obesity and periodontal disease

5/7/14 Obesity and periodontal disease

www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 1/10

J Indian Soc Periodontol. 2010 Apr-Jun; 14(2): 96–100.

doi: 10.4103/0972-124X.70827

PMCID: PMC3110475

Obesity and periodontal disease

Sunitha Jagannathachary and Dinesh Kamaraj

Department of Periodontics, College of Dental Sciences, Davangere, Karnataka, India

Department of Periodontics, Rajas Dental College, Vadakankulam, Tamil Nadu, India

Address for correspondence: Dr. Sunitha Jagannathachary, Department of Periodontics, College of Dental Sciences, Davangere,

Karnataka, India. E-mail: [email protected]

Received October 1, 2009; Accepted April 6, 2010.

Copyright © Journal of Indian Society of Periodontology

This is an open-access article distributed under the terms of the Creative Commons Attribution License, w hich permits unrestricted use,

distribution, and reproduction in any medium, provided the original w ork is properly cited.

Abstract

Obesity is characterized by the abnormal or excessive deposition of fat in the adipose tissue. Its

consequences go far beyond adverse metabolic effects on health, causing an increase in oxidative stress,

which leads not only to endothelial dysfunction but also to negative effects in relation to periodontitis,

because of the increase in proinflammatory cytokines. Thus obesity appears to participate in the

multifactorial phenomenon of causality of periodontitis through the increased production of reactive

oxygen species. The possible causal relationship between obesity and periodontitis and potential

underlying biological mechanisms remain to be established; however, the adipose tissue actively secretes

a variety of cytokines and hormones that are involved in inflammatory processes, pointing toward

similar pathways involved in the pathophysiology of obesity, periodontitis and related inflammatory

diseases. So the aim of this article is to get an overview of the association between obesity and

periodontitis and to review adipose-tissue – derived hormones and cytokines that are involved in

inflammatory processes and their relationship to periodontitis.

Keywords: Adipokines, obesity, periodontal disease

INTRODUCTION

Obesity, defined as a body mass index (BMI) >30.0 kg/m , is a major public health problem today. The

prevalence of obesity has increased substantially over the past decades in most industrialized countries.

Obesity is a risk factor for several chronic diseases, most notably hypertension, type 2 diabetes,

dyslipidemia and coronary heart disease.[1–3] Since adiposity can be considered a systemic disease that

predisposes to a variety of comorbidities and complications that affect overall health, obese persons and

all health professionals including dentists should require awareness regarding obesity. Further, recent

studies have suggested that obesity is also associated with oral diseases, particularly periodontitis.[4–9]

In fact, the adipose tissue secretes several cytokines and hormones that are involved in inflammatory

processes, suggesting that similar pathways are involved in the pathophysiology of obesity and

periodontitis.

DEFINITION AND ASSESSMENT OF OBESITY

The definition of obesity is based on body mass index (BMI, also called Quetelet Index), which is the

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Hypertension

Type 2 diabetes

Cardiovascular disease

ratio of body weight (in kg) to body height (in m) squared.[1] BMI is highly correlated with fat mass

and morbidity and mortality and therefore sufficiently reflects obesity-related disease risk in a wide

range of populations; however, there are some limitations. For example, for the same BMI, older

persons tend to have a higher body fat composition; and therefore, risk assessment by BMI is less

accurate in older people (over 65 years of age).

Body fat distribution is assessed by the measurement of waist circumference, with 102 cm in men and

88 cm in women, respectively, being the cut-off point for abdominal obesity associated with an

increased risk of morbidity.[1] Waist circumference shows a close correlation with the amount of

visceral adipose tissue, and visceral adipose tissue has been shown to be metabolically more active and

to secrete far greater amounts of cytokines and hormones compared with subcutaneous adipose tissue.

[10] Recent large studies have indicated that measurement of waist circumference or waist-hip ratio

may be a better disease risk predictor than BMI, and there is still intensive research ongoing as to

whether BMI, waist circumference or both should be used to assess disease risk[11,12] [Table 1].

Several other diagnostic tools are available to assess body fat composition, such as measurement of

(subcutaneous) skin fold by means of a caliper or ultrasound, bioelectrical impedance analysis (BIA),

densitometry or imaging procedures (Computed tomography, Nuclear Magnetic Resonance); however,

most of these procedures are not readily available in clinical practice and do not add substantial

information for risk assessment in an individual, beyond BMI and waist circumference.

