Melatonin Decreases Alveolar Bone Loss in Rats with Experimental Periodontitis and Osteoporosis: A Morphometric and Histopathologic Study.

BACKGROUND: Periodontitis and post-menopausal osteoporosis include common chronic bone disorders worldwide, with similar etiopathogenetic events. This study evaluated the effect of systemic melatonin administration on the alveolar bone destruction of periodontitis progression in an experimental periodontitis model in osteoporotic rats. METHODS: Forty-four Wistar rats were randomly divided into six experimental groups: control (C; n = 6); osteoporosis (O; n = 6); ligated periodontitis (LP; n = 8); osteoporosis- and periodontitis-induced (O+LP; n = 8); osteoporosis- and periodontitis-induced through 30 mg/kg/day melatonin administration (ML30; n = 8); and osteoporosis- and periodontitis-induced through 50 mg/kg/day melatonin administration (ML50; n = 8). The rats underwent bilateraloophorectomy and were maintained for 4 months to induce osteoporosis. After 4 months, 4-0 silk ligatures were placed submarginally around the mandibular first molar of each rat to induce experimental periodontitis, and melatonin was administered in the ML30 and ML50 groups for 30 days. Changes in alveolar bone levels were clinically measured, and tissues were histopathologically examined. RESULTS: Osteoclastic activity in the LP and O+LP groups was significantly higher than in the other groups (p < 0.05), but was similar in the C, O, and ML30 groups (p > 0.05). RANKL activity was the highest in the O+LP group, while melatonin decreased RANKL activity in the melatonin-administered groups (p < 0.05). Systemically administered melatonin significantly decreased alveolar bone loss in the ML30 and ML50 groups compared with that in the periodontitis groups (p < 0.05). CONCLUSIONS: Melatonin inhibited alveolar bone destruction by decreasing the RANKL expression and inflammatory cell infiltration and increased osteoblastic activity in a rat model with osteoporosis and periodontitis.

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.

Evaluation of apoptosis and hypoxia-related factors in gingival tissues of smoker and non-smoker periodontitis patients.

OBJECTIVE: Smoking causes pathological changes in all tissues, including gingiva and alveolar bone. The aim of present study was to evaluate apoptotic tissue alterations and tissue destruction in smoker and non-smoker periodontitis patients and healthy individuals. METHODS: Gingival biopsy samples from 15 systemically and orally healthy individuals (Group 1), 15 systemically healthy periodontitis patients (Group 2), 15 systemically and orally healthy smokers (Group 3), and 15 systemically healthy smoker periodontitis patients (Group 4) were enrolled in the present study. Clinical periodontal measurements as plaque index (PI), gingival index (GI), and clinical attachment levels (CAL) were recorded, and gingival biopsies were obtained. Biopsy samples were fixed in formalin solution and embedded in paraffin. Fibroblast and inflammatory cell counts were determined via histomorphometrically. Hypoxia-inducible factor alpha (HIF-1α), vascular endothelial growth factor(VEGF), tissue inhibitor of matrix metalloproteinase-1(TIMP-1), matrix metalloproteinases-8(MMP-8) expressions, Bax, Bcl-2, and caspase-3 expressions were evaluated via immunohistochemistry. RESULTS: Demographic data of the study groups were similar. Smoking levels of the smokers were also similar. The highest fibroblast cell counts were observed in healthy controls and the counts were similar in other groups. The highest inflammatory cell counts were found in smoker periodontitis group, and the lowest counts were found in healthy control groups. The differences were statistically significant. HIF-1α and Bax expressions were elevated and Bcl-2 decreased in smoker periodontitis patients compared with healthy individuals. However, there were no differences in VEGF, MMP-8, and TIMP-1 expressions. CONCLUSION: Within limits of present study, it can be suggested that both smoking and periodontitis caused similar decrease in fibroblast counts while causing a dramatic increase in inflammatory cell counts. Increased apoptosis and hypoxia also accompanied to the increased inflammation.

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 vanillic acid on ligature-induced periodontal disease in Wistar rats.

