This course was published in the June 2017 issue and expires June 2020. The authors have no commercial conflicts of interest to disclose. This 2 credit hour self-study activity is electronically mediated.
After reading this course, the participant should be able to:
- Define the concept of cumulative inflammatory burden and its relationship to systemic and oral diseases.
- Discuss the prevalence of obesity and risk of inflammatory-driven diseases, including comorbid conditions and periodontitis.
- Explain the relationship between metabolic syndrome (MetS) and periodontal disease, and a potential assessment tool for MetS risk.
The significant cost associated with delayed intervention in chronic diseases caused by systemic inflammation is widely recognized.1,2 In light of this, we propose a model of risk assessment that will provide an easily implemented strategy to assist oral health professionals in identifying patients at risk for inflammatory-driven comorbid conditions. This model is predicated on the recognition that the cumulative inflammatory burden associated with periodontitis in an obese individual (defined as a body mass index [BMI] ≥30 kg/m2; >30% body fat in women, or >25% body fat in men) may foretell the presence of metabolic disorders, or downstream precipitation of incident diabetes, cardiovascular disease, and other inflammatory-driven conditions. Better patient outcomes—and more efficient use of health care resources—may be realized by implementing this risk assessment model in dental practice.
Much has been written about systemic inflammation and its association with serious comorbid diseases.3,4 Research has provided an understanding of how genetics can modify inflammatory response and the clinical expression of a number of diseases, including coronary artery disease, Alzheimer’s disease, and periodontitis.5 Many sources elicit a state of chronic inflammation and contribute to cumulative inflammatory burden. For example, an imbalance in the intake of omega-6 and omega-3 fats;6 a diet high in red meat, processed foods, refined carbohydrates, and saturated fatty acids; food sensitivities;7 psychosocial stressors; smoking;8 lack of quality sleep;9 environmental toxins;10 infection; and obesity11 all have the potential to add to the inflammatory burden, ultimately promoting cardiometabolic risk. There is a strong rationale for implementing a risk assessment model that considers patients’ cumulative inflammatory burden, which may be amplified by obesity and chronic infection from periodontal disease.
NEW RISK ASSESSMENT MODEL
In white adipose tissue (fat cells), there is a moderate, but continuous increase in the release of a “cocktail” of inflammatory factors that are systemically dumped, including TNF-α, and IL-6 cytokines.12 Hence, obesity is widely recognized as a state of low-grade inflammation,11 fueling the risk for many diseases, including type 2 diabetes,13hypertension,14 dyslipidemia,15 coronary artery disease,16 stroke,17 gallbladder disease,18osteoarthritis,19 sleep apnea and pulmonary dysfunction,20 certain types of cancer,21–23and reproductive abnormalities.24 Periodontal infection, another source of low-grade inflammation, is also fueled by cytokines that mediate inflammation.12 If periodontitis is left untreated, ongoing low-grade bacteremia is produced—and, like obesity, it adds to the cumulative inflammatory burden.25–27 The greater the burden, the greater the risk and incidence of inflammatory-driven disease.
Over the past decade, mounting evidence suggests obesity is also a risk factor for periodontal disease,28–37 independent of other factors, such as age, gender, race, and ethnicity. Furthermore, smoking and insulin resistance may help regulate this relationship.38In a multicentered, randomized controlled trial that studied the effects of periodontal treatment on secondary prevention of cardiovascular disease, Offenbacher et al39 demonstrated that obesity may exert such a dominant influence that when obese individuals undergo periodontal therapy, its presence may nullify the effects of periodontal treatment on high-sensitivity C-reactive protein (hs-CRP), a sensitive marker of systemic inflammation. In other words, an obese patient who undergoes therapy for periodontitis may not be able to realize the full systemic benefits of that treatment.
Studies have suggested a correlation between the severity of obesity and progression of periodontitis. Two of the most noteworthy are the work of Gorman et al40 and Reeves et al.41 Gorman et al monitored 1,038 non-Hispanic white men over 25 years, and found the following:
- For each unit increase in BMI, there was a 5% increase in the hazard of experiencing progression of alveolar bone loss.
- A 1-cm increase in waist circumference was associated with a 1% to 2% increase in the risk of experiencing progression of probing pocket depth and clinical attachment loss. With each 1% increment in baseline waist-height ratio, there was a 3% increase in the risk of experiencing periodontitis progression.40
The study by Reeves et al41 of 2,452 adolescent nonsmokers (ages 17 to 21) noted the following:
- With each 1-kg increase in weight, there was a corresponding 6% increase in the risk of periodontal disease.
- For every 1-cm increase in waist circumference, there was a 5% increase in risk of periodontitis.41
We have hypothesized the presence of obesity and periodontitis may be additive and therefore, in combination, confer a greater cumulative burden of inflammation.42 However, to date, only a few studies have explored this matter. In a cross-sectional study, Zimmerman et al43 observed that compared with obese patients who did not have periodontal disease, leptin and IL-6 levels were elevated in the serum of individuals who were obese and had periodontal disease. These markers did not seem to be affected by scaling and root planing, suggesting that obesity may modulate local and systemic adipokines toward a proinflammatory state, regardless of periodontal treatment.44 Nevertheless, aspects related to periodontal disease severity, number of teeth affected, study design, and sample size may have impacted these outcomes.
Since the 2004 paper by Pozharitskaia et al,45 numerous investigations have looked into the interrelationship between metabolic syndrome (MetS) and periodontitis. MetS is a group of specific metabolic abnormalities that, when combined, imparts a synergistic, enhanced risk for coronary artery disease, stroke, and cardiovascular mortality—an effect that is more pronounced than the individual metabolic components impart alone (eg, hypertension or abdominal obesity).46 As one of the leading causes of death in obese individuals, MetS has a number of definitions; for the purposes of this paper, the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults defines a patient with MetS as exhibiting three or more of the five criteria listed in Table 1.
