Non-surgical periodontal treatment can effectively improve periodontal and circulating inflammatory status. Despite a lack of strong evidence, trends in some results support improved glycemic control after periodontal treatment in patients with diabetes.
Periodontal inflammation is associated with an enhancement of both the M1 and M2 phenotypes of macrophages, in which a phenotypic switch of M2 to M1 might be a critical mechanism in mediating periodontal tissue damage, including alveolar bone loss.
Adiponectin (APN) is an adipocyte-secreted adipokine that exerts well-characterized anti-diabetic properties. Patients with type 2 diabetes (T2D) are characterized by reduced APN levels in circulation and impaired stem cell and progenitor cell mobilization from the bone marrow for tissue repair and remodeling. In this study, we found that APN regulates the mobilization and recruitment of bone marrow-derived mesenchymal stem cells (BMSCs) to participate in tissue repair and regeneration. APN facilitated BMSCs migrating from the bone marrow into the circulation to regenerate bone by regulating stromal cell-derived factor (SDF)-1 in a mouse bone defect model. More importantly, we found that systemic APN infusion ameliorated diabetic mobilopathy of BMSCs, lowered glucose concentration and promoted bone regeneration in diet-induced obesity (DIO) mice. In vitro studies allowed us to identify Smad1/5/8 as a novel signaling mediator of APN receptor (AdipoR)-1 in BMSCs and osteoblasts. APN stimulation of MC3T3-E1 osteoblastic cells led to Smad1/5/8 phosphorylation and nuclear localization and increased SDF-1 mRNA expression. Although APN-mediated phosphorylation of Smad1/5/8 occurred independently from adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1), it correlated with the disassembly of protein kinase casein kinase II (CK2) and AdipoR1 in immunoprecipitation experiments. Taken together, this study identified APN as a regulator of BMSCs migration in response to bone injury. Therefore, our findings suggest APN signaling could be a potential therapeutic target to improve bone regeneration and homeostasis, especially in obese and T2D patients.
BackgroundThe aim of the present study was to describe the characteristics of dental fear of Chinese adult patients with periodontal disease and provide information for clinical assessment.MethodsA total of 1203 dental patients completed questionnaires that included Corach’s Dental Anxiety Scales (DAS), Dental Fear Survey (DFS) and the short-form Dental Anxiety Inventory (S-DAI). Among all the patients, 366 cases were self-reported periodontal disease. The general characteristics were described, such as socio-demographics, dental attendances and oral health behaviors. The statistical analysis was performed by t-test, Mann–Whitney U test and linear regression respectively to evaluate correlations between dental fear and general characteristics according to the three scales.ResultsThe prevalence of dental fear was 74% among 1203 patients, 23.4% of total with high dental fear, while 27.3% in the patients with periodontal disease. The average score of DAS and DFS for patients with periodontal disease was significantly higher than those without periodontal disease. The regression analysis indicated that gender, age, periodontal status, dental attendances and oral health behaviors were correlated with dental fear. Among 366 patients with periodontal disease, gender, dental attendances and oral health behaviors had correlation with dental fear. The analysis of DFS scale exhibited that ‘drilling with handpiece’ and ‘injecting the anesthetic’ were the most important factors to contribute to dental fear.ConclusionsThere was high prevalence of dental fear in Chinese adult patients, particularly in patients with periodontal disease, and high level of dental fear may lead to poor periodontal status.
For patients with T2DM and CP, hyperglycemic status may exacerbate the inflammation state of gingival tissue by activating the NLRP3 pathway, and this abnormal host inflammatory response may contribute to further tissue breakdown.
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