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Definition of Periodontal Disease

“Periodontal disease” does not describe a single disease entity but is a general term encompassing all diseases of the periodontal tissues.

There are many forms of disease which can damage the periodontal tissues, including chronic marginal gingivitis, acute necrotizing gingivitis and periodontitis. All manifest as a reactive immune response to dysbiosis (microbial imbalance) leading to inflammation.

Etiology of Periodontal Disease

How do bacteria cause disease?
Periodontitis is regarded as a condition that is seen in susceptible patients who have an exaggerated inflammatory/immune response to bacterial biofilm and/or reduced levels of antioxidant defence (intracellular molecules present in cells which offer protection from excess inflammatory response). This leads to chronic collateral damage of the periodontal tissues because the host response is unable to successfully remove the biofilm, resulting in the propagation of the periodontal lesion.

Both the quantity and the quality of bacteria that have colonized the gingival sulcus/periodontal pocket can contribute to disease. The quantity causes local gingival inflammation (gingivitis). The quality (species of bacteria) can produce specific virulence factors, especially enzymes, toxins and other metabolic products, all of which have the potential to damage the periodontal tissues (and activate the host's inflammatory/immune response).

Periodontitis is the result of complex interactions between plaque bacteria and the host response.


Role of pathobionts and dysbiosis in periodontitis. ( A ) Pathobionts and associated disease. Pathobionts could be colonized as one of the resident bacteria (commensals) in human bodies without any obvious symptoms. Once dysbiosis is induced by environmental changes ( e.g. , antibiotic treatment, accumulation of other microbes or epithelial barrier disruption), pathobionts cause significant changes in host health. Alternatively, changes in hosts and bacteria, for instance, by genetic variations and immunological defects, affect the virulence of pathobionts, resulting in disease development. (B) Dysbiosis during periodontitis development.

Theory of keystone pathogens and Dysbiosis

The first event at a periodontal site is colonization of the pioneer bacteria that form the biofilm. The pioneer bacteria include Streptococcus species, which strongly interact with host cells. Other indicated biofilm community members are also able to colonize and grow with co-aggregation. Putative pathogens such as F. nucleatum likely act as scaffolds to bridge multiple bacteria and to facilitate colonization by additional biofilm-forming community members. The poor availability of energy sources from foods enforces specific bacteria to obtain energy from host factors by damaging host tissues. These host-damaging bacteria include the red complex bacteria ( P. gingivalis, T. forsythia , and T. denticola ), which possess high protease activity, and toxin-secreting A. actinomycetemcomitans (Aa). Several keystone pathogens, including the red complex bacteria, possess the ability to avoid host detection to optimize their acquisition of energy sources from the host. In addition, the keystone pathogen hypothesis proposes that immunological interference by keystone pathogens further establishes dysbiosis. Finally, environmental changes induced by keystone pathogens facilitate colonization of additional pathobionts that stimulate host immune responses, which results in periodontitis

The major pathogen linked to CP is Porphyromonas gingivalis, with bacterial partners such as Treponema denticola and Tannerella forsythia.

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