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Expression of alpha v beta 6 integrin in periodontal disease Ghannad, Farzin


Integrins are the principal cell surface receptors that mediate cell-to-cell or cell-to-extracellular matrix (ECM) binding, providing adhesion for stationary cells, traction during cell movement and, importantly, translating extracellular matrix cues into intracellular signal transduction pathways. The ανβ6 integrin, an exclusively epithelial integrin, exhibits limited distribution in the body. In adult tissue, ανβ6 integrin is expressed during inflammation, carcinogenesis, and in wound healing. It is not expressed in oral gingival epithelium but it is constitutively expressed in junctional epithelium (JE). Its capability to bind and activate transforming growth factor-β (TGFβ) suggests immune regulation and it could therefore play a protective role against periodontal disease. When comparing hematoxylin and eosin stained paraffin sections of wild-type (FVB) and β6 integrin-knockout mice (β6 -/-) under the light microscope, apical migration of junctional epithelium beyond the cemento-enamel junction (CEJ) resulting in formation of pocket epithelium (PE) was clearly demonstrated only in specimens of β6 integrin-knockout animals. In addition, analysis of defleshed mandibles revealed a significant increase in alveolar bone loss and therefore enhanced exposed root surface area and furcation involvement for knockout mice in comparison to their age matched wild-type animals (FVB). The findings of this study suggest that ανβ6 integrin, exclusively expressed in JE, might play an important role in the pathogenesis of periodontal disease in mice. One possible mechanism could be through its regulatory function in the activation of TGFβ.

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