OBJECTIVE: Vanillic acid, also known as 4-hydroxy-3-methoxy benzoic acid has a potent effect on bone metabolism. The purpose of the present study was to specify the effects of vanillic acid (VA) on preventing inflammation and bone destruction in experimental periodontitis as inflammatory bone disease. To evaluate the effects of VA, osteoblast, osteoclast and inflammatory cell counts, iNOS, CD68, MMP-1, and TIMP-1 levels were determined. METHODS: 32 female Wistar rats were divided into four experimental groups as; Group 1: healthy control (C, n = 8), group 2: Periodontitis (P, n = 8), group 3: periodontitis and 50 mg/kg VA administered group (P + VA-50, n = 8) and group 4: periodontitis and 100 mg/kg VA delivered group (P + VA-100, n = 8). Ligature-induced experimental periodontitis was carried out at mandibular first molar teeth of the right quadrant by placing submarginal 4-0 silk ligatures. VA was administered by oral gavage for 14 days beginning from the first day. Rats were euthanized on the 15th day. Morphological changes in alveolar bone were evaluated via a stereomicroscope. Mandibles were subjected to histological procedures. Osteoblasts, tartrate-resistant acid phosphatase synthesizing osteoclasts and inflammatory cells were counted. Inducible nitric oxide synthase (iNOS), cluster of differentiation (CD)-68, Matrix metalloproteinase (MMP)-1, tissue inhibitor of MMP-1, runt-related x factor-2 (RUNX2), and cyclooxygenase (COX)-2 expressions were determined by immunohistochemistry. RESULTS: The rats in the periodontitis group had the highest alveolar bone loss compared to the other groups. Both doses of VA significantly decreased alveolar bone loss but not the control levels. TRAP-positive osteoclast and inflammatory cell counts were also highest in the P group, and both 50 and 100 mg/kg VA reduced these counts. Control rats had the lowest osteoclast and inflammatory cell counts compared to the other groups. Similar to osteoclast counts, MMP-1, iNOS, CD68, and COX-2 expressions were the highest in the P group compared to the other groups. Both doses of VA significantly decreased these levels. Osteoblast cells were higher in the VA groups compared to the control and periodontitis groups. RUNX2 levels were lower in the periodontitis group compared to the control group. A slight increase was also observed in VA groups. However, the difference in the TIMP-1 levels was significant only between P and VA100 groups. CONCLUSION: VA administration successfully ameliorated periodontitis symptoms by decreasing alveolar bone and collagen destruction, periodontal inflammation, and increasing osteoblastic activity.

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.

Evaluation of the effect of oleuropein on alveolar bone loss, inflammation, and apoptosis in experimental periodontitis.

THE OBJECTIVE: The present study aimed to evaluate the effects of oleuropein on ligature-induced alveolar bone loss. In this respect, osteoblastic activity, osteoclastic activity, inflammatory markers, and apoptosis were evaluated. BACKGROUND: Oleuropein is a flavonoid, which has potent anti-inflammatory and bone-protective effects. METHODS: Thirty-two Wistar rats were divided into four experimental groups as following: control (C, n = 8) group; periodontitis (P, n = 8) group; periodontitis and low-dose oleuropein group (12 mg/kg/day oleuropein, LDO group, n = 8); and periodontitis and high-dose oleuropein group (24 mg/kg/day oleuropein, HDO group, n = 8). Periodontitis was induced via ligatures. Study period was 14 days, and animals were sacrificed at end of this period. Mandibles were examined via a stereomicroscope and underwent histological procedures. Osteoblast, tartrate-resistant acid phosphatase (TRAP)-positive osteoclast, and inflammatory cell counts were determined in hematoxylin-eosin stained sections. Inducible nitric oxide synthase (iNOS), bone morphogenetic protein-4, the cluster of differentiation (CD)-68, cysteine-aspartic proteases-3 (Caspase 3), and B-cell lymphoma-2 (Bcl-2) expressions were evaluated via immunohistochemistry. RESULTS: Periodontitis group had highest alveolar bone loss, and these levels significantly decreased in LDO and HDO groups. Both 12 and 24 mg/kg oleuropein groups significantly increased osteoblast cell counts and decreased TRAP-positive osteoclast and inflammatory cell counts. BMP-4 and bcl-2 expressions were elevated in oleuropein groups while caspase-3 expressions decreased. iNOS and CD68 were higher in periodontitis group compared to control group, but there was no significant difference between other groups. CONCLUSION: Oleuropein successfully decreased alveolar bone loss as a result of decreased osteoclastic activity, inflammation, and apoptosis and increased osteoblastic activity.

