In recent years, researchers have suggested that gum disease, periodontitis, may contribute to the development of cardiovascular disease and neurodegenerative conditions. Leakage of pathogens and harmful metabolites into the bloodstream at the gums, leading to an increased level of chronic inflammation, has been proposed as the important mechanism. This is a reasonable proposition. There is some debate over the degree of risk, however, and it is always possible that periodontitis risk is just as driven by degenerative aging as is the case for risk of cardiovascular disease and neurodegenerative disease, obscuring the effects of periodontitis on other diseases because they will tend to independently co-occur anyway.
Human data typically only allows the determination of correlations between conditions and mechanisms, not causation. There are some ways forward, however. In today's open access paper, researchers employ a Mendelian randomization strategy in order to try to gain some insight into causation between aging, periodontitis, and cardiovascular disease. The result is generally supportive of the present consensus, meaning that aging contributes to both periodontitis and cardiovascular disease, but periodontitis can also contribute to cardiovascular disease. It doesn't add much to the present discussion on the size of these contributions.
Using the NHANES database, a large GWAS database, and Mendelian randomization (MR) analyses, this study investigated the complex relationship between periodontitis, cardiovascular disease (CVD), and biological aging. The results indicated that periodontitis was a risk factor for CVD and that aging plays a mediating role in this association. Gene-level predictive analysis further confirmed the causal effect of periodontitis on small-vessel stroke and revealed the causal effect of biological aging on periodontitis and specific CVD. Simultaneously, the study found that CVD may exacerbate the progression of biological aging.
We observed that an increase in the degree of periodontitis was associated with an increased risk of CVD. Additionally, MR analysis revealed the potential causal effect of periodontitis on small vessel stroke. A number of epidemiologic studies have suggested a significant positive association between periodontitis and CVD, such as CHD and stroke. The possible mechanisms for this association include the systemic inflammation caused by periodontitis. Patients with periodontitis often have elevated levels of inflammatory markers in the blood, such as c-reactive protein and white blood cell count. These biomarkers play a key role in the pathophysiological mechanism of CVD. On the other hand, pathophysiological studies have revealed the potential role of oral bacteria in the formation of atherosclerosis. In addition, further supporting the pathological link between periodontitis and CVD is the observation of pathological changes similar to CVD, such as the formation of atherosclerotic plaques, in animal experimental models following the induction of periodontitis.
We investigated the relationship between periodontitis, CVD, and aging markers. The results indicated that the progression of periodontitis is significantly associated with biological aging. This suggests that periodontitis may not only affect oral health but accelerate the systemic aging process. The presence of periodontitis may aggravate the aging of organisms and even increase all-cause mortality. These findings provide strong evidence for the important role of periodontitis in the mechanism of systemic aging. Furthermore, biological aging was found to be linked to a higher risk of CVD, which aligned with previous research. Our findings also suggest a potential causal relationship between biological aging and periodontitis, as well as a reciprocal causal effect between aging and CVD. In other words, aging contributes to the development of periodontitis and CVD and can also be a potential consequence of CVD. These results underscore the intricate interplay between periodontitis, CVD, and biological aging.
View the full article at FightAging
