Plaque hypotheses

The Plaque hypotheses are theories of plaque bacteria’s role in caries and periodontitis. These theories rely heavily on the postulates of Koch, and the work of Louis Pasteur.

Knowledge of oral disease development has evolved over time. The non-specific plaque hypothesis was developed in the nineteenth century, and posits that the accumulation of all types of dental plaque is responsible for oral disease, regardless of the virulence of the specific pathogens involved. Technological advances in the twentieth century allowed scientists to analyse the chemical changes in the plaque biome from health to disease, and this brought several problems to light. The recently posited keystone-pathogen hypothesis holds that certain malignant pathogens can control the inflammatory disease by proliferating, remodelling and imbalancing a normally benign microbiome.^[1]

Dental plaque biofilm is an essential ætiological agent of the common forms of chronic gingivitis and periodontitis,^[2] and of dental caries.^[3]

The plaque hypothesis applies equally to periodontal disease and dental caries with some differences.

Dental Caries

Specific plaque hypothesis

The specific plaque hypothesis, is the theory which emerged in the 1970's which is said to be responsible for "specific" pathogen and or a particular increase in the number of specific bacteria present within the subgingival plaque. that only a few specific organisms of the biome are responsible for caries.^[4] This was the favoured opinion at the birth of microbiology in the late 19th century, and returned to the surface briefly in the 1990s. However, the theory is proscribed by the fact that caries occurs even in the absence of these bacteria, albeit to a lessor degree.^[5] The specific plaque hypothesis has important implications because the association between S. mutans, lactobacilli and dental caries can be used in diagnosis, treatment and prevention of the disease in groups of subjects as well as in the individual case.

Non-specific plaque hypothesis

The non-specific plaque hypothesis is the theory developed in the 1930s that caries is the result of the combined efforts of all the organisms in the oral biome, and that some patients are merely more susceptible than others.^[6] No specific organisms had been identified at that point that were more cariogenic than others. Thus the amount of plaque in situ was taken to determine the severity of the effect, regardless of its composition.^[7] While this is to a degree true of periodontitis, it could not be proven of caries. Early thoughts of oral caries disease could not be identified to a type of bacteria responsible due to limited technological development in the nineteenth century, which led to the Non-Specific Plaque Hypotheses. Evolving in the 1980’s, not only were a few specific types of bacteria identified as playing a part in disease, differences in virulences of bacteria were then considered as part of the theory that the overall entirety of the microflora could lead to caries disease ^[8] ````

Ecological plaque hypothesis

Ecological plaque hypothesis and the aetiology of dental caries

The ecological plaque hypothesis, a combination of the twain, suggests that there are certain species responsible for pathology, ubiquitous but in insufficient quantities to cause damage in a healthy individual.^[9] Thus biofilm derived diseases are the result of an imbalance in the oral ecology.^[10]

Periodontitis

Specific plaque hypothesis

"The Specific Plaque Hypothesis" was introduced by LoESCHE, who observed concepts by FITZGERALD & KEYES that hamsters and rats that do not develop caries from a high cariogenic diet unless a specific bacteria was introduced such as streptococci. It is understood that specific microorganisms play an importance in both caries and periodontal diseases ^[11]

References

1. Hajishengallis, G; Darveau, RP; Curtis, MA (October 2012). "The keystone-pathogen hypothesis.". Nature reviews. Microbiology 10 (10): 717–25. PMID 22941505.
2. Carranza, [edited by] Michael G. Newman, Henry H. Takei, Perry R. Klokkevold ; editor emeritus, Fermin A. (2012). Carranza's clinical periodontology (11th ed. ed.). St. Louis, Mo.: Elsevier/Saunders. ISBN 978-1-4377-0416-7.
3. Baelum, edited by Ole Fejerskov and Edwina Kidd ; with Bente Nyvad and Vibeke (2008). Dental caries : the disease and its clinical management (2nd ed. ed.). Oxford: Blackwell Munksgaard. ISBN 1405138890.
4. Loesche, W.J (1976). "Chemotherapy of dental plaque infections". Oral science reviews (9): 65–107.
5. Bradshaw, D. J. & Marsh, P. D. (1999). Use of continuous flow techniques in modeling dental plaque biofilms. Methods Enzymol, 310, 279–296
6. Rosier, Bob T.; De Jager, Marko; Zaura, Ejiga; Krom, Bastiaan (16 July 2014). "Historical and contemporary hypotheses on the development of oral diseases: are we there yet?". Frontiers in Cellular and Infection Microbiology. doi:10.3389/fcimb.2014.00092.
7. Theilade, E. (1986): The non-specific theory in microbial etiology of inflammatory periodontal diseases. J Clin Periodontol, 13, 905-911
8. Bob T. Rosier, Marko De Jager, Egija Zaura, and Bastiaan P. Krom."Historical and contemporary hypotheses on the development of oral diseases: are we there yet?" Frontiers in Cellular Infection Microbiology. 16 Jul 2014. Retrieved on 2016-05-01.
9. Miller, W. D. (1890). "The Micro-Organisms of the Human Mouth". The S.S. White Dental MFG.
10. Marsh, P.D (2003). "Are dental diseases examples of ecological catastrophes?". Microbiology (149): 279–294.
11. Emilson CG, Krasse B: Support for and implications of the specific plaque hypothesis. Scand J Dent Res 1985; 93: 96-104. Retrieved on 2016-05-02.