Damaging even when dead: Bacteria from periodontal disease have one more card to play

Dead is dead, right? Well, maybe not, as far as bacteria are concerned. Dr. Richard H. Nagelberg reviews results from a recent study that indicates the periodontal disease battle is far from over even when bacterial death is imminent.

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Dead is dead, right? Well, maybe not, as far as bacteria are concerned. Dr. Richard H. Nagelberg reviews results from a recent study that indicates the periodontal disease battle is far from over even when bacterial death is imminent.


Damaging When Dead Nagelberg 01The more we learn about the bacteria in the mouth, the more we realize that they are very clever little devils. So much effort has gone into a wide variety of strategies to kill the bacteria that cause periodontal disease and understanding the inflammatory response with the thought that dead is dead and the tissue-damaging properties of the periodontal pathogens is done and over with.
Then, along comes a piece of research from 2017 (1) that says, Not so fast. We’re not done with you yet. The objective of this study was to determine if periodontal pathogen-induced death of the macrophages that ingest the bugs causes the release of molecules that participate in the pathogenesis and progression of periodontitis—EVEN IN DEATH.

In the study, macrophages were inoculated with three specific bacteria: Treponema denticola, Porphyromonas gingivalis, and Tannerella forsythia. Upon the demise of the bacteria-stimulated macrophages, a variety of danger signals—including ATP, uric acid, and heat shock protein 60, among others—were released by the dead macrophages.

The conclusion of the study stated: “Inflammatory cell death and endogenous danger molecules released from cells infected with periodontopathogens may play critical roles in the pathogenesis and progression of periodontitis by augmenting immune and inflammatory responses.” (1)

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So, there you have it. It appears as if the macrophages fulfill their destiny of phagocytizing the offending bacteria, butwhen they die, the bacteria that they ingested cause the release of molecules that boost the inflammatory response and participate in the development and progression of periodontitis. This is another classic way in which the bacteria overtake our bodily defenses for their benefit. Even when bacterial death is imminent, they still have a card to play.

One study obviously does not establish a conclusion as fact. But, if affirmed by other studies in the future, this observation would add to our knowledge of how truly complex periodontal disease is.

Reference

1. Jun HK, Jung YJ, Choi BK. Treponema denticola, Porphyromonas gingivalis, and Tannerella forsythia induce cell death and release of endogenous danger signals. Arch Oral Biol. 2017;73(1):72-78. doi: 10.1016/j.archoralbio.2016.09.010. Epub 2016 Sep 26.

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Content Dam Diq Online Articles 2015 10 Richardnagelbergdds Blog 124x124Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact Dr. Nagelberg at gr82th@aol.com.


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