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Structure and function of the tooth–epithelial interface in health and disease
Author(s) -
Pöllänen Marja T.,
Salonen Jukka I.,
Uitto VeliJukka
Publication year - 2003
Publication title -
periodontology 2000
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.725
H-Index - 122
eISSN - 1600-0757
pISSN - 0906-6713
DOI - 10.1034/j.1600-0757.2003.03102.x
Subject(s) - medicine , periodontology , dentistry
Three types of mucous membranes (masticatory, lining, and specialized) line the oral cavity and form the structural boundary between the body and the external environment. Although each type of mucosa protects against mechanical and microbial damage, the epithelia exhibit considerable differences in their histology, thickness and differentiation suitable for the functional demands of their location. Furthermore, the structure of different epithelia reflects their effectiveness as a barrier to the penetration of microbes and noxious agents into the deeper tissues (141,160). Mucosal epithelia are composed of continuously dividing and shedding populations of keratinocytes whose proliferation is confined to the basal layer. The teeth, passing through the gingival masticatory mucosa, create a unique environmental challenge to the protective continuity. At the interface where the healthy gingiva meets the tooth surface the structural continuity is secured by the junctional epithelium attached to the tooth surface by a distinct mechanism known as the epithelial attachment apparatus (143). As opposed to the constantly renewing epithelia, teeth are units of nonshedding surfaces, which provide a solid substratum not only for the attachment of the junctional epithelial cells but also for bacterial colonization and spreading in the oral cavity. At the dentogingival junction the bacterial colonies, exhibiting a variety of virulence factors (68), pose a potential threat to the epithelial attachment. The attachment may be affected directly by bacteria or indirectly through their ability to activate inflammatory and immune processes, which contribute to the composition of the gingival crevice fluid (GCF) and thus to the conditions under which