Sialorrhea is a group of symptoms characterized by excessive accumulation of saliva in the mouth and unconscious overflow from the mouth. It can be divided into physiological sialorrhea and pathological sialorrhea. The etiol-ogy of sialorrhea is complex. Local oral factors, systemic diseases, drug induction or psycho-physiological factors can lead to excessive saliva secretion or excessive saliva storage in the mouth, which can lead to sialorrhea. Physiological sialorrhea generally does not require treatment, while different treatment strategies are needed in cases of pathological sialorrhea. There are many treatments for sialorrhea, including oral and maxillofacial system training, drugs, botulinum toxin injection, surgical treatment, and less commonly, traditional Chinese medicines, radiotherapy and neuromuscular electrical stimulation therapy. For different patients, different treatment methods should be adopted, and the treatment should be gradual. To correct the abnormalities in the oral and maxillofacial regions, the primary disease should be treated, contact with/the use of substances inducing salivation should be stopped, or psychological treatment should be administered, combined with oral and maxillofacial system training; if the effect is not good, invasive treatment, such as surgery, should be considered. At present, there are no unified, clear diagnostic criteria or simple and effective treatments in the clinic. In this paper, the etiology, diagnosis and treatment of sialorrhea, combined with our group's many years of experience in the diagnosis and treatment of sialorrhea, are reviewed to provide a useful reference for the clinical diagnosis and treatment of sialorrhea.

Chronic recurrent parotitis (CRP) is a non-obstructive parotid inflammation in young children or adults, generally associated with recurrent and intermittent swelling of parotid gland, while children are more susceptible. The etiology of this disease is not clear, clinical manifestations are similar to other diseases, and the effective prevention and control measures are lack currently. This paper reviewed the research progress of the etiology of CRP in recent years, and summarized the role of sialography, ultrasonography and sialoendoscopy in diagnosis and treatment, and summarized the main points of diagnosis and differential diagnosis of CRP in children and adults. The relationship and identification of two kinds of CRP and clinically confusing Sjǒgren's syndrome were analyzed.

In the mammalian tooth development system, tooth morphogenesis is strictly regulated by complex genetic networks that govern the formation of different tooth shapes and types. Previous studies about tooth development mainly focused on mandibular teeth; the gene expression pattern of maxillary tooth development and its differences remain largely unknown. RNA sequencing (RNA-seq) analysis was employed to obtain gene expression profiles of the maxillary and mandibular tooth germs at the cap stage. Differential gene expression was assessed using gene ontology enrichment analysis and protein-protein interaction network analysis. The significant differential gene expression data between the maxillary and mandibular tooth germs were validated using quantitative real-time PCR (RT-qPCR) and immunofluorescence (IF). The transcriptome expression profiles of the maxillary and mandibular tooth germs at the cap stage in human fetuses were successfully constructed. Transcriptome analysis revealed shared activation of the TGF-β, WNT, and NOTCH pathways, with the maxillary tooth germs biased toward morphogenesis and signaling and the mandibular tooth germs towards mineralization and metabolism. A total of 687 differentially expressed genes were identified, highlighting regional differences. RT-qPCR and IF validation confirmed the expression of the key genes. Protein–protein interaction analysis identified core regulators, suggesting their pivotal roles in region-specific tooth development. These findings suggest a region-specific regulatory pattern in human cap-stage tooth germ development, with a tendency toward morphological specialization in the maxillary tooth germs, and mineralization-related processes in the mandibular tooth germs.

Circadian rhythm homeostasis refers to the endogenous 24-hour variations that govern biological activities and coordinate physiological processes by integrating hormonal, metabolic, and immune systems to facilitate organismal adaptation to environmental periodicity. The system orchestrates behavioral patterns and physiological rhythms, and its disruption has been implicated in diverse pathologies. Current methods for circadian rhythm assessment include measurement of melatonin levels, sleep diaries, chronotype analysis, rest–activity rhythms, and core body temperature monitoring. Several biomarkers, including hormones, key metabolites, and neurochemical regulators, are also associated with circadian rhythms. In this review, we aim to synthesize the current research on circadian biomarkers, including sample sources, detection methods, classifications, and evolving frontiers. Identifying and validating these biomarkers (e.g. melatonin and glucocorticoids) hold significant promise for advancing precision medicine in circadian rhythm-related disorders, thereby enabling targeted prevention and therapy.

