Periodontitis as a

Component of
Roger B Johnson, DDS, PhD
Professor [)f Anatomy
Professor of Periodontics
Department of Periodontics
& Preventive Sciences
University ol Mississippi Medical Center
Jackson, Mississippi
Hyperinflammation:
Treating Periodontitis in
Obese Diabetic Patients
Abstract
Increasitig evidence points to periodontal disease as a significatii risk factor in the eti-
ology o other diseases with inflammatory components, such as cardiovascular disease
and type 2 diabetes mellitus. Thus, it may be possible to reduce the risk for other dis-
eases with an inflammatory cotnponent by maintaining a healthy periodontium. In
addition to plaque and calculus, other factors such as diet, body weight, lifestyle, and
enNironmental stress complicate the maintenance of a healthy periodontium. It is
becoming more important for the general dentist to address these additional risk fac-
tors in addition to providing conventional treatment for periodontai disease. This
review addresses a multifactorlal approach to the treatment of periodontal disease and
suggests that the "focal theory" of infection may still be relevant for oral inflammation.

Learning Objectives
After reading this article, the reader should be abk to:
explain ihc role of systemic hypcr- describe the role of tumor necrosis
inflammaiion in [he etiology of peri- factor-a in the etiology of both peri-
odontitis, obesity, and type 2 diabetes odoniitis and type 2 diabetes
mellitus. mellitus.
discuss the lifestyle risk factors in the
etiology of periodontitis.

D
uring the past decade, nutner-
ous published research studies
and reviews have promoted a
re-evaluation of the relatiotiship between
the oral and the systetnic health of an
individual.'"' In addition, new risk fac-
tors for periodontal diseases have been
reported, which expands (and possibly
confounds) treattneni options for the
health professional team. The obese dia-
betic dental patient with periodontitLs is
an example oi an individual requiring a
broad scope of treatment by both med-
ical and dental health professionals,
based on the results of these recent stud-
ies. However, a survey of general den-
tists reveals that a very low percentage of
them either screen for diabetes (7%) or
take an active role in diabetes manage-
ment (26%).' A new paradigm for treat-
nicni ol the diabetic dental patient with
periodontitis has emerged lliat provides
a more active role for the dentist in the
overall management of these patients. In
this paradigm, lifestyle risk factors in-
cluding weight control, exercise, diet,
and stress management are added to the
conventional treatment of periodontitis.
The Focal Theory of
Infection Revisited
In 1912, Billings published ihc
first scientific paper using "focal infec-
tion" in the title. This paper described
a theor)' of "focal infection," which was
supported for many years by both
medical and dental health profession-
als. This theory proposed that foci of

500 Compentlium September 2007;28(9):500-505

infection allowed etitrance of pathogenic tnicroorgan-
istns (or their products) into the systemic circulation,
where they could produce infections elsewhere in the
body. The target organs for these bacteria included joints,
the cardiovascular system, and the nervou.s system.
Because oral infections were cotisidered lo he a primary
focus of infection, many unnecessary tooth extractions
were performed for treattnent of systetnic diseases.''
Recent literature suggests that oral infections are a
risk factor for several systemic diseases, resulting in a re-
evaluation of the theory of "focal infection,"' after decades
of rebuke.' " However, the systetnic spread of oral bacte-
ria does not seem to be as destructive to overall health as
the systemic spread of proinflamtnatory cytokines and
acute phase proteins, which arc released from sites of oral
inllamtiiation (Figure),
Systemic Hyperinflammation
Recent evidence suggests that type 2 diabetes melli-
tus, periodontitis, and obesity have cotnmon features,'"
Each of these diseases has an inflammatory component
and releases proinflatntnatory cytokines and acute phase
proteins into the systemic circulation. Taken together, this
release increases the inflammatory- burden viithin the
body.'- A triangular ititeractioti between obesity, diabetes,
and periodontitis has been proposed, suggesting that any
of these diseases affect the incidence and severity o the
others," For instance, periodontitis produces a chronic
hype rinflamtnatory state within the body, which increases
the risk for both obesity and insulin resistance.'*"' Tbese
intetrclationsbips require a "s)'ndemic" approach to treat-
tnent of each of these diseases, which is required when 2
or more linked health problems act synergistically to
increase the burden of either disease individually'" Thus,
disrupting the links between these diseases by treatment of
periodontal disease and patient education aboui inflam-
mation is required for successful patient care, and the den-
tist occupies an excellent position to disrupt those links.
