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.

Mitochondria serve as the primary site for metabolizing the three major nutrients, underscoring their pivotal role in cellular energy metabolism and the regulation of signaling pathways. Mitochondrial homeostatic imbalance is a key pathological cause of the development of many diseases. Hence, preserving mitochondrial homeostasis is vital for the normal growth and development of cells and organisms. Living organisms have evolved intricate regulatory mechanisms to ensure cellular mitochondrial homeostasis. This review focuses on recent advancements in comprehending the mechanisms responsible for maintaining mitochondrial homeostasis and addresses the current challenges in this field. We also provide an overview of the key functions of mitochondria in both physiological and pathological conditions. Emphasizing the potential therapeutic implications, we discuss strategies for preserving mitochondrial homeostasis, recognizing its significance in mitigating various health conditions.

Cisplatin, an anticancer drug, has limited its clinical application due to its severe nephrotoxicity, such as acute kidney injury (AKI). Damaged or dysfunctional mitochondria caused by cisplatin are toxic to the cell by producing reactive oxygen species and releasing cell death factors. Mitophagy is the mechanism of selective degradation of these damaged mitochondria via autophagy, that is critical to cellular homeostasis and viability. In this study, the protective functions of inorganic nitrate against cisplatin-induced nephrotoxicity are assessed. Our results in vitro show that nitrate significantly reduced the apoptosis of HK2 or NRK52E cells induced by cisplatin treatment. Furthermore, dietary nitrate notably alleviates the tubular and glomerular damages as well as the loss of renal function in cisplatin-induced AKI mice models. These protective effects are closely related to downregulation of cell apoptosis and reduction of reactive oxygen species (ROS) generation. Mechanistically, inorganic nitrate treatment promotes the activation of mitophagy mediated by the PINK1-PRKN/PARK2 pathway, which plays an important role in the maintenance of mitochondrial quality, helping renal tubular cells to survive and recover from cisplatin stress. These novel findings suggest that inorganic nitrate supplementation deserve further exploration as a potential treatment in patients with cisplatin-induced renal injury.

Various beneficial biological activities of inorganic nitrate have been revealed in recent decades. Oral bacteria can reduce nitrate to nitrite, which is further reduced to nitric oxide (NO) in the body; this process is known as the nitrate-nitrite-NO pathway. Sialin is a mammalian membrane nitrate transporter that transports nitrate to the salivary glands and secretes it into the oral cavity through the saliva. Recent studies have indicated that nitrate has a protective effect on the salivary glands and other organs by regulating the expression of sialin and maintaining microbial homeostasis. Through the nitrate-nitrite-NO pathway, nitrate can act as a reservoir of NO in vivo and perform a variety of NO-like bioactivities, such as promoting exercise performance, protecting the digestive system, lowering blood pressure, and assisting in tumor treatment. This paper reviews the sources, functions, and possible mechanisms of inorganic nitrate, and discusses the protective role that nitrate promises to play in health and diseases.

Homeostasis is a process of dynamic balance regulated by organisms, through which they maintain an internal stability and adapt to the external environment for survival. In this paper, we propose the concept of utilizing homeostatic medicine (HM) as a strategy to explore health and disease. HM is a science that studies the maintenance of the body's homeostasis. It is also a discipline that investigates the role of homeostasis in building health, studies the change of homeostasis in disease progression, and explores ways to restore homeostasis for the prevention, diagnosis and treatment of disease at all levels of biological organization. A new dimension in the medical system with a promising future HM focuses on how homeostasis functions in the regulation of health and disease and provides strategic directions in disease prevention and control. Nitric oxide (NO) plays an important role in the control of homeostasis in multiple systems. Nitrate is an important substance that regulates NO homeostasis through the nitrate-nitrite-NO pathway. Sialin interacts with nitrate and participates in the regulation of NO production and cell biological functions for body homeostasis. The interactions between nitrate and NO or sialin is an important mechanism by which homeostasis is regulated.