Temporomandibular joint osteoarthritis (TMJOA) is a common degenerative joint disease that can cause severe pain and dysfunction. It has a serious impact on the quality of lives of patients. Since mechanism underlying the pathogenesis of TMJOA is not fully understood, the development of effective tools for early diagnosis and disease-modifying therapies has been hindered. Animal models play a key role in understanding the pathological process of diseases and evaluating new therapeutic interventions. Although some similarities in disease processes between animals and humans are known, no one animal model is sufficient for studying all characteristics of TMJOA, as each model has different translatability to human clinical conditions. For the past 4 decades, TMJOA animal models have been studied by numerous researchers and can be broadly divided into induced, naturally occurring, and genetically modified models. The induced models can be divided into invasive models (intra-articular injection and surgical induction) or non-invasive models (mechanical loading, high-fat diet, and sleep deprivation). Different types of animal models simulate different pathological expressions of TMJOA and have their unique characteristics. Currently, mice, rats, and rabbits are commonly used in the study of TMJOA. This review sought to provide a general description of current experimental models of TMJOA and assist researchers in selecting the most appropriate models for different kinds of research.

The onerous health and economic burden associated with head and neck squamous cell carcinoma (HNSCC) is a global predicament. Despite the advent of novel surgical techniques and therapeutic protocols, there is an incessant need for efficacious diagnostic and therapeutic targets to monitor the invasion, metastasis and recurrence of HNSCC due to its substantial morbidity and mortality. The differential expression patterns of histone deacetylases (HDACs), a group of enzymes responsible for modifying histones and regulating gene expression, have been demonstrated in neoplastic tissues. However, there is limited knowledge regarding the role of HDACs in HNSCC. Consequently, this review aims to summarize the existing research findings and explore the potential association between HDACs and HNSCC, offering fresh perspectives on therapeutic approaches targeting HDACs that could potentially enhance the efficacy of HNSCC treatment. Additionally, the Cancer Genome Atlas (TCGA) dataset, CPTAC, HPA, OmicShare, GeneMANIA and STRING databases are utilized to provide supplementary evidence on the differential expression of HDACs, their prognostic significance and predicting functions in HNSCC patients. Graphical Abstract

Oral squamous cell carcinoma (OSCC) is the most prevalent cancer of the mouth, characterised by rapid progression and poor prognosis. Hence, an urgent need exists for the development of predictive targets for early diagnosis, prognosis determination, and clinical therapy. Dysregulation of lymphoid enhancer-binding factor 1 (LEF1), an important transcription factor involved in the Wnt-β-catenin pathway, contributes to the poor prognosis of OSCC. Herein, we aimed to explore the correlation between LEF1 and histone lysine demethylase 4 A (KDM4A). Results show that the KDM4A complex is recruited by LEF1 and specifically binds the LATS2 promoter region, thereby inhibiting its expression, and consequently promoting cell proliferation and impeding apoptosis in OSCC. We also established NOD/SCID mouse xenograft models using CAL-27 cells to conduct an in vivo analysis of the roles of LEF1 and KDM4A in tumour growth, and our findings show that cells stably suppressing LEF1 or KDM4A have markedly decreased tumour-initiating capacity. Overall, the results of this study demonstrate that LEF1 plays a pivotal role in OSCC development and has potential to serve as a target for early diagnosis and treatment of OSCC.

Periodontal ligament stem cells (PDLSCs) orchestrate alveolar bone remodeling during orthodontic tooth movement (OTM), yet the molecular mechanism translating tension force into coupled osteogenic and anti-osteoclastic responses remains elusive. This study aimed to define the dual mechanosensitive role of PIEZO1 in PDLSCs for simultaneously promoting osteogenesis and suppressing osteoclastogenesis via the Ca²⁺/YAP-TAZ/OPG-RANKL signaling axis. Human PDLSCs were isolated, characterized for mesenchymal markers, and exposed to cyclic tension (10% strain, 0.5 Hz) using a Flexcell system. PIEZO1 was inhibited using GsMTx4 or siRNA, and Ca²⁺ flux was analyzed by live-cell confocal microscopy. Osteogenic (RUNX2, OSX), osteoclastic (RANKL, OPG), and YAP/TAZ signaling markers were assessed using RT-qPCR and Western blot. For in vivo validation, a rat OTM model was established using 40-g NiTi springs. Tooth movement and tension-side alveolar bone remodeling were quantified by micro-CT, while osteogenic and osteoclastic activities were evaluated through immunohistochemistry and TRAP staining. Tension force activated PIEZO1 channels, triggering rapid Ca²⁺ influx and subsequent nuclear accumulation of YAP/TAZ. YAP/TAZ activation transcriptionally upregulated RUNX2 and OSX, concurrently reprogramming the PDLSC secretome to favor Osteoprotegerin (OPG) dominance over RANKL, significantly reducing the RANKL/OPG ratio and thus suppressing osteoclast differentiation. Pharmacological inhibition of PIEZO1 (GsMTx4) or genetic knockdown abrogated Ca²⁺ influx, prevented YAP/TAZ nuclear translocation, and disrupted the RANKL/OPG balance, thereby uncoupling osteogenesis from osteoclast suppression both in vitro and in vivo. This study defines a fundamental mechanotransduction cascade initiated by PIEZO1, wherein Ca²⁺ influx mobilizes YAP/TAZ nuclear translocation to transcriptionally activate osteogenic differentiation and reprogram anti-osteoclastic secretory profiles. Deciphering this mechanocode nominates PIEZO1 as a promising therapeutic target for recalibrating bone remodeling balance and mitigating pathological bone loss during orthodontic therapy.