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Could the end of tooth decay be in sight?

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One of the more important things we can do for longevity is keeping our teeth clean and keeping decay at bay. It might sound strange at first, but it is true. The harm that bacteria causes, especially in the gums, can spread to other tissues and increase inflammation throughout the body.

Some studies show a strong correlation between harmful oral bacteria and mortality rates later in life[1]. The mouth is an easy point of entry for harmful bacteria to invade the body, so it makes sense that maintaining oral hygiene should be an essential part of your health and longevity strategy.

Inflammaging

Inflammation has many sources, including bacterial burden, senescent cell accumulation, protein crosslinks in tissue, and dysfunctional immune responses. All of  these sources unite to create what some researchers refer to as “inflammaging”, first described in 2000, which is a smoldering, chronic background of inflammation[2].

Inflammation plays a key role in the aging process, so the more we can reduce systemic inflammation, the better our prospects for living a healthier and longer life[3]. The level of inflammation increases as we age, leading to increasingly poor wound healing and poor tissue repair and regeneration while encouraging the progression of age-related diseases.



Inflammaging can influence the speed of the aging process and lifespan and is linked to Alzheimer’s disease, Parkinson’s disease, ALS, MS, atherosclerosis, heart disease, age-related macular degeneration, and type 2 diabetes [4-6]. It is also linked to increased cancer risk and increases morbidity and mortality.

Preventing cavities by inhibiting bacteria

Given the nature of the mouth, which is hardly a sterile environment, even the most refined approaches to remove harmful bacteria in the past have failed. The current gold standard is a toothbrush and toothpaste, so what is different this time?

Progress in the fight against bad bacteria in the mouth has been making progress in recent years, and new research is yet another step in that direction[7].

Researchers have succeeded in creating a small molecule that can prevent or resist the formation of tooth cavities in preclinical testing. The molecule blocks the functioning of a key enzyme in oral bacteria to stop it from causing decay. This throws a spanner in the works, jamming the bacterial machinery responsible for making tooth cavities.



Exposure to the molecule causes Streptococcus mutans, the primary bacteria involved in tooth decay, to stop producing a special sticky biofilm it uses to adhere to teeth, allowing these bacteria to eat away at the enamel via production of lactic acid. The molecule appears to selectively target S. mutans and significantly reduced the formation of cavities in rats given a cavity-promoting diet.

Conclusion

The connection between this research and aging may not be immediately obvious, but inhibiting harmful bacteria is an interesting pathway to managing inflammation and reducing bacterial burden.

However, for the time being, while this therapy is being tested and undergoing clinical trials, we will have to fall back on our old faithful toothbrushes.

Literature



[1] Chiu, C. J., Chang, M. L., & Taylor, A. (2016). Associations between Periodontal Microbiota and Death Rates. Scientific reports, 6.

[2] Franceschi, C., Bonafè, M., Valensin, S., Olivieri, F., De Luca, M., Ottaviani, E., & De Benedictis, G. (2000). Inflamm‐aging: an evolutionary perspective on immunosenescence. Annals of the New York Academy of Sciences, 908(1), 244-254.

[3] Xia, S., Zhang, X., Zheng, S., Khanabdali, R., Kalionis, B., Wu, J., … & Tai, X. (2016). An update on inflamm-aging: mechanisms, prevention, and treatment. Journal of immunology research, 2016.

[4] Giunta, B., Fernandez, F., Nikolic, W. V., Obregon, D., Rrapo, E., Town, T., & Tan, J. (2008). Inflammaging as a prodrome to Alzheimer’s disease. Journal of neuroinflammation, 5(1), 51.

[5] Boren, E., & Gershwin, M. E. (2004). Inflamm-aging: autoimmunity, and the immune-risk phenotype. Autoimmunity reviews, 3(5), 401-406.



[6] Franceschi, C., Valensin, S., Lescai, F., Olivieri, F., Licastro, F., Grimaldi, L. M. E., … & Bonafe, M. (2001). Neuroinflammation and the genetics of Alzheimer’s disease: the search for a pro-inflammatory phenotype. Aging Clinical and Experimental Research, 13(3), 163-170.

 

[7] Zhang, Q., Nijampatnam, B., Hua, Z., Nguyen, T., Zou, J., Cai, X., … & Wu, H. (2017). Structure-Based Discovery of Small Molecule Inhibitors of Cariogenic Virulence. Scientific Reports, 7.

 

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About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic, interviewed over 100 of the leading researchers in the field, hosted livestream events focused on aging, as well as attending various medical industry conferences. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, Swiss Monthly, Keep me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project.
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