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.

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

Abstract 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.

The effects of IL-10 gene polymorphism on serum, and gingival crevicular fluid levels of IL-6 and IL-10 in chronic periodontitis.

OBJECTIVE: Anti-inflammatory cytokines play a crucial role in periodontitis by inhibiting synthesis of pro-inflammatory cytokines. The purpose of this study was to evaluate the effect of interleukin-10 (-597) gene polymorphism and genotype distributions on chronic periodontitis (CP) development and IL-6 and IL-10 levels in gingival crevicular fluid (GCF) and serum before and after non-surgical periodontal treatment. MATERIAL AND METHODS: The study population consisted of 55 severe generalized CP patients as CP group and 50 healthy individuals as control group. Plaque index, gingival index, probing depth and clinical attachment level were recorded and GCF and blood samples were taken at both the baseline and the sixth week after non-surgical periodontal treatment. PCR-RFLP procedure was used for gene analyses and cytokine levels were measured via ELISA. RESULTS: IL-10 genotype distribution was significantly different between CP and control groups (p=0.000, OR:7, 95%CI, 2.83-60.25). Clinical measurements significantly improved in the CP group after periodontal treatment (p<0.05). Periodontal treatment significantly decreased GCF IL-6 and IL-10 levels. No significant difference was found in clinical parameters between IL-10 AA and AC+CC genotypes at both the baseline and the sixth week (p>0.05). Sixth week GCF IL-10 levels were significantly lower in patients carrying IL-10 AC+CC genotype compared to the patients carrying IL-10 AA genotype (p<0.05). Serum IL-6 and IL-10 levels were lower in patients carrying the IL-10 AA genotype compared to patients with IL-10 AC+CC genotype, but the difference was not significant (p>0.05). CONCLUSION: IL-10 AA genotype carriers had lower IL-6 and IL-6/10 levels in serum; however, GCF IL-6/10 levels were similar in both genotypes. Within the limitations of our study, a possible association between IL-10(-597) gene polymorphism and CP might be considered.

The effects of IL-10 gene polymorphism on serum, and gingival crevicular fluid levels of IL-6 and IL-10 in chronic periodontitis

Abstract Objective Anti-inflammatory cytokines play a crucial role in periodontitis by inhibiting synthesis of pro-inflammatory cytokines. The purpose of this study was to evaluate the effect of interleukin-10 (-597) gene polymorphism and genotype distributions on chronic periodontitis (CP) development and IL-6 and IL-10 levels in gingival crevicular fluid (GCF) and serum before and after non-surgical periodontal treatment. Material and Methods The study population consisted of 55 severe generalized CP patients as CP group and 50 healthy individuals as control group. Plaque index, gingival index, probing depth and clinical attachment level were recorded and GCF and blood samples were taken at both the baseline and the sixth week after non-surgical periodontal treatment. PCR-RFLP procedure was used for gene analyses and cytokine levels were measured via ELISA. Results IL-10 genotype distribution was significantly different between CP and control groups (p=0.000, OR:7, 95%CI, 2.83-60.25). Clinical measurements significantly improved in the CP group after periodontal treatment (p<0.05). Periodontal treatment significantly decreased GCF IL-6 and IL-10 levels. No significant difference was found in clinical parameters between IL-10 AA and AC+CC genotypes at both the baseline and the sixth week (p>0.05). Sixth week GCF IL-10 levels were significantly lower in patients carrying IL-10 AC+CC genotype compared to the patients carrying IL-10 AA genotype (p<0.05). Serum IL-6 and IL-10 levels were lower in patients carrying the IL-10 AA genotype compared to patients with IL-10 AC+CC genotype, but the difference was not significant (p>0.05). Conclusion IL-10 AA genotype carriers had lower IL-6 and IL-6/10 levels in serum; however, GCF IL-6/10 levels were similar in both genotypes. Within the limitations of our study, a possible association between IL-10(-597) gene polymorphism and CP might be considered.