Evidence of the association between MetS and periodontal disease has been consistent enough that a number of researchers have suggested periodontitis should be considered a component of MetS (Figure 1).47 In addition, mounting evidence suggests that MetS is positively associated with periodontal disease,25,37,47–58 as various studies have concluded:
- There is an association between periodontitis and MetS, independent of other risk factors.31
- Compared to individuals without MetS, the severity and extent of periodontal disease is significantly higher in subjects with MetS.35
- Periodontal therapy may significantly modulate hs-CRP, total leukocytes, serum triglycerides, and high-density lipoprotein cholesterol, which may benefit individuals with MetS and advanced periodontal disease.59
Many individuals have undiagnosed MetS, and thus have not been counseled about the risks inherent to this condition. Given the frequency that patients see their oral health professionals, these clinicians are well positioned to identify patients who have central adiposity (a telling component of MetS) and initiate discussions about cardiometabolic risk. When a patient enters the operatory, the simple task of observing his or her physique can provide valuable clues in identifying whether that individual may be at risk for MetS.
Visceral fat distribution in individuals with an apple-shaped physique, in which weight is concentrated above the waist (Figure 2), is often a sign of MetS.60 This physique, also known as android, is linked to various components of MetS, including hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, and insulin resistance. Patients who present with this body type may be at increased risk for periodontitis. For example, recent evidence from a survey that included 1,287 dentate, nonsmoking, and nondiabetic subjects showed that individuals who present with higher waist circumference and waist-to-height ratio were associated with an increased number of deep pocket probing sites.61
In contrast, patients who have more weight concentrated below their waist (peripheral adiposity or a pear-shaped physique; Figure 2) have a body type that is not usually related to metabolic abnormalities. Generally, these individuals are at a decreased risk for MetS.
In recognition of the possibility that the combination of obesity and/or MetS and periodontitis may amplify a patient’s cumulative burden of inflammation, we introduce two precepts that underpin this proposed risk assessment model.
Inflammatory Priming: Compared with individuals of normal weight, patients who are overweight or obese are “inflammatory primed,” which increases risk for inflammatory-driven diseases, including periodontitis and concomitant systemic sequalea known to be linked to obesity. Because of their overweight or obese status, the question becomes, “What additional systemic impact will periodontal infection contribute to the cumulative inflammatory burden?”
Inflammatory Loading: Once periodontal infection is established in patients who are overweight or obese, a biological cascade of events produces proinflammatory cytokines that could also promote systemic inflammation,62,63 increasing the risk of cardiometabolic diseases. In addition, periodontal disease may exacerbate existing inflammatory-driven diseases; over time, this results in “inflammatory loading.” For example, in an obese individual, periodontitis may elicit complications in type 2 diabetes64 or negatively influence the clinical outcome in cases of coronary artery disease in patients who do not have diabetes.
PANDEMIC OF OBESITY
One of the most ominous threats to the viability of a robust and effective health care system is the pandemic of overweight and obese individuals. Finkelstein et al65 projected a 33% increase in obesity prevalence in the US, and a 130% increase in severe obesity over the next two decades. Given the enormity of this epidemic, its inherent costs, and the potential inflammatory priming associated with adipose tissue, obesity may be the single biggest factor contributing to inflammatory-driven diseases. Periodontitis, however, is also associated with additional risk factors—some of which share a commonality with prevalence markers linked to MetS, such as age, socioeconomic status, smoking, and ethnic background.66
Considering the emerging evidence supporting the interrelationships between obesity and periodontitis, oral health professionals can deliver more effective care by implementing a model of risk assessment that recognizes the importance of reducing patients’ cumulative inflammatory burden, especially in overweight or obese individuals with periodontal disease. This model has the potential to impact not only the periodontal health of obese and overweight patients, but concurrently it could also reduce cardiometabolic risk.
In the past, the responsibility for obesity intervention fell solely to physicians, nurses, dietitians, and other nondental health care professionals. The traditional scope of practice for oral health professionals has not included screening and referral of patients who are obese or at risk for obesity or MetS. However, the sheer magnitude of the obesity epidemic requires all providers to become involved.
Providers from all health care disciplines need to collaborate at the point-of-care to assess patients for the presence of chronic, low-grade inflammation. This must be bilaterally implemented; oral health professionals should move beyond identifying periodontal conditions (or other oral health issues) in isolation of assessing risk for whole-body, inflammatory-driven comorbid diseases. Nondental providers must also recognize that periodontal disease may amplify the cumulative inflammatory burden in a patient who is obese or diagnosed with an inflammatory-driven disease.
Clinicians, health care educators, public health authorities, and policymakers need to be informed of the potential surge in oral health issues that will likely accompany increases in the population of obese individuals, and the concomitant risks associated with inflammatory priming in this population. Accordingly, the development of protocols and clinical tools that will direct care in the individualized management and prevention of oral diseases in patients with metabolic diseases is critical. Close monitoring of the periodontal parameters of obese patients is of obvious importance; however, protocols and clinical tools to assist clinicians in educating patients about the significance of lifestyle modification are essential. These include educational counseling, nutritional assessment, and dietary treatment planning to help reduce a hyperresponsive inflammatory trait, among other clinical measures.
Although somewhat controversial, the concept of using oral health professionals to identify patients who have central adiposity offers promise in mitigating the risk for obesity and preventing metabolic diseases, in addition to benefitting patients’ periodontal health. Adoption of this new model of risk assessment has the potential to modify the trajectory of inflammatory-driven diseases, sustaining health, and, ultimately, prolonging life.
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From Dimensions of Dental Hygiene. June 2017;15(6):38-41.