Gum Disease, Heart Disease and Cholesterol-A Clearer Perspective
Today I want to talk about the connection between gum disease and heart disease. I am going to talk about one specific recent study, and I am going to get more scientific than usual, so forgive me, but the information is too good to ignore.
A brand-new paper published this July in The International Journal of Oral Science by Jin Sook Suh, Sol Kim, Kristina I. Boström, Cun-Yu Wang, Reuben H. Kim & No-Hee Park sheds much light on the connection between gum disease and heart disease while also uncovering more mechanistic details. This paper gives us a better understanding of the inter-relationship of oral infections and the effect on heart disease. (1)
In the study, the researchers used a genetically altered population of mice that make them susceptible to atherosclerosis (fatty deposits in arteries, or heart disease). They are called Apoe knock out mice. The mutation knocks out the receptor Apoe on their cholesterol particles which don’t allow the mice to clear the cholesterol from their bodies, making them develop thickening of the arteries (atherosclerosis) very rapidly. This makes the mice a good proxy for studying heart disease in humans. (2)
They had three groups of mice in the study. All groups were fed a high fat diet for 11 weeks and sacrificed. They were measured for periodontitis, systemic inflammation, and atherosclerosis. The first group was the control group. The second group had a ligature (silk suture or stitch) placed around a tooth to induce gum disease. The third group was the same as the second group but had purified bacterial toxins placed around the tooth as well. The bacterial toxin used was from P. Gingivalis, the main bacteria that causes gum disease. It is called Lipopolysaccharide, or LPS for short. Endotoxin is another name for LPS. LPS is produced by gram negative bacteria and is responsible for causing harm.
The control group did not develop periodontitis (gum disease) or systemic inflammation and had minimal fatty deposits in their aortas. Keep in mind that they were eating a high fat diet. The second and third groups showed severe periodontitis, systemic inflammation, and aortic plaque formation. The third group had slightly worse gum disease due to the LPS but had much more systemic inflammation and plaque formation than the second group. These observations indicate that the development of atherosclerosis is due to systemic inflammation caused by severe periodontitis, and it suggests that the intensity of the atherosclerosis development depends on the magnitude of systemic inflammation caused by severe periodontitis. In other words, periodontitis (gum disease) is a systemic inflammatory condition, it is not just limited to the mouth, and the greater the local gum infection, the greater the systemic inflammation.
Here are the specifics quoted directly from the study, “These observations indicate that the development of atherosclerosis is due to systemic inflammation caused by severe periodontitis. In vitro, P.g. LPS enhanced the secretion of pro-inflammatory cytokines from macrophages and increased the adhesion of monocytes to endothelial cells by upregulating the expression of adhesion molecules from endothelial cells. Moreover, secretory proteins, such as TNF-α, from macrophages induced endothelial–mesenchymal transitions of the endothelial cells.”
Let me translate this for you. The gum disease destroys the tissues around the tooth. Special cells associated with our immune system (Macrophages) secrete chemicals (cytokines) that circulate throughout the body which signal changes in the normal cells that line arteries (endothelial cells). The change causes the cells to attract another specialized reparative cell (monocytes) to “stick” to the artery wall. Other proteins (TNF-α.) secreted by the macrophages causes the lining of the artery to break down, much like the gums do in gum disease. The lining of the artery becomes thick, inflamed, and unstable. In very simplistic terms, the artery can clog and cause a heart attack.
They mention the role of endothelial-to-mesenchymal transition (EndMT) of aortic endothelial cells in heart disease. The paper goes into detail and cites several other studies that discuss the role of EndMT, so I won’t go into detail here, but suffice to say that EndMT is viewed as a critical step for the initiation and progression of atherosclerosis.
Interestingly, no changes in all the normal cholesterol numbers were seen, suggesting that the severity of atherosclerosis is due to the severity of systemic inflammation, not cholesterol numbers (at least in this animal study).
Gum disease causes the immune system to react systemically
Some specialized cells secrete chemicals that alter other cells in the body, especially the ones that line our arteries
The changes cause the artery lining to thicken, become inflamed and unstable
The reaction is worsened by endotoxins (LPS)
The amount of heart disease and inflammation is directly related to the amount of gum disease/inflammation
Inflammation is the cause of heart disease, not fat or cholesterol
Gum disease is unfortunately very common, and the symptoms can be hard to notice by the patient, but the danger is real and can result in loss of life. If you have not been to the dentist lately, I suggest you do so, your life could depend on it!