The impact of vitamin D on clinical parameters and bone turnover biomarkers in ligature-induced periodontitis: An experimental study in rats.

Objectives and Background: Vitamin D has been associated with an increased risk of tooth loss and the severity of periodontal diseases. This study aimed to evaluate the effect of vitamin D on the clinical, radiographic, and serum level changes of bone turnover biomarkers in ligature-induced periodontitis. Methods: A total of 28 rats were included in this study and divided into test groups: Vitamin D supplement (VS), Vitamin D deficient (VD), and control (CG). Ligature-induced periodontal tissue destruction was performed and kept for 21 days. Clinical attachment and radiographic changes were recorded, and serum samples were tested for Osteoprotegerin (OPG), Dickkopf-1 (DKK1), Sclerostin (SOST), and Fibroblast growth factor 23 (FGF23) on the initial and final day of the study. Results: Groups that were made VD exhibited a more significant amount of clinical attachment loss (1.05 ± 0.50 mm) compared to the CG (0.83 ± 0.14 mm) and VS group (0.60 ± 0.13 mm), showing significant differences (p < 0.05). The radiographic alveolar bone loss amount was greater in the VD group compared to the other groups. For serum level assessment, the VD groups also exhibited a statistically significant reduction in the levels of OPG. They showed higher concentrations of DKK1, SOST, and FGF23 than other groups, with significant differences (p < 0.05). Conclusion: The results revealed that Vitamin D may play a role in the progression of periodontal disease. It was found to affect both clinical parameters and bone turnover biomarkers, suggesting its potential impact on the disease process.

Effect of osteoarthritis on alveolar bone loss in experimental periodontitis in rats.

BACKGROUND: There is scarce information about the relationship between periodontal disease and osteoarthritis. This study investigated the effect of surgically induced osteoarthritis on alveolar bone loss in experimental periodontitis in rats. METHODS: 12 rats were divided into test and control groups. On day 1, the animals were anaesthetized, and silk ligatures were ligated around 6 maxillary posterior teeth in each animal from both groups. Surgical induction of osteoarthritis was performed on the left knees in the test group. No knee surgeries were performed in the control group. The ligatures were kept in place for 30 days, at which time the animals were euthanatized, and the maxillae and knee joints were harvested and processed for histological analysis. The alveolar bone loss was assessed using a zoom stereomicroscope. RESULTS: The knee joint histologic sections of the control group showed normal joint features, whereas in the test group there were substantial changes typical of osteoarthritis, including wide joint spaces, prominent monocytic infiltration of the synovium, invasion of periarticular bone, and decreased chondrocyte density. Comparison of the bone height between the groups showed a significantly higher bone loss in the test than in the control group The marginal mean bone height, adjusted for covariates and the intraclass correlation between sites, was 1.19 and 0.78 mm in the test and control groups, respectively (p < .0001). CONCLUSIONS: Surgically induced osteoarthritis leads to greater alveolar bone loss in the experimental periodontitis model in rats.

The influence of cigarette smoking on gingival bleeding and serum concentrations of haptoglobin and alpha 1-antitrypsin.

The objectives of this study were to evaluate the influence of cigarette smoking on gingival bleeding and serum concentrations of cotinine, haptoglobin, and alpha 1-antitrypsin in Malaysian smokers. A total of 197 male smokers and nonsmokers were recruited for this study. Plaque index, bleeding on probing (BOP), and levels of serum cotinine, haptoglobin, and alpha 1-antitrypsin were evaluated. The data were analyzed using SPSS version 20.0, with the significance level set at α ≤ 0.05. Linear regression analyses were performed. The mean cigarette consumption per day was 13.39 ± 5.75 cigarettes; the mean duration was 16.03 ± 8.78 years. Relatively low BOP values (26.05 ± 1.48) and moderate plaque indexes (51.35 ± 11.27) were found. The levels of serum cotinine (106.9 ± 30.71 ng/dL), haptoglobin (76.04 ± 52.48 mg/dL), and alpha 1-antitrypsin (141.90 ± 18.40 mg/dL) were significantly higher in smokers compared to non-smokers. Multiple logistic regression models for all variables and smokers demonstrated observed differences between BOP, the number of cigarettes per day, and duration of smoking, while serum cotinine, haptoglobin and alpha-1 antitrypsin levels showed no significant differences. Duration of smoking (years) and the cotinine level in serum showed a significant correlation with plaque index. The present analysis demonstrated that the duration of smoking in years, but not the number of cigarettes smoked per day, was associated with reduced gingival bleeding in smokers.

In-vivo effect of andrographolide on alveolar bone resorption induced by Porphyromonas gingivalis and its relation with antioxidant enzymes.

Alveolar bone resorption is one of the most important facts in denture construction. Porphyromonas gingivalis (Pg) causes alveolar bone resorption, and morphologic measurements are the most frequent methods to identify bone resorption in periodontal studies. This study has aimed at evaluating the effect of Andrographolide (AND) on alveolar bone resorption in rats induced by Pg. 24 healthy male Sprague Dawley rats were divided into four groups as follows: normal control group and three experimental groups challenged orally with Pg ATCC 33277 five times a week supplemented with 20 mg/kg and 10 mg/kg of AND for twelve weeks. Alveolar bones of the left and right sides of the mandible were assessed by a morphometric method. The bone level, that is, the distance from the alveolar bone crest to cementumenamel junction (CEJ), was measured using 6.1 : 1 zoom stereomicroscope and software. AND reduced the effect of Pg on alveolar bone resorption and decreased the serum levels of Hexanoyl-Lysine (HEL); furthermore the reduced glutathione/oxidised glutathione (GSH/GSSG) ratio in AND treated groups (10 and 20 mg/kg) significantly increased when compared with the Pg group (P < 0.05). We can conclude that AND suppresses alveolar bone resorption caused by Pg in rats.

Environmental tobacco smoke and stress as risk factors for miscarriage and preterm births.

BACKGROUND: Exposure of pregnant women to environmental tobacco smoke has been shown to be associated with low birth weight. Many studies have suggested that stress have a role in the etiology of preterm birth. AIMS: This study carried out from June 2008 to March 2009 to find the relation between environmental tobacco smoke, stress and miscarriage and preterm births. METHODS: A total of 33 subjects consisted of multiparous pregnant women that were in their early third trimester were chosen for this investigation. Subjects were divided into test group women with adverse pregnancy outcome, control group women with successful pregnancy. Four ml of unstimulated whole saliva were collected. The concentrations of cotinine and cortisol were evaluated using commercially available ELISA kit. RESULTS: Pregnancies in which the average standardized cortisol during history of previous miscarriage(s) which occurred within 6th-27th week or/and history of preterm labor which occurred within 28th-36th weeks of gestation, demonstrated higher cortisol level (1.0201 ± 0.1855 ng/ml) compared to control group 0.9757 ± 0.2860 ng/ml (P = 0.323); statistical analysis showed no significant differences. Women of control group were more likely to be environmental tobacco smoke exposed (1.2714 ± 1.7639 ng/ml) than women with miscarriage and preterm births (0.9889 ± 0.5498 ng/ml). CONCLUSION: The results from this primarily study demonstrated no association between cotinine, cortisol, miscarriage and preterm births.