Chronic mucocutaneous candidiasis (CMC) is an infectious phenotype characterized by recurrent or persistent infections caused by Candida species that affect the skin, nails, oral, and genital mucosae for a duration exceeding six months. Current research suggests that CMC is an immunodeficiency disease with a complex pathogenesis. Patients with CMC have various defects in nonspecific and/or specific immunity against Candida infection, resulting in the inability of patients to defend themselves against Candida infection. CMC can be stratified into primary CMC and secondary CMC based on etiology. Primary CMC is often associated with genetic mutations leading to immunodeficiencies in T helper cell 17 and interleukin-17, whereas secondary CMC is frequently linked to factors such as human immunodeficiency virus infection, diabetes mellitus, and immunosuppressive therapy. Primary CMC typically manifests as Candida infections, with distinct genetic mutations often correlating to varied concomitant symptoms. Secondary CMC may present with not only superficial mucosal Candida infections and manifestations of the underlying primary disease but also with invasive fungal infections. Diagnosing CMC requires an integration of medical history and clinical presentation, supplemented by the outcomes of auxiliary diagnostic procedures, including microscopic examination of fungal smear, fungal culture, immunological testing, and genetic sequencing and analysis. Furthermore, confirming primary CMC requires exclusion of the aforementioned secondary factors. At present, antifungal drugs such as triazoles, echinocandins, and polyenes are the main treatment for CMC. Moreover, immunotherapy with biologics such as Janus kinase (JAK) inhibitors provides more options for the clinical treatment of patients with CMC. Gene therapy also has potential clinical application value. In this review, we discuss the etiologies, pathogenesis, clinical manifestations, diagnosis, and treatments of CMC, aiming to provide a reference for the clinical diagnosis and treatment of CMC.

G protein-coupled receptors (GPCRs) are the largest family of membrane proteins in eukaryotes, with nearly 800 genes coding for these proteins. They are involved in many physiological processes, such as light perception, taste and smell, neurotransmitter, metabolism, endocrine and exocrine, cell growth and migration. Importantly, GPCRs and their ligands are the targets of approximately one third of all marketed drugs. GPCRs are traditionally known for their role in transmitting signals from the extracellular environment to the cell's interior via the plasma membrane. However, emerging evidence suggests that GPCRs are also localized on mitochondria, where they play critical roles in modulating mitochondrial functions. These mitochondrial GPCRs (mGPCRs) can influence processes such as mitochondrial respiration, apoptosis, and reactive oxygen species (ROS) production. By interacting with mitochondrial signaling pathways, mGPCRs contribute to the regulation of energy metabolism and cell survival. Their presence on mitochondria adds a new layer of complexity to the understanding of cellular signaling, highlighting the organelle's role as not just an energy powerhouse but also a crucial hub for signal transduction. This expanding understanding of mGPCR function on mitochondria opens new avenues for research, particularly in the context of diseases where mitochondrial dysfunction plays a key role. Abnormalities in the phase conductance pathway of GPCRs located on mitochondria are closely associated with the development of systemic diseases such as cardiovascular disease, diabetes, obesity and Alzheimer's disease. In this review, we examined the various types of GPCRs identified on mitochondrial membranes and analyzed the complex relationships between mGPCRs and the pathogenesis of various diseases. We aim to provide a clearer understanding of the emerging significance of mGPCRs in health and disease, and to underscore their potential as therapeutic targets in the treatment of these conditions.

