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Background: Sclerostin, a glycoprotein, plays a key role in regulating bone mass. In this study, sclerostin levels in the gingival crevicular fluid (GCF) were assessed in patients with Stage III Grade C generalized periodontitis (SIII-GC) and Stage III Grade B generalized periodontitis (SIII-GB). Methods: This cross-sectional study included 30 participants divided equally into three groups: group I (gingival health), group II (SIII-GC), and group III (SIII-GB). Clinical periodontal parameters like plaque index (PI), gingival bleeding index (GBI), probing pocket depth (PD), and clinical attachment level (CAL) were recorded. A sandwich ELISA was used to determine the sclerostin levels in GCF samples. One-way ANOVA and post hoc Tukey tests were used to analyze the clinical parameters and GCF sclerostin levels. The association between GCF sclerostin levels and periodontal parameters was assessed using Pearson's correlation coefficient (r). Results: Patients in groups II and III had much higher sclerostin levels in their GCF than in group I (P≤0.05). In contrast, no significant difference in sclerostin levels was observed between the two diseased conditions (P=0.841). Concerning periodontal parameters, a statistically significant difference was observed between the three groups. There was a positive correlation between the periodontal clinical parameters and the expression levels of sclerostin in GCF (P≤0.05). Conclusion: Increased expression of sclerostin in GCF in patients with periodontitis indicated that it could be considered a reliable biomarker of periodontal disease activity.
RESUMO
Aim: The present study aimed to estimate the serum procalcitonin (PCT) levels in periodontally healthy individuals and chronic periodontitis patients with Type II diabetes mellitus (DM). Materials and Methods: Forty-five male subjects aged 25-60 years were enrolled in the study and grouped as Group I (healthy), Group II (chronic periodontitis), and Group III (chronic periodontitis with Type II DM). Clinical parameters (dental plaque scores, bleeding scores, probing pocket depth, and loss of attachment) and glycemic parameters (random blood sugar and glycated hemoglobin levels) were recorded. Serum procalcitonin levels were analyzed using Raybio® Human Procalcitonin Enzyme-Linked Immunosorbent Assay kit using the sandwich technique. All the data obtained were tabulated and analyzed using SYSTAT 12 statistical software. Kruskal-Wallis test was applied to compare the mean scores between the three study groups, and Spearman's ρ correlation coefficient was used to find out the association. Results: Serum procalcitonin levels were markedly increased in periodontitis group when compared to the healthy group. The mean serum levels of procalcitonin in Group I, Group II, and Group III were 22.52 pg/ml, 64.23 pg/ml, and 185.86 pg/ml, respectively. The variation in the procalcitonin levels was statistically significant at P < 0.001. Conclusion: The expression of procalcitonin in serum was increased to eightfold in the periodontitis group with diabetes in comparison to the healthy group, which shows that periodontal disease can cause the release of procalcitonin.
RESUMO
BACKGROUND: Periodontitis is a highly prevalent inflammatory disease affecting the periodontium that results from an imbalance between periodontopathogens and host mechanisms. Continuous progression of the disease may lead to tissue and bone destruction, eventually resulting in tooth loss. The extent of bone loss depends on the dysregulated host immune response. Various host-elicited molecules play a major role in disease progression. The discovery of the glycoprotein sclerostin and its role as a regulator of bone mass has led to a better understanding of bone metabolism. HIGHLIGHT: Sclerostin, which is primarily expressed by osteocytes, is a negative regulator of bone formation. It is a potent antagonist of the canonical Wingless-related integration site (Wnt) pathway, which is actively involved in bone homeostasis. Sclerostin is known to stimulate bone resorption by altering the osteoprotegerin (OPG)/receptor activator of nuclear factor kappa- ß ligand (RANKL) balance. Additionally, in periodontitis, activation of the inflammatory cascade also increases the synthesis of sclerostin. CONCLUSION: The recently discovered sclerostin antibody has emerged as a positive therapeutic tool for the treatment of metabolic bone diseases. It has been reported to improve bone strength, bone formation, osseointegration around implants and lower the risk of bone fractures in various animal and human models. This review describes the properties and action of sclerostin, its role in periodontal diseases, and the advent and efficacy of sclerostin antibodies.
