Biocompatibility of fiber-reinforced composite (FRC) and woven-coated FRC: an in vivo study.

OBJECTIVES: To investigate biocompatibility and bone contact area of FRC and woven-coated FRC (FRC-C) in rats. MATERIALS AND METHODS: Sixty rats were allocated to three groups: FRC (n=20), FRC-C (n=20), and control group (n=20). Subgroups were determined as 4th (n=10) and 12th weeks (n=10). The specimens were placed in the femur of rats. In the control group, the bone defects were left empty and sutured. Four and 12 weeks after implantation, the rats were sacrificed. Histopathological examinations were performed in a semi-quantitative manner. Twenty rats (n=20) were used for scanning electron microscopy (SEM) examination. Bone contact surfaces were calculated in SEM analysis. A chi-square test was performed to analyze the data. RESULTS: No statistical difference was detected between the 4th and 12th weeks in the quality of bone union. Quality of bone union was lower in FRC compared to the control group in the 4th week (p=0.012) and the 12th week (p=0.017). The periosteal reaction at the 12th week was lower in FRC than in the control group (p=0.021). Bone contact of FRC and FRC-C was 85.5% and 86.3%, respectively. CONCLUSIONS: FRC and FRC-C were biocompatible and showed no inflammation. The woven coating did not increase the quality of bone union and bone contact area, while not reducing biocompatibility. CLINICAL RELEVANCE: The biocompatibility and good bone response of the woven glass fiber net were demonstrated to have the potential as a scaffold for the augmentation of alveolar bone deficiencies and the reconstruction of maxillofacial defects.

Histologic and histomorphometric assessment of eggshell-derived bone graft substitutes on bone healing in rats.

OBJECTIVE: The objective of this study was to histologically and histomorphometrically evaluate the efficacy of the new formulations of eggshell-derived calcium carbonate in rats. STUDY DESIGN: The study was conducted on 30 adult male rats. Four standardized and circular intrabony defects were created in the both maxilla and mandibula of each animal. Three different graft materials were prepared as follows: 1) Material A: Eggshell-derived calcium carbonate combined with carrageenan gel, 2) Material B: Eggshell-derived calcium carbonate combined with xanthan gum gel, and 3) Material C: Eggshell-derived calcium carbonate powder. The right mandibular defect sites were grafted with Material A in all animals, and defects on the left were grafted with Material B. Defects on the right side of maxilla were received Material C in all animals, and all left maxillary defects were remained untreated as controls. The animals were sacrificed either postoperatively on the 15th day, postoperatively on the 30th day or postoperatively on the 45th day. Histomorphometric measurements were made of the areas of newly formed bone, necrotic bone, fibrous tissue and residual graft material. RESULTS: Material A exhibited the highest level of osteoid formation followed by Material B and Material C on the 45th day. In terms of osteoid formation, statistically significant differences were observed between graft materials and controls at 45th day compared to 15th and 30th day (p<0.05). CONCLUSIONS: Eggshell-derived graft substitutes in both gel and powder forms are biocompatible materials which may have the potential to enhance the new bone formation. Key words:Bone graft material, bone defects, eggshell, histopathological evaluation, rat.

A comparative evaluation of the systemic and local alendronate treatment in synthetic bone graft: a histologic and histomorphometric study in a rat calvarial defect model.

OBJECTIVE: The purpose of this study was to compare the relative efficacy of systemic and local alendronate treatment of synthetic bone graft in a rat calvarial defect model. STUDY DESIGN: Forty Wistar rats were divided into 4 groups: experimental animals received alendronate systemically or locally combined with micro-macroporous biphasic calcium phosphate (MBCP) graft material. In the control group, the defect was left empty. On each animal, a 5-mm standardized bone defect was created with a standard trephine bur in calvarium. All animals were killed after 8 weeks. The number of osteoclasts, osteoclast morphology, resorption lacunae, osteoblastic activity, and lamellar bone formation were histopathologically evaluated and the newly formed bone area was analyzed histomorphometrically. RESULTS: Eight weeks after surgery, the number of osteoclasts and the resorption lacunae in the MBCP group using systemic alendronate therapy was significantly higher than those of the other groups (P < .05). Osteoblast number in the MBCP group using systemic alendronate treatment was significantly increased (P < .05). No significant difference was found among all MBCP groups using local or systemic alendronate treatments with regard to new bone formation (P > .05). CONCLUSIONS: Within the limits of the study, alendronate, when administered systemically or locally, did not increase bone regeneration with MBCP graft in the rat calvarial defect model.

Alendronate enhances osseous healing in a rat calvarial defect model.

