Braz J Oral Sci. October-December 2007 - Vol. 6 - Number 23

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Obesity and periodontal disease:why suggest such relationship? Anoverview

Beatriz de Brito Bezerra1Enilson Antnio Sallum2Antnio Wilson Sallum21PhD Student;2ProfessorDepartment of Prosthodontics andPeriodontics, Periodontics Division, PiracicabaDental School, State University of Campinas

Received for publication: September 19, 2007Accepted: November 27, 2007

Correspondence to:Beatriz BezerraDepartamento de Prtese e Periodontiarea de PeriodontiaAv:Limeira, 901Piracicaba/SP BrazilCEP: 13.414-903Phone/fax: +55 19 2106-5301e-mail: biabezerra@fop.unicamp.br

AbstractObesity is a chronic condition that has social and economic implicationsfor public health. It can be associated with periodontal disease sincethe metabolic alterations observed in that condition could have someinfluence in immunity. The elevated levels of lipid and glucose can beassociated with periodontal disease, contributing to an exacerbatedhost inflammatory response, alterations in neutrophil function, andwith the inhibition of macrophage growth factors, reducing tissue-healing capacity. In this way, obese individuals could have higherchances of undergoing tissue destruction in the presence of periodontalinfection. On the other hand, periodontitis may be involved inalterations of lipid metabolism, since gram-negative bacteria couldpromote a rise in cholesterol and triglyceride levels due to chronicexposure to low levels of LPS in circulating blood, leading to theproduction of cytokines, which could initiate the production oflipoproteins by the liver. The objective was to review the literatureabout obesity and periodontal disease and provide a betterunderstanding of their relationship.

Key words:obesity, periodontitis, insulin resistance, hyperlipidemia

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Braz J Oral Sci. 6(23):1420-1422 Obesity and periodontal disease: why suggest such relationship? An overview

IntroductionObesity is a chronic condition, which can be associated withperiodontal disease, since metabolic alterations that arepresent in this condition could have some influence on thehost immunity. Elevations in the levels of lipids and glucosecan be associated with periodontal disease and maycontribute to an exacerbated inflammatory host response,alterations on the neutrophil functions, and the inhibition ofgrowth factors by macrophages, reducing the healingcapacity of the tissues. On the other hand, chronic exposureto bacteria LPS promotes the production of cytokines, whichcontribute to the alteration of the lipid metabolism.

Literature ReviewObesityObesity is a chronic metabolic condition that has publichealth implications because it is a risk factor for manydiseases, such as diabetes, hyperlipidemia, hypertension,atherosclerosis, cardiovascular disease, among others1-2.Three metabolic alterations are responsible for the obesitycharacteristics:(1) Hiperinsulinemia: there is increased production of insulinby beta cells to compensate the resistance in the tissues,especially the adipose, muscular and hepatic ones.(2) Hyperglycemia: since there is a resistance to insulin,the circulating glucose is not taken by the cells and there isan increase of the blood glucose levels.(3) Hyperlipidemia: there is an elevation of the seric levelsof cholesterol and triglyceride due to the lipid metabolismalteration there is an increase in the liver lipogenesis andlipolysis in the adipocytes.These alterations seen in obesity are also found in localizedchronic or generalized acute infections. Cytokines, especiallyTNF-a, produced by the adipose tissue, are the onesresponsible for those alterations. It is known that the adiposetissue stores energy as triglycerides and has a secretoryfunction3, constitutively producing cytokines. Obesity isthen characterized as a chronic inflammatory state that canbe confirmed by the high levels of C-reactive protein1,4.

Insulin ResistanceInsulin resistance is found in obesity and in infections, asthe result of an increased secretion of cytokines by theadipose tissue and the macrophages, which are hyperactivebecause of the hyperlipidemia in obesity5,6.TNF-a interferes in insulin signaling and blocks thetranslocation of the glucose transporter (GLUT-4) to the cellmembrane, as well the assimilation of the circulating glucoseby the cell7; as a result, a state of hyperglycemia can rise.Insulin resistance also interferes with lipid metabolismbecause the adipocytes resistant to insulin cannot assimilatethe circulating fatty acids. Reaching the liver, these fattyacids will be broken down in triglycerides and cholesterol8,

which will worsen the insulin resistance state.Insulin resistance can be the link between periodontaldisease, obesity and diabetes because in these threesituations there is the production of chronic regulatedcytokines. This chronic regulation contributes to the insulinresistance state, leading to metabolic alterations9.

