The majority of dental health-care professionals, and many in the lay public, recognize some level of association between the mouth and the body. Most prominently understood is the impact periodontitis has on a variety of systemic diseases and conditions. Less widely accepted, however, is the positive impact periodontal therapy has on cardiovascular disease (CVD) and its risk factors—despite the number of studies substantiating this effect.
One of the primary risk factors for CVD is hyperlipidemia, which is characterized by elevated levels of a variety of lipids including total cholesterol, triglycerides, LDL cholesterol, and decreased levels of HDL.1 Literature demonstrates a bidirectional relationship between periodontal disease and hyperlipidemia, which are both chronic inflammatory diseases with complex etiologies. Studies as far back as 2010 demonstrated a positive effect of statin treatment on periodontal attachment loss.2 Conversely, a variety of studies demonstrate improvement in serum lipid levels in patients with hyperlipidemia following periodontal treatment.3
Other mechanisms are in play as well. Periodontal pathogens, endotoxins, exotoxins, and inflammatory mediators are released locally in the oral cavity in response to biofilm. These elements can then find their way through the ulcerated lining of the epithelium, enter the bloodstream, and travel throughout the entire body. By this mechanism, the local host response to biofilm can contribute to the systemic burden of inflammation.
However, there is compelling evidence regarding the impact of effective periodontal treatment on chronic inflammation. The inflammatory mediators associated with periodontal disease and atherosclerotic cardiovascular disease (ACVD) include CRP, TNF-, IL-6, and fibrinogen, among others.
A 2018 study cited research concluding nonsurgical periodontal treatment reduced serum levels of C-reactive protein (CRP).4 The article also stated: “This agrees with the results obtained in the meta-analysis performed in the present review, where a decrease in CRP values was noted to be statistically significant when patients were submitted to nonsurgical periodontal treatment in contrast to receiving no treatment at all.”
A significant body of research demonstrates other mechanisms by which periodontal therapy positively affects risk elements of CVD, including improvements in endothelial function and hypertension. But there is currently no proof that chronic inflammatory periodontal disease (CIPD) causes CVD, yet it is reasonable to add CIPD to the list of contributory factors that can raise CVD risk. Proof of a causal link will only be established when it becomes possible to quantify the level of inflammation of oral origin that contributes to the systemic burden of inflammation. It is important to avoid overstating such research findings when speaking with patients. Even though the effect of periodontal therapy on CVD risk factors has been shown, causality has not. The direct effect of periodontal therapy on CVD is indeterminate at this point.
It is important to keep up with research and incorporate the results into our clinical protocols with prudent dialogue. A detailed, thorough review of each patient’s medical and family histories is central to identifying at-risk patients. Informing patients of the potential benefit of periodontal therapy beyond the oral cavity may help motivate them to accept our treatment and home-care recommendations.
Additional studies with longer follow-up periods are needed to determine whether periodontal treatment improves the clinical parameters over time of patients with CVD. Both disease entities are complex and multifactorial. CIPD is one of the most common chronic diseases of humankind globally, coupled with the fact that CVD is among the most common causes of mortality. The need for additional studies is evident. Patients with risk factors for diseases that periodontal disease adversely affects need to be identified and treated comprehensively. Periodontal pocket depths and clinical attachment levels alone are insufficient to determine disease activity. Monitoring gingival inflammation is currently accomplished by observing and documenting bleeding upon probing.
As dental professionals, we are in a unique position to help our patients. If we manage oral inflammation and its associated risk factors, we can contribute to their overall wellness.
References
- Abraham S, Premnath A, Arunima PR, Kassim RM. Critical appraisal of bidirectional relationship between periodontitis and hyperlipidemia. J Int Soc Prev Community Dent. 2019;9(2):112-118. doi:10.4103/jispcd.JISPCD_316_18
- Fajardo ME, Rocha ML, Sánchez-Marin FJ, Espinosa-Chávez EJ. Effect of atorvastatin on chronic periodontitis: a randomized pilot study. J Clin Periodontol. 2010;37(11):1016-1022. doi:10.1111/j.1600-051X.2010.01619.x
- Fu YW, Li XX, Xu HZ, Gong YQ, Yang Y. Effects of periodontal therapy on serum lipid profile and proinflammatory cytokines in patients with hyperlipidemia: a randomized controlled trial. Clin Oral Investig. 2016;20(6):1263-1269. doi:10.1007/s00784-015-1621-2
- Roca-Millan E, González-Navarro B, Sabater-Recolons MM, Marí-Roig A, Jané-Salas E, López-López J. Periodontal treatment on patients with cardiovascular disease: systematic review and meta-analysis. Med Oral Patol Oral Cir Bucal. 2018;23(6):e681-e690. doi:10.4317/medoral.22725
Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact Dr. Nagelberg at [email protected].
