Hyaluronic acid with antioxidants improve wound healing in rats.

Hyaluronic acid (HA) is found in connective tissue and participates in wound healing. We investigated the efficacy of a HA gel (2% hyaluronic acid; 1% antioxidants, coenzyme Q10 and vitamin E; and 5% benzocaine) on healing of palatal wounds in rats. We established two groups of rats: a control group treated with vehicle and an HA group treated with HA gel. The control group was divided into five subgroups and the HA group was divided into four subgroups according to the day on which animals were sacrificed. Wounds were created by elevating 5 mm diameter full thickness flaps. Healed and unhealed wound areas were measured using photographs. Transforming growth factor (TGF)-ß, insulin-like growth factor (IGF), and collagen I and III expressions were determined using immunohistochemistry. The number of fibroblasts increased and inflammatory cells decreased from day 0 to 21 in both groups. The HA group exhibited more fibroblasts by day 7 compared to controls; (TGF)-ß and IGF levels were similar between HA and control groups. HA groups exhibited fewer inflammatory cells than controls on days 3 and 7. We found significant differences in TGF-ß and IGF levels among HA groups between days 3 and 21, and among control groups between days 0 and 21. Collagen I and III levels were greater for the day 3 HA group compared to controls. We observed improved wound healing in HA treated rats within 7 days.

Cinnamic acid decreases periodontal inflammation and alveolar bone loss in experimental periodontitis.

BACKGROUND AND OBJECTIVE: Periodontitis is the chronic destructive disease of the periodontium, which causes severe inflammation in the tissues. Cinnamic acid as an unsaturated carboxylic acid might prevent inflammation and periodontal destruction. The present study aimed to evaluate the effects of cinnamic acid in two different forms as free cinnamic acid and cinnamic acid liposome on experimental periodontitis in Wistar rats. METHODS: Thirty-two female rats were used in the present study. Four main groups were created as follows: C: control group; P: periodontitis group; C-P: free cinnamic acid-administered periodontitis group; and CL-P: cinnamic acid liposome applied group. Periodontitis was induced via ligating 4-0 silk sutures around lower first molar teeth on both right and left mandibles. The study duration was 30 days, and the ligatures were removed from half of the rats in the periodontitis-induced groups. The other half carried the ligatures throughout 30 days, and all rats were euthanized at 30th day. Mandibles were removed and evaluated via stereomicroscope and underwent histological procedures. Inflammatory cell counts, osteoblast, and osteoclast cell counts were determined in hematoxylin-eosin-stained slides, and peroxisome proliferator-activated receptor (PPAR)-γ, cyclooxygenase (COX)-2, receptor activator of nuclear factor κ-B (RANKL), and osteoprotegerin (OPG) expressions were evaluated by immunohistochemistry. RESULTS: Control group had the lowest bone loss, and periodontitis group which kept ligatures had the highest bone loss compared to the other groups. Ligature removal provided significant improvement in bone measurements. Cinnamic acid groups also showed lower bone loss compared to the periodontitis group. The inflammatory cell and osteoclast counts were also higher in the periodontitis group, and both applications of cinnamic acid decreased these values. Osteoblast cells were the lowest in the periodontitis group, and cinnamic acid increased these counts. PPAR-γ and COX-2 levels were higher in the periodontitis group, and cinnamic acid decreased these levels but not to a significant level except for the cinnamic acid liposome ligature removal group, which had significantly lower values in the PPAR-γ and COX-2. OPG levels were lower in the periodontitis group compared to the other groups. Cinnamic acid significantly decreased RANKL and increased OPG levels. CONCLUSION: Periodontitis caused increased inflammation and bone destruction accompanied by increased PPAR-γ, COX-2, and RANKL levels and osteoclast counts. Cinnamic acid decreased osteoclast counts and inflammation and increased osteoblast counts and OPG expression in the present animal model of periodontitis.

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.

Histological evaluation of peri-implant mucosal and gingival tissues in peri-implantitis, peri-implant mucositis and periodontitis patients: a cross-sectional clinical study.

