Systemic circulating inflammatory burden and periodontitis in adolescents.

OBJECTIVES: To analyze the association between systemic inflammatory burden of cardiovascular disease (CVD) risk and periodontitis in adolescents, including mediating pathways triggered by their common risk factors. MATERIALS AND METHODS: Using a population-based sample study (n = 405) of Brazilian adolescents (17-18 years old), direct and mediation pathways triggered by "Socioeconomic Status," "Adiposity," Smoking, and "Blood Pressure" were modelled for the association between the "Systemic Circulating Inflammatory Burden of CVD Risk" (IL-1ß, IL-6, IL-8, TNF-α) and the "Initial Periodontitis" (bleeding on probing (BoP), probing depth (PD) ≥ 4 mm, clinical attachment loss (CAL) ≥ 4 mm), both as continuous latent variables, using structural equation modeling. Sensitivity analysis was performed for the outcomes "Gingivitis" (visible plaque; BoP); "Moderate Periodontitis" (PD ≥ 5 mm and CAL ≥ 5 mm) and periodontitis (CDC-AAP case definition). RESULTS: Higher "Systemic Circulating Inflammatory Burden of CVD Risk" was directly associated with higher "Initial Periodontitis" (standardized coefficient [SC] = 0.178, P value < 0.001). Lower "Socioeconomic Status" (SC = - 0.022, P value = 0.015) and Smoking (SC = 0.030, P value = 0.021) triggered the "Initial Periodontitis", mediated by "Systemic Circulating Inflammatory Burden of CVD Risk". Sensitivity analysis showed a dose-response relationship between "Systemic Circulating Inflammatory Burden of CVD Risk" and "Moderate Periodontitis" (SC = 0.323, P value = 0.021). CONCLUSIONS: "Systemic Circulating Inflammatory Burden of CVD Risk" appeared as an underlying mechanism of early periodontal breakdown in adolescents, also triggered by social vulnerability and smoking. CLINICAL RELEVANCE: The association between periodontitis and CVD in adulthood seems to establish much earlier in life than had been previously studied, giving impetus to preventive approaches focused on their common risk factors.

Impact of natural curcumin on the progression of experimental periodontitis in diabetic rats.

OBJECTIVE: To evaluate the role of natural curcumin (CURC) on experimental periodontitis (EP) in animals with diabetes mellitus (DM). MATERIAL AND METHODS: One hundred rats were assigned to DM + placebo (PLA); DM + CURC; DM + insulin (INS); DM + CURC + INS; and Non-DM. Diabetes was induced by streptozotocin. After 3 days, they were initiated CURC and PLAC solutions and insulin administrations, daily for 30 days. This included a period of 19 days prior to EP induction (ligature at the first mandibular and the second maxillary molar) and then additional 11 days. Specimens from the mandible were processed for morphometric examination of bone level. Gingival tissues from mandibular molars were collected for quantification of IL-1ß, IL-4, IL-6, IL-17, IFN-γ, and TNF-α using a Luminex/MAGpix assay. Gingivae from maxillary molars were subjected to RT-PCR for assessment of Runx2, RANKL, OPG, SIRT, Dkk1, and Sost levels. RESULTS: Lower linear bone loss was detected in ligated molars of DM + CURC + INS vs DM + PLAC and DM + INS groups (P < 0.05). In ligated sites from DM rats treated with CURC + INS, IL-6, IL-1ß, INF-γ, and TNF-α levels were the lowest in comparison with PLAC and/or INS and CURC as monotherapies (P < 0.05). CURC, independently of INS, increased Runx2 and SIRT when compared to DM + PLAC (P < 0.05) in ligated sites, whereas only CURC + INS reduced the RANKL/OPG ratio when compared to DM + PLAC (P < 0.05). CONCLUSION: Natural CURC, when associated with INS, reduces the DM-induced loss of supporting alveolar bone and promotes favorable modulation on osteo-immune-inflammatory mediators.

