The oral epithelial barrier separates the host from the environment and provides the first line of defense against pathogens, exogenous substances and mechanical stress. It consists of underlying connective tissue and a stratified keratinized epithelium with a basement membrane, whose cells undergo terminal differentiation resulting in the formation of a mechanically resistant surface. Gingival keratinocytes are connected by various transmembrane
proteins, such as tight junctions, adherens junctions and gap junctions, each of which has a specialized structure and specific functions. Periodontal pathogens are able to induce inflammatory responses that lead to attachment loss and periodontal destruction. A number of studies have demonstrated that the characteristics of pathogenic oral bacteria influence the expression and structural integrity of different cell-cell junctions. Tissue destruction can be mediated by host cells following stimulation with
cytokines and bacterial products. Keratinocytes, the main cell type in gingival epithelial tissues, express a variety of proinflammatory
cytokines and
chemokines, including
interleukin-1alpha,
interleukin-1beta,
interleukin-6,
interleukin-8 and
tumor necrosis factor-alpha. Furthermore, the inflammatory mediators that may be secreted by oral keratinocytes are
vascular endothelial growth factor,
prostaglandin E2 ,
interleukin-1 receptor antagonist and
chemokine (C-C motif) ligand 2. The
protein family of
matrix metalloproteinases is able to degrade all types of
extracellular matrix protein, and can process a number of bioactive molecules.
Matrix metalloproteinase activities under inflammatory conditions are mostly deregulated and often increased, and those mainly relevant in
periodontal disease are
matrix metalloproteinases 1, 2, 3, 8, 9, 13 and 24.
Viral infection may also influence the epithelial barrier. Studies show that the expression of
HIV proteins in the mucosal epithelium is correlated with the disruption of epithelial tight junctions, suggesting a possible enhancement of human papilloma virus
infection by HIV-associated disruption of tight junctions. Altered expression of
matrix metalloproteinases was demonstrated in keratinocytes transformed with human
papilloma virus-16 or
papilloma virus-18,. To summarize, the oral epithelium is able to react to a variety of exogenous, possibly noxious influences.