Objective: Aim of present study was to evaluate gingival tissue samples obtained from healthy and diseased sites of teeth and dental implants in terms of hypoxia and collagenase activity.Methods: Four study groups were created as Group-1; healthy individuals (H), Group-2; periodontitis patients with stage 3 grade B (P), Group-3; patients with peri-implant mucositis. Group-4; patients with peri-implantitis (P-IMP). Plaque index (PI), gingival index (GI) and probing pocket depth (PPD) were recorded. Gingival and peri-implant mucosal biopsies were obtained. Fibroblast and inflammatory cells were counted. Hypoxia-inducible factor (HIF)-1α, prolyl hydroxylase (PH), matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) levels were determined via immunohistochemistry.Results: Healthy controls had highest fibroblast cell counts and lowest inflammatory cell counts compared to other groups. Peri-implantitis and periodontitis samples had similar fibroblast and inflammatory cell counts, while peri-implant mucositis had higher fibroblast cells and lowered inflammatory cells compared to periodontitis and peri-implantitis samples. HIF-1α, COX-2 and iNOS levels were lowest in healthy controls and increased in other groups. Peri-implant mucositis samples had significantly lower expressions of HIF-1α, COX-2 and iNOS compared to peri-implantitis and periodontitis groups. PH expressions were lower in periodontitis and peri-implantitis groups compared to healthy controls and peri-implant mucositis groups. MMP-8 levels were lower in healthy group compared to other groups while levels were similar in periodontitis, peri-implant mucositis and peri-implantitis groups. TIMP levels were similar in groups.Conclusion: Periodontitis, peri-implantitis, and peri-implant mucositis samples exhibited higher inflammation and lower fibroblast cell counts and tend to have increased tissue collagenase activity, hypoxia and inflammation compared to healthy samples.

Dental hypofunction alters subgingival microorganisms: a pilot study.

BACKGROUND: The aim of this study was to evaluate dental plaque compositions, vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF) 1-alpha levels in gingival crevicular fluid (GCF) at hypofunctional and normofunctional teeth in healthy individuals and chronic periodontitis patients. METHODS: Sixty systemically healthy individuals were enrolled. Study groups were: group 1 hypofunctional healthy group (group 1, N.=15); group 2 hypofunctional periodontitis group (group 2, N.=15); group 3 normofunctional healthy group (group 3, N.=15); and group 4 normofunctional periodontitis group (group 4, N.=15). Clinical periodontal measurements (plaque index, gingival index and clinical attachment level) were recorded. Dental plaque and GCF samples were taken. VEGF and HIF 1-alpha levels in GCF were determined. Subgingival plaque samples were evaluated for 11 different bacterial species as, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Prevotella intermedia, Peptostreptococcus micros, Fusobacterium nucleatum, Campylobacter rectus, Eubacterium nodatum, Eikenella corrodens and Capnocytophaga species. RESULTS: Tannerella forsythia, Peptostreptococcus micros, Eubacterium nodatum levels decreased in hypofunctional healthy and periodontitis groups (P<0.05). Porphyromonas gingivalis levels increased in hypofunctional healthy group and decreased in hypofunctional periodontitis group (P<0.05). There was also a decrease in Eikenella corrodens levels in hypofunctional periodontitis group (P<0.05). There were no difference regarding the Aggregatibacter actinomycetemcomitans, Capnocytophaga spp., Prevotella intermedia and Fusobacterium nucleatum levels among the groups (P>0.05). VEGF and HIF-1α levels in both GCF and serum samples were also similar (P>0.05). CONCLUSIONS: Within the limits of this study, the authors found that the levels of four significant bacterial strains were decreased in both hypofunctional healthy and hypofunctional periodontitis groups compared to normofunctional equivalents. Though not evaluated in this study, this situation could be due to periodontal ligament atrophy and related physiological alterations.

Hypoxia and collagen crosslinking in the healthy and affected sites of periodontitis patients.