Clinical factors associated with salivary flow rate in adults with acromegaly.

OBJECTIVE: To investigate the stimulated salivary flow (SSF) and unstimulated salivary flow (USF) in adults with acromegaly and to identify possible clinical factors associated with salivary flow. STUDY DESIGN: A case-control study was conducted with a group composed of adults diagnosed with acromegaly (n = 29, mean age = 50.2 years) and a control group (n = 29, mean age = 54.3 years). Variables for socio-demographic characterization, lifestyle habits, and diabetes diagnosis, body mass index (BMI), cervical circumference (CC) and abdominal circumference (AC) were collected. USF and SSF variables were analyzed as outcomes. Unpaired t-test, Pearson's correlation, and multivariate regression models were used for statistical analysis. RESULTS: Both groups were 44.8% male and 55.2% female. Diabetes was present in 55.2% of the acromegaly group and in 51.7% of the controls (P = .792). The acromegaly group had a higher USF than the control group (0.50 mL/min versus 0.22 mL/min). SSF showed a direct correlation with CC (r = 0.470, P = .010). Acromegaly was associated with higher USF (standardized coefficient = 0.780, P = .039), and age was inversely related to USF (standardized coefficient = -0.333, P = .013). CONCLUSIONS: The findings suggest that adults with acromegaly have an increased USF and that being older is associated with a decrease in USF.

The influence of periodontal status and serum biomarkers on salivary leptin levels in systemic lupus erythematosus patients.

Objective: This study aimed to investigate the influence of periodontal status, clinical data, and serum markers on salivary leptin levels in patients with systemic lupus erythematosus (SLE). Methods: A case-control study was conducted with 38 patients with SLE and 29 healthy controls. Periodontal data included periodontal probing depth (PPD), clinical attachment level (CAL), and gingival bleeding on probing (BOP). Stimulated saliva samples were collected to analyze salivary leptin levels. Clinical and serum data were collected from the SLE group. Statistical analysis included the t-test, Mann-Whitney test, Spearman correlation coefficient, and a structural equation model. Results: The SLE group had a lower salivary leptin level than the control group (P = 0.002). The model revealed that SLE had an inverse and independent effect on salivary leptin (standardized estimate =  - 0.289, P = 0.023). Moreover, salivary leptin level negatively correlated with the serum levels of triglyceride, creatinine, and leukocytes, positively correlated with the serum total cholesterol, but was not significantly correlated with the periodontal status. Conclusion: These findings suggest that patients with SLE have a lower salivary leptin level. In addition, the level of salivary leptin does not appear to be related to periodontal status in patients with SLE.

Expression of Toll-like receptors 2 and 4 in the saliva of patients with systemic lupus erythematosus and chronic periodontitis.

OBJECTIVE: The aim of this study was to investigate the expression of salivary Toll-like receptors (TRL) 2 and 4 in patients with systemic lupus erythematosus (SLE) and chronic periodontitis (CP). METHODS: A case-control study was conducted with 77 participants (42 SLE and 35 non-SLE) stratified according to CP diagnosis criteria. Periodontal parameters consisted of clinical attachment level (CAL), probing depth (PD), the visible plaque index (VPI), and the gingival bleeding index (GBI). Salivary TRL 2 and 4 expressions were determined by quantitative real-time polymerase chain reaction (RT-PCR). Statistical analysis included Mann-Whitney U test, Kruskal-Wallis test, Spearman's correlation rank, and multiple linear regression. RESULTS: Patients with isolated SLE or CP had higher TLR 2 and TLR 4 expression in their saliva samples (P < 0.05). The group with both SLE and CP had lower TLR 2 and 4 expressions (P < 0.05). TLR 2 and TLR 4 showed significant negative correlations with PD, CAL, and GBI in SLE patients, and a significant positive correlation with periodontal parameters in non-SLE patients. CP was independently associated with reduction of TLR2 and TLR4 expression, even after adjusting for clinical data and current drug use. CONCLUSION: Reduced TRL 2 and 4 expression in saliva was associated with the presence of CP in SLE patients. Key Points • Patients affected by isolated CP or SLE had higher TLR2 and TLR4 expression. • TLR under-expression may be associated with a worse periodontal status in SLE. • Abnormalities in TLRs expression may increase the susceptibility to periodontitis.

