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.

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 Nav1.8^Cre/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 Nav1.8^Cre/ DTA^Lox 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. Graphical