G protein-coupled receptors(GPCRs)are the largest family of membrane proteins in eukaryotes,with nearly 800 genes coding for these proteins.They are involved in many physiological processes,such as light perception,taste and smell,neurotransmitter,metabolism,endocrine and exocrine,cell growth and migration.Importantly,GPCRs and their ligands are the targets of approximately one third of all mar-keted drugs.GPCRs are traditionally known for their role in transmitting signals from the extracellular environment to the cell's interior via the plasma membrane.However,emerging evidence suggests that GPCRs are also localized on mitochondria,where they play critical roles in modulating mitochondrial functions.These mitochondrial GPCRs(mGPCRs)can influence processes such as mitochondrial respi-ration,apoptosis,and reactive oxygen species(ROS)production.By interacting with mitochondrial signaling pathways,mGPCRs contribute to the regulation of energy metabolism and cell survival.Their presence on mitochondria adds a new layer of complexity to the understanding of cellular signaling,highlighting the organelle's role as not just an energy powerhouse but also a crucial hub for signal transduction.This expanding understanding of mGPCR function on mitochondria opens new avenues for research,particularly in the context of diseases where mitochondrial dysfunction plays a key role.Ab-normalities in the phase conductance pathway of GPCRs located on mitochondria are closely associated with the development of systemic diseases such as cardiovascular disease,diabetes,obesity and Alz-heimer's disease.In this review,we examined the various types of GPCRs identified on mitochondrial membranes and analyzed the complex relationships between mGPCRs and the pathogenesis of various diseases.We aim to provide a clearer understanding of the emerging significance of mGPCRs in health and disease,and to underscore their potential as therapeutic targets in the treatment of these conditions.

Oral lichen planus (OLP) is a chronic inflammatory disease occurring in the oral mucosa. Clinically, OLP presents with various lesion morphologies, attributed to differences in host immune responses. T-helper 17 cells (Th17) are a crucial component of the cellular immune response, primarily functioning through the secretion of interleukin 17 (IL-17). IL-17 plays a dual role in the oral mucosa: on one hand, it exerts a protective effect by promoting the recruitment of neutrophils driven by chemokines, enhancing the secretion of antimicrobial peptides, and strengthening the mucosal barrier; on the other hand, it binds to target cells in the mucosal tissue, activating downstream inflammatory signaling pathways such as nuclear factor kappa-B(NF-κB) and mitogen-activated protein kinase(MAPK), thereby initiating a pro-inflammatory cascade. This process increases the secretion of pro-inflammatory factors and promotes the recruitment and activation of immune cells, exacerbating inflammation. Current research extensively explores the correlation between the Th17/IL-17 axis and the pathogenesis and progression of OLP. This paper aims to review these developments to provide a research foundation for further elucidating the immunological mechanisms of OLP. Literature review results indicate that upregulation of Th17 and IL-17 in local lesion tissues and peripheral blood of OLP patients may be a key molecular event in the development of OLP. Compared to non-erosive OLP, higher expression levels of Th17 and IL-17 in the tissues and blood of patients with erosive OLP suggest a positive correlation between Th17/IL-17 and disease severity. Clinical studies demonstrate that targeted drugs against the Th17/IL-17 axis, by directly blocking IL-17 or inhibiting the production of Th17 cells, can effectively improve mucosal damage in OLP patients, showcasing potential as a new target for immune therapy. However, whether Th17 and IL-17 influence the pathogenesis of OLP by regulating the oral microbiome remains unclear. In summary, the Th17/IL-17 axis holds potential value as a new target for the immune therapy of OLP, warranting further in-depth research into its biological functions and signaling mechanisms within the inflammatory process of OLP.

Oral hairy leukoplakia is an oral mucosal disease caused by Epstein-Barr virusinfection of oral squamous epithelial cells.Oral hairy leukoplakia presents as a non-removable,corrugated and wrinkled white plaque sometimes with hair-like projections,typical-ly occurring on the border of the tongue.It is commonly found in patients infected by human immunodeficiency virus,and it can also be seen in immunocompetent and immunocompromised patients who are not infected by human immunodeficiency virus.The pathogenesis of oral hairy leukoplakia is still unclear,and anti-EBV therapy is the main treatment for oral hairy leukoplakia at present.This paper will review the etiology,pathogenesis,risk factors,epidemiology,clinical manifestations,diagnosis and treatment of oral hairy leuko-plakia.

