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Background: The aim of this study is to evaluate the gene expression of immune-inflammatory markers in gingival biopsies of patients with type 2 diabetes with chronic periodontitis (CP). Methods: Gingival biopsies were harvested from systemically and periodontally healthy patients (SPH), systemically healthy patients with CP (SHCP), and patients with better-controlled and poorly controlled diabetes and CP. The levels of mRNA of interleukin (IL)-17, IL-6, IL-23, IL-10, IL-4, interferon-γ toll-like receptor (TLR)-2, TLR-4, osteoprotegerin, receptor activator of nuclear factor-kappa B ligand (RANKL), tumor necrosis factor-s, transforming growth factor-β, transcription factor forkhead box p3, transcription factor orphan nuclear receptor C2 (RORC2), and receptor of advanced glycation end products (RAGE) were evaluated by quantitative real-time polymerase chain reaction. Results: All CP groups presented higher levels of mRNA of TLR-2, TLR-4, IL- 17, RANKL, and RAGE and a higher frequency of IL-17 and TLR-2 mRNA-positive biopsies when compared to SPH (P<0.05). There was a higher frequency of detection of RORC2 in the biopsies from both groups with diabetes compared to the other groups (P<0.05). The frequency of IL-4 mRNA-positive tissues was lower in patients with diabetes compared to SHCP (P<0.05). Conclusion: CP, but not type 2 diabetes mellitus, significantly affected the expressions of the evaluated genes related to the innate and adaptive immune responses. [ABSTRACT FROM AUTHOR]

Background: This study compares the levels of cytokines and bone-related factors in the gingival crevicular fluid (GCF) of systemically healthy patients with chronic periodontitis (CP); and better-controlled, and poorly controlled patients with type 2 diabetes and CP. Methods: Thirty-seven patients with type 2 diabetes and CP and 20 systemically healthy patients with CP were enrolled in this study. The patients with diabetes mellitus were categorized as better-controlled (n = 17; HbAlc levels ≤8%) or poorly controlled (n = 20; glycated hemoglobin values >8%). Levels of tumor necrosis factor-α, interleukin (IL)-4, interferon (1FN)-γ IL-23, 1L-17, soluble receptor activator of nuclear factor-kappa B iigand (sRANKL), and osteoprotegerin (OPG) in GCF of diseased sites were analyzed by enzyme-linked immunosorbent assay. Results: Type 2 diabetes mellitus, as a whole, upregulates the levels of OPG, sRANKL, IFN-γ IL- 17, and IL-23 and down-regulates the production of IL-4 in sites with CP (P<0.05). Better-controlled individuals exhibited the highest levels of IFN-γ whereas poorly controlled patients presented the highest levels of IL-17 (P <0.05). There were no differences in the levels of tumor necrosis factor-s, OPG, and IL-23 among systemically healthy, better-controlled, and poorly controlled patients with diabetes (P>0.05). Conclusions: Increased levels of proinflammatory cytokines and RANKL were observed in the GCF of patients with type 2 diabetes with CP, compared to patients without diabetes. In addition, poor or good glycemic status seems to modulate osteo-immunoinflammatory mediators in a different manner. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the gene expression levels of semaphorins 3A, 3B, 4A, and 4D in both healthy and diseased implants., Materials and Methods: Subjects with peri-implantitis presented clinical attachment loss, probing depth ≥ 5 mm, bleeding on probing and/or suppuration, and radiographic bone loss > 4 mm. Peri-implant tissue biopsy specimens were sampled for analysis of the mRNA expression levels for semaphorins 3A, 3B, 4A, and 4D. A real-time polymerase chain reaction was performed, and the gene expression levels of semaphorins in relation to the housekeeping gene were analyzed by using the nonparametric Mann-Whitney test (P < .05)., Results: Thirty-five subjects (16 men, 19 women; mean age: 54.12 ± 2.34 years) with implant-supported restorations, using screw-shaped dental implants with internal or external hexagon were enrolled in this study. Higher levels of semaphorins 3A and 4D were detected in the peri-implantitis compared with the healthy tissues (P = .0011 and P = .0404, respectively), whereas Sem4A levels were significantly higher in the control group (P < .0001). Differences between groups in the expression levels of Sem3B were not significant., Conclusion: Advanced peri-implantitis lesions showed higher levels of gene expression for Sem3A and Sem4D and lower levels of Sem4A in comparison to tissues obtained from a healthy dental implant.

