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Objectives: To establish an inflammation grading system for radioactive iodine‐induced sialadenitis (RAIS) based on spiral computed tomography (CT), ultrasonography and sialography. Methods: In all, 120 RAIS patients (18 males and 102 females) were retrospectively included. Spiral CT, ultrasonography and sialography appearances were analysed and categorized as follows: grade I, approximately normal or mild sialadenitis; grade II, moderate sialadenitis; and grade III, severe sialadenitis. Adenitis severity was analysed relative to sex, age, RAI treatment sessions and cumulative doses. Results: Spiral CT showed heterogeneous (78.9%) and atrophic changes (36.8%) in the parotid glands (PGs) and duct ectasia (24.8%) in the submandibular glands (SMGs). Ultrasonography showed heterogeneous echogenicity (54.3%) and diminished gland size (30.2%) in PGs and duct ectasia in SMGs (34.7%). Sialography showed duct obliteration in 25.3% PGs and 3.2% SMGs. Statistical analysis showed good consistency among the three imaging grading results. The incidence and severity of PG lesions were significantly higher than that of SMGs (p < 0.001). As for PGs, adenitis severity was associated with both treatment sessions and cumulative doses; but in SMGs, disease severity was only related to treatment sessions. Conclusions: A grading system for severity of RAIS was established based on spiral CT, ultrasonography and sialography appearances. [ABSTRACT FROM AUTHOR]

Objectives: Confirm that stem cells from human exfoliated deciduous teeth‐derived exosomes (SHED‐exos) can limit inflammation‐triggered epithelial cell apoptosis and explore the molecular mechanism. Methods: SHED‐exos were injected into the submandibular glands (SMGs) of non‐obese diabetic (NOD) mice, an animal model of Sjögren's syndrome (SS). Cell death was evaluated by western blotting and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labelling staining. Results: SHED‐exos treatment promoted the saliva flow rates of NOD mice, accompanied by decreased cleaved caspase‐3 levels and apoptotic cell numbers in SMGs. SHED‐exos inhibited autophagy, pyroptosis, NETosis, ferroptosis, necroptosis and oxeiptosis marker expression in SS‐damaged glands. Mechanistically, Kyoto Encyclopedia of Genes and Genomes analysis of exosomal miRNAs suggested that the rat sarcoma virus (RAS)/mitogen‐activated protein kinase kinase (MEK)/extracellular signal‐regulated kinase (ERK) pathway might play an important role. In vivo, the expression of Kirsten RAS, Harvey RAS, MEK1/2 and p‐ERK1/2 was upregulated in SMGs, and this change was blocked by SHED‐exos treatment. In vitro, SHED‐exos suppressed p‐ERK1/2 activation and increased cleaved caspase‐3 and apoptotic cell numbers, which were induced by IFN‐γ. Conclusion: SHED‐exos suppress epithelial cell death, which is responsible for promoting salivary secretion. SHED‐exos inhibited inflammation‐triggered epithelial cell apoptosis by suppressing p‐ERK1/2 activation, which is involved in these effects. [ABSTRACT FROM AUTHOR]

Objective: To analyse the histopathological features of eosinophilic sialodochitis by using terminal duct biopsy. Methods: Sixty‐five patients with suspected eosinophilic sialodochitis and four with chronic obstructive sialadenitis were prospectively enrolled. Clinical features, laboratory tests and sialograms were comparatively analysed. Terminal duct biopsy of the parotid or submandibular glands was performed concomitantly with endoscopy‐assisted duct dilatation to determine the histopathological features of eosinophilic sialodochitis. Results: Based on eosinophil quantification, the samples of suspected patients were scored as 'definite', 'highly suspected' and 'negative' in 26 (40%), 15 (23.1%) and 24 (36.9%) cases, respectively. Gland types and peripheral blood eosinophil counts were significantly different among these three groups. The proportions of itching glands, mucus plug exudations and elevated immunoglobulin E levels were higher in the 'definite' group than in the other two groups; however, the intergroup differences were insignificant. The primary pathological features of eosinophilic sialodochitis were abundant eosinophils and lymphocytes infiltrated around the duct, degranulation of eosinophils, extensive fibrosis and scattered mastocytes. Periductal eosinophils were not found in cases of chronic obstructive sialadenitis. Conclusion: Our findings suggest that terminal duct biopsy is safe and valuable for the pathological confirmation of eosinophilic sialodochitis, and can be used simultaneously with endoscopy‐assisted duct dilatation. [ABSTRACT FROM AUTHOR]

Tight junctions (TJs) are cell–cell interactions that localize at the most apical portion of epithelial/endothelial cells. One of the predominant functions of TJs is to regulate material transport through paracellular pathway, which serves as a selective barrier. In recent years, the expression and function of TJs in salivary glands has attracted great interest. The characteristics of multiple salivary gland TJ proteins have been identified. During salivation, the activation of muscarinic acetylcholine receptor and transient receptor potential vanilloid subtype 1, as well as other stimuli, promote the opening of acinar TJs by inducing internalization of TJs, thereby contributing to increased paracellular permeability. Besides, endothelial TJs are also redistributed with leakage of blood vessels in cholinergic‐stimulated submandibular glands. Furthermore, under pathological conditions, such as Sjögren's syndrome, diabetes mellitus, immunoglobulin G4‐related sialadenitis, and autotransplantation, the integrity and barrier function of TJ complex are impaired and may contribute to hyposalivation. Moreover, in submandibular glands of Sjögren's syndrome mouse model and patients, the endothelial barrier is disrupted and involved in hyposecretion and lymphocytic infiltration. These findings enrich our understanding of the secretory mechanisms that link the importance of epithelial and endothelial TJ functions to salivation under both physiological and pathophysiological conditions. [ABSTRACT FROM AUTHOR]