Oral hairy leukoplakia is an oral mucosal disease caused by Epstein-Barr virusinfection of oral squamous epithelial cells.Oral hairy leukoplakia presents as a non-removable,corrugated and wrinkled white plaque sometimes with hair-like projections,typical-ly occurring on the border of the tongue.It is commonly found in patients infected by human immunodeficiency virus,and it can also be seen in immunocompetent and immunocompromised patients who are not infected by human immunodeficiency virus.The pathogenesis of oral hairy leukoplakia is still unclear,and anti-EBV therapy is the main treatment for oral hairy leukoplakia at present.This paper will review the etiology,pathogenesis,risk factors,epidemiology,clinical manifestations,diagnosis and treatment of oral hairy leuko-plakia.

Bitter taste in the mouth is a prevalent clinical symptom that refers to a spontaneous bitterness in the mouth after excluding external factors such as diet,and belongs to the phantogeusia of dysgeusia.The etiology and mechanism of bitter taste in the mouth re-main unclear.Studies have shown that bitter taste in the mouth is mainly associated with multiple factors such as diseases,medications and nutrition.In addition,effective and reliable treatments have also not yet been developed.This paper reviews the latest research ad-vances in the etiology,mechanism and treatment of bitter taste in the mouth,with the aim of providing reference for the clinical man-agement of patients with mouth bitterness.

Aging of craniofacial skeleton significantly impairs the repair and regeneration of trauma-induced bony defects, and complicates dental treatment outcomes. Age-related alveolar bone loss could be attributed to decreased progenitor pool through senescence, imbalance in bone metabolism and bone-fat ratio. Mesenchymal stem cells isolated from oral bones (OMSCs) have distinct lineage propensities and characteristics compared to MSCs from long bones, and are more suited for craniofacial regeneration. However, the effect of epigenetic modifications regulating OMSC differentiation and senescence in aging has not yet been investigated. In this study, we found that the histone demethylase KDM4B plays an essential role in regulating the osteogenesis of OMSCs and oral bone aging. Loss of KDM4B in OMSCs leads to inhibition of osteogenesis. Moreover, KDM4B loss promoted adipogenesis and OMSC senescence which further impairs bone-fat balance in the mandible. Together, our data suggest that KDM4B may underpin the molecular mechanisms of OMSC fate determination and alveolar bone homeostasis in skeletal aging, and present as a promising therapeutic target for addressing craniofacial skeletal defects associated with age-related deteriorations.
Aging ; Cell Differentiation ; Facial Bones/physiology* ; Humans ; Jumonji Domain-Containing Histone Demethylases/genetics* ; Mesenchymal Stem Cells/cytology* ; Osteogenesis ; Osteoporosis

In order to improve the scientific research ability of the postgraduates of Oral Medicine, based on the characteristics of this discipline, our team has adopted a teamwork-based, interest-driven, clinical work and scientific research combined, multiple disciplines interacted pattern of scientific research training of postgraduates. After several years of practice, some achievements have been made in promoting the scientific literacy and ability of independently undertaking clinical practice and scientific research of Oral Medicine, and the average number of publication of postgraduates increased annually. During the university, doctoral students published 2.4 papers in average, and master students published 1.9 papers in average.

To evaluate the application of medical magnifying loupes in diagnosis of oral mucosal diseases. Twenty-four patients with plaque-type oral lichen planus or homogeneous oral leukoplakia were inspected by naked eyes or assistance with magnifying loupes. Histopathological results were used as the gold standard to evaluate the sensitivity, specificity and accuracy of the two methods in clinical diagnosis. Questionnaires were used to evaluate the subjective effect of magnifying loupes on the diagnosis efficiency of oral mucosal diseases and to explore the most suitable parameters for application. The sensitivity, specificity and accuracy of medical magnifying loupes for the identification of plaque-type oral lichen planus and homogeneous oral leukoplakia were 94.74%, 100.00% and 95.83%, respectively, which were significantly higher than those of naked eye inspection (89.47%, 80.00% and 87.50%). The effective rate of magnifying loupes assisted diagnosis was 91.76% according to physicians' subjective evaluation. The most suitable parameters were 3.5 times magnification and working distance. The medical magnifying loupes can effectively improve the efficiency of the inspection and diagnosis of oral mucosal diseases, and have the characteristics of convenience and real-time. The recommended clinical parameters are 3.5 times magnification and working distance.
Efficiency ; Humans ; Lenses ; Surveys and Questionnaires