Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/111022
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Host modulation: controlling the inflammation to control the infection
Author: Bartold, P.
Van Dyke, T.
Citation: Periodontology 2000, 2017; 75(1):317-329
Publisher: Blackwell Publishing
Issue Date: 2017
ISSN: 0906-6713
1600-0757
Statement of
Responsibility: 
P. Mark Bartold, Thomas E. Van Dyke
Abstract: Historically, 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'.
Keywords: Humans; Periodontal Diseases; Disease Progression; Disease Susceptibility; Inflammation; Host-Pathogen Interactions; Microbiota
Rights: © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
RMID: 0030074836
DOI: 10.1111/prd.12169
Grant ID: http://purl.org/au-research/grants/nhmrc/1023747
http://purl.org/au-research/grants/nhmrc/627143
Appears in Collections:Dentistry publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.