Oral epithelial membrane‐associated mucins and transcriptional changes with Sjögren's syndrome

Abstract

Objectives To determine expression and localization of membrane‐associated mucins within human keratinized and non‐keratinized oral epithelia, and to explore transcriptional changes associated with primary Sjögren's syndrome. Subjects and Methods Mucin transcripts and glycoproteins were determined by RT‐PCR and immunohistochemistry, respectively, in oral keratinized (hard palate) and non‐keratinized (buccal) epithelia obtained from three cadavers. Mucin transcripts assessed by quantitative PCR were compared between cells harvested by brushing buccal and palatal epithelia of 25 female primary Sjögren's syndrome patients vs 25 healthy age‐matched female control subjects. Results In hard palate, MUC4 is absent and MUC1 localized to deeper cell layers. Both mucins are within the apical layers of buccal epithelium. MUC15 is localized throughout all palatal cell layers and in all but the basal layer of buccal epithelia. MUC16, MUC20, and MUC21 glycoproteins are localized within all but the basal cell layer of both tissue types. In buccal cells of primary Sjögren's patients, MUC21 transcripts are down‐regulated 3.4‐fold and MUC20 2.6‐fold. Dysregulation of select epithelial mucins may therefore contribute to xerostomia. Conclusions Differential expression of multiple mucins and down‐regulation in Sjögren's syndrome support further study of oral epithelial mucin physiology and pathophysiology, including their functions in hydration and lubrication of the oral mucosal pellicle.

Differences in perceived intra-oral dryness in various dry-mouth patients as determined using the Regional Oral Dryness Inventory

“…Notably, they show that SS patients had significantly higher RODI scores (median score 4.00) for the posterior palate than controls did (median score 3.00). This can be explained by the fact that except for the palatal salivary flow rate [ 29 , 30 ], the UWS flow rate in SS patients is reduced [ 20 , 29 – 34 ]. Indeed, the number of patients with xerostomia was higher in SS patients [ 29 , 30 , 32 ].…”

Surfactant Protein A and Microbiome Composition in Patients With Atraumatic Intraoral Lesions

“…Repeating the differential abundance analysis adjusting for smoking, Bifidobacterium dentium is no longer significant (Table 3 Block 2). Adjusting for both smoking and SP-A levels removes the final eight OTUs from significance (Table 3 Block 3). When the differential abundance species lists are considered collectively, of the 16 bacterial species initially associated with intraoral lesions, all are more strongly influenced by smoking or SP-A levels.…”

“…It also provides the first line of defense against harmful microbes and chemical substances, and intact mucosa is a major component of innate immunity [ 1 ]. Intraoral lesions are ulcerous conditions of the mucosa that appear with many medical conditions, including autoimmune disorders, diabetes, and Sjogren syndrome [ 2 , 3 ]. The multifactorial nature of this condition also implicates host genetics, nutrition, stress levels, changes in hormone levels, and immune responses.…”

Regulation of mucin 1 expression and its relationship with oral diseases

“…The presence of secretory granules and extracellular matrix for mucins indicates that ectopic exocytosis may be due to 1) alterations in the cytoskeleton (actin microfilament), 2) changes in the secretory pathway (Rab GTPase -Ras superfamily of small G protein; guanosine triphosphate hydrolase enzyme) involved in membrane recognition and fusion of vesicles, 3) alterations in membrane fusion receptors (SNARE proteinssoluble N-ethylmaleimidesensitive factor attachment protein receptor) (Wang et al, 2008). These changes result in a disturbed mucin distribution and its secretion by ductal and acinar cells of the minor salivary glands explains the cytoplasmic accumulation of MUC1 in SS patients (Prez-Vilar, 2007;Culp, Stewart & Wallet, 2019).…”