Proinflammatory Cytokines and
Systemic Hyperinflammation
Focal sites of inflamtnation release proinflammatory
cytokines, such as tumor necrosis factor (TNF)-a and
interleukin (IL)-6,''"'* which may initiate and maintain a
systemic hyperinflatnmatory state.-"-^ IL-6 is an acute
phase protein, which stimulates the liver to produce
additional IL-6, an etiologic factor for serious diseases,
including septicemia.
Obesity as a Risk Factor for Systemic
Hyperinflammation
Adipose tissue produces cytokines and acute phase
proteins proportional to its mass and functions as a
major site of chronic inflammation in obese individuals.''
Adipose tissue produces lL-^''"* and TNF-a,-' which
contribute lo systemic hyperinflammation and insulin
Compendium September 2007;28(9):500-505
FigureGingivitis associoted wiih denlol plaque. The gingiva features erylhe
mo and is enlarged due to edema It readily bleeds when iouched ar probed.
resistance. Obesity enhances the synthesis and release of
TNF-ct and IL-16 and is reduced after weight loss.'" Re-
cent evidence suggests that obesity, in addition to being a
risk factor for type 2 diabetes,^'''" is also a risk factor for
periodontitis.'^^''"
Type 2 Diabetes Mellitus as a Risk Factor for
Systemic Hyperinflammation
Type 2 diabetes primarily affects adults and repre-
sents 90% to 95% of the total nutnbcr of persons with
diabetes." The cause of type 2 diabetes is insulin resis-
tance, with some degree of insulin deficiency and hyper-
lipidemia. TNF-a is an etiologic factor for pcriodoniitis
and also blocks the insulin receptor, which contributes to
insulin resistance and type 2 diabetes.'^ In addition, bolh
cytokines induce hyperlipidemia, a feature o both obesi-
ty and type 2 diabetes.'^ '" Type 2 diabetes is associated
with older age (18% of the population aged 65 or greater
have the disease), obesity, fatnily bistor); and race/ethnic-
ity'' African Americans are 1.7 times as likely to have
type 2 diabetes compared witb the general population.
Increased serum concentrations of TNF-ct and IL-l|i,
have been reported in people with diabetes, which are
risk faciors for the development of systemic hyperinflam-
mation under appropriate conditions.'''^''
Periodontitis as a Risk Factor for
Hyperinflammation
Sites of periodontal inflammation release numerous
cytokines into the systemic circulation, includitig IL-6,
IL- I, and TNF-a. The gingival sulcular epithelial surfaee
area ranges from 8 cm' to 20 cml"" Thus, if the entire peri-
odontium were infected, the lesion would be of similar
size to the pahn of an adult hand, which would not be
considered to be a trivial infection elsewhere in the body.
However, because periodontitis is hidden and often pres-
etits no debilitating symptoms, the disease often becomes
chronic and undertreated. In addition, bacteria associated
wilh periodontitis also have been identified at sites distant
from the oral cavity, where tbey produce inllammation."
These bacteria can be released from the periodontium
501
1 into ihe systemic circulation during chewing or after
minor manipulation of the gingiva. For example, gingival
irritation coincident lo chewing gum has heen reported to
increase serum levels of haelena within 40% of diabetic
patienis witb pcriodontilis, compared with a 12% increase
wilhin the blood of diabetic patients without periodonti-
tis.'" Gingival irritation during toothbrushing may have a
similar effect.
