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Journal of oral rehabilitation · 1999

The effect of diabetes mellitus on histopathological changes in the denture-supporting tissues under continuous mechanical pressure in rat.

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Mori S, Sato T, Hara T, Shirai H, Maruo Y, Minagi S

Аннотация

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.

Предметные рубрики MeSH

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты