Zuolin Jin

Structural craniofacial abnormalities, particularly mandibular asymmetry (MA), are increasingly recognized as key drivers of orofacial pain and emotional comorbidities, although the underlying neural mechanisms remain unclear. This study aims to develop a preclinical MA model to investigate the dynamic interplay between craniofacial structural defects and neurobehavioral dysfunction. Longitudinal behavioral phenotyping including von Frey filaments test as well as open field and elevated plus maze tests reveals progressive sensory hypersensitivity and anxiety‐like behaviors, with computational ethology revealing subtle but consistent alterations in the naturalistic behaviors. Whole‐brain activity mapping reveal hyperactivation in the anterior cingulate cortex (ACC), whereas multi‐omics profiling reveal cell type‐specific transcriptional changes and synaptic reorganization within this region. Functional investigation including sparse labeling, electrophysiology, western blotting, and chemogenetics demonstrate that the ACC modulation regulated both pain and anxiety. These findings establish a causal association between structural craniofacial defects and maladaptive neural circuit remodeling, with the ACC emerging as a critical therapeutic target. The study provides a comprehensive framework for understanding how anatomical abnormalities translate into persistent neurological dysfunction and offers new avenues for mechanistically informed intervention.

Background. miR‐205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR‐205 in cardiac ischemia/reperfusion (I/R) injury remain unknown. The aim of this research is to reveal whether miR‐205 could regulate cardiac I/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis. Methods. Levels of miR‐205 and Rnd3 were examined in the hearts with I/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia/reperfusion (MI/R) injury. The primary neonatal cardiomyocytes underwent hypoxia/reoxygenation (H/R) to simulate MI/R injury. Results. miR‐205 levels were significantly elevated in cardiac tissues from I/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI/R injury. Furthermore, inhibiting miR‐205 alleviated MI/R‐induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR‐205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR‐205 reduced oxidative stress in H/R‐treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR‐205 inhibitor in MI/R injury. Conclusions. We conclude that inhibiting miR‐205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI/R injury. miR‐205 inhibitor‐induced Rnd3 activation is a valid target to treat MI/R injury.

Background: To analyze the sagittal positions of the mandibular prominence and maxillary central incisors in adult Chinese Han men to establish their aesthetic profile characteristics. Methods: Seventy-four Chinese Han men aged 18 to 40 years underwent cone beam computed tomography for detecting the distances between Glabella and Subnasale, Subnasale and Menthon of soft tissue, Condyle and Gonion, Pogonion and Pogonion's Anterior Limit Line, Facial Axis point of maxillary central incisor and the Goal Anterior Limit Line as well as the angle of the Occlusal Plane. Dolphin Imaging and Photoshop software packages were used to generate silhouette profiles. Thirteen orthodontists assessed the silhouette profiles and assigned visual analog scale scores. Scores >70 were assigned to the aesthetic (group 1), scores of 60to 70 to the general (group 2), scores of 50 to 60 to the acceptable (group 3), and scores of P = .046) and Facial Axis-Goal Anterior Limit Line (−0.61 ± 2.54 mm vs 1.70 ± 2.62 mm, P = .038) there were significant differences. Conclusion: Compared with the unaesthetic profile group, the sagittal positions of the maxillary central incisors were slightly posterior, and the chin was slightly anterior in adult Chinese Han men with an aesthetic profile.

Osteoporosis is a metabolic disease that results in the progressive loss of bone mass, which, in postmenopausal women, is related to oestrogen deficiency. Periostin (POSTN) plays a key role in the early stages of bone formation. However, whether POSTN participates in oestradiol regulation of osteogenic differentiation of bone marrow stromal cells (BMSCs) from ovariectomised (OVX) rats remains unclear. In vivo, using microcomputed tomography (micro‐CT), immunohistochemistry, and dynamic analysis of femurs, we found that 17β‐E2 promotes bone formation and POSTN expression at the endosteal surface. In vitro, 17β‐E2 upregulated POSTN expression in OVX‐BMSCs. POSTN overexpression activated the Wnt/β‐catenin signalling pathway and enhanced osteogenic differentiation of OVX‐BMSCs. Furthermore, knockdown of Postn blocks the involvement of 17β‐E2 in the osteogenic differentiation of OVX‐BMSCs. Collectively, our study indicated the role of POSTN in the osteogenesis and stemness of OVX‐BMSCs and proves that 17β‐E2 reduces osteoporosis and promotes osteogenesis through the POSTN‐Wnt/β‐catenin pathway. POSTN could, therefore, be a novel target gene for anti‐osteoporosis therapies.

Periodontitis is a chronic infectious disease which would damage the connective tissue and alveolar bone. Inflammation micro-environment could destroy the osteogenic differentiation ability of PDLSCs, which would induce the periodontitis. Long non-coding RNA (lncRNA) had a very wide range of biological functions, including chromosomal inactivation and differentiation, pluripotent reprogramming, and apoptosis. Nowadays, many lncRNAs have been discovered regulating PDLSCs osteogenesis. Recent studies have demonstrated that lncRNAs were upregulated or down regulated in periodontitis tissues.

HPDLSCs derived from periodontal ligament tissues contribute to tooth development and tissue regeneration. Exploring the effects of long noncoding RNAs (lncRNAs) in the process of osteogenic differentiation of periodontal ligament stem cells would provide novel therapeutic strategies for tissue regeneration. The expression levels of lncRNA, which significantly changed during osteogenic differentiation, were observed by real-time quantitative PCR (q-PCR). Then, we screened for osteogenic-related lncRNA, which was initially named lncRNA-TWIST1. Moreover, we detected the mRNA expression levels of TWIST1 and osteogenesis-related genes after upregulating and downregulating lncRNA-TWIST1 in PPDLSCs (periodontal mesenchymal stem cells from periodontitis patients) and HPDLSCs (periodontal mesenchymal stem cells from healthy microenvironment), respectively. The osteogenic degree was verified by detecting ALP activity and alizarin red staining. LncRNA-TWIST1 decreased the mRNA levels of TWIST1 and promoted osteogenic differentiation in PPDLSCs, which was confirmed by the increase in osteogenesis-related gene levels (Runx2, ALP, and OCN), the increase in ALP activity, and the formation of more osteogenic nodules. In contrast, downregulating lncRNA-TWIST1 decreased the expression of osteogenesis-related genes, ALP activity, and osteogenic nodules both in PPDLSCs and in HPDLSCs. LncRNA-TWIST1 promoted osteogenic differentiation both in PPDLSCs and in HPDLSCs by inhibiting the TWIST1 expression. LncRNA-TWIST1 may be a novel therapeutic strategy to regenerate dental tissues.

Periodontal ligament stem cells (PDLSCs) can repair alveolar bone defects in periodontitis in a microenvironment context-dependent manner. This study aimed to determine whether different extracellular matrices (ECMs) exert diverse effects on osteogenic differentiation of PDLSCs and accurately control alveolar bone defect repair.

The aim of this paper is to investigate the effect that bone marrow mesenchymal stem cells (BMMSCs) - endothelial progenitor cells (EPCs), BMMSCs and EPCs sheets have on repairing maxillary alveolar defects in ovariectomized (OVX) rats. In this study, after identification using multi-lineage differentiation and flow cytometry, BMMSCs and EPCs were isolated from female rats. The BMMSCs-EPCs, BMMSCs and EPCs sheets were detected by hematoxylin-eosin (H&E) staining, alkaline phosphatase (ALP) staining and qRT-PCR. Defects were created in maxillary alveoli and repaired with BMMSCs-EPCs, BMMSCs and EPCs sheets in OVX rats. The repair effects were determined by histological staining and micro-CT analysis at 2, 4 and 8 weeks after implantation. We aim to clarify whether BMMSCs-EPCs sheets are more effective in repairing alveolar bone defects than are BMMSCs and EPCs sheets in OVX rats. The results show that the osteogenic potential and the effect of bone repair are greater in the BMMSCs-EPCs sheet group and that this group has a higher ability to repair alveolar bone defects in OVX rats. These results suggest that BMMSCs-EPCs sheets have potential in clinical applications for treating humans with osteoporosis.