Parodontitis: scary biofilm

4. August 2011
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An inflammation of the gums doesn't ruin in the long run only the teeth. The released bacteria are conveyed to many other regions of the body as well. In Zurich, a young group of researchers is trying to fully understand the inflammatory process by putting it in a culture dish.

In some areas of our world, over 90 percent of the population suffers from inflammation of the tooth-supporting tissues. In the mouths of patients from developed countries there is in a frequency of more than one in ten advanced periodontitis. Even with intensive cleaning and antibiotics, the mixture of aggressive bacteria can then no longer be driven from their respective sockets around the tooth.

“Periodontitis is a widespread health problem affecting the health of the whole person. At the same time it’s still unknown exactly how the inflammatory processes occur and why some people develop severe periodontal disease and others do not.” Nagihan Bostanci has been studying for more than ten years in this field. For almost a year she has been directing a working group at the University of Zurich which wants to get a better picture of what happens around the tooth. With that in mind, she has established an in-vitro model of bacterial biofilms. This should provide researchers with explanations at the molecular level of what happens in the encounter between pathogenic bacteria and periodontal tissue.

Close proximity with “joint weapons-production”

If bacteria – often even different species – unite in such biofilms, they get a significant evolutionary advantage, because only very few enzymes manage to split their sturdy shield of extracellular polysaccharides. Therefore it’s no wonder that, as experts estimate, in about 60-70 percent of all infections such biofilms occur. The close proximity of bacterial cells’ joint “foot-patrols” also influences the expression of proteins there. Pseudomonas aeruginosa switches on its cell-membrane pumps which effectively remove antibiotics, for example, from within. Glucosyltransferases from Streptococcus mutans allow the synthesis of insoluble long chain sugars out of low molecular weight units. They may help with the adhesion to the tooth, but also serve as a nutrition storage during low-sugar diet periods. Subgingival biofilm thus closes itself off impenetrably and from there starts its attack into the tissue.

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Chronic inflammatory reactions in the body and in the mouth are similar. Many features of periodontitis are also found in Crohn’s disease, polyarthritis, in cystitis or even with diabetes.

Periodontitis, diabetes and heart disease

There are significant connections between diabetes and periodontal infections: diabetics – especially those in whom the condition is poorly controlled – are much more likely to suffer periodontal disease, which is then usually more aggressive. Poorer response to therapy and weaknesses in the immune system reduce the chance of a quick effective cure. Longitudinal studies have also shown that periodontal disease can even lead to an increase in blood glucose levels and therefore may worsen existing diabetes. The greater the inflammation in the mouth, the more likely the bacteria will have a chance to get into the blood and inflict damage there. The messengers produced reduce the sensitivity of insulin receptors and can increase blood sugar levels.

Meta-studies have also shown a link between periodontal and cardiovascular disease. Effective treatment improves endothelial function and hence reduces the risk of heart attack and stroke.
Those who do not pay attention to their weight also do their teeth no good. Obesity is also associated with inflammation of the tooth. A higher BMI means in many cases even more periodontal lesions in the mouth. It’s probable that adipokines play a role in these processes. These messengers from fat tissue increase inflammation. These mediators are also to be found in the sulcus and the gingival tissues.

Biofilm and gums in the petri dish

Of the approximately 700 types of bacteria that are active in the human mouth, Bostanci picked out the top 10 and grew them in the laboratory as a biofilm. The model on which this was based was the work of an American group that had already two years ago undertaken similar experiments. A publication from the researcher, which appeared a few months ago in Cellular Immunology, describes the increased production of interleukin-1ß messenger and IL-18 when fibroblast of the gum and the culture supernatant of the biofilm come together. Depending on whether it is a supragingival or subgingival biofilm, the fibroblasts activate different genes.

The increased production of caspases is indicative of the aggressive strategy of the pathogen. This protein-splitting enzyme plays an important role in the programmed suicide of cells. With respect to increase in bone resorption of the jaw, RANKL and it’s antagonist OPG are responsible. RANKL is a ligand of the transcription factor NFkB and triggers the development of osteoclasts, ie. bone-destroying cells. Osteoprotegerin (OPG), by contrast, blocks these ligands.

As DocCheck learned via conversation with Bostanci, the exciting results of this research project should in the coming months appear in journals. The data could also give information on which way future drugs could thwart the strategy of bacterial biofilms. This might possibly include other persistent infections beyond the oral cavity.

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Pharmacist Jennifer Fall
Pharmacist Jennifer Fall

Very imformative. Good job.

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