Evidence that metyrapone in the presence of inflammation modulates cytokine mRNA expression.

OBJECTIVE: Metyrapone (MT) has been used clinically to decrease glucocorticoid levels in human and animal studies. However, the potential effects of MT in the presence of inflammation are poorly understood. Thus, the aim of this study was to evaluate the effects of the administration of MT on the mRNA levels of pro-inflammatory cytokines in the presence of inflammation induced by the well-established model of ligature-induced periodontitis in rats. MATERIAL AND METHODS: Sixty animals were randomly assigned into three experimental groups of 20 rats each: G1-control; G2-periodontal disease (PD) induced by cotton ligature; G3-PD associated with 3 daily doses of MT (50mg/kg/3×3h). After 30 days, all animals were killed by decapitation. Blood samples were taken and the concentrations of corticosterone and catecholamines measured. Marginal tissues around ligated and non-ligated teeth were harvested and gene expression was assessed by quantitative polymerase chain reaction technique (qPCR). Moreover, the area of interradicular bone loss (ABL) was histometrically determined. RESULTS: Data analysis showed that: (i) ligature placement resulted in a significant ABL, as compared to non-ligated sites of G1 group; (ii) mRNA levels of all the pro-inflammatory factors assessed (INF-γ, TNF-α, IL-1ß and IL-6) were increased in the PD group (G2) (p<0.05) when compared to G1; (iii) there were no significant differences in corticosterone and catecholamine plasmatic levels between the three groups; (iv) MT administration, in the presence of inflammation, induces an increased ABL and significantly increased mRNA levels of all pro-inflammatory cytokines analyzed (p<0.05). CONCLUSION: Within the limits of this study, it can be concluded that MT in the presence of inflammation may modulate expression of pro-inflammatory cytokines, regardless of its effect on plasma corticosterone levels.

Chronic stress may modulate periodontal disease: a study in rats.

BACKGROUND: The present study aimed to evaluate whether chronic stress (CS) affects ligature-induced periodontal disease and to investigate the impact of CS on the mRNA levels of interleukin (IL)-1beta, -1 receptor antagonist, -6, and -10, interferon-gamma (IFN-gamma), receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoprotegerin in the gingival tissues of rats. METHODS: Sixty male Wistar rats were assigned randomly to three groups: G1 (control; non-ligated sites), G2 (periodontal disease), and G3 (periodontal disease associated with restraint stress for 12 hours/day for the entire study). After 30 days, all animals were sacrificed by decapitation. Blood samples were taken, and the concentrations of corticosterone and catecholamines were measured as biomarkers of CS. Marginal tissues around ligated and non-ligated teeth were harvested, and gene expression was assessed by quantitative polymerase chain reaction. Moreover, the area of bone loss (ABL) was determined histometrically. RESULTS: Data analysis showed that CS increased serum levels of stress biomarkers (P <0.05), ligature placement resulted in a significant ABL compared to non-ligated sites, CS significantly increased the amount of ABL in inflamed sites (P <0.001), and CS significantly increased mRNA levels of proinflammatory (IL-1beta and -6 and IFN-gamma) and anti-inflammatory (IL-10) cytokines and proresorptive factor (RANKL) in ligated sites (P <0.05). CONCLUSION: CS significantly increased bone loss resulting from ligature-induced periodontitis by a local increase in proinflammatory and proresorptive factors.

A systematic review of stress and psychological factors as possible risk factors for periodontal disease.

