The effect of hyperlipidemia on bone graft regeneration of peri-implantal created defects in rabbits.

AIM: It is reported that hyperlipidemia affects quality and density of bone and adversely affects wound healing. The effect of hyperlipidemia on implant osseointegration and peri-implant defect regeneration has not been fully explained. The purpose of this study was to examine the effects of hyperlipidemia on the healing potential of the materials used for peri-implant bone regeneration and implant stability. MATERIALS AND METHODS: Twelve male, New Zealand rabbits were used in this study. Half of the rabbits were fed a 2% cholesterol diet for 8 weeks to induce hypercholesterolemia. Peri-implant defects (7 mm diameter) were created in the tibias of rabbits and placed implants (3.3 mm in diameter). This study was conducted as a split-mouth design. Animals were randomly divided into two groups: (1) hypercholesterol+autogenous graft group and hypercholesterol+xenograft group (n = 6), and (2) autogenous graft and xenograft groups as controls (n = 6). At 8 weeks after surgery, the rabbits were euthanized. During implant surgery and at 8 weeks, implant stability was measured with resonance frequency analysis (RFA values). Bone-to-implant contact (BIC) was analyzed via histomorphometric analysis. RESULTS: Hyperlipidemic groups showed significantly lower BIC values than those of the control groups at 8 weeks (p < 0.05). According to baseline RFA readings, there was no significant difference between control and hyperlipidemic groups (p Ëƒ 0.05). The hypercholesterol+autogenous graft group had significantly lower RFA readings and BIC values than the hypercholesterol+xenograft group at 8 weeks (p < 0.05). CONCLUSION: Within the limitations of this study, it was found that hyperlipidemia may negatively affect the implant stability especially in the autogenous group and also, may decrease peri-implant bone regeneration. However, further studies are necessary to confirm these results more.

The effect of luteolin in prevention of periodontal disease in Wistar rats.

BACKGROUND: Periodontal disease is the chronic infectious disease of the periodontium. Because of irreversibility, prevention of disease is one of the most important goals of periodontal treatment. The aim of this study was to evaluate the effect of luteolin, a powerful anti-inflammatory agent, on the prevention of experimental periodontitis by determining morphological and histological tissue alterations. METHODS: This study consisted of 28 rats and four experimental groups: healthy control group (C, n = 6); periodontitis group (P, n = 6); periodontitis and 50 mg/kg luteolin administered group (L-50, n = 8); and periodontitis and 100 mg/kg luteolin administered group (L-100, n = 8). Experimental periodontitis was induced via ligature method around lower right first molar teeth. All rats were euthanized 11 days after. The severity of periodontal destruction was determined by measuring alveolar bone loss under a stereomicroscope. Osteoblast and inflammatory cell counts were counted on hematoxylin-eosin-stained slides and osteoclasts were counted on tartrate-resistant acid phosphatase-stained slides. The levels of inducible nitric oxide synthase (iNOS), bone morphogenetic protein (BMP)-2, matrix metalloproteinase (MMP)-8, tissue inhibitor of MMP (TIMP)-1, receptor activator of nuclear factor κB ligand (RANKL), and osteoprotegerin (OPG) were determined by immunohistochemistry. RESULTS: The highest alveolar bone loss was observed in the periodontitis group and the luteolin administration decreased bone loss in both groups. Osteoblast cell number was higher and osteoclast and inflammatory cell numbers were lower in the P group compared to C, L-50, and L-100 groups. Luteolin, dose-dependently increased osteoblast cell counts. Luteolin attenuated periodontal inflammation in both L-50 and L-100 groups. Like osteoblast cell numbers, BMP-2 expressions were also elevated in luteolin groups. Both doses of luteolin significantly increased TIMP-1 and BMP-2 expressions and decreased MMP-8 levels. iNOS expressions increased in P group and L-100 significantly decreased iNOS levels. RANKL increased and OPG decreased in P group and 100 mg/kg luteolin increased OPG and decreased RANKL levels significantly. CONCLUSIONS: Within the limits of present experimental study, luteolin successfully improved periodontal health in a ligature-induced experimental periodontitis model in Wistar rats. The decrease in inflammation, osteoclastic and collagenase activity and increase in osteoblastic activity are possibly involved in this process.

The effect of colchicine on alveolar bone loss in ligature-induced periodontitis.

Colchicine is widely used in the treatment of several inflammatory diseases due to its anti-inflammatory effect, but effects on bone metabolism are unclear. The aim of this study was to evaluate the effects of systemically-administered colchicine on healthy periodontium and experimentally-induced periodontitis. In total, 42 male Wistar rats were included in this study. A non-ligated group constituting the negative control group (Control, C, n = 6) and a ligature-only group forming the positive control group (LO, n = 12) were created separately. Twelve rats were treated with 0.4 mg/kg colchicine and another 12 with 1 mg/kg colchicine. In the colchicine-administered groups, right mandibles constituted the ligated groups (1 mgC-L or 0.4 mgC-L) and left mandibles formed the corresponding non-ligated controls (1mgC or 0.4mgC). Silk ligatures were placed at the gingival margin of the lower first molars. The animals were euthanized at different time-points of healing (11 or 30 days). Alveolar bone loss was clinically measured and TRAP+ osteoclasts, osteoblastic activity, and MMP-1 expression were examined histologically. There was no increase in alveolar bone loss with either colchicine dose in healthy periodontium (p > 0.05) and the highest level of alveolar bone loss, TRAP+ osteoclast number, and MMP-1 expression were measured in the LO group (p < 0.05). The 0.4 mgC-L group showed less alveolar bone loss at 11 days (p < 0.05), but greater loss at 30 days. The 1 mgC-L group showed higher osteoblast number than the other ligated groups (p < 0.05) at both time-points. In summary, colchicine did not increase alveolar bone loss in healthy periodontium and also may tend to reduce periodontitis progression. However, further extensive study is necessary to understand the mechanism of colchicine action on alveolar bone loss in periodontitis.