Periodontal disease is the most common disease on the planet that affects people. However, what may be unknown is that this disease has a potential to cause or even aggravate life threatening conditions such as diabetes, heart disease, respiratory diseases and cancer. Initially, it was believed that bacteria causing periodontal disease were responsible for other diseases and body complications. Further extensive research carried out to establish this association has, in fact, identified inflammation as the main link between periodontal disease and other diseases. Therefore, inflammation treatment not only has benefits of dealing with periodontal diseases but also plays a major role in chronic inflammatory conditions management.
According to a new study published in the most recent issue of PLOS Pathogens, Dr. Darveau together with his colleagues have managed to successfully come up with a medical explanation to explain the link between periodontal diseases commonly known as gum diseases and vascular inflammation. A recent journal publication by the Chair of the Department of Periodontics co-authored by Dr. Richard Darveau explains how bacterium responsible for periodontal disease causes blood vessel inflammation outside of the oral cavity after the body’s immune response fails to fight the bacterium.
Dr Darveau said “We had published earlier that this mechanism could be used by P. gingivalis to evade host detection, and this paper is the first to demonstrate it in an animal model of disease.”
The group of colleagues which included Boston’s University School of Medicine Dr. Caroline Attardo Genco, Dr. Darveau and other scholars made discoveries that expected to shed more light on the assertion that chronic inflammation indeed heightens the dangers of serious diseases such as diabetes, cancer and heart disease.
Porphyromonas gingivalis is the main subject of discussion in The PLOS Pathogens paper. This pathogen is responsible for gum disease and is linked to atherosclerosis. P. gingivalis together with gram negative bacteria consists of an outer layer coating with lipids and sugars. The immune system swings into action after recognizing sections of this coating. On the other hand, the outer coat is modified by P. gingivalis to prevent a counter attack from the immune system.
The outer surface of P. gingivalis, which has a specific lipid known as lipid A was the basis of the research focus. The lipid interacts with TLR4.P, which is a host’s immune system crucial regulator. Various versions of lipid A can be produced by gingivalis and scholars were faced with the responsibility of how these changes interfere with immune response causing inflammation because the pathogen is allowed to survive.
In summary, the research concluded that P. gingivalis makes changes to the structure of the lipid A to escape the host’s defense system and instead pave the way for chronic infection causing systemic low-grade inflammation which is persistent in nature. The research also revealed “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.”