Interaction of Periodontitis, Diabetes,
and Obesity
Because several chronic inflammatory conditions
share some common features with periodontitis, there is
a potential for interactions between them.^' Patients witb
type 2 diabetes are known to have a 2-fold increased risk
lor also having periodontitis.^*"'' In contrast, evidence
suggests that a person wiih periodontitis has an increased
risk lor developing type 2 diabetes."^ Once periodontitis
is established in a diahetie host, metaholic control of dia-
betes becomes more difficult because of the constant re-
lease of periodontal pathogenic hacteria and TNI-'-a into
ihe systemic circulation.
I
Recent studies report that diabetic patients with
severe periodontitis had a 6-fold worsening of glycmie
control during a 2-year period/" In addition, diabetic pa-
tients wilh severe periodontitis have an increased risk for
other complications of type 2 diahetes, including vascu-
lar, kidney, and retinal diseases. In an 11-year study, 82%
of diabetie patients with severe periodontitis experienced
one or more major circulatory diseases, including heart
attack, siroke, or peripheral vascular diseases, compared
with 21% of the diahelic patients without periodontitis.^^*"
These severe diabetic complications occurred despite sim-
I ilar HbAi,. levels between the groups.
Obesity also has been established as a risk factor for
both periodontitis and type 2 diahetes. Obese persons
I have more than a lO-fold increased risk for developing
type 2 diahetes*'^ and a 3-foId increased risk for develop-
ing periodontitis." In addition, those who consumed a
heailhy diei were 40% less likely to have periodontitis.'"
I
The distrihution of body fat has heen reported to have a
crucial role in the association between obesity and peri-
odontitis, with upper lx)dy olx-sity, waist-to-bip ratio (WHR),
and body mass index (BMl) being the most important
risk factors,'""
I Psychosocial Factors as Risk Factors for
Periodontitis and Hyperinflammation
Individuals with periodoniitis or individuals with
many missing teeth are very likely to assess their oral
health as fair or poor, which adversely affects their qual-
ity of life,'' These adverse effects include difficulties wilh
eating and relaxing, avoiding social engagements, self-
conscious feelings, and pain or discomfort.''
Major lifestyle stresses are also signihcant risk factors
for periodtintitis and also adversely affeet glycmie con-
502 Compendium September 2007;28(9):500-505
trol.'" Individuals living within the lowest tertile of the
socioeconomic score are reported lo be 1.8 times more
likely lo have periodoniiiis than those in the highest lertile
of the socioeconomic score." Those with less than a high
school education are twice as likely to liave periodontitis.
Individuals who are married, employed, and have few neg-
ative life events have a lower risk for periodontitis com-
pared with those who are unmarried, unemployed, and/or
experienced negative life events.'^ In addition, persons
with low job satisfaetion have greater risk for periodonii-
tis ihan persons witb high job satisfaction." Persons who
believe that they have personal control of ihcir destiny
have decreased risk for periodontitis, compared with those
who feel no control.'"'"' '' In addition, persons with clinical
depression and loneliness have an increased risk for peri-
odontitis.'** Those engaged in regular exercise programs
have lower serum IL-6 than those not engaged in regular
exercise.'"'"''- The important conclusion of these studies is
that individual lifestyle stress plus individual stress coping
strategics, taken together, have significant effects on the
risk for periodontitis and also often complicate the treat-
ment of type 2 diahetes,
A new paradigm for treatment
of the diabetic dental patient with
periodontitis has emerged that provides
a more active role for the dentist in
the overall management of these patients.
