以保存。我们得出结论，炎症和牙周炎先于糖尿病患者的牙槽骨恶化。研究发现，通过增加骨改建速度，牙周组织基本不会受到I型糖尿病的短期有害影响。
Type I 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’s 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. Micro-computed tomographic (μCT) imaging and in vivo fluorochrome labeling were also employed 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 to 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 cementum-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. Periodontium was found to be mostly preserved from short-term detrimental effects of Type I Diabetes through increased bone remodeling rate.
影响因子：
3.5
作者：
Sima C;Rhourida K;Van Dyke TE;Gyurko R
通讯作者：
Gyurko R