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，并抵制治疗。本实验采用链脲佐菌素(STZ：65 mg/kg)诱导的糖尿病大鼠(ODUS/ODU)。对照组(ODUS/ODU，不含STZ)。注射STZ后1个月和3个月，分别腹腔注射液体石蜡。4天后，测量口袋探查深度(PPD)，并采集血样和腹腔巨噬细胞。为了阐明糖尿病对牙周病变的影响，我们研究了糖尿病患者和非糖尿病患者牙周组织中巨噬细胞的趋化和吞噬功能。注射链脲佐菌素后1个月和3个月，合并糖尿病的ODUS/ODU患者的产后抑郁程度明显高于非糖尿病患者(P&lt；0.001)。合并糖尿病的ODUS/ODU患者注射STZ后3个月的PPD比1个月时的PPD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&lt；0.01)。在这两个实验期，糖尿病组的巨噬细胞吞噬功能比非糖尿病组明显受到抑制(p&lt；0.001)。注射STZ 3个月后，合并糖尿病的ODUS/ODU患者的巨噬细胞趋化功能明显受到抑制。这些结果表明，糖尿病影响了ODUS/ODU巨噬细胞的趋化和吞噬功能。因此，宿主防御机制减弱，并加重牙周病。

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.