Oral infections and gum disease usually lead to gum inflammation and tooth loss in the oral cavity but a recent study shows that a pathogen associated with periodontal disease can increase the risk of atherosclerosis.  According to the study published in PLOS Pathogens, the periodontal disease pathogen Porphyromonas gingivalis can evade the immune system and cause inflammation throughout the body.

P. gingivalis is a gram-negative bacteria with an outer layer made up of sugars and lipids.  This coating is recognized by the immune system which launches a multi-pronged immune reaction to fight the bacteria.  However like other types of gram-negative bacteria, P. gingivalis can change their outer coating to evade the attack from the immune system.

What Was Tested

The study was done by Caroline Attardo Genco from the Boston University School of Medicine in collaboration with Richard Darveau from the University of Washington School of Dentistry.  They focused on a specific lipid from the coating of P. gingivalis called lipid A which interacts with TRL4, a main regulator of the immune system.  P. gingivalis produces many versions of lipid A and the researchers hoped to discover how the immune system’s response changed with each type and contributed to the pathogen’s ability to evade the response and cause inflammation throughout the body.

The researchers produced two different versions of lipid A on strains of genetically modified P. gingivalis.  One version of lipid A, the agonist, activated TLR4 and the other version of lipid A, the antagonist, interacted with TRL4 but prevented it from activating.  They concluded that when P. gingivalis produces antagonist lipid A, the pathogen becomes resistant to the responses of the immune system and can survive in the body.  The researchers then exposed atherosclerosis-prone mice to P. gingivalis with the TRL4 antagonist strain and found that inflammation of their blood cells became worse which made them more likely to fully develop atherosclerosis.


Genco and Darveau conclude that “P. gingivalis modifies its lipid A structure in order to evade host defenses and establish chronic infection leading to persistent systemic low-grade inflammation.”  Their conclusion continues, “Uniquely among gram-negative pathogens, P. gingivalis evasion of TRL4-mediated host immunity results in progression of inflammation at a site that is distant from local infection by gaining access to the vasculature.”