Drug-Induced Gingival Overgrowth—a Review

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  • Kataoka Masatoshi
    Division of Gene Expression, Institute for Genome Research, The University of Tokushima
  • Kido Jun-ichi
    Department of Periodontology and Endodontology, Institute of Health Bioscience, The University of Tokushima Graduate School
  • Shinohara Yasuo
    Division of Gene Expression, Institute for Genome Research, The University of Tokushima Health Technology Research Center, National Institute of Advanced Industrial Science and Technology (AIST), Japan Faculty of Pharmaceutical Sciences, The University of Tokushima
  • Nagata Toshihiko
    Department of Periodontology and Endodontology, Institute of Health Bioscience, The University of Tokushima Graduate School

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  • Drug-Induced Gingival Overgrowth--a Review
  • Drug-Induced Gingival Overgrowth—a Review

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Abstract

Drug-induced gingival overgrowth is a side effect associated with 3 types of drugs: anticonvulsants (phenytoin), immunosuppressive agents (cyclosporine A), and various calcium channel blockers for cardiovascular diseases. Gingival overgrowth is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components with various degrees of inflammation. Although the mechanisms of these disorders have not been elucidated, recent studies suggest that these disorders seem to be induced by the disruption of homeostasis of collagen synthesis and degradation in gingival connective tissue, predominantly through the inhibition of collagen phagocytosis of gingival fibroblasts. The integrins are a large family of heterodimeric transmembrane receptors for extracellular matrix molecules. α2β1 integrin serves as a specific receptor for type I collagen on fibroblasts, and α2 integrin has been shown to play a crucial role in collagen phagocytosis. Actin filaments, which are assembled from monomers and oligomers, are involved in collagen internalization after binding to integrins. Furthermore, the implication of intracellular calcium in the regulation of integrin-mediated binding activity and gelsolin activity, known as a calcium-dependent actin-severing protein, is also described. In this review, we focus on collagen metabolism in drug-induced gingival overgrowth, focusing on the regulation of collagen phagocytosis in fibroblasts.

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