Studies on leukocyte function of periodontal desease and diabetes mellitus

许多研究表明，糖尿病患者的牙周病变进展迅速，且对治疗有抵抗性。本研究采用注射链脲佐菌素（STZ: 65mg/kg，静脉注射）致糖尿病的天然牙龈炎大鼠（ODUS/Odu）和不注射STZ的对照大鼠（ODUS/Odu）。注射STZ后1个月和3个月分别腹腔注射液体石蜡。4 d后，我们测量了大鼠的口袋探测深度（PPD），并采集了大鼠的血液样本和腹腔巨噬细胞。为了阐明糖尿病对牙周病变的影响，我们在有糖尿病和没有糖尿病的情况下，研究了巨噬细胞的趋化性和吞噬作用。注射STZ后1个月和3个月，合并糖尿病的ODUS/Odu组PPD明显深于未合并糖尿病的ODUS/Odu组（p<0.001）。糖尿病患者在注射STZ后3个月PPD比在注射STZ后1个月PPD更深。注射STZ 3个月后，血糖与甘油三酯、血红蛋白A_1C呈高度正相关（p<0.01）。在两个实验阶段，糖尿病组巨噬细胞的吞噬能力明显高于非糖尿病组（p<0.001）。注射STZ 3个月后，糖尿病患者的巨噬细胞趋化性明显低于非糖尿病患者。这些结果表明糖尿病影响了ODUS/Odu巨噬细胞的趋化作用和吞噬作用。因此，宿主防御机制减弱，使牙周病恶化。

Many studies have shown that periodontal lesions in diabetic patients progress rapidly and resist treatment. Herein, we use the naturally occurring gingivitis rat (ODUS/Odu) with diabetes mellitus induced by injection of streptozotocin (STZ : 65mg/kg, i.v.) and the control rat (ODUS/Odu without STZ). One and 3 months after STZ injection, we intraperitoneally injected liquid paraffin. Four days later, we measured the pocket probing depth (PPD), and collected the blood sample and peritoneal macrophages from these rats. To elucidate the effect of diabetes on periodontal lesions, the chemotaxis and phagocytosis of macrophages were studied in ODUS/Odu with and without diabetes. One and 3 months after STZ injection, the PPD in the ODUS/Odu with diabetes was significantly deeper than in ODUS/Odu without diabetes (p<0.001). PPD was deeper at 3 months after STZ injection than at 1 month in ODUS/Odu with diabetes. Three months after STZ injection, there was a high positive correlation between blood glucose and triglycerides, or hemoglobin A_1C (p<0.01). In both experimental periods, the phagocytosis of macrophages in the diabetes group was significantly more suppressed than in that without diabetes (p<0.001). Three months after STZ injection, the macrophage chemotaxis was more suppressed in ODUS/Odu with diabetes than in those without diabetes. These findings stuggest that diabetes mellitus affects the chemotaxis and phagocytosis of macrophages in ODUS/Odu. Therefore, the host defense mechanism weakens, and worsens periodontal disease.