Prevalence

Over the period 1960-1980, the prevalence of overweight and obesity among adults and of overweight

among children, was relatively constant. Above 13% of adults were obese, and 5% of children were

overweight. However, data from the National Health and Nutrition Examination Survey III (1989-

1991) showed that obesity in adults and overweight in children had markedly increased in comparison

to the previous survey. Those trends continued such that approximately 31% of American adults now

meet the criteria for obesity. More than 65% of the United States adult population has a body mass

index of ≥25 kg/m2, and 15.8% of children aged 6-11 years and 16.1% of adolescents aged 12-19 years

are overweight. Thus in a relatively short time period, the prevalence of obesity among adults has

doubled, and the prevalence of overweight among children and adolescents has tripled. In the year

2004, approximately 34.1% of the US population was overweight; and about 32.2%, obese.[1,7]

Obesity-related diseases

Overweight and obesity have long been recognized as important determinants of elevated

blood pressure levels. It is well established that weight gain is consistently associated with increased

blood pressure, and that weight loss decreases blood pressure independent of changes in sodium intake.

Compared with normal-weight individuals, obese persons have an up to 5 times higher risk of

hypertension, and up to two thirds of cases of hypertension can be attributed to excess weight.

Mechanisms that have been implicated in the development of obesity-related hypertension include

increased sympathetic nerve activity, sodium and volume retention, renal abnormalities, insulin

resistance, hyperleptinemia and increased secretion of angiotensinogen from adipocytes.[3,13]

The relationship between obesity and type 2 diabetes is particularly close. Obese persons

have a more than 10-fold increased risk of developing type 2 diabetes compared with normal-weight

persons. Type 2 diabetes develops due to an interaction between insulin resistance and beta cell failure.

Several factors, including lipotoxicity and glucose toxicity, as well as obesity-derived cytokines, have

been implicated in these processes.[8,14]

Obese persons have an about 1.5-fold increased risk for cardiovascular disease

(including coronary heart disease and cerebrovascular disease), and between 10% and 15% of all cases

of cardiovascular disease can be attributed to overweight and obesity. Obesity is also associated with an

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/table/T0001/



Osteoarthritis

Respiratory disorders

Metabolic syndrome

about 2-fold higher risk of heart failure and a 50% increased risk of atrial fibrillation.[10,15]

Obesity is associated with bone knee and hip arthritis, and with arthritis involving the

carpometacarpal joints of the hand. Recent studies have proved that being overweight antedates the

development of knee osteoarthritis and increases the risk of radiographic progression.[16]

Visceral fat accumulation results in restrictive respiratory function with reduced

forced vital capacity and expiratory reserve volume. Obesity is the major reversible risk factor for

obstructive sleep apnea syndrome. The prevalence rises from 2% to 4% in the general population to a

prevalence of at least 40% in morbidly obese patients. Orofacial findings of this syndrome includes a

retrognathic mandible, narrow palate, large neck circumference, long soft palate, tonsillar hypertrophy,

nasal septal deviation and relative macroglossia. Waist circumference tends to be a better predictor of

this syndrome than body mass index.[16,17]

The metabolic syndrome is a concept that encompasses metabolic abnormalities

that co-occur to a greater degree than would be expected by chance alone, and which predisposes

individuals at a high risk to develop cardiovascular disease. Although the exact underlying cause of

metabolic syndrome is unknown, the more recent definitions emphasize the focus on abdominal obesity

as its core component (International Diabetes Federation, 2005). This approach is supported by a

growing number of studies showing that the adipose tissue itself is capable of producing several

hormones and proteins, which are involved in the development of obesity-related diseases.[16,18]

MORTALITY

Whether overweight and obesity affect disease prognosis and total mortality is an ongoing area of

research, and recently published studies have found contradictory results. For example, although obesity

increases the risk of heart failure, the studies found that among persons with prevalent heart failure,

obese individuals are likely to have a better prognosis than non-obese individuals. This is likely due to

the fact that lower BMI reflects wasting processes in this patient group (as in other chronic diseases).

Further, several studies have found a U-shaped association between BMI and total mortality, with a

minimum at a BMI of approximately 25.0 kg/m ,.[19] However, it has been argued that these analyses

may be confounded by smoking (smokers are usually leaner than nonsmokers but have a higher risk of

mortality) or underlying prevalent chronic diseases (individuals with chronic diseases often have lower

body weight). Clearly, further studies are needed to examine the effect of obesity on morbidity, disease

prognosis and mortality.[20]

Association between obesity and periodontal disease

It has been suggested that obesity is second only to smoking as the strongest risk factor for

inflammatory periodontal tissue destruction.[21] The first report on the relationship between obesity

and periodontal disease appeared in 1977, when Perlstein et al. observed histopathologic changes in the

periodontium in hereditary obese Zucker rats. Using ligature-induced periodontitis, they found alveolar

bone resorption to be greater in obese animals compared with non-obese rats. Also, it seemed that under

healthy oral conditions, obesity per se does not promote pathologic periodontal alterations; however, in

response to bacterial plaque accumulation, periodontal inflammation and destruction were more severe

in obese animals.[4] Later on, the hypothesis of obesity as a risk factor for periodontal disease was

supported by epidemiological studies.