AIM: The aim of this study was to evaluate the effect of alendronate on osseous wound healing in an experimental model. METHODS: Critical size defects were created in calvaria of 40 male Wistar rats. The animals were divided into four groups of 10 animals each: autogenous bone graft group; autogenous bone graft with systemic alendronate group (0.01 mg/kg body weight per day for 8 weeks); autogenous bone graft with local alendronate group (1mg/mL for 5 min); non-treatment (control) group. Animals were sacrificed after 8 weeks; osteoblast number, lamellar bone formation, and area of newly formed bone were analysed. RESULTS: The osteoblast number significantly increased in the autogenous bone graft with local alendronate group compared to the autogenous bone graft group (p<0.05). Both systemic and local application of the alendronate significantly increased the new bone formation compared to the autogenous bone graft group (p<0.05) with no significant difference between local or systemic use (p>0.05). Local alendronate and autogenous bone graft use significantly increased the total bone area compared to autogenous bone graft alone (p<0.05). CONCLUSION: Alendronate enhances the new bone formation by autogenous bone graft in the rat calvarial defect model suggesting that the inhibition of the osteoclastic activity allows an increased rate of bone apposition, which could be applicable to the inflammation-induced destruction of the periodontal tissues during disease.

N-acetylcysteine, a thiol antioxidant, decreases alveolar bone loss in experimental periodontitis in rats.

BACKGROUND: The purpose of this study was to analyze the morphometric and histopathologic changes associated with experimental periodontitis in rats in response to systemic administration of N-acetylcysteine (NAC). METHODS: Forty-three Wistar rats were divided into five experimental groups: non-ligated (NL) group (n = 10), ligature only (LO) group (n = 10), and groups that were administered NAC systemically (7, 35, or 70 mg/kg body weight per day [NAC7, NAC35, and NAC70 groups, respectively]; n = 8, 9, and 6). Silk ligatures were placed at the gingival margin of the lower first molars in a mandibular quadrant. The study duration was 11 days, and the animals were sacrificed at the end of this period. Changes in alveolar bone levels were measured clinically and tissues were histopathologically examined to assess the differences among the study groups. RESULTS: At the end of 11 days, the alveolar bone loss was significantly higher in the LO group compared to NL, NAC7, NAC35, and NAC70 groups (P <0.05). There was no statistically significant difference in the osteoclast numbers among the study groups (P >0.05), whereas the effect of NAC was dose-dependent. CONCLUSION: NAC prevented alveolar bone loss in the rat model, in a dose-dependent manner, when administered systemically.

A morphometric and histopathologic evaluation of the effects of propolis on alveolar bone loss in experimental periodontitis in rats.

BACKGROUND: Propolis collected by honeybees from various plant sources is a resinous hive product possessing a broad spectrum of biologic activities. Propolis has been used extensively in the diet to improve health and prevent disease. The purpose of this study was to analyze the morphometric and histopathologic changes associated with experimental periodontitis in rats in response to the systemic administration of propolis. METHODS: Forty Wistar rats were divided into four experimental groups: non-ligated (NL; N = 10); ligature only (LO; N = 10); and systemic administration of ligature and propolis (100 mg/kg body weight per day [Pro100; N = 10] or 200 mg/kg body weight per day [Pro200; N = 10]). Silk ligatures were placed at the gingival margin of the lower first molars in both mandibular quadrants. The study duration was 11 days, and the animals were sacrificed at the end of this period. Changes in alveolar bone levels were clinically measured, and tissues were histopathologically examined to assess the differences among the study groups. RESULTS: At the end of 11 days, alveolar bone loss was significantly higher in the LO group compared to the NL, Pro100, and Pro200 groups (P <0.05). Osteoclast numbers in the LO group were significantly higher than those of the NL, Pro100, and Pro200 groups (P <0.05). Both dosages of propolis significantly reduced the periodontitis-related bone loss, but the differences between the two propolis groups were not statistically significant (P >0.05). CONCLUSION: The findings of this study provide morphologic and histologic evidence that propolis, when administered systemically, prevents alveolar bone loss in the rat model.

Effect of periodontal treatment on IL-1beta, IL-1ra, and IL-10 levels in gingival crevicular fluid in patients with aggressive periodontitis.