Treatment of the Obese Diabetic Dental Patient
with Periodontal Disease
Because bO% of tbe US population is either over-
weight or obese, ihe chances of treating an obese diabetic
patieni are good."^ Because ihe common risk factors for
obesity, periodoniiiis, and type 2 diahcies include systemic
hyperinilannnation, therapies that reduce inllammalion,
in general, should decrease ihe incidence of any of these
diseases. Some oral health researchers arc recommending
proactive patient managemeni, such as monitoring hlood
glucose levels, communicating with ihe patient's physi-
cian, and adjusting ihe frequency of dental visiis, for treat-
tiient of diabetic dental patients'^"; however, recent stud-
ies suggest that the rates of proactive patient management
acliviiies by tlcntists arc quite low.' In addition, smoking
cessation programs have been shown to be valuable for the
treatment of periodontitis, obesity, and type 2 diabetes"*;
however, only 18% of dentists provide these services.^
While prophylaxis, curettage, and surgery are classical
approaches to treating periodontitis, recent evidence sug-
gests that diabetic patients may require additional lypcs of
treatment to resolve periodontal inllainmation. The combi-
nation of mechanical debridemeni and systemic antibiotics
has been reported to improve both pcriodontilis and
glycmie control,^"" Thus, prevention and control of peri-
odontitis must be considered an integral pan of diabetes
control.*^ Recent studies suggest that successful treatment
of periodontitis not only has beneficial effects on daily
glycmie control"''"' bul also on HbAt^. levels, a long-term
assessment of glycmie control."" Tbese effects probably
t)ccur because of reducing semm TNF-a concentrations
coincident to periodontitis control''" In addition to conven-
tional periodontal therapy, diabetic patients with periodon-
litis would benefit from implementation of changes in
lifeslyle, such as stress management, smoking cessation,
did counseling, and weight control. Thus, treatment of
periodontitis could include an assessment and monitoring
of WHR and BMl in addition to a program for increasing
physical activity.
Conclusion
It is important for diabetic patients to be concerned
about both obesity and periodoniitis, and ihey should be
encouraged to have regular dental visits as part of their
overall health treatment. Diabetic patietits willing to
comply wilh periodonlal disease prevention and treat-
ment programs may minimize development of future dia-
betic complications. While there remains some contro-
versy about the associations between periodontal and
systemic diseases, if those theories are correct the signif-
icance of the associations is of vital importance. In addi-
tion, the associations between the diseases should be
excellent motivation for patients to accept treatment for
periodonlal diseases and to maintain the health of their
teeth and oral tissues.
References
1. CosicnntiJ, Keller D. Oral pcriopathogens and systemic effects.
GenDenl. 2007:55:210-215.
2. Kim J, Amar S. Periodonlal disease and systemic conditions: a
bidireciional relaiionship. Odontology. 2006;94:10-21.
3. Al"Zahrani MS, Kayal RA, Bissada NF Periodontiiis and car-
din vascular disease: a review o shared risk faclors and new
findings siipporiing a catisaliiy hypothesis. Qiiiii'sscncc ni.
200ii;.7:li-ia
4. Rosenstein ED, Greenwald RA. Kttshncr L). ct al. Hypothesis:
Uie htimoral immune response to oral bacteria provides a siim-
uUis ft)r ihe dcvelopmeni of rheumatoid arlhritis.
/rijimmaiofi. 2004;28:311-318.
5. Kunzel C, Lulla E, Lamster IB. Managcmcnl tif ihe palient who
smokes and the diabetic patient in the dental office. J Pehmhnlol
2006;77:.331-340.
(>. Gibbons RV Germs, Dr, Billings, and the theory of focal infec-
tion. Clin Infec Dis. 1998:27:627-633.
7. Demmcr RT. Dcsvarieux M. Periodontal infections and cardio-
vascuiar disease: the heari nf ilie inaiier. / Am Den Assoc. 2006;
n7(siippt):14S-20S.
8. Xiong X, Buekens P, Fraser WD, el ai. Periodontal disease and
adverse pregnancy outcomes: a systema[ic review. BJOG. 2006;
113:135-143.
'). Manila KJ, Pusslnen PJ, Paju S, Dental infections and cardio-
vascular diseases: a review.,/ Periodontol 2005;76(suppl 11):
2085-2088.
10. Jin LJ, Chiu GK, Corbet EF; Are periodontal diseases risk fac-
tors for certain systemic disorderswhat matters to medical
praciilioners? Hong Kong Med J. 2003;9:31-37.
i I. Mouisopoulos NM, Madianos PN. Low-grade inflammalion in
Compendium September 2007;28(9):500-505
chronic infectious diseases: paradigm of periodontat infec-
tions. Ann N YAaid Sei. 200C>;108:25i-264.
12. Donahue RP, Wu T. Insulin resistance and periodonlal disease:
an epidemiologic overview of research needs and future direc-
tions. Ann Periodonloi 2001;6: II9-124.