BACKGROUND: Clinical observations and epidemiologic studies suggest that some negative life events and psychological factors may contribute to an increased susceptibility to periodontal disease. The aim of the present study was to systematically review the evidence from case-control studies, cross-sectional studies, and prospective clinical trials reporting on the influence of stress and psychological factors on periodontal disease. The focused question addressed in this systematic review was whether the scientific evidence is enough to consider stress and psychological factors as risk factors for periodontal disease. METHODS: A literature search was conducted using two databases (MEDLINE and the Cochrane Oral Health Group specialist trials register) in addition to searching reference lists of original and review articles. The search strategy used was the combination of the terms: "stress," "periodontal disease," and "psychosocial disorders." Studies were selected if they were published in dental journals between January 1, 1990 and April 1, 2006; only human studies and studies with adults and middle-aged subjects were included. Suitable variables included control for the potential effect of confounding factors, adequate criteria to define periodontal disease, adequate criteria for establishing stress, and methodologic quality. Only English-language articles were considered, and unpublished data were not sought. Two reviewers independently extracted information regarding quality and study characteristics in duplicate. The studies were assessed regarding their methodologic characteristics, statistical analysis, characteristics of the periodontal outcome measures, and psychological measurements. RESULTS: Of the 58 articles identified in the search, 10 were excluded because they were reviews and 34 did not comply with the selection criteria. Fourteen articles (seven case-control studies, six cross-sectional studies, and one prospective clinical trial) were included in the analysis; their quality and main study characteristics were assessed according to the criteria preestablished in the protocol of the study. With regard to the results of the studies, 57.1% found a positive outcome between psychosocial factors/stress and periodontal disease, 28.5% observed a positive outcome for some characteristics and a negative outcome for others, and 14.2% found a negative outcome. CONCLUSIONS: Within the limitations of this systematic review, the majority of studies showed a positive relationship between stress/psychological factors and periodontal disease. However, in the future, well-designed and more representative studies should be considered to confirm these factors as a risk for periodontal disease.

Resveratrol Inhibits Periodontitis-Related Bone Loss in Rats Subjected to Cigarette Smoke Inhalation.

BACKGROUND: Alternative therapeutic approaches have been explored to modulate host response to periodontal disease. Knowledge of new strategies to treat periodontitis is particularly relevant in patients presenting augmented risk to periodontitis, such as smokers. The aim of this study is to investigate the impact of resveratrol (RESV) on progression of experimental periodontitis (EP) in the presence of cigarette smoke inhalation (CSI). METHODS: Rats were assigned to one of three groups: 1) CSI+RESV (n = 20); 2) CSI+placebo (n = 20); and 3) non-CSI (n = 20). CSI was initiated 1 week prior to initiation of RESV or placebo administration (systemically for 30 days) and was continued until the end of the study. EP was induced around the first mandibular and second maxillary molars using ligatures. Specimens from the mandible were processed for morphometric and microcomputed tomography examination of bone volume/levels. Gingival tissues surrounding mandibular molars were collected for quantification of interleukin (IL)-1ß, IL-4, IL-6, IL-17, and tumor necrosis factor-α using an assay system. Additional analyses of immunoinflammatory mediator performance (T-helper Type 17 [Th17]/Th2 and Th1/Th2 cell levels) were performed according to Th cell responses in gingival tissues. Gingival tissues of maxillary molars were subjected to real-time polymerase chain reaction for assessment of osteoprotegrin, runt-related transcription factor-2, receptor activator of nuclear factor-kappa B ligand (RANKL), sclerostin, and Dickkopf Wnt signaling pathway inhibitor 1 levels. RESULTS: Higher linear alveolar bone loss (ABL) and lower interradicular bone density were detected in ligated molars in the CSI+placebo group (P <0.05). IL-4 level was the highest, and Th17/Th2 levels were the lowest in RESV-treated rats compared with placebo rats (P <0.05). RESV reduced expression of messenger RNA for RANKL in animals receiving CSI (P <0.05). CONCLUSION: RESV inhibits EP and CSI-induced supporting ABL and has a beneficial effect on osteo-immunoinflammatory markers.

