Excessive oxidative response, unbalanced immunomodulation, and impaired mesenchymal stem cell function in periodontitis in diabetes makes it a great challenge to achieve integrated periodontal tissue regeneration. Here, a polyphenol-mediated redox-active algin/gelatin hydrogel encapsulating a conductive poly(3,4-ethylenedioxythiopene)-assembled polydopamine-mediated silk microfiber network and a hydrogen sulfide sustained-release system utilizing bovine serum albumin nanoparticles is developed. This hydrogel is found to reverse the hyperglycemic inflammatory microenvironment and enhance functional tissue regeneration in diabetic periodontitis. Polydopamine confers the hydrogel with anti-oxidative and anti-inflammatory activity. The slow, sustained release of hydrogen sulfide from the bovine serum albumin nanoparticles recruits mesenchymal stem cells and promotes subsequent angiogenesis and osteogenesis. Moreover, poly(3,4-ethylenedioxythiopene)-assembled polydopamine-mediated silk microfiber confers the hydrogel with good conductivity, which enables it to transmit endogenous bioelectricity, promote cell arrangement, and increase the inflow of calcium ion. In addition, the synergistic effects of hydrogen sulfide gaseous-bioelectric coupling promotes bone formation by amplifying autophagy in periodontal ligament stem cells and modulating macrophage polarization via lipid metabolism regulation. This study provides innovative insights into the synergistic effects of conductivity, reactive oxygen species scavenging, and hydrogen sulfide on the periodontium in a hyperglycemic inflammatory microenvironment, offering a strategy for the design of gaseous-bioelectric biomaterials to promote functional tissue regeneration in immune-related diseases.

To measure the validity and reliability of a Chinese version of Child Oral Health Impact Profile (COHIP) and to assess oral health-related quality of life (OHRQoL) with regard to gender, age, and cleft types in Chinese children with orofacial cleft (OFC). A total of 120 patients with OFC (8-15 years old) and their parents were investigated with COHIP in the West China Hospital of Stomatology. Items were divided into oral symptoms, functional well-being, emotional well-being, school, and peer interaction subscales, and scores on all subscales were compared between and within groups. The internal consistency measured by Cronbach α was satisfactory in children’s sample (0.85) and parents’ sample (0.90). The correlation between children’s and parents’ questionnaires was moderate to weak (Pearson r = 0.34), which was also supported by moderate intraclass correlation coefficients. The OHRQoL of children differed significantly from parents on the overall COHIP, functional well-being, emotional well-being, and school subscales. Older children had poor OHRQoL, functional well-being, and emotional well-being. Girls had poor emotional well-being. Children with cleft lip and palate and cleft palate performed worse on the overall COHIP, functional well-being, and school subscales. Parents, boys, and younger children had better treatment expectations and global health perceptions. The Chinese version of COHIP is a reliable and valid tool to assess OHRQoL in Chinese children with OFC. Parents’ reports could not replace children’s answers but add complementary information. Children’s gender, age, and cleft types should be considered in OHRQoL assessment and individual treatment plan.

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.