Holzhausen Marinella, Garcia Daniele Fakoury, Pepato Maria Teresa, Marcantonio Elcio
Department of Periodontology, Dental School of Araraquara, Faculty of Pharmaceutical Sciences of Araraquara, State University of Sao Paulo (UNESP), Araraquara, Sao Paulo, Brazil.
J Periodontal Res. 2004 Jun;39(3):188-93. doi: 10.1111/j.1600-0765.2004.00723.x.
It is well known that the multiple direct and indirect consequences of hyperglycemia in diabetic individuals have been linked to a number of abnormal host effector mechanisms that could lead to an increased risk of developing periodontal disease.
The aim of this study was to investigate the effect of short-term experimental diabetes and insulin therapy on the severity of alveolar bone loss in rats, and the effect of experimental periodontitis on glycemic control.
Seventy-two male Wistar rats were divided into four groups: group I animals were submitted to dental ligature around lower right first molars (ligated); group II consisted of streptozotocin (STZ)-diabetic, ligated rats; group III represented STZ-diabetic, unligated rats; and group IV consisted of insulin-treated (6 U/day), STZ-diabetic, ligated rats. Blood glucose of all diabetic rats was monitored at regular intervals. Standardized digital radiographs were taken after killing at 7, 15 and 30 days to measure the amount of bone loss about the mesial root surface of the first molar tooth in each rat.
No significant (p < 0.05) changes in plasma glucose levels of insulin-treated diabetic rats were found among the different examinations after the beginning of insulin therapy. Rats from group II showed significantly greater increases in mean plasma glucose levels at 15 and 30 days after ligature placement compared with rats from group III (p < 0.05). Furthermore, in spite of the significant alveolar bone loss progression that was observed in groups I, II and IV (p < 0.00001; two-way anova), no significant differences among these groups regarding the severity of bone loss (p = 0.77) and no significant interaction between treatment group and time (p = 0.81) were found.
Within the limits of this study, it can be suggested that the severity of periodontal disease was not affected by short-term diabetes, and that experimental periodontitis increased blood glucose levels in uncontrolled diabetic rats.
众所周知，糖尿病患者高血糖的多种直接和间接后果与许多异常的宿主效应机制有关，这些机制可能导致患牙周病的风险增加。
本研究旨在探讨短期实验性糖尿病和胰岛素治疗对大鼠牙槽骨丧失严重程度的影响，以及实验性牙周炎对血糖控制的影响。
将72只雄性Wistar大鼠分为四组：第一组动物在右下第一磨牙周围进行牙结扎（结扎组）；第二组由链脲佐菌素（STZ）诱导的糖尿病结扎大鼠组成；第三组为STZ诱导的糖尿病未结扎大鼠；第四组为由胰岛素治疗（6 U/天）的STZ诱导的糖尿病结扎大鼠组成。定期监测所有糖尿病大鼠的血糖。在处死7、15和30天后拍摄标准化数字X线片，以测量每只大鼠第一磨牙近中根面的骨丧失量。
胰岛素治疗的糖尿病大鼠在开始胰岛素治疗后的不同检查中，血浆葡萄糖水平无显著（p < 0.05）变化。与第三组大鼠相比，第二组大鼠在结扎放置后15天和30天的平均血浆葡萄糖水平显著升高（p < 0.05）。此外，尽管在第一、二和四组中观察到明显的牙槽骨丧失进展（p < 0.00001；双向方差分析），但这些组之间在骨丧失严重程度方面无显著差异（p = 0.77），且治疗组与时间之间无显著交互作用（p = 0.81）。
在本研究的范围内，可以认为短期糖尿病不影响牙周病的严重程度，且实验性牙周炎会使未控制的糖尿病大鼠血糖水平升高。
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