Relationship between hyperlipidemia and periodontal diseaseThe relationship between periodontal disease andhyperlipidemia has already been studied by other authors5,6,10-12

, who verified that patients with periodontal disease couldpresent elevated levels of triglycerides and cholesterol. Thisis because the systemic involvement, since the periodontalinfection is a chronic one. Moreover, chronic exposure tobacteria LPS promotes the recruitment of defense cells,specifically macrophages that secrete TNF-a e IL-1b,increasing lipogenesis and lipolysis and leading to a state ofhyperlipidemia5.The increased lipid levels promote alterations, for example,phagocytosis and chemotaxis alterations of the defense cells(polimorphonuclear cells and macrophages). These cellsrelease a greater amount of growth factors by themacrophages, which impair tissue healing5.

Why suggest such a relationship?New evidences7,9,13,14 have been showing that insulinresistance is a link between obesity and periodontal diseasedue to the TNF-a produced in both conditions. TNF-aproduced by the adipose tissue helps exacerbate theperiodontal disease and the one produced by periodontaldisease helps perpetuate the insulin resistance seen inobesity.Periodontal disease may also unbalance lipid metabolismworsening the hiperlipidemic state in the obese patients5,6,10-12

. In a case-control study by Noack et al.15 the patients withhyperlipidemia had higher periodontal inflammation than thecontrol patients, with a higher percentage of sites and sextantswith probing depth (PD) 3.5mm.A positive relationship between the obesity indicators, bodymass index (BMI) and waist-hip ratio (WHR), and periodontaldisease was found in some studies14,16-18. Furthermore, asignificant correlation between BMI and the plasmaticconcentrations of TNF-a4, which may suggest that obesitymay lead to an exacerbation of the periodontal diseasebecause of the higher load of circulating cytokines.Nevertheless, the BMI is not a good obesity indicatorbecause it is based on the total fat of the patient. Waist-hipratio is a more reliable indicator since it measures the waistcircumference, which shows a close correlation with theamount of visceral adipose tissue19. Visceral adipose tissuewas shown to be metabolically active and to secrete a greatamount of cytokines and hormones, this way beingresponsible for some metabolic alterations19, such as insulin

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resistance and lipid profile alterations. In addition, in the hiparea, there is the greatest amount of muscle in the body, andits mass and function are closely related to the systemicsensitivity to insulin20. This way, many studies are using theWHR as an obesity indicator and have found a strongerpositive relationship with periodontal disease than theBMI11,14,16-17.

Final considerationsObesity is characterized by a chronic inflammatory state,which can worsen the preexisting periodontal disease.Periodontal disease has shown to induce metabolicalterations in the lipid metabolism contributing to thehyperlipidemic state of obesity.Further studies are necessary to elucidate the realrelationship between obesity and periodontal disease.Molecular biology studies are necessary to betterunderstand the mechanism and biological foundation of theassociation between obesity, periodontal disease and insulinresistance. Longitudinal studies are also necessary to showa causal relationship. However, before any progress in theunderstanding of this relationship, periodontists shouldcounsel obese patients in relation to the possible oralcomplications of obesity, to diminish morbidity for theseindividuals. This counseling should include the measurementof BMI and WHR for periodontal risk evaluation on a regularbasis21.

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15. Noack B, Jachmann I, Roscher S, Sieber L, Kopprasch S,Lck C et al. Metabolic diseases and their possible link to riskindicators of periodontitis. J Dent Res. 2000; 71: 898-903.

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17. Wood N, Johnson RB, Streckfus CF. Comparison of bodycomposition and periodontal disease using nutritionalassessment techniques: Third National Health and NutritionExamination Survey (NHANES III). J Clin Periodontol. 2003;30: 321-7.

18. Dalla Vecchia CF, Susin C, Rsing CK, Oppermann RV, AlbandarJM. Overweight and obesity as risk indicators for periodontitisin adults. J Periodontol. 2005; 76: 1721-8.

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21. Pischon N, Heng N, Berninmoulin J-P, Kleber B-M, WillichSN, Pischon T. Obesity, inflammation and periodontal disease.J Dent Res. 2007; 86: 400-9.

Braz J Oral Sci. 6(23):1420-1422 Obesity and periodontal disease: why suggest such relationship? An overview