Oral health care workers and scientists have know for many years that bacteria cause periodontitis (gum disease); however, they were not sure exactly what bacteria was response.
Recently the bacteria that causes periodontitis (gum disease) has been identified by a University of Michigan study. This bacterium is known as NI1060. It was also found that this triggers a normally protetive protein in the oral cavity called Nod1 to trigger bone destroying cells. In normal circumstances Nod1 fights harmful bacterium in the body. Hence, it was that the bacteria that causes gum disease triggers a one-two punch by also causing normally protective proteins to then destroy more bone.
In normal cases No1 helps to fight infection by recruiting neutrophils which are blood cells that act as bacterial killers. Nod1 also removes harmful bacteria during infection. When periodontitis (gum disease) occurs NI1060 will cause Nod1 to trigger neutrophils and also osteoclasts which are cells that destroy bone.
The researchers are encouraged by the results in that they can help to better develop personalized therapy for dental patients.
Periodontitis (gum disease) has been discussed on this site before numerous times. In one blog post it is discussed how Gum Disease Is More Common With Old Age, how Periodontal disease (gum disease) might increase the time it takes to become pregnant, and how Omega 3 Fatty Acids Are Inversely Proportional to Periodontitis. In this post it is discussed how eating certain foods such as eating nuts, peanut butter, margarine, and salmon, can help you have more omega 3 fatty acids in your diet which can help reduce the chances of getting periodontitis (gum disease). In addition, one could take a supplement such as fish oil.
Source: Yizu Jiao, Youssef Darzi, Kazuki Tawaratsumida, Julie T. Marchesan, Mizuho Hasegawa, Henry Moon, Grace Y. Chen, Gabriel Núñez, William V. Giannobile, Jeroen Raes, Naohiro Inohara. Induction of Bone Loss by Pathobiont-Mediated Nod1 Signaling in the Oral Cavity. Cell Host & Microbe, 2013; 13 (5): 595