Salivary levels of calcium, phosphorus, potassium, albumin and correlation with serum biomarkers in hemodialysis patients.

OBJECTIVES: Evidences suggest that hemodialysis patients have reduced salivary flow and changes in the composition of salivary secretion. These changes may reflect local and systemic disorders. The objectives of this study were to compare the salivary levels of calcium (Ca), phosphorus (P), potassium (K) and albumin in hemodialysis patients and healthy subjects, and to investigate a possible correlation between their serum and salivary levels. DESIGN: A case-control study was conducted with 60 hemodialysis patients (HD group) and 37 systemically healthy individuals (control group). Stimulated saliva samples were collected for biochemical analysis (Ca, P, K and albumin). Serum data were collected in the HD group. Statistical analysis included t-test, Pearson correlation and simple linear regression. RESULTS: The HD group exhibited higher salivary levels of Ca, P, and albumin (p<0.05). There was a significant positive correlation between serum PTH and salivary phosphorus (r=0.342, p=0.009), and between serum PTH and salivary potassium (r=0.306, p=0.020). An increase of 100 pg/dL in serum PTH was associated with an elevation of salivary P levels (0.34 mg/dL, p=0.009), and salivary K levels (0.20 mmol/dL, p=0.02), in the HD group. CONCLUSIONS: The findings suggest that HD patients present increased levels of salivary components (Ca, P, and albumin), and changes commonly observed in HD patients, such as hyperparathyroidism, appear to have an influence on salivary composition.

Bone filling around titanium implants may benefit from smoking cessation: a histologic study in rats.

BACKGROUND: Although a harmful effect of smoking on titanium implants has been documented, only a few studies have investigated the benefits of smoking cessation. Thus, this study histologically investigated whether smoking cessation influences bone healing around titanium implants and comparatively evaluated temporary versus complete cessation protocols. METHODS: Sixty-six male Wistar rats were randomly assigned to one of four groups: control (N = 16); CSI, intermittent cigarette smoke inhalation (CSI) throughout the entire 150-day experiment (N = 17); P-CSI, CSI 83 days prior to implant placement (N = 17); or R-CSI, CSI for 83 days, cessation 7 days before and 21 weeks after implant placement, and return to CSI for 39 days (N = 16). The animals were sacrificed and the degree of bone-to-implant contact (BIC) and the bone area (BA) within the limits of the implant threads obtained for cortical (zone A) and cancellous bone (zone B). RESULTS: Intergroup analysis (Kruskal-Wallis test, alpha = 0.05) demonstrated a significant effect of CSI on BA (P <0.05) and that temporary or complete CSI cessation protocols resulted in values similar to those of the control group (P >0.05) 88.91% +/- 4.29%; 80.66% +/- 6.55%; 84.27% +/- 6.96%; 85.71% +/- 4.7% in zone A, and 51.28% +/- 6.49%; 38.69% +/- 10.78%; 48.87% +/- 8.47%; 49.47% +/- 8.04%; in zone B for groups CTRL, CSI, P-CSI, and R-CSI, respectively. CONCLUSION: Within the limits of the present investigation, temporary and complete CSI cessation reversed the effect of smoke exposure on bone healing around titanium implants in both cortical and cancellous bone.

Smoking cessation may present a positive impact on mandibular bone quality and periodontitis-related bone loss: a study in rats.

