Nakamura-Kiyama Mariko, Ono Kentaro, Masuda Wataru, Hitomi Suzuro, Matsuo Kou, Usui Michihiko, Nakashima Keisuke, Yokota Makoto, Inenaga Kiyotoshi
Division of Physiology, Kyushu Dental University, 2-6-1, Manazuru, Kokurakitaku, Kitakyushu, Fukuoka 803-8580, Japan; Division of Periodontology, Kyushu Dental University, 2-6-1, Manazuru, Kokurakitaku, Kitakyushu, Fukuoka 803-8580, Japan.
Division of Physiology, Kyushu Dental University, 2-6-1, Manazuru, Kokurakitaku, Kitakyushu, Fukuoka 803-8580, Japan.
Arch Oral Biol. 2014 Feb;59(2):125-32. doi: 10.1016/j.archoralbio.2013.11.001. Epub 2013 Nov 8.
This study was designed to investigate the mechanism of salivary dysfunction in an experimental periodontitis rat model and to examine the improvements in salivary secretion following treatment of the experimental periodontitis.
In the experimental periodontitis rat model, which included a unilateral ligature for 4 weeks around the second upper molar, several salivary functions were investigated. Changes in the salivary function were evaluated 4 weeks after removal of the ligature in some rats.
The periodontitis model showed significant reductions in the weight of the bilateral major salivary glands and pilocarpine-induced salivary secretion. The model also showed an increase in the number of apoptotic cells in bilateral salivary glands. According to Ca(2+) imaging and Western blotting, there were no differences in the muscarine-induced intracellular Ca(2+) mobilization in acinar cells or in the M3 receptor and AQP5 expression levels in the salivary glands between the sham and the periodontitis model. Following removal of the ligature, differences in the weights of salivary glands and pilocarpine-induced salivary secretion between the sham and the periodontitis model animals were not found.
These results suggest that experimental periodontitis leads to hyposalivation and that relief from it improves salivary function. It is likely that lower levels of salivary secretion are caused by the decrease of functional acinar cells in salivary glands in the experimental periodontitis model, and the bilateral gland effects in the unilateral periodontitis model are caused by systemic rather than by local effects.
本研究旨在探讨实验性牙周炎大鼠模型中唾液功能障碍的机制，并检测实验性牙周炎治疗后唾液分泌的改善情况。
在实验性牙周炎大鼠模型中，对大鼠上颌第二磨牙进行单侧结扎4周，研究多项唾液功能。部分大鼠在去除结扎4周后评估唾液功能的变化。
牙周炎模型显示双侧主要唾液腺重量和毛果芸香碱诱导的唾液分泌显著减少。该模型还显示双侧唾液腺中凋亡细胞数量增加。根据钙成像和蛋白质印迹分析，假手术组和牙周炎模型组之间，腺泡细胞中毒蕈碱诱导的细胞内钙动员、唾液腺中M3受体和水通道蛋白5表达水平均无差异。去除结扎后，假手术组和牙周炎模型组动物之间唾液腺重量和毛果芸香碱诱导的唾液分泌差异未被发现。
这些结果表明，实验性牙周炎导致唾液分泌减少，而缓解牙周炎可改善唾液功能。在实验性牙周炎模型中，唾液分泌水平降低可能是由于唾液腺中功能性腺泡细胞减少所致，单侧牙周炎模型中的双侧腺体效应是由全身而非局部效应引起的。
