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UBC Theses and Dissertations

Experimental diabetes in ß6 integrin deficient mice Aurora, Saljae


Objectives: Periodontal disease involves transformation of the junctional epithelium (JE) to a pocket epithelium (PE). Integrin avß6 is constitutively expressed in the healthy IF but not in PE. Mice deficient of this integrin (ß6-/-) exhibit increased periodontal bone loss and PE migration. Thus, avß6 integrin in JE may have a protective role against periodontal disease. As diabetes aggravates periodontal disease, we hypothesized that diabetic ß6-/- mice would develop more advanced periodontal disease compared to nondiabetic mice. Furthermore, we hypothesize that re-introduction of ß6 integrin under the cytokeratin 14 (Ki 4) gene promoter in the ß6-/- strain, would restore protection against periodontal disease. Methods: Wild-type (WIT), ß6-/-, ß6 integrin over-expressing (Kl4ß6; ß6 integrin expression is driven by Ki 4 promoter) and ß6 integrin rescue (ß6-rescue; cross-breed of ß6-/- and K14ß6 mice) mice were induced to develop diabetes by injections of streptozotocin, and confirmed diabetic 2 weeks later (Blood glucose >306 mg/dl (17 mmollL). Control animals were exposed to the citrate vehicle only. Four months later, mice were sacrificed. Mandibles were dc-fleshed and imaged for quantification of periodontal bone loss. Maxillae were decalcified and sectioned for histological assessment of epithelial migration and inflammation. Results: Diabetic ß6-/- mice (71% mortality) exhibited significantly higher death rates as compared to non-diabetic WT and K14ß6 groups. Epithelial migration for the ß6-/- strain was significantly higher than that seen in the W/T and the K14ß6 strains. (P

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