Analysis of IL-6, IL-10 and NF-κB Gene Polymorphisms in Aggressive and Chronic Periodontitis.

OBJECTIVE: Pro-inflammatory cytokines, interleukin-6 (IL-6), demonstrated to be suppressed by interleukin-10 (IL-10) are known to be regulated by the transcription factor nuclear factor-κB(NF-κB). The aim of this study was to ascertain the association between genetic polymorphism of these genes (IL-6(-174), IL-10(-597) and NF-κB1-94ins/del)) and chronic/aggressive periodontitis. METHODS: Forty-five patients with chronic periodontitis (CP), 58 patients with aggressive periodontitis (AP) and 38 periodontally healthy subjects were included in this study. Genomic DNA was isolated from whole blood samples. The NF-κB, IL-6, and IL-10 polymorphisms were determined by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: Among subjects for the ins/ins genotypes of NF-κB1 gene, the AA genotypes of IL-10 presented a higher frequency in chronic periodontitis group than in healthy controls (p=0.023). A statistically significant difference in genotyping frequencies between AP group and healthy controls was observed for the IL-6 gene. The AA genotype of IL-10 was overrepresented in CP and AP groups compared to healthy controls (OR=9.93, 95% CI: 2.11-46.7, OR=5.7, 95% CI: 1.22-26.89, respectively). CONCLUSIONS: Within the limits of this study, it can be concluded that the IL-10 (-597) AA genotype is associated with susceptibility to chronic/aggressive periodontitis and IL-6 (-174) GG genotypes and G allele seems to be associated with aggressive periodontitis. Clinical relevance: The results of the current study indicate that IL-6 and IL-10 genotypes seem to be associated with aggressive periodontitis. Also, the AA genotypes of IL-10 presented a higher frequency in chronic periodontitis subjects with carrying NF-κB1 ins/ins genotypes.

IL-6 and IL-10 gene polymorphisms in patients with aggressive periodontitis: effects on GCF, serum and clinic parameters.

Genetic variations observed in cytokines affect periodontitis susceptibility. The aim of this study was to investigate interleukin(IL)-6(-174) and IL-10(-597) gene polymorphisms in generalized aggressive periodontitis (GAgP) patients. Also, we aimed to evaluate the effects of IL-6 and IL-10 gene polymorphisms on the clinical outcomes of non-surgical periodontal therapy and cytokine levels in gingival crevicular fluid(GCF) and serum. Fifty-three patients with GAgP and 50 periodontally healthy individuals were included in this study. Clinical parameters, GCF and blood samples were collected at baseline and at 6-week. Non-surgical periodontal therapy was performed in patients with GAgP. Gene analysis were determined by PCR-RFLP(polymerase chain reaction-restriction fragment length polymorphism) and cytokine levels were determined by enzyme-linked immunosorbent assay(ELISA).GAgP patients showed significant improvement on clinical parameters after periodontal therapy(p<0.05). In the GAgP group, IL-6 GG genotype and G allele frequency were higher than in the control group. GCF IL-6 level was also significantly lower at 6-week in the GAgP group. Higher GCF IL-10 levelswere observed in patients carrying the IL-6 GG genotype than in those carrying the GC+CC genotype at baseline. In conclusion, IL-6(-174) and IL-10(-597) gene polymorphisms were found to be associated with GAgP and genotype distribution did not affect the outcome of non-surgical periodontal therapy, while patients with IL-6(-174) GG genotype had higher levels of GCF IL-10 levels.

Evaluation of IL-1ß, IL-1ra, and IL-10 levels and outcome of periodontal therapy in chronic periodontitis with familial Mediterranean fever.

