Bartold, P.M.Van Dyke, T.E.2018-03-142018-03-142017Periodontology 2000, 2017; 75(1):317-3290906-67131600-0757http://hdl.handle.net/2440/111022Historically, periodontal disease (gingivitis and periodontitis) has been recognized as being primarily of bacterial origin. However, recent evidence indicates that while bacteria are necessary for disease development they are not sufficient for the clinical manifestation of the many and varied forms of periodontal disease. It is becoming increasingly apparent that it is the host inflammatory response to the subgingival bacteria that is responsible for the tissue damage and, most likely, progression of the disease. We explore the concept that it is the subgingival microenvironment modified by the inflammatory response that leads to a change from a commensal to pathogenic microbiota. In this review, we examine the evidence for the emerging paradigm supporting the central role of inflammation rather than specific microbiota in the pathogenesis of periodontitis, and that by controlling the inflammation, it is possible to control the infection. As an extension of this, we propose a working model for the ongoing monitoring of periodontal patients using the medical model of 'treat to target'.en© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.HumansPeriodontal DiseasesDisease ProgressionDisease SusceptibilityInflammationHost-Pathogen InteractionsMicrobiotaJournal article003007483610.1111/prd.121690004066560000102-s2.0-85026628622368209Bartold, P.M. [0000-0002-5695-3877] [0000-0002-6225-3084]