To consider the answer of these questions, we need to look at the pathogenesis of periodontal disease.
It has been well established that plaque is essential for initiation of gingivitis, the progression of gingivitis to periodontitis and its further deterioration (Mild à Moderate à Severe) is related to immune-inflammatory imbalance. In simple words, it is the imbalance with a domination of aggressive host immuno-inflammatory response over reparative capacity or anti-inflammatory response of the body. When this balance is maintained or reparative response dominates, the disease does not progresses further (the periodontal pockets cannot heal without elimination of biofilm by debridement). The immune-inflammatory imbalance in favour of disease progression is driven by:
While plaque is necessary for initiating process of periodontal disease, the disease progression is taken over by body’s immuno-inflammatory response (imbalance).
There are some bugs (microorganisms) which are infamous for their destructive potential and may possibly contribute to immune imbalance:
Robert Koch, very well known for isolating Bacillus anthracis (1877), the Tuberculosis bacillus (1882) and Vibrio cholerae (1883) and for his development of Koch’s postulates to link a bacteria with infection; the above 4 bacteria fulfill most if not all the postulates, modified for periodontitis by Socransky and coworkers.
Presence of these bacteria, individually or combination, were not as predictive of periodontal disease progression as their absence being noticeable in stable sites. In fact, the bleeding on probing from periodontal pockets, which is a clinical sign of immuno-inflammatory imbalance, can provide source of nutrition (blood) and so increase the red complex bacteria in the deep pockets. Thus, it is hard to establish a cause-response-relationship of the presence of red complex with deep pockets. Alternatively, the presence is governed by ecological factors such as anaerobic environment of deep pocket along witn increased protein and heme content from exudation and bleeding from pockets.
Regarding microbiology, now we know that “we don’t know a lot compared to what we know”. There are around 500 microorganisms can be found in periodontal pocket area, as characterized by studying 16s sequencing. Many of them are not yet characterized and we don’t know how they can contribute to periodontal pathology and potentially contribute towards an immuno-inflammatory imbalance.
Overall, we don’t rely on microbiological assessment in treating/monitoring severe cases of periodontitis, we probably rely more on clinical signs of immuno-inflammatory imbalance like bleeding on probing.
