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An essential challenge in diabetic periodontal regeneration is achieving the transition from a hyperglycemic inflammatory microenvironment to a regenerative one. Here, we describe a polydopamine (PDA)-mediated ultralong silk microfiber (PDA-mSF) and metformin (Met)-loaded zeolitic imidazolate framework (ZIF) incorporated into a silk fibroin/gelatin (SG) patch to promote periodontal soft and hard tissue regeneration by regulating the immunomodulatory microenvironment. The PDA-mSF endows the patch with a reactive oxygen species (ROS)-scavenging ability and anti-inflammatory activity, reducing the inflammatory response by suppressing M1 macrophage polarization. Moreover, PDA improves periodontal ligament reconstruction via its cell affinity. Sustained release of Met from the Met-ZIF system confers the patch with antiaging and immunomodulatory abilities by activating M2 macrophage polarization to secrete osteogenesis-related cytokines, while release of Zn2+also promotes bone regeneration. Consequently, the Met-ZIF system creates a favorable microenvironment for periodontal tissue regeneration. These features synergistically accelerate diabetic periodontal bone and ligament regeneration. Thus, our findings offer a potential therapeutic strategy for hard and soft tissue regeneration in diabetic periodontitis.

Periodontitis is one of the most prevalent infectious inflammatory diseases, characterized by irreversible destruction of the supporting tissues of teeth, which is correlated with a greater risk of multiple systemic diseases, thus regarded as a major health concern. Dysregulation between periodontal microbial community and host immunity is considered to be the leading cause of periodontitis. Comprehensive studies have unveiled the double‐edged role of immune response in the development of periodontitis. Immune senescence, which is described as age‐related alterations in immune system, including a diminished immune response to endogenous and exogenous stimuli, a decline in the efficiency of immune protection, and even failure in immunity build‐up after vaccination, leads to the increased susceptibility to infection. Recently, the intimate relationship between immune senescence and periodontitis has come into focus, especially in the aging population. In this review, both periodontal immunity and immune senescence will be fully introduced, especially their roles in the pathology and progression of periodontitis. Furthermore, novel immunotherapies targeting immune senescence are presented to provide potential targets for research and clinical intervention in the future. : Review on the effects of immune cells and immune senescence on periodontitis.

The underlying mechanisms and treatment of painful temporomandibular disorders (TMDs) are important but understudied topics in craniofacial research. As a group of musculoskeletal diseases, the onset of painful TMD is proved to be a result of disturbance of multiple systems. Recently, emerging evidence has revealed the involvement of neuroimmune interactions in painful TMD. Inflammatory factors play an important role in peripheral sensitization of temporomandibular joint (TMJ), and neurogenic inflammation in turn enhances TMJs dysfunction in TMD. Furthermore, centralized neuroimmune communications contribute to neuron excitability amplification, leading to pain sensitization, and is also responsible for chronic TMD pain and other CNS symptoms. Therapeutics targeting neuroimmune interactions may shed light on new approaches for treating TMD. In this review, we will discuss the role of neuroimmune interactions in the onset of painful TMD from the peripheral and centralized perspectives, and how understanding this mechanism could provide new treatment options. Insights into the neuroimmune interactions within TMJs and painful TMD would broaden the knowledge of mechanisms and treatments of this multifactorial disease. Reviews neuro‐immune interactions that influence TMD pain sensitization and chronicity; describes the implications this has for treatment.

Background. It is necessary for dental students and dentists to apply their temporomandibular disorders (TMDs)-related knowledge to clinical practice. The current study aimed to evaluate the knowledge and awareness of postgraduate dental students and practicing dentists regarding etiology, diagnosis, and treatment of TMD in western China and thus provide suggestions on TMD curricula design to get postgraduate students and dentists better prepared for TMD diagnosis and treatment. Methods. This observational and descriptive cross-sectional study was conducted among postgraduate students and practicing dentists in western China. Twenty-five reorganized knowledge questions in four domains were selected from the published literature and were evaluated with answer options from “strongly agree” to “strongly disagree,” and “I don’t know.” “Consensus” is defined as more than 50% of respondents in a group agree or disagree with a statement. Chi-square tests were performed for comparisons between the two groups. Results. A total of 132 postgraduate dental students and 123 dentists completed the questionnaire. Around 75% of postgraduate students and 85% of dentists claimed that they have never participated in systematic training in TMD. Nine statements in etiology, diagnosis, treatment, and prognosis of TMD had different consensus between the two groups. And the dentist group tended to agree more with 12 statements in the questionnaire. Conclusions. The majority of Chinese dentists and dental students have not taken any TMD courses and possess limited knowledge of TMD. Curriculum reform for predoctoral education, postgraduate education, and continuing education is needed to augment knowledge and skills for TMD diagnosis and treatment.

Bone stromal cells are critical for bone homeostasis and regeneration. Growing evidence suggests that non-stem bone niche cells support bone homeostasis and regeneration via paracrine mechanisms, which remain to be elucidated. Here, we show that physiologically quiescent SM22α-lineage stromal cells expand after bone injury to regulate diverse processes of intramembranous bone regeneration. The majority of SM22α-lineage cells neither act as stem cells in vivonor show their expression patterns. Dysfunction of SM22α-lineage niche cells induced by loss of platelet-derived growth factor receptor β (PDGFRβ) impairs bone repair. We further show that PDGFRβ-triggered hydrogen sulfide (H2S) generation in SM22α-lineage niche cells facilitates osteogenesis and angiogenesis and suppresses overactive osteoclastogenesis. Collectively, these data demonstrate that non-stem SM22α-lineage niche cells support the niche for bone regeneration with a PDGFRβ/H2S-dependent regulatory mechanism. Our findings provide further insight into non-stem bone stromal niche cell populations and niche-regulation strategy for bone repair.

Objective. To assess the differences in hyoid bone position in patients with and without temporomandibular joint osteoarthrosis (TMJOA). Methods. The present cross-sectional study was conducted in 427 participants whose osseous status was evaluated using cone-beam computed tomography and classified into normal, indeterminate osteoarthrosis (OA), and OA. The hyoid bone position and craniofacial characteristics were evaluated using cephalograms. Patients were divided into the normal group (N = 89), indeterminate OA group (N = 182), and OA group (N = 156). Descriptive statistics, one-way analysis of variance, and age- and sex-based stratified analyses were performed. P<0.05 was considered statistically significant. Results. The differences in Hy to MP, Hy-RGn, Hy to C3-RGn, C3-RGn, and Go-Hy-Me among the three groups were statistically significant. The differences in the Frankfort-mandibular plane angle, saddle angle, articular angle, gonial angle, ramus height, and posterior facial height were statistically significant. After adjusting age and sex, the Hy-RGn and C3-RGn in the normal group were significantly greater than the OA group. No statistical differences were observed in the hyoid measurements in the stratified analyses in males or subjects less than 18 years old. The differences in Hy to MP, Hy to C3-RGn, and Go-Hy-Me in female patients among the three groups were statistically significant. The differences in Hy to SN, Hy to FH, Hy to PP, Hy to MP, Hy-RGn, Hy-C3, Hy to C3-RGn, Go-Hy-Me, Hy-S, and C3-Hy-S in adults were statistically significant. Conclusion. The differences in the hyoid bone position, mainly relative to the mandible, were statistically significant in patients with or without TMJOA. The difference pattern varied among different age and sex groups. Clinical evaluation of the hyoid position must consider the age and sex of patients. Longitudinal studies are required to clarify the causal relationship between TMJOA and hyoid bone position.