Present study suggests that diseased sites of periodontitis with stage 3 grade B and C had decreased fibroblast cell density, hypoxia-inducible factor (HIF) and vascular endothelial growth factor (VEGF) expressions while increased inflammatory cell counts compared to both healthy sites of the periodontitis patients and healthy controls. Collagen maturation enzymes also decreased in the diseased sites. Objective: The present study aimed at determining markers of hypoxia and collagen crosslinking in healthy and diseased gingiva from healthy individuals and periodontitis patients. Methods: Group-1; healthy individuals, Group-2; healthy sites of periodontitis patients-stage 3 grade B, (H-GradeB) Group-3; diseased sites of periodontitis patients-stage 3 grade B, (D-GradeB). Group-4; healthy sites of periodontitis patients-stage 3 grade C, (H-GradeC). Group-5; diseased sites of periodontitis patients-stage 3 grade C, (D-GradeC). Plaque index (PI), gingival index (GI) and clinical attachment levels (CALs) were recorded. Gingival biopsies were obtained. Fibroblast and inflammatory cells were counted. HIF-1α, prolyl hydroxylase (PH), VEGF, lysyl oxidase (LOX) and lysyl hydroxylase (LH) levels were determined via immunohistochemistry. Results: Fibroblast cell counts were lower in D-GradeC and D-GradeB than other groups. C group had highest fibroblast cell counts. Inflammatory cell counts were highest in the D-GradeC and lowest in C group. HIF-1α levels were highest in C group and decreased in diseased sites. Lowest value was observed in D-GradeC group. VEGF, PH, and LH levels were higher in the control group compared to other groups. LOX levels were similar in the groups except for D-GradeC. LOX levels were similar in the groups except for D-GradeC which is significantly lower than those of the control group and healthy sites. Conclusions: The results revealed that diseased sites of periodontitis patients had decreased fibroblast cells, HIF and VEGF expressions while increased inflammatory cells. Collagen crosslinking tend to decrease with disease regardless of stage and grade of disease.

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.

Assessment of local and systemic 25-hydroxy-vitamin D, RANKL, OPG, and TNF levels in patients with rheumatoid arthritis and periodontitis.

The present study aimed to evaluate proinflammatory cytokine and vitamin D levels in rheumatoid arthritis (RA) and chronic periodontitis (CP) patients and healthy individuals before and after initial periodontal treatment. Overall, 17 CP patients with RA (RA + CP), 18 systemically healthy CP patients (CP), and 18 healthy controls (C) were included. Clinical periodontal measurements were recorded and gingival crevicular fluid (GCF) and blood samples were recorded. RA + CP and CP patients received nonsurgical periodontal treatment. Vitamin D, tumor necrosis factor (TNF)-α, receptor activator of nuclear factor-KB ligand (RANKL), and OPG levels were determined in GCF and serum. Baseline clinical parameters were similar in all periodontitis groups (P > 0.05) but were higher than that in controls (P < 0.05). Periodontal treatment improved clinical parameters in all periodontitis groups (P < 0.05). GCF vitamin D levels were higher in RA + CP and CP groups than in healthy controls, but these levels decreased in the RA + CP group after periodontal treatment (P < 0.05). Serum RANKL and GCF TNF-α levels in RA patients decreased after periodontal treatment (P < 0.05). Within the limitations of this study, the results suggested that GCF vitamin D levels are increased in RA patients and decrease after periodontal treatment; therefore, local vitamin D levels might be an important indicator of periodontal bone loss.

The effect of commercial conjugated linoleic acid products on experimental periodontitis and diabetes mellitus in Wistar rats.

OBJECTIVE: The aim of present study was to determine the effects of conjugated linoleic acid enriched milk on alveolar bone loss, hyperglycaemia, oxidative stress and apoptosis in ligature-induced periodontal disease in diabetic rat model. METHODS: 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 + L, n = 8) group, 5; ligature and conjugated linoleic acid (CLA) (L + CLA, n = 8) group, 6; STZ, ligature and CLA group (STZ + L + CLA, n = 8) group. Diabetes mellitus was induced by 60 mg/kg streptozotocin. Rats were fed with CLA enriched milk for four weeks. Silk ligatures were placed at the gingival margin of lower first molars of mandibular quadrant. The study duration was four weeks 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. Inducible nitric oxide synthase (iNOS) and Bax protein expressions, serum interleukin-1ß (IL-1ß), low-density lipoprotein (LDL), high-density lipoprotein (HDL) and triglyceride levels and tartrate resistant acid phosphatase (TRAP)+ osteoclast numbers were also evaluated. RESULTS: At the end of four weeks, alveolar bone loss was significantly higher in the STZ + LO group compared to the other groups (p < .05). CLA decreased alveolar bone loss in L + CLA and STZ + L + CLA groups. CLA significantly decreased TRAP + osteoclast numbers and increased osteoblastic activity compared to the STZ + L group (p < .05). Diabetes and CLA increased Bax protein levels (p < .05) however CLA had no effect on iNOS expression (p > .05). CONCLUSION: Within the limits of this study, commercial CLA product administration in addition to diet significantly reduced alveolar bone loss, increased osteoblastic activity and decreased osteoclastic activity in the diabetic Wistar rats.

