Trigeminal neurons control immune-bone cell interaction and metabolism in apical periodontitis.

Apical periodontitis (AP) is an inflammatory disease occurring following tooth infection with distinct osteolytic activity. Despite increasing evidence that sensory neurons participate in regulation of non-neuronal cells, their role in the development of AP is largely unknown. We hypothesized that trigeminal ganglia (TG) Nav1.8+ nociceptors regulate bone metabolism changes in response to AP. A selective ablation of nociceptive neurons in Nav1.8Cre/Diphtheria toxin A (DTA)Lox mouse line was used to evaluate the development and progression of AP using murine model of infection-induced AP. Ablation of Nav1.8+ nociceptors had earlier progression of AP with larger osteolytic lesions. Immunohistochemical and RNAscope analyses demonstrated greater number of macrophages, T-cells, osteoclast and osteoblast precursors and an increased RANKL:OPG ratio at earlier time points among Nav1.8Cre/ DTALox mice. There was an increased expression of IL-1α and IL-6 within lesions of nociceptor-ablated mice. Further, co-culture experiments demonstrated that TG neurons promoted osteoblast mineralization and inhibited osteoclastic function. The findings suggest that TG Nav1.8+ neurons contribute to modulation of the AP development by delaying the influx of immune cells, promoting osteoblastic differentiation, and decreasing osteoclastic activities. This newly uncovered mechanism could become a therapeutic strategy for the treatment of AP and minimize the persistence of osteolytic lesions in refractory cases.

Capsaicin-sensitive Innervation Modulates the Development of Apical Periodontitis.

INTRODUCTION: Nociceptive neurons play a critical role in the detection of stimuli evoking actual or potential tissue injury. In addition, they are involved in neurogenic inflammation by the peripheral release of neuropeptides such as calcitonin gene-related peptide (CGRP). The dental pulp and periradicular tissues are innervated by capsaicin-sensitive neurons known to release CGRP. However, the role of these capsaicin-sensitive neurons in the development of apical periodontitis is largely unknown. The aim of this study was to evaluate the contribution of peptidergic neurons to the development of apical periodontitis. METHODS: Neonatal Sprague-Dawley rats were injected with vehicle (control group) or a single subcutaneous capsaicin dose to cause the selective ablation of peptidergic neurons (neonatal capsaicin group). Ablation of capsaicin-sensitive neurons was verified with confocal microscopy, capsaicin-induced eye-wipe nocifensive behavior test, and by measurement of immunoreactive CGRP levels in the dental pulp. Five weeks after ablation, standardized pulp exposures were made in the mandibular left first molars. Mandibles were harvested at 7, 14, 21, and 28 days after pulp exposure and imaged with micro-computed tomography (µCT) to quantify apical lesion volume. Data were analyzed by using 2-way ANOVA analysis with Bonferroni post hoc test. RESULTS: Rats in the control group displayed a robust capsaicin-induced nocifensive behavior, which was nearly abolished in the neonatal capsaicin group. In addition, the neonatal capsaicin group showed a significant depletion of susceptible neurons and CGRP in the dental pulp compared with control. Importantly, micro-computed tomography analysis showed larger periradicular lesions at 7 and 14 days after pulp exposure in the neonatal capsaicin group when compared with control. CONCLUSIONS: Results identify a protective role for capsaicin-sensitive neurons in the initial phase of apical periodontitis. Thus, interventions or disorders that alter activity of capsaicin-sensitive fibers are likely to alter the development of apical periodontitis.

Photodynamic therapy as an adjunctive to scaling and root planing in treatment of chronic periodontitis in smokers.

OBJECTIVE: To compare photodynamic therapy (PDT) as an adjunctive treatment of chronic periodontitis with scaling and root planing (Sc/Rp) in smokers. METHODS: This is a split-mouth, single-masked randomized controlled clinical trial conducted at the Faculty of Dentistry, King Abdulaziz University, Jeddah, Saudi Arabia between May 2010 and March 2011. Fifty-four teeth with probing depth of ≥5mm at one or more periodontal sites in 20 smokers diagnosed with moderate to severe chronic periodontitis were selected. In each patient, at least one tooth was randomly assigned to Sc/Rp plus PDT (test group) and the contra-lateral tooth was assigned to Sc/Rp only (control). Plaque index (PI), bleeding on probing (BOP), probing depth (PD), recession and clinical attachment level (CAL) were recorded at baseline and 3 months after the periodontal treatment. Descriptive statistics and Wilcoxon signed ranked test were used for data analysis. RESULTS: There was a statistically significant improvement in PD, CAL, BOP, and PI after periodontal treatment in both groups. No statistically significant differences between the 2 groups in any of the periodontal parameters were found at baseline (p>0.05), but a statistically significant greater reduction in PD (p=0.028) and CAL (p=0.044) in the test compared to the control group was found at the 3-month follow up. CONCLUSION: Photodynamic therapy might have an additional benefit to scaling and root planing when treating smokers affected with periodontitis.

Self reported halitosis in relation to glycated hemoglobin level in diabetic patients.

OBJECTIVE: This study was conducted to examine the relationship between the glycated hemoglobin level (HbA1c) and halitosis status among diabetic patients affected with periodontitis and to examine if there is a relationship between halitosis and different periodontal parameters. METHODS AND MATERIALS: Consecutive type 2 diabetic patients were recruited from patients presented for treatment at a University hospital. Age, gender and smoking were recorded. A structured questionnaire on patients' perception of their oral health, halitosis and diabetes severity and control was completed. Peripheral blood samples were obtained and analyzed for HbA1c levels. In addition, periodontal clinical parameters including probing depth, clinical attachment level, bleeding on probing and plaque scores were recorded. RESULTS: A total of 38 type 2 diabetic patients were selected. The mean age was 52.1 (±8.8) years. Sixteen subjects (42.1%) reported halitosis. Of these, 62.5% were females, and only one subject was a current smoker. The mean levels of HbA1c were significantly different between those with and without halitosis, mean 9.6 (±2) and 8.2 (±1.6), respectively (p=0.03). No significant differences were found in the mean periodontal parameters between those with and without halitosis. CONCLUSION: The results of this study suggest an association between halitosis and increased levels of HbA1c. Further studies are needed to explain the nature of this association.