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.
Clinical and microbiological benefits of strict supragingival plaque control as part of the active phase of periodontal therapy