Mandibular homeostasis depends on mesenchymal stromal cells (MSCs), whose site-specific characteristics critically influence osteogenesis. While phosphoinositide signaling has been extensively studied in limb osteogenesis, its role in mandibular homeostasis remains poorly understood. Despite shared mechanisms underlying hard tissue homeostasis, this study uncovers a distinct regulatory function for Pip5k1a in mandibular osteogenesis, contrasting the previously established role of Pip5k1c in limb osteogenesis. Single-cell transcriptomic analysis revealed unique transcriptional profiles between mandibular MSCs (MdMSCs) and limb MSCs (LbMSCs), with Pip5k1a being highly expressed in MdMSCs and their osteo-lineages. Functional assays demonstrated that Pip5k1a inhibition significantly reduced osteoblastic differentiation while promoting adipogenesis in MdMSCs, underscoring its essential role in osteogenic fate determination. Enrichment of Pip5k1a expression in the mandibular periosteum and endosteum further supports its specialized role in mandibular biology. These findings highlight site-specific molecular mechanisms in bone remodeling and position Pip5k1a as a promising therapeutic target for mandibular bone diseases, such as periodontitis and fractures.

Homeostasis constitutes a dynamic equilibrium process through which an organism sustains internal stability and adjusts to its external environment. A crucial aspect of this process involves a cascade of redox reactions, generating energy (such as adenosine triphosphate, ATP) and synthesizing essential cellular components (such as nucleic acids) from nutrients to support diverse biological functions. Intracellular redox imbalance, resulting from disruptions in the equilibrium between oxidants and antioxidants, is a hallmark event in numerous pathophysiological processes. This review encapsulates the concept of cellular redox homeostasis, examines the factors and processes contributing to regulatory roles in redox homeostasis, and elucidates how cellular functions can be modulated by targeting these molecular mechanisms. Future advancements will necessitate the development of precise assessment methods for redox homeostasis, the judicious selection of oxidative modulators based on disease characteristics, the rationalization of delivery systems, and the creation of precise interventions. These interventions must consider various factors to achieve optimal modulation either positively or negatively and meet therapeutic goals across different diseases.

Many tissues and organ systems have intrinsic regeneration capabilities that are largely driven and maintained by tissue-resident stem cell populations. In recent years, growing evidence has demonstrated that cellular metabolic homeostasis plays a central role in mediating stem cell fate, tissue regeneration, and homeostasis. Thus, a thorough understanding of the mechanisms that regulate metabolic homeostasis in stem cells may contribute to our knowledge on how tissue homeostasis is maintained and provide novel insights for disease management. In this review, we summarize the known relationship between the regulation of metabolic homeostasis and molecular pathways in stem cells. We also discuss potential targets of metabolic homeostasis in disease therapy and describe the current limitations and future directions in the development of these novel therapeutic targets.

Micrognathia is a severe craniofacial deformity affecting appearance and survival. Previous studies revealed that multiple factors involved in the osteogenesis of mandibular bone have contributed to micrognathia, but concerned little on factors other than osteogenesis. In the current study, we found that ectopic activation of Fgf8 by Osr2-cre in the presumptive mesenchyme for masseter tendon in mice led to micrognathia, masseter regression, and the disrupted patterning and differentiation of masseter tendon. Since Myf5-cre;Rosa26R-Fgf8 mice exhibited the normal masseter and mandibular bone, the possibility that the micrognathia and masseter regression resulted directly from the over-expressed Fgf8 was excluded. Further investigation disclosed that a series of chondrogenic markers were ectopically activated in the developing Osr2-cre;Rosa26R-Fgf8 masseter tendon, while the mechanical sensing in the masseter and mandibular bone was obviously reduced. Thus, it suggested that the micrognathia in Osr2-cre;Rosa26R-Fgf8 mice resulted secondarily from the reduced mechanical force transmitted to mandibular bone. Consistently, when tenogenic or myogenic components were deleted from the developing mandibles, both the micrognathia and masseter degeneration took place with the decreased mechanical sensing in mandibular bone, which verified that the loss of mechanical force transmitted by masseter tendon could result in micrognathia. Furthermore, it appeared that the micrognathia resulting from the disrupted tenogenesis was attributed to the impaired osteogenic specification, instead of the differentiation in the periosteal progenitors. Our findings disclose a novel mechanism for mandibular morphogenesis, and shed light on the prevention and treatment for micrognathia.