Higher expression of Th1/Th2-related cytokines in the intestine of Wistar rats with ligature-induced periodontitis.

OBJECTIVE: This study aimed to investigate the impact of ligature-induced periodontitis (LIP) on histopathological and immunological outcomes in the colon of Wistar rats. BACKGROUND: It has been repeatedly shown that inflammatory bowel disease (IBD) patients are at higher risk of developing periodontitis and presenting worse oral health than non-IBD patients. However, whether the chronic inflammatory process around teeth contributes to the pathophysiology of IBD needs to be further explored. MATERIALS AND METHODS: Thirteen Wistar rats were allocated into LIP (n = 7) and controls (n = 6). Half of the colon was processed for histopathological analyses and immunohistochemical (CD45); the other half was homogenized for immunological analyses. Periodontal destruction was confirmed by measuring the distance from the cementum-enamel junction to the mandible's apical position of the mesial interproximal bone. The immunological analyses were performed with the Bio-Plex Th1/Th2 assay. RESULTS: There was a significantly higher interproximal bone loss in LIP compared to controls. The LIP group showed a moderate infiltrate of inflammatory cells, predominantly mononucleated cells in the intestinal tissues. There was significantly higher expression of GM-CSF, IFN-γ, IL-1α, IL-1ß, IL-2, IL-4, IL-5, IL-10, IL-12 (p70), IL-13, and TNF-α in the intestinal tissues of LIP group compared to controls. CONCLUSION: Ligature-induced periodontitis was associated with an overexpression of Th1/Th2-related cytokines in the colon of Wistar rats.

Gingival recession treatment with enamel matrix derivative associated with coronally advanced flap and subepithelial connective tissue graft: a split-mouth randomized controlled clinical trial with molecular evaluation.

OBJECTIVES: The goal of this study was to evaluate the impact of enamel matrix derivative (EMD) on periodontal healing after root coverage (RC) surgery, involving CAF in combination with SCTG, and to assess the molecular profile, verifying the inflammation level in early stage (1 and 2 weeks). MATERIALS AND METHODS: Thirty-two recessions (RT1) were submitted to periodontal surgery with (test) or without (control) EMD. The clinical parameters analyzed on the day of surgery and 6 months after the surgical procedure were as follows: recession height and width, keratinized tissue height, percentual root coverage, and the gingival thickness of keratinized tissue. Moreover, the main inflammatory biomarkers and growth factors (IL-1ß, IL-6, IL-8, FGF, MIP-1α and ß, PDGF, TNF-α, and VEGF) were evaluated at baseline, 7, and 14 days after procedures. RESULTS: The average root coverage was significantly higher in the test group as compared to the control group (86% vs. 66%, p = 0.008). The test side had significantly lesser final RH compared to the control side (p = 0.01). Also, there was a significant reduction of RW in both groups, with more significant results in the test group. KTH and GT were not significantly different at any time and group. After 14 days, the immunological analysis showed an increase of VEGF (p = 0.03) on the test group compared to the control side. CONCLUSION: The use of EMD in RC surgeries resulted in a significantly higher RC, as well as a significant increase in VEGF expression, suggesting that EMD may contribute to the angiogenic and healing process. CLINICAL RELEVANCE: EMD provided better results in root coverage treatment when associated with CAF and SCTG, beyond a greater releasing of angiogenic growth factor (VEGF), which enhanced the result.

Immunological Traits of Patients with Coexistent Inflammatory Bowel Disease and Periodontal Disease: A Systematic Review.

This systematic review assessed studies that evaluated the immunological traits of patients with both inflammatory bowel disease (IBD) and periodontal disease. An electronic search for literature was conducted on PubMed, Embase, Scopus, Cochrane and Web of Science. Studies that evaluated the immunological response in patients with IBD and periodontal disease were considered eligible for inclusion. A total of 6 cross-sectional studies of 275 patients were included. Immunological analyses were performed in gingival crevicular fluid, saliva, serum, intestinal and gingival biopsies. Four studies identified that the presence of IBD and periodontal disease was associated with higher levels of prostaglandin E2, aMMP8, IL-18 and S100A12, respectively, when compared to patients without the coexistence of both diseases. Furthermore, another study identified higher aMMP-8 levels with increasing severity of periodontitis in Crohn's disease patients. The quality of overall evidence ranged from high to low due to the observational nature of contributing studies. The coexistence of IBD and periodontal disease seems to be associated with a more responsive inflammatory reaction compared with individuals having one or the other. More randomized controlled studies evaluating the coexistence of IBD and periodontitis are required to better explore the immunological interplay between them.

Impact of non-surgical periodontal treatment on salivary expression of cytokines related to bone metabolism.

We aimed to evaluate the impact of non-surgical periodontal treatment on the salivary expression of leptin, TNF-α, sclerostin, parathyroid hormone, osteoprotegerin, osteopontin, osteocalcin, IL-6, IL-1ß and fibroblast growth factor 23 in patients with chronic periodontitis after 1 year of follow-up. Fifteen patients with chronic periodontitis (56.0 ± SD 9.6 years) and 15 subjects with gingivitis (39.7 ± SD 4.4 years) were included in the study. Clinical periodontal parameters, such as probing pocket depth (PPD), clinical attachment level (CAL), % of plaque and bleeding on probing (BOP) were evaluated, and non-stimulated whole saliva was collected from all patients before periodontal treatment and after 1 year of follow-up. A bead-based multiplex assay measured cytokines. In the chronic periodontitis group, periodontal treatment significantly improved clinical parameters and reduced the salivary levels of IL-1ß, leptin and TNF-α (p = 0.002, 0.007 and 0.015, respectively). In the gingivitis group, there were also significant improvements in the mean patient %BOP, % Plaque, CAL and PPD. However, there were no significant changes in the cytokine's salivary levels. In conclusion, chronic periodontitis patients showed a significant reduction in the salivary levels of leptin, TNF-α and IL-1ß 1 year after periodontal treatment and a significant improvement in their clinical periodontal parameters suggesting that periodontal treatment alone can downregulate important cytokines associated with bone metabolism.

Nitric oxide and oral diseases: can we talk about it?

Nitric oxide (NO) is a short-lived intercellular messenger with multiple biological implications, such as regulation of blood pressure, inhibition of platelet adhesion and aggregation, bacterial-challenge and cytokine stimulation, and regulation of mineralized tissue function. NO synthase (NOS) catalyses the conversion of cationic amino acid L-arginine to L-citrulline and NO. Recently there is an increasing interest in the role of NO in the physiopathology of periodontal disease (PD). PD is a chronic inflammatory disease of the attachment structures of the teeth, which is found in 40-50% of most adult populations worldwide and may result in tooth loss. The potential sources of NO in periodontum are inflammatory cells, keratinocytes, fibroblasts, osteoclastics and blood vessels. Etiological periodontitis factors, such as inflammatory cytokines and periodontopathogens are evolved in enhanced NO levels, which may be part of a nonspecific natural defense mechanism or may lead to periodontal damage. This review gives detail of recent research data focusing on NO bioavailability and its involvement in periodontitis pathogenesis and the modulation of NO for better control of this disease.