You are on page 1of 10

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): 96100.
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: dr_sunithaj@yahoo.co.in
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, which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work 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.[13] 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.[49]
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
1
1
2
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 2/10
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
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 3/10
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
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 4/10
Leptin
Adiponectin, resistin and other adipose-tissuederived 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-tissuederived 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-tissuederived hormones and cytokines (adipokines) inflammatory markers
Adipose tissue secretes proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-) and
interleukin-6 (IL-6). TNF- 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-tissuederived 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
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 5/10
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.[2830] 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-, IL-1 and IL-6.[28] It has been suggested
that the secretion of TNF- 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- 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
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 6/10
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-
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
REFERENCES
1. Expert Panel. Executive summary of the clinical guidelines on the identification, evaluation, and
treatment of overweight and obesity in adults. Arch Intern Med. 1998;158:185567. [PubMed: 9759681]
2. Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, et al. Prevalence of obesity,
diabetes, and obesity-related health risk factors, 2001. JAMA. 2003;289:769. [PubMed: 12503980]
3. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with
overweight and obesity. JAMA. 1999;282:15239. [PubMed: 10546691]
4. Perlstein MI, Bissada NF. Influence of obesity and hypertension on the severity of periodontitis in
rats. Oral Surg Oral Med Oral Pathol. 1977;43:70719. [PubMed: 266151]
5. Saito T, Shimazaki Y, Koga T, Tsuzuki M, Ohshima A. Relationship between upper body obesity and
periodontitis. J Dent Res. 2001;80:16316. [PubMed: 11597023]
6. Saito T, Shimazaki Y, Kiyohara Y, Kato I, Kubo M, Iida M, et al. Relationship between obesity,
glucose tolerance, and periodontal disease in Japanese women: the Hisayama study. J Periodontal Res.
2005;40:34653. [PubMed: 15966913]
7. Wood N, Johnson RB, Streckfus CF. Comparison of body composition and periodontal disease using
nutritional assessment techniques: Third National Health and Nutrition Examination Survey (NHANES
III) J Clin Periodontol. 2003;30:3217. [PubMed: 12694430]
8. Genco RJ, Grossi SG, Ho A, Nishimura F, Murayama Y. A proposed model linking inflammation to
obesity, diabetes, and periodontal infections. J Periodontol. 2005;76:207584. [PubMed: 16277579]
9. Dalla Vecchia CF, Susin C, Rsing CK, Oppermann RV, Albandar JM. Overweight and obesity as risk
indicators for periodontitis in adults. J Periodontol. 2005;76:17218. [PubMed: 16253094]
10. Pouliot MC, Desprs JP, Lemieux S, Moorjani S, Bouchard C, Tremblay A, Nadeau A, et al. Waist
circumference and abdominal sagittal diameter: best simple anthropometric indexes of abdominal
visceral adipose tissue accumulation and related cardiovascular risk in men and women. Am J Cardiol.
1994;73:4608. [PubMed: 8141087]
11. Wang Y, Rimm EB, Stampfer MJ, Willett WC, Hu FB. Comparison of abdominal adiposity and
overall obesity in predicting risk of type 2 diabetes among men. Am J Clin Nutr. 2005;81:55563.
[PubMed: 15755822]
12. Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, et al. Obesity and the risk
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 7/10
