TY - JOUR
T1 - Type 1 diabetes mellitus leads to gingivitis and an early compensatory increase in bone remodeling
AU - Yuan, Xue
AU - Amin, Vedanshi
AU - Zhu, Tianli
AU - Kittaka, Mizuho
AU - Ueki, Yasuyoshi
AU - Bellido, Teresita M.
AU - Turkkahraman, Hakan
N1 - Publisher Copyright:
© 2022 The Authors. Journal of Periodontology published by Wiley Periodicals LLC on behalf of American Academy of Periodontology.
PY - 2023/2
Y1 - 2023/2
N2 - Background: 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. Methods: 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). Results: 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. Conclusions: 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.
AB - Background: 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. Methods: 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). Results: 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. Conclusions: 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.
KW - bone remodeling
KW - diabetes mellitus
KW - gingivitis
KW - inflammation
KW - periodontitis
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U2 - 10.1002/JPER.22-0192
DO - 10.1002/JPER.22-0192
M3 - Article
AN - SCOPUS:85146341214
SN - 0022-3492
VL - 94
SP - 277
EP - 289
JO - Journal of periodontology
JF - Journal of periodontology
IS - 2
ER -