In 1998, Saito et al. analyzed 241 healthy Japanese individuals and showed, for the first time, an

association between obesity and periodontal disease in humans. In addition, studies have indicated that

the fat distribution pattern plays a crucial role in the association with periodontitis.[6,7] Another recent

study by Saito et al. concluded that obesity is associated with deep periodontal pockets, independent of

glucose tolerance status. Genco et al. analyzed National Health and Nutrition Examination Survey

(NHANES III) data and demonstrated that BMI was positively correlated with the severity of

2



Leptin

Adiponectin, resistin and other adipose-tissue–derived cytokines

periodontal attachment loss; they found that this relationship is modulated by insulin resistance.[8]

The underlying biological mechanisms for the association of obesity with periodontitis are not well

known; however, adipose-tissue–derived cytokines and hormones may play a key role. Fat tissue is not

merely a passive triglyceride reservoir of the body, but also produces a vast amount of cytokines and

hormones, collectively called adipokines or adipocytokines, which in turn may modulate periodontitis.

[22]

Adipose-tissue–derived hormones and cytokines (adipokines) inflammatory markers

Adipose tissue secretes proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and

interleukin-6 (IL-6). TNF-α and IL-6 are the main inducers of acute-phase hepatic protein production,

including C-reactive protein (CRP) [Figure 1].

Leptin is a pleiotropic cytokine, secreted by adipocytes, which is involved in a variety of biological

processes, including energy metabolism, endocrine functions, reproduction and immunity. Leptin is

thought to act as a “lipostat” that regulates adipose tissue mass. As a negative feedback mechanism,

elevated leptin concentrations result in increased energy expenditure, decreased food intake and a

negative energy balance. In contrast, most overweight and obese persons show resistance to leptin at

the receptor level and therefore have higher leptin levels than non-overweight individuals.[16]

In addition, leptin has been shown to be involved in bone metabolism. Although reported data appear

somewhat conflicting, evidence exists that leptin may decrease bone formation via central nervous

pathways and may stimulate bone formation via direct peripheral effects on bone cells. The net result

on bone formation may depend on various general and bone-specific factors, such as species, age,

gender, serum leptin levels, blood-brain barrier permeability, bone tissue, skeletal maturity and

signaling pathways.[23]

In periodontal disease, leptin regulation has still to be examined, especially with respect to the

epidemiological association between obesity and periodontitis. One study implied decreasing leptin levels

in gingival biopsies with increasing pocket-probing depths, which would be contrary to the cited data on

other inflammatory diseases.[24]

Adiponectin is a circulating hormone

secreted by adipose tissue that is involved in glucose and lipid metabolism and which accounts for about

0.05% of total serum proteins. Contrary to other adipose-derived hormones, adiponectin levels are

reduced in persons with obesity, insulin resistance or type 2 diabetes. Adiponectin improves insulin

sensitivity and may have anti-atherogenic and anti-inflammatory properties, and low plasma

adiponectin levels have been shown to predict type 2 diabetes and coronary heart disease in humans.

Experimental models suggest that adiponectin could play a role as a mediator of inflammation;

however, the exact role of adiponectin in inflammatory diseases remains to be elucidated.[25,26]

Resistin belongs to a family of resistin-like molecules (RELM) and has been reported to be secreted by

adipocytes and to cause insulin resistance in animal models. However, studies have shown that the

biology of resistin differs substantially between species, and many aspects, specifically its association

with obesity and its effects on insulin sensitivity in humans, remain controversial. Current evidence

suggests that, in humans, resistin is more closely related to inflammatory processes than to insulin

resistance. Whether or not resistin plays a role in inflammatory periodontal disease remains to be

defined.[27]

As more and more adipose-tissue–derived cytokines and hormones are being discovered, the complexity

of the endocrine network of which these mediators are a part becomes more and more apparent. Recent

additions to this list of adipokines include visfatin, which elicits insulin-like effects, and serum-retinol–

binding protein 4 (RBP4). Regarded initially as markers mainly related to weight regulation and insulin

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resistance, it has become clear that hormones like leptin, resistin or adiponectin are involved in a variety

of functions and diseases, including cardiovascular disease, diabetes and inflammatory diseases.[27]

Association of periodontitis with obesity-related chronic diseases

Proinflammatory cytokines may play a crucial role in the close relationship among periodontitis, obesity

and chronic diseases. In fact, this association may be multidirectional [Figure 2].[28] For example, it

has been well established that inflammation is an essential component in the development of

atherosclerosis, and observational studies showed that periodontitis is associated with a moderately, but

significantly, higher risk of coronary heart disease.[28–30] Interventional studies that examined the

effects of antibiotic treatment on cardiovascular risk have generally failed to show any beneficial effect;

however, these studies have mostly been of short duration (less than 1 year of treatment) and have

investigated the effects on secondary prevention only. Inflammatory diseases like periodontitis induce

the production of proinflammatory cytokines such as TNF-α, IL-1 and IL-6.[28] It has been suggested

that the secretion of TNF-α by adipose tissue triggered by LPS from periodontal gram-negative bacteria

promotes hepatic dyslipidemia and decreases insulin.

