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.