From an article in ScienceDaily dated July 10, 2014 …
“P. gingivalis can produce a number of different lipid A versions, and the researchers wanted to clarify how these modify the immune response and contribute to the ability of the pathogen to survive and cause inflammation — both locally, resulting in oral bone loss, and systemically, in distant blood vessels.”
The researchers (from Boston University School of Medicine in collaboration with Richard Darveau, at the University of Washington School of Dentistry) conclude, "P. gingivalis modifies its lipid A structure in order to evade host defenses and establish chronic infection leading to persistent systemic low-grade inflammation … P. gingivalis evasion of TLR4-mediated host immunity results in progression of inflammation at a site that is distant from local infection by gaining access to the vasculature."
ADDITIONAL READING …
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