AIM: The aim of this study was to examine the effect of phase I periodontal treatment on the levels of interleukin (IL)-1beta, IL-1ra, and IL-10 in gingival crevicular fluid (GCF) in patients with generalized aggressive periodontitis (G-AgP). MATERIAL AND METHODS: Data were obtained from 15 patients with aggressive periodontitis and 15 healthy controls. GCF was collected from at least four pre-selected sites (one shallow, at least two moderate, or at least one deep pockets) in patients with G-AgP. In the healthy group, GCF samples were collected from one site. The cytokine levels were determined by an enzyme-linked immunosorbent assay. Probing depth, clinical attachment level (CAL), gingival and plaque indices, and bleeding on probing were measured. The GCF sampling and clinical measurements were recorded at baseline and 6 weeks later after periodontal treatment. RESULTS: IL-1beta levels were significantly higher at the moderate and deep pocket sites compared with the shallow sites (p<0.05). After periodontal therapy, IL-1beta levels were significantly reduced in the moderate and deep pocket sites (p<0.05). IL-1ra levels at baseline of the moderate and deep pocket sites were significantly lower than the control sites (p<0.05). IL-10 levels were similar in all pockets and did not change after periodontal therapy. CONCLUSIONS: The periodontal treatment improves the clinical parameters in G-AgP, and this improvement is evident in deep pocket sites for pocket depth and CAL values. These results confirm that IL-1beta is effective for evaluating the periodontal inflammation and can thus be used as a laboratory tool for assessing the activity of periodontal disease.

Monitoring of buccal epithelial cells by alkaline comet assay (single cell gel electrophoresis technique) in cytogenetic evaluation of chlorhexidine.

During the last few years, there has been increasing interest in buccal epithelial cells for cytogenetic evaluation of different materials. In the present study, the use of these cells and peripheral lymphocytes for cytogenetic evaluation of chlorhexidine digluconate (CHX) with comet assay (single cell gel electrophoresis, or SCGE) is reported. This technique detects DNA strand breaks in individual cells in alkaline conditions. Thirteen volunteers were requested to rinse their mouths with 0.12% CHX solution for 18 days. Buccal epithelial cells and peripheral blood lymphocytes were obtained from all participants at baseline and the end of the experimental period. One hundred cells per subject were analysed for the DNA damage. A statistical increase was observed in the damaged buccal and blood cells after the CHX application. The mean grade of damage in buccal cells was statistically different from that in blood cells. Due to minimal absorption of chlorhexidine into the tissues and low concentrations of free chlorhexidine in the oral cavity, the DNA damage produced by chlorhexidine in lymphocytes was lower than in buccal epithelial cells. As chlorhexidine does not accumulate in the body, the frequencies of DNA damage could be transient. Detected DNA damage after CHX use might be the indication of an earlier effect, before DNA repair begins, and could be reversible.

Level of neopterin, a marker of immune cell activation in gingival crevicular fluid, saliva, and urine in patients with aggressive periodontitis.

BACKGROUND: Neopterin, a marker of cellular immune activation, is produced by human macrophages after induction by interferon gamma that is secreted by T lymphocytes. Neopterin concentrations in diverse body fluids have been reported to increase in parallel with bacteria in the clinical course of infections. Therefore, determination of neopterin in body fluids was thought to be useful for predicting the prognosis and diagnosis of aggressive forms of periodontal disease, in which the cell-mediated immune response plays an important role in immunopathogenesis. The aim of the present study was to observe the role of neopterin in the pathogenesis of aggressive periodontitis (AgP). METHODS: Thirteen individuals who were systemically and periodontally healthy and 16 systemically healthy individuals diagnosed with AgP were recruited for this study. Mixed saliva and urine samples were collected from each subject. Gingival crevicular fluid (GCF) samples were obtained from 6 teeth with > or =5 mm probing depth (PD). After evaluation of GCF amount from paper strips, enzyme-linked immunosorbent assay (ELISA) was employed to determine the amount of neopterin in urine, saliva, and GCF. RESULTS: The amount of neopterin in urine and saliva measured 235.77+/-405.31 micromol neopterin/mol creatinine and 9.85+/-7.66 nmol/l, respectively, for the AgP group and 225.45+/-100.72 micromol neopterin/mol creatinine and 5.25+/-5.76 nmol/l, respectively, for controls. The present data demonstrate that, while salivary neopterin levels were found to be significantly different between periodontitis and control subjects, there were non-significant differences in urine neopterin levels. The amount and concentration of neopterin in GCF measured was 18+/-12.75 nmol/l and 3.67+/-2.40 nmol/ml for the AgP group and 2.51+/-1.72 nmol/l and 3.88+/-4.50 nmol/ml for the control group. When total amounts of neopterin are taken into consideration, a significant difference between AgP and controls is shown; however, no significant difference in net concentration of neopterin was found between both groups. CONCLUSIONS: This study is the first report to evaluate the involvement of neopterin in AgP and this might be considered of value in understanding periodontal disease mechanisms.