The biopsychosocial model suggests that temporomandibular disorders (TMDs) often coexist with mental health disorders, particularly depression and anxiety, affecting a significant portion of the global population. The interplay between TMDs and mental health disorders contributes to a complex comorbidity, perpetuating a cycle of mutual influence and reinforcement. This review investigates the neurobiological mechanisms and epidemiological evidence supporting the shared etiology of TMDs and mental health disorders, exploring potential shared vulnerabilities and bidirectional causal relationships. Shared vulnerabilities between TMDs and mental health disorders may stem from genetic and epigenetic predispositions, psychosocial factors, and behavioral aspects. Inflammatory cytokines, neurotransmitters, neurotrophins, and neuropeptides play pivotal roles in both peripheral and central sensitization as well as neuroinflammation. Brain imaging studies suggest that TMDs and mental health disorders exhibit overlapping brain regions indicative of reward processing deficits and anomalies within the triple network model. Future research efforts are crucial for developing a comprehensive understanding of the underlying mechanisms and confirming the reciprocal causal effects between TMDs and mental health disorders. This review provides valuable insights for oral healthcare professionals, stressing the importance of optimizing treatment strategies for individuals dealing with concurrent TMDs and mental health issues through a personalized, holistic, and multidisciplinary approach.

Chronic pain and mental health disorders, such as depression and anxiety, frequently co-occur and share underlying mechanisms involving neuronal excitability and synaptic transmission. The inwardly rectifying potassium channel 4.1 (Kir4.1), predominantly expressed in glial cells, is crucial for maintaining extracellular potassium and glutamate homeostasis. Dysregulation of Kir4.1 leads to altered neuronal activity, contributing to both chronic pain and mental health disorders. In chronic pain, downregulation of Kir4.1 impairs potassium buffering and glutamate clearance, increasing neuronal excitability and enhancing pain signaling through peripheral and central sensitization. In mental health disorders, impaired Kir4.1 function disrupts neurotrophic factor secretion and neuroinflammatory pathways, leading to mood disturbances. This review primarily summarizes findings from preclinical studies to examine the relationship between Kir4.1 and the pathogenesis of chronic pain and mental health disorders, discussing its molecular structure, expression patterns, and functional roles. Furthermore, we explore therapeutic strategies targeting Kir4.1, including pharmacological modulators and gene therapy approaches, emphasizing its potential as a novel therapeutic target.

Objective: This retrospective clinical study aimed to compare root resorption between the surgery-first approach (SFA) and conventional orthognathic approach (COA) using cone-beam computed tomography (CBCT). Methods: Forty-one skeletal class III patients who underwent combined orthognathic surgery and non-extraction orthodontic treatment were included. According to surgical timing, participants were divided into the conventional orthognathic approach (COA) group (n=21) and the surgery-first approach (SFA) group (n=20). Root length and volume were measured on pre- and post-treatment CBCT scans. Intra-group changes in root dimensions were analyzed using paired t tests. Inter-group differences were evaluated using independent-samples t tests for tooth-specific analyses and a linear mixed model for overall assessment. Results: Root resorption was observed in both groups after treatment completion. Compared with the COA group, the SFA group exhibited a lower prevalence of mild-to-moderate root resorption and a higher proportion of unaffected teeth. Significant inter-group differences in root length reduction were observed across all maxillary teeth and mandibular incisors ( P <0.05). The linear mixed model revealed a reduction of 0.21 mm in overall root resorption in the SFA group ( P =0.002), although its clinical significance may be limited. Regarding volume loss, no significant differences were observed between the groups, except for the maxillary central incisors ( P =0.037). Consistent with these findings, the linear mixed model demonstrated no significant difference in volume loss between the two groups ( P =0.238). Conclusion: Compared with COA, SFA did not increase the risk of root resorption and might have a protective potential in non-extraction cases.