肥胖2型糖尿病大鼠高血糖影响牙髓创面愈合

IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Journal of Oral Biosciences Pub Date : 2025-08-09 DOI:10.1016/j.job.2025.100683

Rosa Baldeon-Gutierrez , Naoto Ohkura , Nagako Yoshiba , Shintaro Takahara , Susan Gomez-Kasimoto , Takako Ida , Naoki Edanami , Kunihiko Yoshiba , Shoji Takenaka , Yuichiro Noiri

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引用次数: 0

摘要

目的：2型糖尿病患者的高血糖与伤口愈合延迟有关，但其潜在机制尚不清楚。巨噬细胞分化为促炎和抗炎亚型，在炎症的发生、维持和消退中起着至关重要的作用。在2型糖尿病患者中，高血糖可能会干扰成牙细胞样细胞的分化并引起持续的促炎极化。方法选用8周龄自发性糖尿病Torii脂肪大鼠（2型糖尿病模型大鼠）和Sprague-Dawley大鼠（对照组，每组4只）。左上颌第一磨牙切髓，7天后用三氧化二矿聚集体盖上观察。分析骨桥蛋白的表达以评估伤口愈合的开始。采用巢蛋白和-平滑肌肌动蛋白的免疫荧光分析来评价成牙细胞样细胞的分化。计数促炎和抗炎巨噬细胞中的双阳性细胞。此外，对增殖细胞核抗原（PCNA）、Thy1和CD146进行评估，以评估细胞增殖和间充质干细胞。结果模型大鼠炎症持续，未形成修复性牙本质。模型大鼠巨噬细胞的促炎反应增强，抗炎反应减弱。结论高血糖会干扰巨噬细胞极化和成牙细胞样细胞分化，从而影响该模型的创面愈合。

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Hyperglycemia in obese type 2 diabetes mellitus rats affects pulp wound healing

Objective

Hyperglycemia in individuals with type 2 diabetes mellitus is associated with delayed wound healing, although the underlying mechanism remains unclear. Macrophages play a crucial role in the initiation, maintenance, and resolution of inflammation by polarizing into proinflammatory and anti-inflammatory subtypes. Hyperglycemia may interfere with odontoblast-like cell differentiation and cause persistent proinflammatory polarization in individuals with type 2 diabetes mellitus.

Methods

Eight-week-old spontaneously diabetic Torii fatty rats (model rats for type 2 diabetes mellitus) and Sprague-Dawley rats (control group, four rats per group) were used. The upper left first molars underwent pulpotomy and were capped with mineral trioxide aggregates for observation after seven days. Osteopontin expression was analyzed to assess the initiation of wound healing. Immunofluorescence analysis of nestin and alpha-smooth muscle actin was used to evaluate odontoblast-like cell differentiation. Double-positive cells among proinflammatory and anti-inflammatory macrophages were counted. Furthermore, the proliferating cell nuclear antigen (PCNA), Thy1, and CD146 were evaluated to assess cell proliferation and mesenchymal stem cells.

Results

Inflammation persisted in the model rats, and no reparative dentin was formed. Macrophages in the model rats showed an increased proinflammatory response and a reduced anti-inflammatory response.