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The etiopathogenesis of periodontal disease results from complex interaction between infectious agents, mainly including bacteria, and host cellular and humoral immune responses. However it is thought that bacteria-induced pathogenesis is not sufficient alone to explain all biological and clinical features of the destructive periodontal disease. The main hypothesis is that herpesviruses, such as Epstein-Barr Virus, may participate as well by altering epithelial gingival cell biology and consequently may promote the initiation and progression of periodontitis.
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Interventional model
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23 participants in 3 patient groups
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Vanina OLIVERI, ARC promoteur; Severine VINCENT, PH
Data sourced from clinicaltrials.gov
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