Nicotine is associated with increased incidence of periodontal disease and poor response to therapy. This article aimed at identifying the expression of Matrix metalloproteinases-2 (MMP2) and Vascular endothelial growth factor (VEGF) proteins on extracellular matrix, fibrous distribution and angiogenetic development in periodontitis caused by nicotine effects on periodontal membrane. In this experimental study, the groups were divided into nicotine and control groups. While the nicotine groups in rats (n=6) were administered 2mg/kg Nicotine sulphate for 28 days, the control group in rats (n=6) were only administered 1,5 ml physiologic saline solution subcutaneously for 28 days. Histological sections were prepared and immunohistochemically stained for MMP2 and VEGF. The sections were stained with Trichrome-Masson were observed under light microscope. VEGF and MMP2 immunoreactivity of periodontal gingiva and dentin was assessed by immunohistochemical staining. In conclusion, nicotine effect reduces Matrix metalloproteinases production and disrupt collagen synthesis and causes periodontitis. We observed that nicotine increases periodontitis by disrupting periodontal membrane and prevent tooth to anchor in dental alveoli by disrupting epithelial structure.
Background: The objective of this study was to investigate whether long term formaldehyde inhalation may affect periodontal membrane and alveolar bone loss leading to periodontitis. The negative effects of formaldehyde were described using vascular endothelial growth factor (VEGF), matrix metallopeptidase 2 (MMP-2) and osteonectin antibodies involved in the extracellular matrix and angiogenetic development. Materials and methods: Thirty adult Wistar albino rats were used in this study. Rats were divided into two groups: a control group (n = 15) and formaldehyde administered group (n = 15). Formaldehyde group was exposed to inhalation of 10 ppm formaldehyde 8 hours a day, 5 days a week for 5 weeks. Maxillary bone regions were dissected under anaesthesia. After fixation in 10% formaldehyde solution, tissues were passed through graded ethanol series to obtain paraffin blocks. Five-micrometre histological sections were cut with RM2265 rotary microtome stained with Masson trichrome and VEGF, MMP-2 and osteonectin antibodies for examination under Olympus BH-2 light microscopy. Results: The present study revealed that congestion in blood vessels, degeneration of collagen fibres and alveolar matrix around alveolar bone were observed to be more significant in formaldehyde group than the control group (p ≤ 0.001). Interestingly, VEGF expression in the formaldehyde group was the most significant finding between the two groups (p < 0.001). When compared inflammation, MMP-2 and osteonectin expressions were significant (p < 0.01) in the formaldehyde group. Conclusions: It was suggested that formaldehyde toxicity decreased the expression of MMP-2 and in osteoblasts as well as affecting the retention of MMP levels in tooth cavity, which is very low in collagen fibres. But, vice versa for the expression of VEGF in dilated vascular endothelial cells and osteocytes in alveolar bone. As a conclusion, formaldehyde disrupts the periodontal membrane and may cause collagen fibres degeneration by affecting the alveolar bone matrix.
Purpose To investigate the effects of allopurinol administration on osteoinductive reaction and bone development with graft material. Methods Thirty-six Wistar albino rats were divided into 3 groups. In the control group, calvarial bone defect was only created without any treatment. In the Defect + Graft group, allograft treatment was performed by forming 8 mm calvarial bone defect. In the Defect + Graft + Allopurinol group, alloplastic bone graft was placed in the calvarial bone defect and then, allopurinol (50 mg/kg/day) treatment was intraperitoneally applied for 28 days. Results Histopathological examination revealed inflammation, congestion in the vessels, and an increase in osteoclast cells in the defect area. We also observed that new osteocyte cells, increase in connective tissue fibers, and new bone trabeculae. Osteopontin expression was positive in osteoblast cells and lacunated osteocyte cells were located in the periphery of the new bone trabeculae. Osteopontin expression was also positive in osteoblasts and osteocytes cells of new bone trabeculae in the graft site. Conclusion It has been shown that allopurinol treatment in rat calvaria defects may induce osteoblastic activity, matrix development, mature bone cell formation and new bone formation when used with autogenous grafts.
Purpose: To evaluate histologically and immunohistochemically the bone regeneration after application of simvastatin on tibial bone defects in rats. Methods: Sixty Wistar albino rats were divided into 3 groups as control (6 mm tibial bone defect), defect + graft (allograft treatment), and defect + graft + simvastatin (10 mg/kg/day) for 28 days. Results: Histopathological examination revealed inflammation in control group (defect group), congestion in blood vessels, and an increase in osteoclast cells. In defect + graft group, osteoclastic activity was observed and osteocyte cells were continued to develop. In defect + graft + simvastatin group, osteocytes and matrix formation were increased in the new bone trabeculae. Osteopontin and osteonectin expression were positive in the osteclast cells in the control group. Osteoblasts and some osteocytes showed a positive reaction of osteopontin and osteopontin. In defect + graft + simvastatin group, osteonectin and osteopontin expression were positive in osteoblast and osteocyte cells, and a positive expression in osteon formation was also seen in new bone trabeculae. Conclusion: The simvastatin application was thought to increase bone turnover by increasing the osteoinductive effect with graft and significantly affect the formation of new bone.
FARUK. E. R.; DEVECI, E.; KALKANLI, S. & DEVECI, B.The effects of nicotine on the incisive teeth and expression of vimentin in rats. Int. J. Morphol., 31(2):516-519, 2013. SUMMARY:Nicotine is an alkaloid toxic effects of oral cavity. In this study,14 adult Sprague-Dawley rats weighing 230-260 mg (±10 mg) were used as experimental animal. The rats of experimental group (n=6) were nicotinized systemically with nicotine sulphate, 2mg/kg subcutaneously, daily in period of 28 days. Pulp, alveolar bone tissue, periodontal membrane and gingival epithelial junction were investigated in these regions in incisive teeth longitudinal cross-section. Thinning of the collagen fibers in the pulp tissue, vascular congestion, and inflammatory cell infiltration were observed. Mesenchymal tissues that is stained positive for vimentin lay underneath the epithelium. A strong expression of vimentin can be observed in formed periodontal ligament.
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