Periostin, an extracellular matrix protein functioning as an important structural mediator and adhesion molecule, has been shown to be an important regulator of connective tissue integrity. This study aimed to evaluate the levels of periostin in chronic periodontitis (CP) and aggressive periodontitis (AgP) compared to non-periodontitis (NP). Individuals were submitted to gingival crevicular fluid (GCF) and saliva sampling. Periodontal examination consisted of plaque index (PI), gingival index (GI), probing depth (PD), bleeding on probing (BOP), and clinical attachment level (CAL) measurements. Assays for periostin were performed by an enzyme-linked immunosorbent assay. Periodontitis patients presented more severe clinical indices compared to the NP group (p < 0.001). The mean GCF level of periostin was lowest in the AgP group as compared to the other groups and was lower in the CP group as compared to the NP group (p < 0.001). Increased levels of periostin were observed in the saliva of patients with AgP as compared to the CP and NP groups (p < 0.05). There was a negative relationship between GCF periostin levels and clinical parameters (p < 0.01), whereas a positive correlation was observed between salivary periostin levels and full-mouth GI and CAL scores (p < 0.01). To our knowledge, this is the first report investigating periostin levels in GCF and saliva in aggressive periodontitis. The results suggest that subjects with CP and AgP exhibit a different periostin profile. Periostin in GCF may have a protective role against periodontal disease. Furthermore, salivary periostin concentrations may have a promising diagnostic potential for the aggressive forms of periodontal disease.

Background:The inflammasome modulates the release of key proinflammatory cytokines associated with periodontal disease pathogenesis. The aim of this study was to evaluate the expression of proteins that regulate the inflammasome, namely pyrin domain-only proteins (POPs), caspase activation recruitment domain (CARD)-only proteins, and tripartite motif-containing (TRIM) proteins, in periodontal diseases.

The aim of this study was to evaluate the efficacy of the anti-inflammatory effects of propolis on the systemic and local effects on experimental periodontitis and diabetes. Fifty-six Wistar rats were divided into seven groups: (1) negative-control (NC), (2) periodontitis (P), (3) diabetes (D), (4) diabetes+periodontitis (DP), (5) periodontitis+propolis (P-Pro), (6) diabetes+propolis (D-Pro), and (7) diabetes+periodontitis+propolis (DP-Pro). Periodontitis was induced by ligature placement and diabetes was induced by streptozotocin injection. Propolis (Pro) was administrated by oral gavage (100 mg/kg/day). On day 21, plasma was obtained for analysis and alveolar bone level was evaluated using histomorphometric analysis. Compared to NC the final blood glucose levels for D-Pro was not significantly different (P=.052), however, D, DP, and DP-Pro were significantly different. There were no statistically significant differences in blood glucose concentrations between P and P-Pro, between D and D-Pro, and between DP and DP-Pro. All groups showed significantly more alveolar bone loss compared with NC. A significant difference in bone loss was found between P and P-Pro, and DP and DP-Pro, however there was no difference between D and D-Pro. Plasma interleukin 1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and matrix metalloproteinase-8 (MMP-8) levels were not significantly different among groups. In conclusion, propolis reduced fasting blood glucose levels in diabetes. In addition, propolis might be beneficial as an adjunct treatment of diabetes associated periodontitis and periodontitis without diabetes.

Background Caspases are key mediators of apoptosis. Caspase‐8 mediates extrinsic, and caspase‐9 initiates the intrinsic pathway of apoptosis. Apoptosis Inducing Factor (AIF), a mitochondrial proapoptotic protein, mediates cell death by a caspase‐independent process. Because apoptosis is involved in periodontal disease, this study evaluated caspase‐8, ‐9, and AIF in periodontal disease. Methods Twenty periodontally healthy volunteers (Group Healthy), 20 patients with generalized aggressive periodontitis (Group AgP), and 20 patients with generalized chronic periodontitis (Group CP) were included in this study. Levels of caspase‐8, ‐9, and AIF were evaluated in gingival crevicular fluid (GCF) of all participants via enzyme‐linked immunosorbent assays. Results AIF was significantly higher in the AgP (P = 0.07) and CP groups (P = 0.01) than the Healthy group, and similar to the CP and AgP groups (P > 0.05). Caspase‐8 was significantly higher in the CP and Healthy groups than the AgP group (P = 0.00), and similar between Healthy and CP groups (P > 0.05). Caspase‐9 was significantly higher in the AgP group than the Healthy group (P = 0.01), and similar between Healthy and CP groups (P > 0.05). Conclusions The mitochondrial‐centered intrinsic pathway involving caspase‐9 and AIF, and the extrinsic pathway involving caspase‐8 are significant for aggressive periodontitis. The intrinsic pathway involving caspase‐independent AIF is also significant for chronic periodontitis.

