Microbiological basis for periodontal therapy

Abstract

The search for the etiologic agents of periodontal diseases started in the Golden Era of medical bacteriology, when the etiologic agents of many bacterial infections were isolated and characterized. After the initial enthusiasm in establishing the infectious nature and the true agents of periodontal diseases, this concept was virtually ignored for the next four decades. Until the early 1970s treatment regimens based on the non-specific plaque hypothesis were directed towards a non-specific reduction in plaque amount. Later, the specific plaque hypothesis established the role of some microorganisms such as A. actinomycetemcomitans, P. gingivalis, T. forsythensis, T. denticola, P. intermedia and F. nucleatum in different forms of periodontal diseases. It was recently suggested that these suspected periodontal pathogens seem to not act alone and interactions between species, especially the balance between pathogenic and beneficial species affect both progression of disease and response of tissues to periodontal therapy. Nowadays it is well established that one of the goals of therapy is to control such periodontal pathogens. Among the most commonly used therapies to treat periodontal infections are scaling and root planing (SRP), supragingival plaque control and periodontal surgeries. Many studies confirmed the reduction of "red complex" species by SRP, and apically repositioned flap can lead to an additional beneficial effect in the subgingival microbiota by decreasing levels of "red" and "orange complexes" species. Furthermore, the level of plaque control maintained by the patients has been considered a crucial step in preventing recurrence of destructive periodontitis.

The Biological Activity of Propolis-Containing Toothpaste on Oral Health Environment in Patients Who Underwent Implant-Supported Prosthodontic Rehabilitation

“…One of them, the so-called “red complex,” consisting of Tannerella forsythensis , Porphyromonas gingivalis, and Treponema denticola, is strongly associated with increased depth of periodontal and/or peri-implant pockets as well as bleeding when a probe is inserted [3]. Results of clinical and microbiological investigations also indicate that Prevotella intermedia or Fusobacterium nucleatum, among others, are potential etiological factors causing periodontitis and peri-implantitis problems [4]. Reduction of the number of those pathogenic micro-organisms could potentially influence the epidemiology of periodontium diseases, reducing their amount and intensification.…”

Associations Between Periodontitis and Chronic Obstructive Pulmonary Disease: The 2010 to 2012 Korean National Health and Nutrition Examination Survey

“…Periodontitis is a common infectious disease affecting tissues supporting teeth 1 . Risk factors for periodontal disease include: 1) poor oral hygiene; 2) diabetes mellitus (DM); 3) smoking; 4) low socioeconomic status; 5) age; and 6) stress 2 .…”

Associations Among Oral Hygiene Behavior and Hypertension Prevalence and Control: The 2008 to 2010 Korea National Health and Nutrition Examination Survey

“…Periodontitis is defined as a chronic inflammatory disease of microbial origin, which is characterized by a progressive loss of alveolar bone around the teeth as well as pocket formation around the teeth and/or gum recession. 33,34 The present authors believe that although periodontitis is not seen yet, inflammatory and immune reactions could take place by local bacteria, host immune response, and reactive oxygen species produced by locally infiltrating neutrophils. Previously, it was shown that individuals who cleaned their teeth at least twice a day had less visible plaque compared with those who cleaned their teeth less than once a day or never.…”

“…It is also important to note that in this study, oral behavior is associated with the prevalence of hypertension even in the population without periodontitis. Periodontitis is defined as a chronic inflammatory disease of microbial origin, which is characterized by a progressive loss of alveolar bone around the teeth as well as pocket formation around the teeth and/or gum recession 33,34 . The present authors believe that although periodontitis is not seen yet, inflammatory and immune reactions could take place by local bacteria, host immune response, and reactive oxygen species produced by locally infiltrating neutrophils.…”