13. Genco RJ, Grossi SG, Ho A, et al. A proposed model linking
inflainmaiion lo ohcsiiy, diabetes, and periodontal inleclions. /
Periodomol 2005;76(suppl 11):2075-2084.
14. Nishimura F, Murayama Y, Periodonlal inflammation and in-
sulin resistancelessons from obesity._/ Dent Res. 2001;80:1690-
1694.
15. Eesta A, D'Agostino R, Howard G, et al. Chronic suhctinical
inflammation as part ol the insulin resistance syndrome: ihe
Insulin Rcsisiance Atherosclerosis Study (tR.-\Si. Cirdiiiilion.
2000:102:42-47.
16. Singer M. .AltS and ihe heallh crisis oi ibc US urban poor: ihe
perspective of critical medical anthropology. Soc Seien Med.
1994:39:931-948.
!7. D'Aiuto F, Parkar M, Andreou G, et al. Periodontitis and sys-
temic inflammation: control of the local infecilon is associated
wilh a reduction in serum inflammalory markers. J Dfril Res,
2004;83:156-160.
18. Fbersole JL, Cappelli D, Acule-phase rcactants in infections
and inflammatory diseases. Periodontol 2000. 2000:23:19-49.
19. Geeris SO. Nys M. De MP, etal. Systemic release of cndotoxins
induced by gentle mastication: associaiion with periodontitis
severity. J Periodontol. 2002;73:73-78,
20. Lalla E, Lamster IB, Feit M, et al. Blockade of RAGE suppress-
es pcriodonlilis-associated bone loss in diabelic mice. J Clin
Jrm'i(.2OOO;IO5:1117-l24.
21. Lalla E, L.amsier IB. Scbmidi AM. Enhanced inicraciion of
advanced glycaiion end products with their cellular recep-
!or RAGE: implications for the pathogenesis of accel-
erated periodontal disease in diabetes. Arm Periodontol 1998;3:
13-19.
22. Grossi SG. Treatment of periodonlal disease and control of dia-
heies: an assessment of the evidence and need for future
research. Ann Periodonlol 2001:6:138-143.
23. Mohamed-AIi V, Goodnck S. Rawesh A, et al. Subcutaneous adi-
pose tissue releases intcrleukin-ft, bul not tumor necro.sis factor-
alpba, m vivo. J Clin Emhcrinoi Metah. l'-)97;82:4196-4200.
24. Bastard JP, Jardel C, BrucUert E, et al. Elevated levels of inter-
leukin 6 are reduced in serum and subcutaneous adipose tis-
sue of obese women after weight loss. J Clin Endocrinol Metah.
2000:85:3338-3342.
25. Kern P, Ranganaihan S, Li C, et al. Adipose tissue tumor necro-
sis factor and interleukin-6 expression in human obesity and
insulin resistance. .Am / Pliy.'ii! Endocrinol Metah. 2001:280:
E745-E751.
26. Ramos HJ, \ u Y, Romanova I, et al. Is obesiiy an iullammatory
disease? Surgery. 2003;134:329-335.
27. Mokdad AH, Ford ES, Bowman BA, el al. Prevalence of obesi-
ty, diabetes, and obesity-related health risk factors. JAMA.
2003:289:76-79.
28. Must A, SpadanoJ, Coakley EH, el al. The disease burden asso-
ciated with overweight and obesity. jAMA. 1999:282:1323-1529.
29. Dalla Vecchia CF, Susin C, Rosing CK, et al. Overweight and
nbesity as risk indicators for periodoniitis in adults, ] Perio-
donlol 2003;76:172t-1728.
30. Saito T, Shimazaki Y, Koga T, et al Relationship between upper
body obesiiy and periodontitis.) Dent Res. 2001;80:1631-1636.
31. Saiio T, Shimazaki Y. Sakamolo M. Obesity and periodoniitis.
N EngiJ Met!. l9'8:339:482-483.
