Nishimoto Taiki, Kodama Yasushi, Matsuura Tetsuro, Ozaki Kiyokazu, Taniguchi Yoshihiko
Laboratory of Clinicopathological Therapeutics, Faculty of Pharmaceutical Sciences, Hiroshima International University, 5-1-1 Hirokoshingai, Kure, Hiroshima 737-0112, Japan.
Laboratory of Pathology, Faculty of Pharmaceutical Sciences, Setsunan University, 45-1 Nagaotoge-cho, Hirakata, Osaka 573-0101, Japan.
J Toxicol Pathol. 2017 Jan;30(1):47-55. doi: 10.1293/tox.2016-0054. Epub 2016 Nov 6.
Diabetes and salivary gland dysfunction are major factors that induce dental caries in experimental animals, but there are no reports analyzing the association of dental caries and salivary glands in an animal model of diabetes mellitus (DM). To clarify the initial development of dental caries and preceding salivary gland disorder, we performed a histopathological analysis on teeth and salivary glands in diabetic Wistar rats 7 weeks after alloxan treatment (DM group) in comparison with nondiabetic rats (Non-DM group) and functional analysis on saliva secretion during the experimental period. Pilocarpine-induced salivary fluid secretion in diabetic rats gradually decreased with continuous hyperglycemia from immediately after alloxan treatment to the time of autopsy. Histopathologically, Oil Red O-positive lipid droplets accumulated in the acinar cells of the parotid gland. No tooth was stereoscopically defined as having dental caries in any of the rats in either group; however, the external appearance remarkably changed owing to occlusal wear in almost all molars in the DM group. The initial lesions of dental caries, appearing as micro-defects in dentin with bacterial colonization on the molar surface, were identified using histopathological analysis, and the incidence in the DM group was more than twice that in the Non-DM group. In conclusion, hyperglycemia simultaneously induces initial caries development and enhances spontaneous occlusal wear in molar teeth of Wistar rats 7 weeks after alloxan treatment. The parotid gland dysfunction caused by hyperglycemia may be mostly involved in the pathogenesis of occlusal wear as well as in dental caries in this diabetic model.
糖尿病和唾液腺功能障碍是实验动物发生龋齿的主要因素，但尚无关于糖尿病（DM）动物模型中龋齿与唾液腺关联的分析报告。为阐明龋齿的初始发展及先前存在的唾液腺疾病，我们对用四氧嘧啶处理7周后的糖尿病Wistar大鼠（DM组）的牙齿和唾液腺进行了组织病理学分析，并与非糖尿病大鼠（非DM组）进行比较，同时对实验期间的唾液分泌进行了功能分析。从四氧嘧啶处理后即刻到尸检时，随着持续高血糖，毛果芸香碱诱导的糖尿病大鼠唾液分泌逐渐减少。组织病理学上，腮腺腺泡细胞中积累了油红O阳性脂滴。两组大鼠中均未在立体显微镜下明确任何一颗牙齿患有龋齿；然而，DM组几乎所有磨牙由于咬合磨损外观发生了显著变化。通过组织病理学分析确定了龋齿的初始病变，表现为磨牙表面牙本质的微缺损并伴有细菌定植，DM组的发病率是非DM组的两倍多。总之，高血糖在四氧嘧啶处理7周后同时诱导Wistar大鼠磨牙的初始龋齿发展并加剧自发咬合磨损。高血糖引起的腮腺腺功能障碍可能在该糖尿病模型的咬合磨损发病机制以及龋齿发病中起主要作用。
