Despite good oral hygiene, localised oral inflammation can affect distant healthy areas in mouth

oral inflammation
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New research from the US shows that localised gingivitis—the first stage of periodontal disease—can induce changes in the oral microbiome and can lead to immune responses in distant healthy parts of the mouth. Furthermore, the timing and intensity of such responses can vary among individuals.

The study is by researchers from the University of Washington, Rutgers University, King Abdulaziz University, and the Department of Oral Health Research at the Colgate Palmolive Company, and is published in Proceedings of the National Academy of Sciences.

Existing research shows that humans can exhibit different immune responses to bacterial and viral pathogens. Within the mouth, differing immune responses to microbial invasion have been similarly observed. In this study, the researchers sought to observe and describe contrasts in microbial gingival inflammation induced in study subjects.

The research involved 21 adults between the ages of 18 and 35 in good general health. Fourteen days before the experimental phase began, each volunteer received a professional teeth cleaning to establish normal oral health.

As this was a split-mouth design study, two weeks later, each subject received a personalised acrylic intraoral stent to cover a randomly assigned test site of three teeth on the upper maxilla (either #3, 4, and 5 or #12, 13, and 14). The three teeth located contralateral to each test site were considered the control site.

For the next 21 days, the test subjects covered the test sites with their stents while they maintained regular oral hygiene and brushed the rest of their teeth with toothpaste containing fluoride. During this three-week period, the researchers induced gingival inflammation, taking gingival samples on days 0, 4, 7, 14, and 21, and noting the timing of the amounts and types of oral bacteria and bleeding on probing observed in each volunteer.

As the study proceeded, the healthy control sites (on which the volunteers maintained regular oral hygiene) exhibited indicators of gingival inflammation similar to those seen in the test sites, but which developed to a lesser extent and at a slower pace.

Interestingly, based on the test subjects’ bacterial responses, the researchers were able to categorise each as one of three inflammatory responder types: high, low, or slow. High-IRTs and slow-IRTs exhibited more vulnerability than low-IRTs to high inflammation, with longer development periods of bacterial loads in slow-IRTs. The IRT groups did not reflect notable differences in sex and age.

These results are important because they add to existing knowledge of how inflammation in a localised area can ultimately affect healthy tissues in a distant area and possibly lead to infection. Moreover, despite maintaining oral hygiene, each study subject developed varying levels of oral inflammation at different rates according to their specific inflammatory responder type.

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