OBJECTIVES: This study aimed to examine the IL-1ß, IL-1ra, and IL-10 cytokine levels in gingival crevicular fluid (GCF) and serum of familial Mediterranean fever (FMF) and chronic periodontitis (CP) patients, and their response to nonsurgical periodontal therapy. MATERIALS AND METHODS: A total of 50 patients, 15 FMF patients with generalized chronic periodontitis (FMF-CP), 15 systemically healthy patients with generalized chronic periodontitis (CP), ten systemically and periodontal healthy controls (HC), and ten periodontally healthy FMF patients (FMF-HC) were enrolled in the study. The cytokine levels in GCF and serum were determined by ELISA. Probing depth, clinical attachment level, and gingival and plaque indices in each participant were also measured. The GCF and clinical parameters at baseline and 6 weeks were recorded. RESULTS: The study indicated statistically significant healing of the clinical parameters in both FMF-CP and CP groups after periodontal treatment. GCF IL-1ß levels at 6 weeks in FMF-CP group were significantly lower than the CP group (p < 0.05), and GCF IL-1ra levels were significantly decreased at 6 week in the FMF-CP group (p < 0.05). GCF IL-10 levels were significantly higher in the FMF-CP group than in the other groups at baseline and 6 weeks (p < 0.05). There were no significant differences in serum-IL-1ß, IL-1ra, and IL-10 levels either FMF-CP or CP groups at baseline or 6 weeks (p > 0.05). CONCLUSIONS: The results of our study suggested that there was a positive correlation between gingival inflammation and serum cytokine levels in FMF patients and also colchicine treatment showed protective effects on GCF cytokine levels in FMF-CP group. CLINICAL RELEVANCE: Following treatment, GCF IL-1ß and GCF IL-1ra levels were decreased in FMF-CP group. GCF IL-10 levels were increased in FMF-CP group compared to other groups. Also, the serum cytokine levels associated with periodontal inflammation in FMF patients.

IL-6 and IL-10 gene polymorphisms in patients with aggressive periodontitis: effects on GCF, serum and clinic parameters

Abstract Genetic variations observed in cytokines affect periodontitis susceptibility. The aim of this study was to investigate interleukin(IL)-6(-174) and IL-10(-597) gene polymorphisms in generalized aggressive periodontitis (GAgP) patients. Also, we aimed to evaluate the effects of IL-6 and IL-10 gene polymorphisms on the clinical outcomes of non-surgical periodontal therapy and cytokine levels in gingival crevicular fluid(GCF) and serum. Fifty-three patients with GAgP and 50 periodontally healthy individuals were included in this study. Clinical parameters, GCF and blood samples were collected at baseline and at 6-week. Non-surgical periodontal therapy was performed in patients with GAgP. Gene analysis were determined by PCR-RFLP(polymerase chain reaction-restriction fragment length polymorphism) and cytokine levels were determined by enzyme-linked immunosorbent assay(ELISA).GAgP patients showed significant improvement on clinical parameters after periodontal therapy(p<0.05). In the GAgP group, IL-6 GG genotype and G allele frequency were higher than in the control group. GCF IL-6 level was also significantly lower at 6-week in the GAgP group. Higher GCF IL-10 levelswere observed in patients carrying the IL-6 GG genotype than in those carrying the GC+CC genotype at baseline. In conclusion, IL-6(-174) and IL-10(-597) gene polymorphisms were found to be associated with GAgP and genotype distribution did not affect the outcome of non-surgical periodontal therapy, while patients with IL-6(-174) GG genotype had higher levels of GCF IL-10 levels.

Ozone Therapy Enhances Osseous Healing in Rats With Diabetes With Calvarial Defects: A Morphometric and Immunohistochemical Study.