Type 2 diabetes and decreased insulin sensitivity are associated with the production of advanced

glycation end products (AGE), which trigger inflammatory cytokine production, thus predisposing to

inflammatory diseases such as periodontitis. These observations suggest a potential interaction among

obesity, periodontitis and chronic disease incidence, although present studies are insufficient to conclude

whether such associations are causal. Thus in addition to being a risk factor for type 2 diabetes and

coronary heart disease, obesity-related inflammation may also promote periodontitis. Conversely,

periodontitis, once it exists, may promote systemic inflammation and thereby increase the risk of

coronary heart disease. In this context, it is interesting to note that periodontal treatment has been

shown to reduce circulating TNF-α and serum levels of glycosylated hemoglobin, and has beneficial

effects on the control of type 2 diabetes [Figure 3].[5,8,31]

Assessment in dental practice

Until recently, a definite diagnosis of obesity was only rarely made by physicians, and body weight or

body height was rarely measured in clinical practice. Further, it has been shown that about 25% of

obese persons have been misclassified, by subjective estimation of the physician, as having normal

weight. In future, if obesity is to be acknowledged as a multiple-risk-factor syndrome for overall and

oral health, general and oral risk assessment in the dental office should include the evaluation of body

mass index on a regular basis. Although there is still research ongoing as to whether BMI or waist

circumference or both are a better disease risk predictor, the assessment of waist circumference in

addition to BMI seems advisable, based on current obesity guidelines. Besides the suggested association

between periodontal disease and obesity, periodontists need to be aware of the potential health problems

related to obesity and should take them into account during treatment.[27,32]

It has been suggested that supine patient positioning should be avoided, to maximize the pulmonary

mechanics. Impaired chest expansion decreases vital capacity and tidal function, which compromises

tissue oxygenation. These conditions put the obese person at high anesthetic and surgical risk. Wound-

healing processes are dependent on sufficient tissue oxygenation. Also, higher incidences of infections

and post-surgical hematoma formation have been reported among obese persons. The vulnerability to

wound complications increases morbidity and mortality of obese persons. Also, a close collaboration

with the general physician and the dietician may be beneficial to ensure effective periodontal treatment.

[27,32]

CONCLUSION

Obesity is a complex disease, and its relationship to oral status has been realized by the scientific





community in recent years. Periodontists must be aware of the increasing numbers of obese persons

and of the significance of obesity as a multiple-risk-factor syndrome for overall and oral health.

Proinflammatory cytokines may be a multidirectional link among periodontitis, obesity and other

chronic diseases. The adipose tissue is a large reservoir of biologically active mediators, such as TNF-α

and other adipokines. Studies have demonstrated a close involvement of the adipokines – such as leptin,

resistin and adiponectin – in inflammatory processes. However, their role in periodontal inflammation

has yet to be defined. Although this relationship needs further investigation, periodontists should counsel

obese persons regarding the possible oral complications of obesity, to diminish morbidity for these

individuals. This includes the measurement of body mass index and waist circumference for periodontal

risk assessment on a regular basis.

Footnotes

Source of Support: Nil

Conflict of Interest: None declared

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Figures and Tables

Table 1

Classification and definition of overweight and obesity (based on expert panel, 1998)

Disease risk relative to norm al weight circum ference and waist

Classification BMI (kg/m ) Men≤102 cm Wom en≤88 cm Men>102 cm Wom en>88 cm

Underweight <18.5 — —

Normal 18.5-24.9 — —

Overweight 25.0-29.9 Increased High

Obese - Class I 30.0-34.9 High Very high

Obese - Class II 35.0-39.9 Very high Very high

Obese - Class III ≥40 Extremely high Extremely high

Established for non-Asian populations. The recently proposed classification for Asian population is

BMI<18.5, underweight, 18.5-22.9, normal weight; 23.0-24.9, overweight 25.0-29.9, obese class I;

≥30.0 obese class II (WHO/IASO/IOTF, 2000).

Disease rick for type 2 diabetes, hypertension, and cardiovascular\disease.

Figure 1

Different roles of adipokines

Figure 2

†

2

†



Model linking periodontitis and obesity with inflammationrelated chronic diseases

Figure 3



A proposed model linking inflammation to obesity , diabetes and periodontal infections

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