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Commensal Damage

June 11, 2013

Aggregatibacter actinomycetemcomitans

Photo courtesy of Dr. Daniel Fine’s laboratory, New Jersey Dental School


Spring is here, and bright colors are back in the garden. But imagine that the usual harmony of purples, reds, blues, and whites gave way this spring to just a few dominant flowers. That’s analogous to what happens to the microbial flora of people with chronic periodontitis. A small subset of bacterial species becomes dominant in the subgingival crevice, the space between the tooth and gum. These dominant species then expand their numbers and spread into the tooth’s supportive structures, or periodontium, causing immune cells to respond excessively and destructively to the challenge.

A long-standing assumption was the disruptive species must be oral pathogens that had discovered a way to become dominant in the subgingival crevice. But a recent research surprise is while some oral pathogens may be guilty of upsetting the immunological balance that leads to all of the above, it is the formerly benign commensal bacteria that opportunistically expand in number, spill into the periodontium, and turn infectious. This discovery has raised important new research questions about which commensal species tend to be most opportunistic and how they succeed in damaging the supportive bone in the tooth socket. Answering these questions will go far toward developing better treatments for chronic periodontitis.

In the May 15 issue of the journal Cell Host & Microbe, NIDCR grantees and colleagues offer two fascinating answers in mouse studies. First, the researchers show some commensals have learned to stimulate the Nod1 protein receptor on innate immune cells as their exploitable mechanism of choice to assist them on their way to infect the periodontium. Nod1, a pattern recognition receptor, senses small molecules related to polymers in the cell wall of bacteria.

Second, the researchers discovered that a specific commensal bacterium, known as NI1060, is especially adept at stimulating Nod1 and alone sufficient to induce bone resorption. Interestingly, they sequenced the genome of NI1060 and found that it shares over 1,500 genes with Aggregatibacter actinomycetemcomitans, or Aa. The latter is strongly associated with an aggressive form of periodontitis in children and adolescents. A subsequent database search suggested to them that the bacteria are mouse and human counterparts. The scientists concluded, “Our studies suggest that inhibition of NI1060-related bacteria like Aa and/or targeting Nod1 signaling might be beneficial for the prevention and/or treatment of periodontitis.”

The study is titled, “Induction of Bone Loss by Pathobiont-Mediated Nod1 Signaling in the Oral Cavity,” and is published in the May 15 issue of the journal Cell Host & Microbe. The authors are: Yizu Jiao, Youssef Darzi, Kazuki Tawaratsumida, Julie T. Marchesan, Mizuho Hasegawa, Henry Moon, Grace Y. Chen, Gabriel Nunez, William V. Giannobile, Jeroen Raes, and Naohiro Inohara.

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This page last updated: February 26, 2014