Composition of hemidesmosomes in basal keratinocytes of normal buccal mucosa and oral lichen planus

Abstract

Oral lichen planus (OLP) is a chronic inflammatory disease displaying ultrastructural disturbances in epithelial hemidesmosomes. The expression of several key hemidesmosomal components in OLP as well as in normal buccal mucosa is, however, unknown. The aim of the study was therefore to examine intracellular and extracellular components involved in hemidesmosomal attachment, in OLP (n = 20) and in normal buccal mucosa (n = 10), by immunofluorescence. In normal buccal mucosa, laminin‐α3γ2, integrin‐α6β4, CD151, collagen α‐1(XVII) chain, and dystonin showed linear expression along the basal membrane, indicating the presence of type I hemidesmosomes. Plectin stained most epithelial cell membranes and remained unphosphorylated at S4642. In OLP, most hemidesmosomal molecules examined showed disturbed expression consisting of discontinuous increases, apicolateral location, and/or intracellular accumulation. Plectin showed S4642‐phosphorylation at the basement membrane, and deposits of laminin‐α3 and laminin‐γ2 were found within the connective tissue. The disturbed expression of hemidesmosomal proteins in OLP indicates deficient attachment of the basal cell layer, which can contribute to detachment and cell death of basal keratinocytes seen in the disease.

Junctional complexes in epithelial cells: sentinels for extracellular insults and intracellular homeostasis

“…Hemidesmosomes are anchoring structures at the basement membrane that link intermediate filaments with the extracellular matrix via integrin proteins [20]. These types of junctions have been found in most of our major organs, including the epithelium of the skin [21][22][23][24][25], the digestive system (oral cavity, esophagus, stomach, and intestine) [26][27][28][29][30][31][32][33][34][35][36], the nasal cavity and trachea [37][38][39][40][41][42][43][44], and excretory organs such as kidney and bladder [45][46][47][48]. Tight junctions and desmosomes are also detected in the alveolus epithelium [49][50][51].…”

Cortactin expression in a Norwegian cohort of human papilloma virus negative oral squamous cell carcinomas of the mobile tongue

“…Primary cell cultures were established from oral mucosal tissue obtained after third molar extractions as described recently [30]. In brief, the epithelial sheet and the connective tissue were separated by tissue digestion, then cut into small pieces prior to cell isolation through enzymatic treatment.…”

Role of Hemidesmosomes in Oral Carcinogenesis: A Systematic Review

“…A total of 15 studies, comprising 12 in vitro, 1 in vivo and 2 in vivo and in vitro studies, examined changes to individual α6 and/or β4 subunits at different stages of oral carcinogenesis [6,[24][25][26][27][28][29][30][31][32][33][34][35][36][37]. Expression of α6 in OSCC and oral leukoplakia (OL) lesions was higher compared to normal mucosa, while β4 expression was increased in OSCC lesions with negligible changes in OL lesions [25].…”

“…A total of 12 studies, comprising 11 in vitro and 1 in vivo, specifically examined alterations in the hemidesmosomal integrin α6β4 heterodimer [24][25][26][27][28][29][30][33][34][35][36][37]. An in-vitro study on human primary OSCC tumours demonstrated increased α6β4 expression in aggressive lesions compared to non-metastatic growths, but reduced expression in PD and recurring tumours [27,34,36].…”