Background: Damage of tissue repair and dysfunction of the oral mucosa are usually associated with the diabetic condition. Apoptosis plays a functional role in limiting diabetic repair. Russell bodies, an uncommon finding that may be associated with chronic inflammatory conditions. Although insulin is the mainstay of diabetes treatment, it has prominent side effects. Episodes of severe hypoglycemia and increased mortality rate are associated with insulin therapy. Cod liver oil (CLO) is an important source of long-chain omega-3 (ω-3) fatty acids that have antioxidant and anti-inflammatory properties.
Objective: The present study was designed to determine the adaptive apoptotic alterations accompanying diabetes in the buccal mucosa with the possibility of occurrence of the so-called Russell bodies and the possible role of long-chain ω-3 fatty acids versus insulin supplementation in enhancement of the buccal mucosa in streptozotocin (STZ)-induced diabetic rats.
Design: Sixty adult male Swiss albino rats (200-250 gm) were selected for this study. The animals were randomly divided into four groups (fifteen rats each): Group I (Control group), Group II (Diabetic untreated group), Group III (Insulin treated group) and Group IV (Cod liver oil treated group). At the end of the experimental period (four weeks), the rats were sacrificed and the specimens were obtained from the mucosa of the cheek of both sides. The sections were examined histologically, immunohistochemically and histomorphometrically. Statistical analysis: Data obtained from histomorphometric analysis were statistically described in terms of mean ± standard deviation (± SD).
Results: Histopathologic examination of Group I revealed the normal histological features of the buccal mucosa. In Group II several histological changes in the epithelial layer of the buccal mucosa were noticed. These changes include; atrophy in the epithelium, evidences of cells undergo degeneration, nuclear changes, ill-defined cell membrane, cytoplasmic vacuolations, thickening of stratum granulosum (hypergranulosis) which was accompanied by hyperkeratosis. Moreover, the lamina propria showed differential orientation and arrangement of the collagen fiber bundles, areas of degeneration and hyalinization in addition to fibroblasts that showed signs of degeneration. Furthermore, the lamina propria was strongly infiltrated by inflammatory cells and invaded by multiple Russell bodies scattered throughout the connective tissue (C.T) and dilated blood vessels (BVs); lined by swollen endothelial cells and engorged with red blood cells (RBCs) were observed. Some of these changes were still observed in Group III that received insulin treatment. Treatment with CLO in Group IV resulted in histological features resembling nearly those of the control group (Group I). The least immuno-expressions for caspase-3 and CD-138 were detected in Group I, followed by Group IV, then Group III and subsequently Group II. The histomorphometric analysis supported the previous results as Group I showed the highest mean epithelium thickness, followed by Group IV, then Group III and the least value was for Group II. On the other hand, Group I showed the least mean keratin thickness and the least mean area percentage of both caspase-3 and CD-138 immunoreactivities, followed by Group IV, then Group III and the highest values were for Group II. There was statistically highly significant difference between the studied groups.
Conclusions: Diabetes has deleterious effect on the structure of the buccal mucosa. The raised levels of capase-3 in diabetic buccal mucosa are related to increased Russell bodies (Mott cells) formation. Insulin can't completely inhibit the complications of diabetes. However, ω-3 fatty acids present in CLO can inhibit to a great extent the abnormalities caused by diabetes.