Current concepts in periodontal pathogenesis.
Periodontal research over the last 40 years has been remarkably prolific. We now understand that severe periodontitis affects approximately 10-15% of the population (representing a large number of individuals in the UK) and gingivitis and mild periodontitis affect a majority of people. Microbiological research has identified some of the key pathogens that are implicated in periodontal disease. Plaque bacteria exist in biofilms, which have evolved to protect individual organisms within the subgingival bacterial community. For this reason, root surface instrumentation (RSI) remains the cornerstone of periodontal treatment, and is necessary to disrupt the subgingival biofilm mechanically and reduce the bacterial bioburden. Although bacteria are necessary for periodontal disease to occur, a susceptible host is also required. The immune-inflammatory response that develops in the gingival and periodontal tissues in response to the chronic presence of plaque bacteria results in destruction of structural components of the periodontium leading, ultimately, to the clinical signs of periodontitis. The nature of the host response is determined primarily by genetic factors and environmental and acquired factors such as smoking. The host response is essentially protective in nature, but both under-activity (hypo-responsiveness) and over-activity (hyper-responsiveness) of aspects of the host response can result in enhanced tissue destruction. The purpose of this paper is to review current thinking in periodontics with special reference to periodontal epidemiology, microbiology, and pathogenesis.
Preshaw
Philip M
PM
School of Dental Sciences, University of Newcastle upon Tyne, UK.
Seymour
Robin A
RA
Heasman
Peter A
PA
D018441:Biofilms; D003773:Dental Plaque / Q000382:microbiology*; D012534:Dental Scaling; D018450:Disease Progression; D005891:Gingivitis / Q000473:pathology; D006801:Humans; D018836:Inflammation Mediators / Q000009:adverse effects; D010518:Periodontitis / Q000453:epidemiology / Q000209:etiology* / Q000628:therapy; D012307:Risk Factors; D016745:Root Planing
D018836:Inflammation Mediators