Diffusion tensor imaging of the hippocampus in chronic cigarette smokers.

PURPOSE: Previous studies have demonstrated neuronal dis-integrity in chronic smokers using diffusion tensor imaging (DTI). However, assessment of hippocampal DTI has not been performed in this group. The purpose of this study was to investigate the hippocampal integrity in chronic smokers and non-smokers and to compare this to memory performance. METHODS: We used in vivo DTI to measure the differences in hippocampal integrity between 88 chronic smoker and 88 non-smoking subjects. DTI was performed on a 3T scanner. We administered a verbal learning test to assess new verbal learning capabilities. The immediate recall (IR) was administered immediately after test procedure and delayed recall (DR) after 15min. RESULTS: Mean values of fractional anisotropy (FA) for non-smokers and smokers were 0.46 and 0.40, respectively (p<0.05). Mean IR word number for non-smokers and smokers was 11.6, 9.04, respectively (p<0.05). The mean word number of DR for non-smokers and smokers was 10.2, 7.2, respectively (p<0.05). CONCLUSIONS: This is the first study of hippocampal DTI assessment in the chronic smokers. We found that decreased hippocampal FA associated with neuronal dis-integrity and worse memory performance in chronic smokers than non-smokers. We also found a low positive correlation hippocampal FA values with memory performance in nonsmoking group.

The Effect of Melatonin on Bone Loss, Diabetic Control, and Apoptosis in Rats With Diabetes With Ligature-Induced Periodontitis.

BACKGROUND: The aim of this study examines the effect of systemic melatonin administration on proinflammatory cytokine levels, apoptosis, alveolar bone loss (ABL), lipid metabolism, and diabetic control in in rats with diabetes mellitus (DM) and ligature-induced periodontitis. METHODS: Fifty-two male Wistar rats were used in this study. Study groups were as follows: 1) non-ligated control (NL, n = 6); 2) streptozotocin (STZ, n = 8); 3) STZ and melatonin (STZ+Mel, n = 8); 4) ligature (L, n = 6); 5) ligature and melatonin (L+Mel, n = 8); 6) STZ and ligature (STZ+L, n = 8); and 7) STZ, ligature, and melatonin (STZ+L+Mel, n = 8). DM was induced by intraperitoneal injection of a single dose of STZ (60 mg/kg). Melatonin was administered by intraperitoneal injection of a dose of 10 mg/kg/day for 4 weeks. Silk ligatures were placed subgingivally around the mandibular right first molars. The study period was 4 weeks, and animals were sacrificed at the end of 4 weeks. Morphometric analysis of bone loss was performed. Tissues were histopathologically examined. Inducible nitric oxide synthase (iNOS) and B-cell lymphoma-2-associated X (bax) protein expressions, serum interleukin (IL)-1ß levels, and tartrate-resistant acid phosphatase-positive (TRAP+) osteoclast numbers were also evaluated. RESULTS: After 4 weeks, the highest ABL was observed in the STZ+L group, and the difference was significant (P <0.05). Systemically administered melatonin significantly decreased ABL in the STZ+L+Mel group compared with that in the STZ+L group (P <0.05). TRAP+ osteoclast numbers were the highest in the STZ+L group, and melatonin significantly decreased osteoclast numbers (P <0.05) but had no effect on iNOS, IL-1ß, or bax levels. CONCLUSIONS: Within the limits of this study, it can be concluded that systemic melatonin treatment may decrease osteoclastic activity and reduce ABL in the model using rats with DM.

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.

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.