of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet.
2005;366:16409. [PubMed: 16271645]
13. Haslam DW, James WP. Obesity. Lancet. 2005;366:1197209. [PubMed: 16198769]
14. Stumvoll M, Goldstein BJ, van Haeften TW. Type 2 diabetes: principles of pathogenesis and therapy.
Lancet. 2005;365:133346. [PubMed: 15823385]
15. Wilson PW, DAgostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as
determinants of cardiovascular risk: the Framingham experience. Arch Intern Med. 2002;162:186772.
[PubMed: 12196085]
16. Ritchie CS. Obesity and periodontal disease. Periodontol. 2007;44:15463.
17. Magliocca KR, Helman JI. Obstructive sleep apnea: diagnosis, medical management and dental
implications. J Am Dent Assoc. 2005;136:11219. [PubMed: 16161367]
18. Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2005;365:141528.
[PubMed: 15836891]
19. Flegal KM, Graubard BI, Williamson DF, Gail MH. Excess deaths associated with underweight,
overweight, and obesity. JAMA. 2005;293:18617. [PubMed: 15840860]
20. Willett WC, Hu FB, Colditz GA, Manson JE. Underweight, overweight, obesity, and excess deaths.
JAMA. 2005;294:551. [PubMed: 16077044]
21. Nishida N, Tanaka M, Hayashi N, Nagata H, Takeshita T, Nakayama K, et al. Determination of
smoking and obesity as periodontitis risks using the classification and regression tree method. J
Periodontol. 2005;76:9238. [PubMed: 15948686]
22. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab.
2004;89:254856. [PubMed: 15181022]
23. Thomas T, Gori F, Khosla S, Jensen MD, Burguera B, Riggs BL. Leptin acts on human marrow
stromal cells to enhance differentiation to osteoblasts and to inhibit differentiation to adipocytes.
Endocrinology. 1999;140:16308. [PubMed: 10098497]
24. Johnson RB, Serio FG. Leptin within healthy and diseased human gingiva. J Periodontol.
2001;72:12547. [PubMed: 11577959]
25. Lindsay RS, Funahashi T, Hanson RL, Matsuzawa Y, Tanaka S, Tataranni PA, et al. Adiponectin
and development of type 2 diabetes in the Pima Indian population. Lancet. 2002;360:578.
[PubMed: 12114044]
26. Pischon T, Girman CJ, Hotamisligil GS, Rifai N, Hu FB, Rimm EB. Plasma adiponectin levels and
risk of myocardial infarction in men. JAMA. 2004;291:17307. [PubMed: 15082700]
27. Pischon N, Heng N, Bernimoulin JP, Kleber BM, Willich SN, Pischon T. Obesity, inflammation, and
periodontal disease. J Dent Res. 2007;86:4009. [PubMed: 17452558]
28. Beck JD, Offenbacher S. Systemic effects of periodontitis: epidemiology of periodontal disease and
cardiovascular disease. J Periodontol. 2005;76:2089100. [PubMed: 16277581]
29. Dietrich T, Garcia RI. Associations between periodontal disease and systemic disease: evaluating the
strength of the evidence. J Periodontol. 2005;76:217584. [PubMed: 16277591]
30. Mattila KJ, Pussinen PJ, Paju S. Dental infections and cardiovascular diseases: a review. J
Periodontol. 2005;76:20858. [PubMed: 16277580]
31. Nishimura F, Iwamoto Y, Mineshiba J, Shimizu A, Soga Y, Murayama Y. Periodontal disease and
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 8/10
diabetes mellitus: the role of tumor necrosis factor-alpha in a 2-way relationship. J Periodontol.
2003;74:97102. [PubMed: 12593603]
32. Kempers KG, Foote JW, DiFlorio-Brennan T. Obesity: prevalence and considerations in oral and
maxillofacial surgery. J Oral Maxillofac Surg. 2000;58:13743. [PubMed: 10670591]
Figures and Tables
Table 1
Classification and definition of overweight and obesity (based on expert panel, 1998)
Disease risk relative to normal weight circumference and waist
Classification BMI (kg/m ) Men102 cm Women88 cm Men>102 cm Women>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

5/7/14 Obesity and periodontal disease


www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 9/10
Model linking periodontitis and obesity with inflammationrelated chronic diseases
Figure 3
5/7/14 Obesity and periodontal disease
www.ncbi.nlm.nih.gov/pmc/articles/PMC3110475/?report=printable 10/10
A proposed model linking inflammation to obesity, diabetes and periodontal infections
Articles from Journal of Indian Society of Periodontology are provided here courtesy of Medknow Publications

You might also like