BACKGROUND: It has been previously shown that cigarette smoke inhalation (CSI) enhances bone loss in ligature-induced periodontitis. In this study, the hypothesis that the interruption of smoke exposure would reverse the impact of CSI on mandibular bone quality and periodontitis-related bone loss was tested. METHODS: Fifty-three Wistar rats were randomly assigned to one of the following groups: group 1: control, N = 16; group 2: 83 days of CSI prior to ligature placement, N = 17; or group 3: 90 days of CSI before and 60 days after ligature placement, N = 20. Animals were sacrificed 60 days after ligature placement, the jaws removed and immediately radiographed for photodensitometry analysis. Bone loss was histometrically evaluated. RESULTS: CSI did not affect unligated sites in either condition (P >0.05); however, smoke inhalation during the whole experimental period significantly enhanced bone loss in ligated teeth (P < 0.05). Moreover, similar levels of bone loss were observed for ligated teeth between the control and cessation groups (0.90 +/- 0.33 mm(2); 0.96 +/- 0.32 mm(2); 1.64 +/- 0.65 mm(2); groups 1, 2 and 3, respectively). Radiographically, continuous exposure to cigarette smoke promoted a significantly reduced bone density (1.74 +/- 0.38 aluminum equivalence [Al eq]; 1.74 +/- 0.14 Al eq; and 0.68 +/- 0.10 Al eq for groups 1, 2, and 3, respectively). CONCLUSIONS: Within the limits of the present investigation, it can be assumed that CSI may enhance bone loss in ligature-induced periodontitis, and negatively impact mandibular bone quality. Additionally, smoke exposure cessation seems to reverse its impact on mandibular bone, and, therefore, may be of clinical relevance.

Bone density around titanium implants may benefit from smoking cessation: a histologic study in rats.

PURPOSE: This study tested the hypothesis that interruption of cigarette smoke inhalation (CSI) would reverse its impact on bone quality around implants. MATERIALS AND METHODS: Sixty-nine rats were assigned to 1 of 4 groups. Group 1 (n = 16) was the control group; group 2 experienced CSI for the duration of the study (150 days); group 3 experienced CSI for 83 days prior to implant placement, until 7 days prior to implant placement, when CSI ceased; and for group 4, CSI exposure was temporarily halted from 7 days before implantation to 21 days afterward. Bone density (the proportion of mineralized bone in a 500-microm-wide zone lateral to the implant) was calculated for each specimen (mean +/- SD). RESULTS: In the cortical bone, a slight difference in bone density was noted between the groups (97.66% +/- 3.69% for group 1, 98.30% +/- 0.95% for group 2, 98.83% +/- 0.73% for group 3, and 98.11% +/- 1.14 for group 4; P > .05). In contrast, continuous exposure to cigarette smoke (group 2) significantly decreased density in the cancellous bone in comparison to the other groups (25.69% +/- 9.41% for group 1, 18.08% +/- 6.0% for group 2, 25.46% +/- 5.42 for group 3, and 26.20% +/- 6.77% for group 4; P < .05), with no significant differences between groups 1, 3, and 4 (P > .05). DISCUSSION: The results support the concept that the effects of cigarette consumption on dental implants may be reversible, and therefore suggest that smokers may realize satisfactory outcomes if they cease smoking, even temporarily. CONCLUSION: In conclusion, smoking may affect bone quality around titanium implants in cancellous bone, and cessation could result in a return toward to the levels of the control group.

Effects of a Mikania laevigata extract on bone resorption and RANKL expression during experimental periodontitis in rats.

OBJECTIVES: The Mikania laevigata extract (MLE) (popularly known in Brazil as "guaco") possesses anti-inflammatory properties. In the present study we tested the effects of MLE in a periodontitis experimental model in rats. We also investigated possible mechanisms underlying such effects. MATERIAL AND METHODS: Periodontal disease was induced by a ligature placed around the mandibular first molars of each animal. Male Wistar rats were divided into 4 groups: non-ligated animals treated with vehicle; non-ligated animals treated with MLE (10 mg/kg, daily); ligature-induced animals treated with vehicle and ligature-induced animals treated with MLE (10 mg/kg, daily). Thirty days after the induction of periodontal disease, the animals were euthanized and mandibles and gingival tissues removed for further analysis. RESULTS: Morphometric analysis of alveolar bone loss demonstrated that MLE-treated animals presented a decreased alveolar bone loss and a lower expression of the activator of nuclear factor-κB ligand (RANKL) measured by immunohistochemistry. Moreover, gingival tissues from the MLE-treated group showed decreased neutrophil migration myeloperoxidase (MPO) assay. CONCLUSIONS: These results indicate that MLE may be useful to control bone resorption during progression of experimental periodontitis in rats.

