Cigarette smoke and alendronate are two different exogenous stimuli involved in the pathogenesis of oral diseases, but their actual role in altering the epithelial barrier and function has not been thoroughly investigated, yet.
To evaluate the morphological chronic effect of both agents, biopsies of normal human keratinized oral mucosa are collected respectively from smoking women (n = 5) and from osteoporotic women undergoing chronic oral therapy with alendronate (n = 6). Both groups are compared to age and sex-matched controls. The acute effects of smoke are investigated in a three-dimensional model of human oral mucosa organotypic cultures (n = 5) after exposure to the mainstream smoke coming from one single cigarette. Morphological analysis by light and transmission electron microscopy is performed on all considered samples.
Chronic smoke and chronic alendronate treatment affect keratinocyte terminal differentiation and intercellular adhesion impairing desmosomal molecular composition and morphology, in a stress specific and time exposure related manner. Desmoglein 3 and desmoglein 1 distribution are altered respectively after chronic smoke and chronic alendronate treatment. Epithelial proliferation is also impaired in the alendronate treated group. On the contrary, after three hours from cigarette smoke exposure, the first significant response of the oral epithelium comes from the immediately suprabasal keratinocytes, without impairment of the epithelial junctional apparatus and apoptosis induction.
The collected data highlight differences in the acute and chronic response of the oral epithelium to cigarette smoke. Moreover, reported results support the crucial signaling role of desmosomal cadherins in the oral epithelium and introduce a new issue in oral biology: the specific response of human oral mucosa to different physico-chemical stresses