BACKGROUND: Bone healing is impaired in diabetes mellitus (DM) cases. The aim of this study is to investigate, both morphometrically and immunohistochemically, the effect of gaseous ozone on bone healing in diabetic rat calvarial defects treated with xenografts. METHODS: DM was induced with 50 mg/kg intraperitoneal streptozotocin in 56 male Wistar rats. Study groups were as follows: 1) empty defect (control, n = 14); 2) xenograft (XG, n = 14); 3) empty defect treated with ozone therapy (control + ozone, n = 14); and 4) xenograft and ozone application (XG + ozone, n = 14). Critical-size defects were created in all rats. Bovine-derived xenograft was applied to XG groups. Gaseous ozone was applied on the operation day and daily for 2 weeks (140 ppm at 2 L/d, 2.24 mg). Rats were sacrificed at 4 or 8 weeks post-surgery. Total bone area, newly formed bone, and residual graft material were measured histomorphometrically. Osteocalcin and bone morphogenic protein (BMP)-2 expression was evaluated immunohistochemically. RESULTS: Osteoclast numbers in the XG + ozone group were higher than the other groups at week 4 (P <0.05). XG + ozone group revealed more total bone area and new bone area than the XG group at weeks 4 (P <0.05) and 8 (P >0.05). Residual graft materials were decreased in the XG + ozone group and the same group revealed more BMP-2 positivity compared with other groups. Osteocalcin positivity in XG groups was higher than in control groups. CONCLUSION: Within the limitations of this DM animal study, gaseous ozone application accelerates xenograft resorption and enhances bone regeneration, especially in the early stages of bone healing.

The effect of boron on alveolar bone loss in osteoporotic rats.

BACKGROUND/PURPOSE: The aim of this study is to investigate the effects of systemically administered boric acid on osteoporosis-related bone alterations, alveolar bone loss, receptor activator of nuclear factor kappa-b ligand (RANKL) expressions, and mandibular bone density in experimental periodontitis model in osteoporotic rats. MATERIALS AND METHODS: Thirty-six male Wistar rats were separated into five study groups: nonligated control (C, n = 6) group; periodontitis (P, n = 6) group; osteoporosis (O, n = 8) group; osteoporosis + periodontitis (O+P, n = 8) group, and osteoporosis + periodontitis with 50 mg/kg/d boric acid (BA50, n = 8) group for 15 days. Osteoporosis was created with intraperitoneal injection of 80 mg/kg retinoic acid for 15 days. Silk ligatures (4/0) were placed around the mandibular right first molar teeth to induce experimental periodontitis. After induction of osteoporosis and periodontitis, rats were sacrificed at Day 15. Alveolar bone loss was evaluated with a stereomicroscope by measuring the distance from the cement-enamel junction to the alveolar crest. Density measurements were performed on radiographs. RANKL and tartrate-resistant acid phosphatase (TRAP) staining were performed on histological slides. RESULTS: Alveolar bone loss was significantly higher in the O+P group than those of the other groups (P < 0.05). Boric acid decreased bone loss (P < 0.05). TRAP + osteoclast numbers were highest in the P group and lowest in the control group. The differences in TRAP + osteoclast numbers among control, P, O+P, and BA50 groups were significant (P < 0.05). There were no significant differences in RANKL expression and mandibular bone density (P > 0.05). CONCLUSION: Within limitations of this study, we conclude that boric acid may decrease alveolar bone loss in a rat model with periodontitis and osteoporosis.

Prevalence of periodontal disease in patients with Familial Mediterranean Fever: a cohort study from central Turkey.

OBJECTIVE: The aim of this study was to compare the periodontal status in patients with Familial Mediterranean Fever (FMF) and in those without this disease. METHOD AND MATERIALS: 84 subjects clinically diagnosed with FMF and 75 systemically healthy controls, matched by age and gender, were recruited. All FMF patients were on a regular daily colchicine treatment and during attack-free periods. Gingival Index (GI), Plaque Index (PI), probing pocket depth (PD), and clinical attachment level (CAL) were measured in all subjects. To evaluate periodontal disease further, patients were stratified into fi ve groups. Education information and smoking habits were recorded. RESULTS: The FMF patients and healthy controls were comparable for age, gender, and smoking status (P>.05). The FMF patients had significantly higher PI and GI values and lower PD and CAL values than those of the control group (P<.05). However, there was no significant difference among all groups in terms of periodontal disease severity (P>.05). In the FMF-severe periodontitis group, higher PI and GI values were seen (P<.05). However, there was no significant difference between the FMF-severe periodontitis group and the controls with severe periodontitis regarding the PD and CAL values (P>.05). CONCLUSION: Patients with FMF using colchicine did not manifest higher attachment loss compared to age- and sex-matched systemically healthy controls.

