Oral-Systemic Dentistry: 
Reducing Heart Disease and Diabetes Risk

Heart disease remains the number one cause of death worldwide, claiming over 17 million lives each year. Yet traditional risk factors such as smoking and cholesterol levels account for only half of these deaths - with systemic inflammation appearing to fill in much of the predictive equation (Corson 2008).

Over the past 2 decades, chronic low grade inflammation has been shown to play a major part in the initiation, progression and rupture of atherosclerotic plaques - the primary mechanism of heart attacks and strokes. Kolodgie found that three quarters of sudden death cases were due to plaque rupture and thrombosis (Corson et al 2008). As one of the key contributors to systemic inflammation, periodontal biofilm (bacteria) has been closely scrutinized for its possible role in coronary artery disease. 

Because atherosclerosis is an inflammatory disease, inflammatory markers like hsCRP and Lp-PLA2  can be used to evaluate the risk of a heart attack or stroke. A metaanalysis (Corson et al 2008) including more than 25 prospective studies found that patients in the top LP-PLA2 quintile had twice the risk for coronary artery disease when compared to patients in the bottom quintile, independent of other risk factors. With both LP-PLA2 and hsCRP elevation, the risk of stroke and coronary events was magnified 11 times, respectively 3 times. Conversely, low values in both markers consistently identified patients with lowest CVD risk. 

Both insulin resistance and hsCRP are increased in patients with sleep apnea - an increase that correlates with the severity of the apnea (see "Sleep Apnea: Understanding the Cardiometabolic Vicious Cycle").  

According to a joint paper published by the Journal of Cardiology and Journal of Periodontology (Friedewald et al 2009), periodontal disease is also a significant risk factor in the development of coronary artery disease and its acute events. Moderate to severe periodontitis increases levels of hsCRP (a marker of systemic inflammation predictive of future heart attacks and the onset of hypertension, diabetes and stroke). Increased carotid intima-media thickness, which correlates with an elevated risk for heart attack and stroke in patients without CVD histories, is common in patients with periodontitis.  The same landmark paper concludes that non-diabetic adults with periodontal disease develop Type 2 diabetes more often than those without periodontal disease, with glycemic control being adversely affected by the severity of the periodontal condition. Another recent study published in Diabetes Care found that  A1c levels increased five times faster in the presence of periodontal disease. Other systematic reviews and meta-analyses have found that periodontitis was significantly associated with coronary heart disease and stroke, and that it favored the deposition of atherosclerotic plaques (Spahr 2006). 

A large controlled study (Spahr et al. 2006) found a very significant association (OR 1.92) between the total number of  periodontal bacteria present in a patient's tissues and the presence of heart disease. An even higher association (OR 2.70) was found between the quantity of a certain species (A. actinomycetemcomitans) and cardiovascular disease, while another independent correlation was identified with the number of P. intermedia pathogens.  Patients with heart disease had approximately twice as many periodontal bacteria when compared to healthy controls. Other recent studies found periodontal bacteria in 73% of heart plaques and an increased attachment of immune cells to the aortic artery wall with periodontitis, suggesting that periodontal pathogens play a significant role in the formation of hemorrhagic plaques (Corson 2008, Miyajima 2014)

Treatment of periodontal disease and sleep apnea has a clear impact on cardiovascular and diabetes control (see http://www.aasmnet.org/articles.aspx?id=5175, Gallegon, Guest)  Recent studies suggest that the standard Perio Protect method (scaling/root planing plus subgingival antimicrobial delivery) can reduce  the LP-PLA2 by as much as 37% at 3 months (Keller 2014), while effective control of sleep apnea has been shown to significantly reduce blood pressure, glucose levels and insulin sensitivity (Iftikhar 2103, Sleep Review 2015). At the same time, because some of the physiological changes associated with sleep apnea and periodontitis may be hard to reverse, it is important to address both conditions from a preventive standpoint, with early recognition and definitive interventions, thus minimizing the overall cardiovascular and metabolic risk. 


Cardiologist Jason Wischmeyer  Talking About the Oral Systemic Link and Coordinated Inflammatory Risk Management 



Sleep Disorders and the Heart: What Do Cardiologists Need to Know? / MAYO CLINIC 

Sleep apnea research: The HeartBEAT Study 
NHLBI (National Heart, Lungs and Blood Institute - NIH) 

Sleep Apnea: Why Snoring is Bad for your Heart / PENN MEDICINE

Findings Link Sleep Apnea to Cardiovascular Disease 
UPMC - University of Pittsburgh Medical Center

Mechanisms of Insulin Resistance in Sleep Apnea
Speaker: Christopher P. O'Donnell
Meeting: ADA 72nd Scientific Sessions (2012)

Sleep Apnea and Diabetes Risk
Speaker: Naresh M. Punjabi
Meeting: ADA 72nd Scientific Sessions (2012)

Relationship Between Obstructive Sleep Apnea and Diabetes Risk–A Meta-Analysis
Speaker: Kazuya Fujihara
Meeting: ADA 72nd Scientific Sessions (2012)

Obstructive Sleep Apnea and Type 2 Diabetes
Speaker: Esra Tasali
Meeting: ADA 57th Annual Advanced Postgraduate Course (2010)

Obstructive Sleep Apnea: A Cardiometabolic Risk Factor
Speaker: Eric Olson
Meeting: ADA 67th Scientific Sessions (2007)

Sleep Apnea and Sleep Deprivation: The Less You Sleep, the More you Eat! / MAYO CLINIC


Gallegos, L., T. Dharia, and A. B. Gadegbeku. "Effect of continuous positive airway pressure on type 2 diabetes mellitus and glucose metabolism." Hospital practice (1995) 42.2 (2014): 31-37. 

Guest, Julian F., et al. "Clinical outcomes and cost-effectiveness of continuous positive airway pressure to manage obstructive sleep apnea in patients with type 2 diabetes in the UK." Diabetes Care 37.5 (2014): 1263-1271.

Friedewald, Vincent E., et al. "The American Journal of Cardiology and Journal of Periodontology Editors' Consensus: Periodontitis and Atherosclerotic Cardiovascular Disease♦." Journal of periodontology 80.7 (2009): 1021-1032.

Corson, Marshall A., Peter H. Jones, and Michael H. Davidson. "Review of the evidence for the clinical utility of lipoprotein-associated phospholipase A 2 as a cardiovascular risk marker." The American journal of cardiology 101.12 (2008): S41-S50.

Keller, Duane C. "Systemic Lp-PLA-2 cardiovascular marker response to direct medication delivery periodontal treatment." Cardiovascular System 2.1 (2014): 8.

Miyajima, Shin-ichi, et al. "Periodontitis-activated monocytes/macrophages cause aortic inflammation." Scientific reports 4 (2014).

Iftikhar, Imran H., et al. "Effect of oral appliances on blood pressure in obstructive sleep apnea: a systematic review and meta-analysis." Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 9.2 (2013): 165.

Sleep Review Magazine, April 6, 2015. "In Resistant Hypertension, Sleep Apnea Treatment Results in Greater Blood Pressure Reduction"