Plaque Hypothesis

Microbiologic Specificity of Periodontal disease

1. Non-specific Plaque Hypothesis
2. Specific Plaque Hypothesis
3. Ecological Plaque Hypothesis
4. Keystone Pathogens Hypothesis

Non- Specific Plaque Hypothesis

“Periodontal disease results from the elaboration of noxious products by the entire plaque flora”- Theilade in 1986. 

According to proponents of this concept, the quantity of plaque was important rather than the quality of microorganisms present. They believed; When only small amount of plaque are present they are neutralized by host. Similarly, large amount of plaque produces large amount of noxious products, which would essentially overwhelm the hosts defense causing tissue destruction. Most of if not all periodontal treatment including debridement and oral hygiene maintenance is founded on this hypothesis.

This theory is now discarded because:

1. Some individuals with considerable amount of plaque and calculus as well as gingivitis never developed destructive periodontitis.

2. Individuals with periodontitis demonstrated considerable site specificity in pattern of disease.

3. Individuals with very less plaque developed destructive periodontal disease as in Aggressive periodontitis. 

Updated Non specific Plaque hypothesis 

Theilade’s statement (1986) that “any microbial colonization of sufficient quantity in the gingival crevice causes at least gingivitis." It was supported by the fact that a non-pathogenic plaque (i.e., not causing gingivitis in the absence of oral hygiene) had never been observed.

Specific Plaque Hypothesis(Loesche 1989)

States that only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganism. This concept predicts that plaque harboring specific bacterial pathogens results in periodontal disease because these organisms produce substances that mediate the destruction of host tissues.

Eg: A actinomycetemcomitans as pathogen in localized aggressive periodontitis

Ecological Plaque Hypothesis

Proposed by Marsh & Co-workers (1991). 

1. The bacterial composition of plaque remains relatively stable despite regular exposure to minor environmental perturbations. This stability (microbial homeostasis) is due in part to a dynamic balance of both synergistic and antagonistic microbial interactions. However, homeostasis can break down, leading to shifts in the balance of the microflora, thereby predisposing sites to disease. 

Eg: frequent exposure of plaque to low pH leads to inhibition of acid-sensitive species and the selection of organisms with an aciduric physiology, such as mutans streptococci and lactobacilli.

Similarly, The subgingival microflora shifts from being mainly Gram-positive to being comprised of increased levels of obligately anaerobic, asaccharolytic Gram-negative organisms.

It is proposed that disease can be prevented or treated not only by targeting the putative pathogens but also by interfering with the processes that drive the breakdown in homeostasis.

Keystone Pathogen Hypothesis

George Hajishengallis and colleagues (2012) proposed,“keystone pathogen” hypothesis which believes that, "certain low-abundance microbial pathogens can produce inflammatory disease by remodelling a normally benign microbiota into a dysbiotic one." It was developed by observing the characteristics of Red Complex (P. gingivalis) with the role of host immune response critical. 

P. gingivalis can inhibit the production of IL-8 which delays the recruitment of neutrophils preventing proper neutrophil wall formation, of which was proposed that it could facilitate initial microbial colonization of the periodontium. This mechanism is called the local chemokine paralysis.