Year : 2021 | Volume
: 25 | Issue : 2 | Page : 93--94
Dynamic concepts of periodontal etiology
Department of Periodontology, J. N Kapoor D.A.V (C) Dental College and Hospital, Yamunanagar, Haryana, India
Department of Periodontology, J. N Kapoor D.A.V (C) Dental College and Hospital, Yamunanagar, Haryana
|How to cite this article:|
Pandit N. Dynamic concepts of periodontal etiology.J Indian Soc Periodontol 2021;25:93-94
|How to cite this URL:|
Pandit N. Dynamic concepts of periodontal etiology. J Indian Soc Periodontol [serial online] 2021 [cited 2021 Apr 16 ];25:93-94
Available from: https://www.jisponline.com/text.asp?2021/25/2/93/310575
Periodontology as a speciality is concerned with tissues that are always in a state of flux and are further interconnected with the rest of the systems of our body. The zone of the initiation of the disease process is also somewhat unique, where hard tissue of the tooth structure is jutting out from the soft tissues and thereby making this area even more susceptible to the onslaught of bacterial toxins actually.
We have witnessed a sea of change in the way the etiological concepts have developed in understanding the etiology of these chronic inflammatory conditions but the certainty of these hypotheses are still not established. Initially the diseases were thought to be degenerative in nature (W.J Younger 1894) until the time Loe et al. in 1965 established the role of dental plaque in Gingivitis & Periodontitis which led to the hypothesis that if we allow the bacteria to accumulate on the tooth surfaces, it will lead to the initiation of an inflammatory reaction in the periodontal tissues.
Socransky & Haffajee in a series of studies between 1920 and 1960's concluded that periodontitis results from some defect in the immune response of the patient, trauma from occlusion, nutritional deficiency or disuse atrophy. They further placed emphasis on the role of calculus, rough surfaces of the restorations and systemic diseases in periodontal disease development.
In 1994, with the advent of new diagnostic techniques like DNA-DNA hybridization, and response of the disease to the use of antibiotics, studies again reestablished the concept that periodontitis results from the bacteria and is infectious in nature. Then the concept of Specific plaque Hypothesis came into existence which was based on the observation that some patients with abundant amounts of plaque did not display any attachment loss while some individuals with scanty amounts of plaque showed advanced bone and attachment loss. This discrepancy could only be explained by assigning the bacteria into various categories depending on their degree of virulence and therby we could explain the pathogenesis of severe forms of periodontitis like Aggressive Periodontitis and associated with systemic diseases. This hypothesis also could not be fully validated because of the fact that the bacteriologists found it difficult to culture some periodontopathogens, and thus, their role could not be established in the pathogenesis of the disease as such. As there is a gap or a latent period between the presence of the etiological agents and the occurrence of the disease, even the presence of virulent organisms does not necessarily mean that the present disease condition is the result of these interactions.
Further in 1990's the detection of viruses in the periodontal lesions led to the concept of viral synergy with bacteria in propagation of the periodontal disease. Various mechanisms like exaggerated host response along with potentiation of bacterial virulence was implicated. But some studies proved to disregard this hypothesis also.
Marsh introduced the term dysbiosis and the theory of ecological succession, stating that the bacteria which colonize teeth initially change the local environment and the bacteria which thrive in that environment only survive. Although the concept of bacterial specificity seems to enjoy the consensus among the scientific community for past so many years but, latest research using the molecular techniques put more emphasis on the wide variety of organisms which have missed the detection by more conventional methods like culturing and even DNA-DNA checkerboard with limited capacity to detect all the periodontal pathogens.
A part of the etiology related with the progression of periodontitis may be explained by the concept that inflammation may be central to the development of specific pathogenic flora at the local site. It is because of this understanding that we are trying to control the disease by modulating the host response by the use of anti-inflammatory agents. The resolution of the inflammation may lead to the change of the micro flora to a much healthier complex.
There has always been a yearning to reach a proper system of cause and effect in any disease by the scientific community and diseases affecting the periodontium are no exception. Since it is a multifactorial disease with complex interactions between the risk factors, it is difficult to ascertain a specific role to each component and the research thus goes on…
Future research in this field will be directed towards the characterization of the combined gene expressions and their interactions in the bacterial plaque rather than concentrating on the individual species. This type of revelation will lead to the exploration of more novel methods to manage this chronic disease condition.