Resistin as potential biomarker for chronic periodontitis: A systematic review and meta-analysis.

OBJECTIVES: To determine the serum and gingival crevicular fluid (GCF) levels of resistin between individuals with chronic periodontitis (CP) and those without CP, and to evaluate the role of resistin in CP. MATERIALS AND METHODS: The addressed focused question was "Is there a difference in the resistin levels between individuals with CP and those without CP?" four electronic databases: Medline, PubMed (National Institutes of Health, Bethesda), EMBASE, and Science direct databases from 1977 up to March 2016 for appropriate articles addressing the focused question. EMBASE and Medline were accessed using OVID interface which facilitated simultaneous search of text words, MeSH or Emtree. Unpublished studies (gray literature) were identified by searching the Open-GRAY database and references of the included studies (cross referencing) were performed to obtain new studies. In-vitro studies, animal studies, studies that reported levels of other cytokines but not resistin, letters to the editor and review papers were excluded. RESULTS: Ten studies were included. Nine studies compared resistin levels between CP and periodontally healthy (H) individuals and reported higher mean serum and GCF levels of resistin in CP patients than the H controls. Two studies showed comparable resistin levels from GCF and serum between diabetes mellitus with CP (DMCP) and CP groups. Three studies included obese subjects and showed comparable serum and GCF resistin levels between obese subjects with CP (OBCP) and CP subjects. CONCLUSIONS: CP patients were presented with elevated levels of GCF or serum resistin as compared with H individuals. Resistin modulates inflammation in chronic periodontal disease and may be used as surrogate measure to identify subjects at risk for periodontitis. Resistin levels in patients with CP and systemic inflammatory disorders such as diabetes, obesity, or rheumatoid arthritis was not significantly higher than the levels in patients with only CP.

Aberrant proteins featured in the saliva of habitual betel quid chewers: an indication of early oral premalignancy?

Prolonged chewing of betel quid is known to cause oral diseases, including cancer. The present study was performed to screen for aberrant proteins in the saliva of habitual betel quid chewers compared to nonchewers. Saliva of female subjects (n = 10) who had been chewing betel quid for more than 20 years and nonbetel quid chewers (n = 10) of the same gender and range of age was analyzed by gel-based proteomics. Increased structural microheterogeneity of saliva haptoglobin beta chains indicated by shifts of focused spots similar to that earlier reported in patients with oral squamous cell carcinoma, and their relatively higher abundance compared to nonbetel quid chewers, were detected in saliva protein profiles of all chewers. In addition, the majority of the betel quid chewers also showed significant higher abundance of hemopexin, alpha-1B glycoprotein, alpha1-antitrypsin, complement C3, and transthyretin. These proteins had previously been associated with several different cancers. Our data demonstrated different forms of protein aberration in the saliva of betel quid chewers, which may be indicative of early oral precancerous conditions.

Scanning Electron Microscopic study of Piper betle L. leaves extract effect against Streptococcus mutans ATCC 25175

INTRODUCTION: Previous studies have shown that Piper betle L. leaves extract inhibits the adherence of Streptococcus mutans to glass surface, suggesting its potential role in controlling dental plaque development. OBJECTIVES: In this study, the effect of the Piper betle L. extract towards S. mutans (with/without sucrose) using scanning electron microscopy (SEM) and on partially purifed cell-associated glucosyltransferase activity were determined. MATERIAL AND METHODS: S. mutans were allowed to adhere to glass beads suspended in 6 different Brain Heart Infusion broths [without sucrose; with sucrose; without sucrose containing the extract (2 mg mL-1 and 4 mg mL-1); with sucrose containing the extract (2 mg mL-1 and 4 mg mL-1)]. Positive control was 0.12 percent chlorhexidine. The glass beads were later processed for SEM viewing. Cell surface area and appearance and, cell population of S. mutans adhering to the glass beads were determined upon viewing using the SEM. The glucosyltransferase activity (with/without extract) was also determined. One- and two-way ANOVA were used accordingly. RESULTS: It was found that sucrose increased adherence and cell surface area of S. mutans (p<0.001). S. mutans adhering to 100 µm² glass surfaces (with/without sucrose) exhibited reduced cell surface area, fuffy extracellular appearance and cell population in the presence of the Piper betle L. leaves extract. It was also found that the extract inhibited glucosyltransferase activity and its inhibition at 2.5 mg mL-1 corresponded to that of 0.12 percent chlorhexidine. At 4 mg mL-1 of the extract, the glucosyltransferase activity was undetectable and despite that, bacterial cells still demonstrated adherence capacity. CONCLUSION: The SEM analysis confrmed the inhibitory effects of the Piper betle L. leaves extract towards cell adherence, cell growth and extracellular polysaccharide formation of S. mutans visually. In bacterial cell adherence, other factors besides glucosyltransferase are involved.