Mori S, Sato T, Hara T, Shirai H, Maruo Y, Minagi S
Department of Removable Prosthodontics, Okayama University Dental School, Okayama City, Japan.
J Oral Rehabil. 1999 Jan;26(1):80-90. doi: 10.1046/j.1365-2842.1999.00354.x.
The histopathological changes in denture-supporting tissues of streptozotocin-induced diabetes mellitus rat were studied in relation to continuous mechanical pressure exerted through an experimental denture base. The experimental dentures were designed to load continuous mechanical pressures (3.4, 1.5 or 0.5 kPa) to the hard palate of the molar region of a rat. From the results of this study, the following conclusions were drawn: the streptozotocin-induced diabetic condition (1) tended to prolong the appearance period of a shortened epithelial ridge, and weakened the phenomenon, (2) reduced the appearance period and severity of the compression of epithelium, (3) delayed the time of manifestation of the proliferative change in the recovery process of the shortened epithelial ridge, and weakened the phenomenon, (4) prolonged the appearance period of the compressed lamina propria mucosae, and enhanced the phenomenon, (5) reduced the number of osteoclasts, (6) lowered the threshold for induction of the osteoclastic bone resorption to between 1.5 and 0.5 kPa, (7) inhibited the appearance of osteoblast which follows the disappearance of osteoclasts, (8) did not induce any inflammatory change, and (9) tended to enhance the longitudinal change of the continuous mechanical pressure. The histopathological changes in the denture-supporting tissues of the streptozotocin-induced diabetes mellitus rat related highly to the longitudinal change of the continuous mechanical pressure exerted through the denture base. From the results of this study, it was suggested that the streptozotocin-induced diabetic condition lowers the tolerance of the denture-supporting tissues to continuous mechanical pressure.
研究了链脲佐菌素诱导的糖尿病大鼠义齿支持组织的组织病理学变化，并将其与通过实验性义齿基托施加的持续机械压力相关联。实验性义齿被设计为对大鼠磨牙区硬腭施加持续机械压力（3.4、1.5或0.5 kPa）。从本研究结果得出以下结论：链脲佐菌素诱导的糖尿病状态（1）倾向于延长缩短上皮嵴的出现时间，并减弱该现象，（2）减少上皮受压的出现时间和严重程度，（3）延迟缩短上皮嵴恢复过程中增殖性变化的表现时间，并减弱该现象，（4）延长压缩固有层黏膜的出现时间，并增强该现象，（5）减少破骨细胞数量，（6）将破骨细胞性骨吸收的诱导阈值降低至1.5至0.5 kPa之间，（7）抑制破骨细胞消失后成骨细胞的出现，（8）未诱导任何炎症变化，（9）倾向于增强持续机械压力的纵向变化。链脲佐菌素诱导的糖尿病大鼠义齿支持组织的组织病理学变化与通过义齿基托施加的持续机械压力的纵向变化高度相关。从本研究结果表明，链脲佐菌素诱导的糖尿病状态降低了义齿支持组织对持续机械压力的耐受性。