32. Wood N.Johnson RB, Sireckfus CF Comparison of body com-
position and periodonlal disease using nutritional assessmeni
lechniques: Third National Health and Nutrition Examination
Survey (.NHANES 111)../ Clin Periodontol 2OO3;3O:32i-327.
503
33. Centers lor Disease Control and Prevention. National diabeies
fact sheet: general information and national csiimates on dia-
betes in the Uniied States, 2005. Atlanta, Ga: US Departmeni
of Health anil Human Services, Centers for Disease Control
and Prevention, 200').
34. Paz K, Hemi R, LeRoith D, et al, A molecular basis for insulin
resistance. J Blol Chem. I997;272:29911-2*JQ18.
35. Hotamisligil GS. Mechanisms of TNF-alpha-induced insulin
resistance. ExpClin Eriicnio Diabetes. 1999:107:119-125.
36. Moller DE. Potential role of TNF-alpha in the pathogenesis of
instiiin resistance and type 2 diabetes. TITI.S Endocriml
Metab. 200;ll:212-217.
37. Peraldi P. Spiegelman B. TNF-alpha and instilin-resistance: sum-
mar>' and fuutre prospects. Mol Cell Biochem. 1998;182:169-175.
38. Qi C, Pekala PH. Tumor necrosis factor-alpha-induced insulin
trsistance in adipocytes. Pwc Soc Exp Biol Med. 2OOO;223:128-l 35,
39. lacopino AM. Periodontitis and diabeies interrelationships:
rote of inflammation. Ann Periodonlol. 200! ;6:125-137.
40. Salvt GE, Beck jD, Offenbachcr S. PGn2. IL-I beta, and TNF-
alpha responses in diabetics as modifiers of periodontal dis-
ease expression. Ann Periodtmtoi 1998;3:40-50.
41. Hujoel PP, White BA, Garcia RI,ct al. The deniogingival epithe-
liai stirface area revisited. JPeriodoni Res. 2001:36:48-55,
42. Ford PJ, Gemmeil E, Chan A, et al. inflammalion, heat shock pro-
teins and periodonial pathogens in atherosclerosis: an immuno-
histologie study. Oral Microbiol imniuno. 2006;2l :206'2l 1.
43. lacopino AM, Cutler CW. Pathophysiologica! relationships
between periodontitis and sysiemic disease: recent concepts
involving serum lipids.,/ Pci iodoniol. 2000:71:1375-1384.
44. Mealey BL Periodontal implications: medically compromised
patients. Ann Periodonlol. I996;l:256-321.
45 Papapanou PN, Periodontal diseases: epidemiology. Ann Peiio-
dontoi 1996:1:1-36.
4ti. Taylor GW, Burt BA, Becker MP et al. Severe periodontitis and
risk for poor glycmie control in latients with non-insulin-
dependent diabetes melliius. J. Pniodoniol. 1996:67:1085-1093-
47. Thorstensson H, Kuylenstierna J. Hugoson A. Medical sta-
tus and complications in relation to periodoncal disease experi-
ence in insulin-dependent diabetics../ Clin Periodontol. 1996:23:
194-202.
48. Saremi A, Nelson RG, Tulloch-Reid M, et ai. Periodontal dis-
ease and mortality in type 2 diabetes. Diabetes Care. 2005:
28:27-32.
49. Field AE. Coakley EH, Must A, et al. Impact of overweight on
the risk of developing common chronic diseases during a 10-
year period. Airti Intern Med. 2001:161:1581-1586.
50. Al-Zahrani MS, Borawski EA, Bissada NF Periodontitis and
three health-enhancing behaviors: maintaining normal weight,
engaging in recommended level of exercise, and consuming a
high-quality \el. j Peiiodonlol. 2005:76:1362-1366.
51. Cunha-Cruz J, Hujoel PR Kressin NR. Oral health-related
quahty of life of periodontal patients. J Periodonial Res. 2007;
42:169-176.
504 Compendium September 2007:28(9):500-505
52. Croucher R, Marcenes WS, Torres MC. el al. The relationship
between lite-events and periodoniitis. A case-control study.,/
Clin Periodonlol 1997:24:39-43.