The histopathological and morphometric investigation of the effects of systemically administered boric acid on alveolar bone loss in ligature-induced periodontitis in diabetic rats.

OBJECTIVE: The purpose of this study was to evaluate the effects of systemically administered boric acid on alveolar bone loss, histopathological changes and oxidant/antioxidant status in ligature-induced periodontitis in diabetic rats. MATERIALS AND METHODS: Forty-four Wistar rats were divided into six experimental groups: (1) non-ligated (NL, n = 6) group, (2) ligature only (LO, n = 6) group, (3) Streptozotocin only (STZ, n = 8) group, (4) STZ and ligature (STZ+LO, n = 8) group, (5) STZ, ligature and systemic administration of 15 mg/kg/day boric acid for 15 days (BA15, n = 8) group and (6) STZ, ligature and systemic administration of 30 mg/kg/day boric acid for 15 days (BA30, n = 8) group. Diabetes mellitus was induced by 60 mg/kg streptozotocin. Silk ligatures were placed at the gingival margin of lower first molars of the mandibular quadrant. The study duration was 15 days after diabetes induction and the animals were sacrificed at the end of this period. Changes in alveolar bone levels were clinically measured and tissues were histopathologically examined. Serum total antioxidant status (TAS), total oxidant status (TOS), calcium (Ca) and magnesium (Mg) levels and oxidative stress index (OSI) were evaluated. Primary outcome was alveolar bone loss. Seconder outcome (osteoblast number) was also measured. RESULTS: At the end of 15 days, the alveolar bone loss was significantly higher in the STZ+LO group compared to the other groups (p < 0.05). There was no significant difference in alveolar bone loss between the STZ+LO 15 mg/kg boric acid and STZ+LO 30 mg/kg boric acid groups (p > 0.05). Systemically administered boric acid significantly decreased alveolar bone loss compared to the STZ+LO group (p < 0.05). The osteoblast number in the BA30 group was significantly higher than those of the NL, STZ and STZ+LO groups (p < 0.05). Inflammatory cell infiltration was significantly higher in the STZ+LO group the other groups (p < 0.05). Serum TAS levels were significantly higher in the NL and LO groups than the other groups (p < 0.05). The differences in TOS levels were not found to be significant among all the groups (p > 0.05). The OSI values of the BA30 group were significantly lower than the STZ+LO group (p < 0.05). Also, the differences in serum calcium and magnesium levels were insignificant among the all groups (p > 0.05). CONCLUSION: Within the limits of this study, it can be suggested that BA, when administered systemically, may reduce alveolar bone loss in the diabetic rat model.

A novel platelet concentrate: titanium-prepared platelet-rich fibrin.

We developed a new product called titanium-prepared platelet-rich fibrin (T-PRF). The T-PRF method is based on the hypothesis that titanium may be more effective in activating platelets than the silica activators used with glass tubes in Chouckroun's leukocyte- and platelet-rich fibrin (L-PRF) method. In this study, we aimed to define the structural characteristics of T-PRF and compare it with L-PRF. Blood samples were collected from 10 healthy male volunteers. The blood samples were drawn using a syringe. Nine milliliters was transferred to a dry glass tube, and 9 mL was transferred to a titanium tube. Half of each clot (i.e., the blood that was clotted using T-PRF or L-PRF) was processed with a scanning electron microscope (SEM). The other half of each clot was processed for fluorescence microscopy analysis and light microscopy analysis. The T-PRF samples seemed to have a highly organized network with continuous integrity compared to the other L-PRF samples. Histomorphometric analysis showed that T-PRF fibrin network covers larger area than L-PRF fibrin network; also fibrin seemed thicker in the T-PRF samples. This is the first human study to define T-PRF as an autogenous leukocyte- and platelet-rich fibrin product. The platelet activation by titanium seems to offer some high characteristics to T-PRF.