Cannabidiol decreases bone resorption by inhibiting RANK/RANKL expression and pro-inflammatory cytokines during experimental periodontitis in rats.

Cannabidiol (CBD) is a cannabinoid component from Cannabis sativa that does not induce psychotomimetic effects and possess anti-inflammatory properties. In the present study we tested the effects of CBD in a periodontitis experimental model in rats. We also investigated possible mechanisms underlying these effects. Periodontal disease was induced by a ligature placed around the mandible first molars of each animal. Male Wistar rats were divided into 3 groups: control animals; ligature-induced animals treated with vehicle and ligature-induced animals treated with CBD (5 mg/kg, daily). Thirty days after the induction of periodontal disease the animals were sacrificed and mandibles and gingival tissues removed for further analysis. Morphometrical analysis of alveolar bone loss demonstrated that CBD-treated animals presented a decreased alveolar bone loss and a lower expression of the activator of nuclear factor-kappaB ligand RANKL/RANK. Moreover, gingival tissues from the CBD-treated group showed decreased neutrophil migration (MPO assay) associated with lower interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha production. These results indicate that CBD may be useful to control bone resorption during progression of experimental periodontitis in rats.

Direct capping of human pulps with a dentin bonding system and calcium hydroxide: an immunohistochemical analysis.

Pulp capping is a treatment where a protective agent is applied to an exposed pulp to allow the maintenance of its vitality and function. The present study analyzed the immunohistochemical expression of fibronectin and type III collagen in human dental pulps submitted to direct pulp capping with calcium hydroxide [Ca(OH)2] or the Single Bond adhesive system (SBAS). The results demonstrated that both proteins were not expressed in the SBAS group, although in the group capped with Ca(OH)2 a diffuse labeling in the extracellular matrix was initially observed, followed by a late expression in the odontoblast-like layer and beneath the dentin bridge. It seems that application of adhesive systems in direct contact with healthy pulps will not lead to expression of proteins that are believed to be essential for pulpal repair. Moreover, Ca(OH)2 showed good biocompatibility properties with the dental pulp tissue, inducing the expression of reparative molecules, and therefore remains the material of choice for the treatment of accidental pulp exposures.

Effects of a Mikania laevigata extract on bone resorption and RANKL expression during experimental periodontitis in rats

OBJECTIVES: The Mikania laevigata extract (MLE) (popularly known in Brazil as "guaco") possesses anti-inflammatory properties. In the present study we tested the effects of MLE in a periodontitis experimental model in rats. We also investigated possible mechanisms underlying such effects. MATERIAL AND METHODS: Periodontal disease was induced by a ligature placed around the mandibular first molars of each animal. Male Wistar rats were divided into 4 groups: non-ligated animals treated with vehicle; non-ligated animals treated with MLE (10 mg/kg, daily); ligature-induced animals treated with vehicle and ligature-induced animals treated with MLE (10 mg/kg, daily). Thirty days after the induction of periodontal disease, the animals were euthanized and mandibles and gingival tissues removed for further analysis. RESULTS: Morphometric analysis of alveolar bone loss demonstrated that MLE-treated animals presented a decreased alveolar bone loss and a lower expression of the activator of nuclear factor-κB ligand (RANKL) measured by immunohistochemistry. Moreover, gingival tissues from the MLE-treated group showed decreased neutrophil migration myeloperoxidase (MPO) assay. CONCLUSIONS: These results indicate that MLE may be useful to control bone resorption during progression of experimental periodontitis in rats.