Are Biofilm Infections Different?

Socransky and Haffajee 2002

When having revised a popular textbook on Periodontology for undergraduates for its 3rd edition I slightly updated a table which I had used in teaching for a decade. It was once published in an important article by late Sigmund Socransky and Anne Haffajee [1] where these two most influential authors in Oral Microbiology made their point that biofilm infections are in fact different (and difficult to target). The table is featured on the first page of the article but may easily be overlooked. But it contains important ideas which are still valid. Socransky and Haffajee differentiate acute, chronic delayed and biofilm infections and present respective examples. While many acute infections are fortunately  self-limiting and require just supportive treatment [2] chronic infections need antibiotics since the host does not properly cope with the causative agents. I have added as typical examples acute necrotizing ulcerative gingivitis, or ANUG, which in most cases resolves under oral hygiene improvement and cautious scaling (supported by antiseptics), and necrotizing ulcerative periodontitis, or NUP, which is longstanding and indicates that the host, for instance due to immune suppression in the course of HIV infection, elicit an improper, impaired response. Antibiotics are not indicated in the former case while they are in the latter; usually metronidazole is the drug of first choice [3]. If the causative agent in delayed infection is known, therapy involving suitable antibiotics is easy. In the past, that was not the case for example for syphilis (Treponema pallidum) where all kinds of mercury treatment had been applied. The deiseas ecould only be cured after the detection of penicillin. The same holds, for example, for gastrointestinal ulcers caused by Helicobacter pylori, which has been proven only in the 1980s. Gastric ulcers are now easily treated by high dosages of antbiotics after the bug had been identified.

The treatment of biofilm infections is much more difficult. For instance, periodontal bacteria which elicit host responses which ultimately may lead to loss of periodontal tissue support, are largely protected in the very complex biofilm. In any case, treatment has to start with disrupting the biofilm. Since most periodontal pathogens are sensitive to oxygen, changing the ecology is another treatment goal, i.e., pocket reduction or elimination and proper (surgical) treatment of involved furcations. Antiseptics such as chlorhexidine or essential oils are effective as well.

There might be indications for supportive antibiotic therapy. There are patients awfully difficult to treat. There is definitely a short-term beneficial effect after adjunct antibiotics in terms of probing pocket reduction and gain of clinical attachment. But it is unclear how long it will last, whether anatomical defects such as infrabony defects and furcation involvements are influenced in the long run and whether primary outcomes such as tooth loss are affected at all [4].

Notes

[1] Socransky SS, Haffajee AD. Dental biofilms: difficult therapeutic targets. Periodontol 2000 2002; 28: 12-55.

[2] This is unfortunately not known by many doctors who proactively or on patients’ demands would prescribe too frequently broad-spectrum (due to lack of knowledge about the causative agent(s)) antibiotics in acute infections.

[3] Note that either diseases are rarely seen in industrialized countries nowadays. The most recent comprehensive study on the bacteria involved in ANUG and noma in children in Niger  has been conducted by Bolivar et al. (2012), see pdf here.

[4] Biofilms are the preferred colonization pattern of bacteria. They can be found everywhere in nature at the bottom of flowing and standing waters and in any sanitary facility. Consider, for instance, a common toilet. You will find a brush and an antiseptic close to it. And throwing remaining tetracycline tablets into it is prohibited. Deliver them to your next pharmacy.

12 March 2013 @ 11:02 am.

Last modified March 12, 2013.

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