Alloxan had been recognized as having a direct nephrotoxic effect different from its diabetogenic action. We encountered previously unreported granulomatous tubulointerstitial nephritis with severe luminal and interstitial mineralization in one diabetic rat after one week of alloxan administration. Histopathologically, many dilated and occluded proximal and distal tubules were segmentally observed in the cortex and outer medulla. The tubular lumen contained minerals and cell debris. Tubular epithelial cells were degenerated and piled up, and they protruded into the lumen, where they enveloped minerals. Mineralization was observed mainly in the tubular lumen, and to some extent in the subepithelium and interstitium. The mineralization beneath the tubular epithelium was often continuous from the subepithelium to the interstitium. In these lesions, the tubular basement membrane was disrupted by mineralization, and a granuloma with multinuclear foreign-body giant cells was formed in the interstitial areas.
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.
Several studies indicated that both obesity and diabetes are related to dental caries development, but their involvement remains unclear. Thus, we investigated the effect of obesity and diabetes on dental caries development using obese Zucker fatty (ZF) rats, obese Zucker diabetic fatty (ZDF) rats, and Zucker lean (Lean) rats as controls. Eight ZF, 6 ZDF, and 7 Lean male rats were studied. We macroscopically examined the mandibular and maxillary molars and evaluated soft X-ray photographs for caries development. From each group, 5 mandibles and maxillae were examined histologically. The ZF rats' average body weight was more than twice that of the other 2 groups, but the ZDF and Lean rats had comparable body weights. The average triglyceride and total cholesterol levels were elevated in the ZF and ZDF rats, but the ZF rats' average triglyceride and total cholesterol levels were three times and twice, respectively, those of the ZDF rats. The ZDF rats became diabetic after 13 weeks of age and demonstrated a high blood glucose level (>500 mg/dL) after 23 weeks of age. The ZF rats had a significantly higher blood glucose level than that of Lean rats after 23 weeks of age but had about one-half that of the ZDF rats. The ZDF rats had significantly more molar caries and greater alveolar bone resorption than the other two groups; the ZF rats' caries and bone resorption were moderately higher than those of the Lean rats. Histopathologically, crown caries progressed to apical periodontitis in 20% and 50% of the ZF and ZDF rats' molars, respectively, corresponding to the alveolar bone resorption on the soft X-ray film. Dyslipidemia and hyperglycemia may involve dental caries development and obesity or diabetes could enable lesion progression to apical periodontitis in Zucker rats; diabetes enhances dental caries to a greater extent than obesity. J ou rna l o f D ia be tes & M e ta bolism
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