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Closer To An Effective Treatment For Gum Disease In Smokers

ScienceDaily (May 13, 2009) — Scientists in the USA have discovered why smokers may be more prone to chronic gum disease (periodontitis). One of the bacteria responsible for this infection responds to cigarette smoke – changing its properties and the way it infects a smokers mouth.

The study published recently in the Society for Applied Microbiology journal Environmental Microbiology, showed that the bacterium Porphyromonas gingivalis adapts and changes its DNA and membrane proteins in response to cigarette smoke.

Several genes of P. gingivalis associated with its virulence (infectivity), detoxification, oxidative stress mechanisms and DNA repair are altered by exposure to cigarette smoke. As a result, the expression of a number of the proteins in the cell membrane is changed. This affects important characteristics of the bacterial cells themselves and how the immune system recognizes this pathogen.

This could explain why smokers are more likely to be resistant to treatment for periodontitis and are more susceptible to oral disease caused by infection with P. gingivalis.

Finding an effective treatment for smokers infected with P. gingivalis will be easier now that these changes in the bacterium's 'properties' have been identified.

University of Louisville researcher, Dr David Scott said: "It has long been known that smokers are more susceptible to periodontitis than are non-smokers. However, the reasons why are not so clear. Our study shows, for the first time, that components in cigarette smoke alter key characteristics of a major bacterial pathogen which, subsequently, changes how our immune system reacts to it. It may turn out that we need to develop alternate treatment plans for smokers and non-smokers".

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Adapted from materials provided by Wiley-Blackwell, via EurekAlert!, a service of AAAS.

Journal Reference:

  1. Bagaitkar et al. Tobacco-induced alterations to Porphyromonas gingivalis-host interactions. Environmental Microbiology, 2009; 11 (5): 1242 DOI: 10.1111/j.1462-2920.2008.01852.x
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