Purpose: There is interest in establishing hypoglycemiant agents able to contain/revert the impact of diabetes mellitus on osseointegration. The purpose of this study was to assess the possible effect of metformin in reversing the negative effects of hyperglycemia on the healing of bone surrounding implants inserted in rats., Materials and Methods: Rats (10 per group) were assigned to one of the following groups: DM group: type 2 diabetic rats deprived of metformin (M) treatment; MDM group: type 2 diabetic rats under M treatment (40 mg/kg/day, starting on the 15th day after implant placement); control group: nondiabetic rats without M treatment. At 30 days after streptozotocin injection, titanium implants were placed in tibiae. Animals were euthanized 30 days after implant surgery. Bone-to-implant contact (BIC), bone area (BA), and the number of receptor activator of nuclear factor κB ligand (RANKL)- and osteoprotegerin (OPG)-stained cells were assessed in cortical and medullary areas., Results: The percentages of BIC and BA in the cortical bone were reduced in the DM and MDM groups compared with the control group (P < .05). The percentage of BA in the medullary region was reduced in the DM group compared with the control group (P < .05). The MDM group showed the greatest number of OPG-stained cells, while the DM group presented the greatest ratio of RANKL/OPG in the medullary area (P < .05)., Conclusion: Metformin did not modulate the damaging effect of hyperglycemia on bone healing around implants at histometric levels, but increased the expression of OPG and decreased the RANKL/OPG ratio in the medullary area, yielding some molecular benefits in the osseointegration of implants under the hyperglycemic state.

There is scarce evidence on suitable approaches for the treatment of unresponsive or residual periodontal sites in diabetic patients. This study assessed the effects of surgical debridement (SD) and nonsurgical debridement (NSD), associated with amoxicillin and metronidazole, on clinical and immunological outcomes of residual pockets and adjacent healthy sites in patients with type 2 diabetes. A split-mouth, randomized controlled trial was conducted in 21 patients presenting at least 2 residual pockets in contralateral quadrants 12 months after basic nonsurgical periodontal therapy. Patients received systemic antibiotics, and contralateral quadrants were assigned to receive SD or NSD. The changes in clinical parameters were evaluated from baseline to 12 months. Local levels of 14 cytokines and chemokines were measured with multiplex bead immunoassays at baseline and 3 and 12 months after therapy. There were no statistically significant differences between SD and NSD for changes in clinical parameters from baseline to 12 months (P > 0.05). There was a significantly greater increase in the levels of granulocyte-macrophage colony-stimulating factor and interleukin 6 from baseline to 3 months in the healthy sites adjacent to residual pockets receiving SD (P < 0.05). A significant decrease in the levels of monocyte chemoattractant protein-1 and macrophage inflammatory protein 1α occurred from baseline to 12 months in the residual pockets treated by SD (P < 0.05). In conclusion, SD and NSD resulted in similar clinical benefits at 12 months. The short-term increase in the levels of proinflammatory biomarkers in SD sites probably can be attributed to tissue trauma and healing, and the long-term decrease in the levels of chemotactic factors in residual pockets treated by surgery may reflect remission of infection and stable wound healing in these sites at 12 months.

Purpose: To evaluate the effects of caffeine and/or estrogen deficiency on trabecular bone area (TBA) and bone healing in rats., Materials and Methods: Rats were divided into groups (n=15/group) as follows: control, caffeine, ovariectomy (OVX), and caffeine/OVX. Critical-sized defects were created in the tibiae (57 days after beginning caffeine administration and 43 days after OVX). The intact femurs were evaluated for TBA and the number of positive cells for tartrate-resistant acid phosphatase (TRAP), receptor activator of nuclear factor-κB ligand (RANKL), and osteoprotegerin (OPG). In the defects, bone healing, the number of TRAP+ and RANKL/OPG+ cells, and gene expression of bone morphogenetic protein (BMP)-2, BMP-7, osteopontin, and CBP/p300-interacting-transactivator-with-ED-rich-tail-2 (CITED-2) were evaluated., Results: Bone healing was poorer in defects of the caffeine group than in those of the control group. The femurs of the OVX and OVX/caffeine groups presented lower TBAs and higher RANKL/OPG+ cell ratios. The number of TRAP+ cells was higher in femurs of the caffeine group and in defects of the OVX group. The caffeine/OVX group presented the highest RANKL/OPG+ cell ratio in femurs and defects. The OVX group presented the highest expression of BMP-2, BMP-7, and CITED-2., Conclusion: Caffeine affected bone healing, while estrogen deficiency mainly affected TBA, but no significant deleterious synergic effects of both conditions were observed.

Purpose: To evaluate the effects of the lercanidipine on bone healing (BH) and bone density (BD) in the tibiae of spontaneously hypertensive rats (SHR), using histometric and tartrate-resistant acid phosphatase (TRAP) expression analyses., Materials and Methods: Wistar and SHR were assigned to one of the following groups: normotensive rats (NTR) (n = 15), untreated SHR (n = 15), and lercanidipine-treated SHR (n = 15). The latter group was treated daily with lercanidipine for 6 weeks. Two weeks after the beginning of drug administration, a critical-sized surgical defect was created in the right tibia of all groups, whereas the contralateral tibia remained without defect. The animals were killed 30 days after the creation of the bone defect., Results: There were no significant differences among the groups for BH, trabecular BD, and the number of TRAP+ cells in the newly formed cortical bone (P > 0.05). SHR presented significantly lower cortical BD and increased cortical levels of TRAP+ cells, when compared with NTR and lercanidipine-treated SHR (P < 0.05)., Conclusion: SHR presented a lower cortical BD and increased levels of TRAP+ cells. In addition, the treatment of SHR with lercanidipine during 6 weeks was able to revert the deleterious effects of hypertension on cortical BD and on the number of TRAP+ cells in the tibia of SHR.