Department of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Histol Histopathol. 2012 Oct;27(10):1297-306. doi: 10.14670/HH-27.1297.
We have previously shown that diabetes increases dental caries, and periodontitis might be a secondary change resulting from dental caries in spontaneous diabetic rodent models. However, the lesions in these models were slow to manifest, and the intensity and frequency were mild and varied among individuals. The goal of this study was to confirm the reproducibility of caries development in chemically induced diabetic rats and investigate whether alloxan, which induces immediate and severe hyperglycemia in experimental animals, increases the lesions. Female F344 rats were examined 13 and 26 weeks after dosing of alloxan. Alloxan injection induced severe hyperglycemia in two-thirds of the rats. Progressive molar caries and periodontitis were already induced in all diabetic rats 13 weeks after dosing of alloxan, although the lesions were not observed in nondiabetic rats. Histopathologically, dental caries initially developed in the crown, then spread into the dental root, entered the periodontal connective tissue via the apical foramen, and progressed to periodontitis. In conclusion, alloxan-induced severe hyperglycemia is capable of causing rapid-onset and progressive dental caries and periodontitis in rats.
我们之前已经表明，糖尿病会增加龋齿的发生，而牙周炎可能是自发糖尿病啮齿动物模型中由龋齿引起的继发性变化。然而，这些模型中的病变表现缓慢，其强度和频率在个体之间是轻微且不同的。本研究的目的是确认化学诱导的糖尿病大鼠中龋齿发展的可重复性，并研究是否会诱导立即和严重高血糖的 1,6-二羟己酮增加病变。雌性 F344 大鼠在给予 1,6-二羟己酮 13 和 26 周后进行检查。三分之二的大鼠在给予 1,6-二羟己酮后会出现严重的高血糖。尽管在非糖尿病大鼠中未观察到病变，但在所有糖尿病大鼠中，在给予 1,6-二羟己酮 13 周后，已经诱导出进行性磨牙龋齿和牙周炎。组织病理学上，龋齿最初在牙冠中发展，然后扩散到牙根，通过根尖孔进入牙周结缔组织，并进展为牙周炎。总之，1,6-二羟己酮诱导的严重高血糖可导致大鼠快速发生和进行性龋齿和牙周炎。