Background: Studies evaluating the relationship between oral health status and obesity have provided conflicting data. Therefore, there is a great need to investigate and clarify the possible connection in a comprehensive sample. Aims: To assess the relationship of obesity and oral health status among children and adolescents aged 6 to 17 yearsold. Study Design: Cross-sectional study. Methods: Data were obtained from 4,534 children and adolescents (2,018 boys and 2,516 girls). Questionnaires were sent home prior to examination; afterwards, anthropometric and dental data were collected from participants. Community Periodontal Index (CPI) and number of decayed, missing, and filled teeth in the permanent dentition (DMFT), and deciduous dentition (dmft) index were used to measure oral health status. Height, body weight, body mass index (BMI), waist circumference (WC), and body fat percentage were analyzed. Results: For DMFT scores, healthy (score=0) girls and boys had significantly higher BMI and WC values than unhealthy (score>1) girls and boys (p<0.05). Healthy girls had higher fat percentage values than unhealthy girls (p<0.05). In terms of CPI scores, healthy boys had lower BMI and WC values than unhealthy boys (p<0.05). According to multiple binary logistic regression results for model 1, BMI predicted DMFT scores in both genders but CPI scores only in boys. No beverage consumption predicted DMFT scores in boys, while milk consumption predicted DMFT scores in girls. No meal skipping predicted CPI scores in boys. For model 2, WC predicted DMFT scores in both genders and CPI scores only in boys. Milk consumption predicted DMFT scores only in girls. No meal skipping predicted CPI scores for both gender (p<0.05). According to DMFT, there were significant differences between the frequencies of the BMI groups (normal weight, overweight and obese) at the age of 7 (girls only), 9, 10, and 16 (boys only) years and overall (only girls) (p<0.05). According to CPI, significant differences between the frequencies of the BMI groups at the age of 16 (boys only) and 17 (girls only) were seen (p<0.05). Conclusion: Periodontal and dental status appears to correlate with nutritional habits and obesity. Obesity and dental/periodontal diseases are multifactorial diseases that follow similar risk patterns and develop from an interaction between chronic conditions originating early in life. It is important for all health professionals to educate patients at risk about the progression of periodontal and dental diseases and the importance of proper oral hygiene.

Within the limits of this study, salivary/GCF cortisol and DHEA levels were suggested to be related with more severe and aggressive forms of periodontal disease.

The purpose of this clinical study is to comparatively investigate the interleukin-33 (IL-33) levels in gingival crevicular fluid (GCF), saliva and plasma of patients with periodontal disease as well as periodontally healthy subjects and the association between these levels and clinical parameters. GCF, saliva and plasma samples were collected from systemically healthy, non-smoker chronic periodontitis patients (CP group, n = 20), gingivitis patients (G group, n = 20) and periodontally healthy control groups (H group, n = 20). Full-mouth clinical periodontal parameters were also recorded. IL-33 levels were determined by ELISA. The total amount of GCF IL-33 was greater in the G and CP groups compared to the H group (p < 0.05). The GCF IL-33 concentration was significantly lower in the CP group than in the H and G groups (p < 0.001). Salivary or plasma IL-33 levels were similar in the study groups. The total amount of GCF IL-33 was positively correlated with the GI, PI and BOP (%) (p < 0.05). Considering the present findings, the increase in total amounts of GCF IL-33 may have a role in the pathogenesis of periodontal disease.

These finding suggest that colchicine has a prophylactic potential for the prevention of periodontal tissue destruction through anti-inflammatory, anti-oxidative, anti-apoptotic, and bone-protective effects.