Tonight I attended a fascinating presentation that shared new research on how periodontal pathogens are directly related in the pathogenesis of atherosclerosis and am going to attempt to explain it to you to make it tangible and easy to understand.  Most of this information I learned in my periodontal residency but so much of the detailed science is easily forgotten over the years. The bottom line is that as a profession we continue to accumulate a massive amount of data on this topic and the conclusion is undeniable; poor oral health significantly increases your risk of premature death.  Tonight I heard a cardiologist share the following statistics:
  • Cardiovascular disease (namely heart attack and stroke) have been the number one cause of death for almost 100 years
  • The average age for heart attacks for men is 65 and women is 72
  • Cardiovascular disease on average reduces life expectancy by 17 years
This got me thinking, what would you do to get 17 more years of your life?  Would you have made oral health a higher priority in your life if you knew it meant seeing your grand children grow into adults? Or maybe be able to walk your daughter down the aisle once she finally found a man you’d be proud to call your son? Think about it.  And all you would have needed to do is commit a little more effort to your oral health. I wish it was easier to convey this message to our patients, but perhaps if we ourselves understood a little better how important oral health really is for our overall well-being and improved quality of life, we might better be able to explain it to our patients.  So here it goes…
First, a biochemistry refresher.  Apolipoprotein B (Apo B) is a protein that is the main constituent of lipoproteins (“bad” cholesterol like LDL, HDL, & VLDL). Basically, Apo B is like an anchor that allows LDL to stick to the intimal layer of the arterial wall. The periodontal pathogen P. gingivalis (p.g.) causes the formation of more Apo B and thus increases that “stickiness” of LDL to the inner wall of your arteries.  As if that’s not bad enough, toxins produced from periodontal pathogens enter the bloodstream through the microulcerations in the inflamed periodontal pocket and directly damages the endothelial lining of arteries.  Some of the toxins produced by these sinister bacteria cause physical breakage of the chemical bonds that seal the inner structure of the arteries (Google “F. nucleatum”, “cadherins”, and “endothelium” for details). Anyways, these leaky areas in the arterial endothelium allow access for those Apo B-laden LDLs to get into the inner arterial wall (intima) to begin with.  So at this point we have bacterial toxins causing physical damage to the lining of the artery and facilitating cholesterol accumulation inside the wall of the arteries.  To further complicate things, bacterial toxins also stimulate the muscle cells inside the artery wall to duplicate (“intimal hyperplasia”), actually MIGRATE from the muscle layer into the intimal layer, AND attract the cholesterol balls (LDL, HDL, & VLDL) to stick to displaced muscle cells by increasing their velcro-like proteoglycan receptors (which bond to the Apo B proteins covering the cholesterol balls).  And there you have it! The formation of atherosclerotic plaques induced by toxins produced from naughty bacteria that have overstayed their welcome in their oral homes.  I won’t even discuss the myriad of effects from inflammatory cytokines that are also significantly elevated in the blood stream as a result of the chronic inflammation caused by these naughty critters. Just google IL-6, CRP, TNF gamma, or TGF beta for further proof that gum disease can have much worse effects that just tooth loss.