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Gingivitis

Jose R Kina

Department of Surgery and Integrated Clinic, Araçatuba School of Dentistry, Sao Paulo State University – UNESP. Rua José Bonifácio, Araçatuba, Brazil. kinajr@hotmail.com

Eunice FU Kina

Private Dentistry, Specialist in Periodontology, Endodontics and Dental Prosthesis. Avenida dos Holandeses, São Luis, Brazil.

DOI: 10.15761/JDRR.1000112

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Key words

gingivitis, periodontitis, bacterial plaque, predisposing risk factor

Since Loe, Theilade, and Jensen in 1965 published the research: ‘’Experimental gingivitis in man’’; this research became a landmark proving that periodontal disease has as main etiologic factor the accumulations of plaque around the teeth [1,2]. The researchers studied a group of individuals with previously excellent oral hygiene and healthy gingivae. After 9–21 days without oral hygiene eleven experimental individuals developed substantial accumulations of plaque and generalized mild gingivitis. The specific rate of development of gingivitis was closely linked with the rate of plaque accumulation. Bacteriological changes were verified in the bacterial plaque around the gingival margin during the experiment. The correlation between time and quality and quantity of bacterial plaque accumulation was equal for all subjects. The gingival condition was correlated with the composition of the plaque. However, it was found that gingivitis could not be diagnosed clinically at approximately the same time as the complex flora was established for all individuals. The first individual developed gingivitis in day 9 and the other individuals developed gingivitis in subsequent days until the last one, be diagnosed with gingivitis in day 21. This detail shows that individuals were susceptible to different times of the bacterial plaque accumulation and also to different quantities and qualities of bacterial plaque accumulation, since, the quality and quantity of bacterial plaque accumulation was equal for all subjects when was harvested and was checked in a specific day. When oral hygiene was instituted, the bacterial plaque in most areas was controlled. The gingival inflammation disappeared one day after the plaque control establishment. The main conclusion of this research was: bacterial plaque accumulation may cause gingivitis and bacterial plaque control may induce gingival health. However, some questions arise from this historical research [3]: 1- why some individuals developed gingivitis in day 9 and other individuals developed gingivitis in subsequent days, until the last one be diagnosed with gingivitis in day 21, if the bacterial flora was equal for all individuals in a determined time. The answer is: gingivitis present multifactorial aetiology and each individual respond in different ways from different qualities and quantitates of the bacterial plaque attack, depending of the local and general predisposing factors which may be associated with a specific moment of the fragility of the individual. 2- Why the teeth should be brushed 3 time per day if only after 9–21 days without oral hygiene eleven experimental individuals developed substantial accumulations of plaque and generalized mild gingivitis. 3- If it may take up to 21 days of plaque accumulation for some individuals to present gingivitis, how much plaque accumulation would be required to induce periodontitis. This condition is impossible to be studied in humans. Only without oral hygiene will be impossible to induce periodontitis experimental in animals. To establish periodontitis experimental in animals a local or general predisposing risk factor will be essential to in association with bacterial plaque provoke periodontitis [4]. Then gingivitis and periodontitis are considered diseases with multifactorial etiologic factors. Why the focus of the treatment of these alterations is bacterial plaque control which all individuals present and is impossible to establish an efficient control, if researchers still cannot know what kind of bacteria really initiate these alterations. It would not be easier to control the predisposing risk factors that only some individuals possess than establish a program of the bacterial plaque control. These arguments should be studied and answered to improve the prevention and treatment of gingivitis and periodontitis.

References

  1. Loe H, Theilade E, Jensen Sb (1965) Experimental gingivitis in man. J Periodontol 36: 177–187. [CrossRef]
  2. Theilade E, Wright WH, Jensen SB, Löe H (1966) Experimental gingivitis in man. II. A longitudinal clinical and bacteriological investigation. J Periodontal Res 1: 1–13. [CrossRef]
  3. Kina JR, Suzuki TYU, Kina J, Kina M, Kina EFU (2013) Reparative phase events on periodontal disease progression: interpretation and considerations. Int J Microbiol Res 5: 439–444.
  4. Lindhe J, Hamp S, Löe H (1973) Experimental periodontitis in the beagle dog. J Periodontal Res 8: 1–10. [CrossRef]

Editorial Information

Editor-in-Chief

Ibrahim El-Sayed M. El-Hakim
Ain Shams University, Egypt

Article Type

Short Commentary

Publication history

Received : March 07, 2019
Accepted : March 16, 2019
Published : March 21, 2019

Copyright

©2019 Kina JR. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation

Kina JR, Kina EFU (2019) Gingivitis. J Dent Res Rep 2: DOI: 10.15761/JDRR.1000113.

Corresponding author

Jose Ricardo Kina

Department of Surgery and Integrated Clinic, Araçatuba School of Dentistry, Sao Paulo State University – UNESP. Rua José Bonifácio, 1193. Zip code: 16015-050, Araçatuba, Brazil.

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