53. Borrell LN, Burt BA, Warren RC, et al. The role of individtial
and neighborhood social laclors on periodontitis: the Thini
National Health and Nutrition Examination Survey. J
Periodonlol. 2006:77:444-453.
54. Marcenes WS, Sheiham A. The relationship between work
stress and oral health status, Soc Sd Mec- 1992:35:1511-1520.
55. Linden GJ. Mtillally BH. Freeman R. Stress and ihe progres-
sion ol periodonial disease. J CJiii Periodonioi 1996:23:675-
680.
56. Genco RJ, Ho AW, Grossi SG, el al. Relationship of stress, dis-
tress and inadequate coping behaviors to periodontal disease.
J Periodonioi. 1999:70:711-723.
57.Genco RJ, Ho AW, Kopman J, et al. Models to evaluate the role
of stress in periodontal disease. Ann Petiodontol. 1998:3:288-
302.
58. Monteiro da Silva AM, Oakley DA, Newman HN, et al.
Psychosocial factors and adult onset rapidly progressive peri-
odontitis. J did Periodomol 199fi:23:789-794.
59. Al-Zahrani MS, Borawski EA, Bissada NH Increased physical
activity reduces prevalence of periodontitis. J Dem. 2005:33:
703-710,
60. Karjalaiiien S, VanHamaki M, Kanto D, et al. Long-term phys-
ical inactivity and oral health in Finnish adults with intellec-
tual disability. .Actii Odontol Suind. 2002:60:50-55.
61. Merchant AT, Pitiphat W. Rimm EB, ei al. Increased physical
activity decreases periodontitis risk in men. Etir J Epidemiol.
2003:18:891-898.
62. Wakai K, Kawamura T, Umemura O, et al. Associations of
medical status and physical fitness with periodontal disease. J
Clin Periodonlol. 1999:26:664-672.
fi3. Pischon N. Heng N, Bernimoulin JP et al. Obesity, inflamma-
lion, and peridontal disease. J Dnif Rf-s, 2007:86:400-409.
64. Matthews DC. The relationship between diabetes and peri-
odontal disease. J Can Dent Assoc. 2002:68:161-164.
65. Hein C, Small D. Combating diabetes, obesity, periodontal dis-
ease and interrelated inflammatory conditions with a syndem-
ic approach. Grand Rounds Oral-Sys Med. 2006:2:36-47a.
66. Promsudthi A, Pimapansri S, Deerochanawong C, et al. The
effect of periodontal therapy on uncontrolled tj^ie 2 diabetes
tnellitus in older subjects. Oral Dis. 2005:11:293-298.
67, Grossi SG, Skrepcinski FB, DeCaro T. el al. Response to peri-
odontal therapy in diabetics and smokers. J Pt-riodontoi.
1996:67:1094-1102.
68. Grossi SG, Skrepcinski FI, DeCaro T, et al. Treatment of peri-
odontal disease in diabetics reduces glycated ht-moglobiii. /
Periodontoi 1997:68:713-719.
69. lwamoto Y, Nishimura R Nakagawa M, etal. The effect of antimi-
crobial pcriodontal treatment on circulating tumor necrosis fac-
tor-alpha and glycated hemoglobin level in patients with type 2
diabetes.; Periodonlol. 2001:72:774-778.
 QuizlWhich of the following statements is true?
a. Most general dentists screen patients for
6. If the entire periodontium were infected, the
lesion would be of similar size to which of the
diabetes mellitus. following?
b. Most general detitists actively manage the a. palm of the adult hand
diabetic patient. b. upper eyelid
c. Most general dentists do not take an active c. nail-bed of the thumb
role in diabetes management. d. anterior surface of the forearm
d. Most general dentists screen for diabetes
and actively manage the diabetic patient. 7. Diabetic patients with severe periodontitis
have an increased risk for which of the following
Type 2 diabetes, periodontitis, and ohesity: eomplications of type 2 diabetes?
a. have an inflammatory component. a. vascular disease
b. release proinflammatory cytokines. b. kidney disease
c. release acitte phase proteins. c. retinai disease
d. all of the ahove d. all of the above

3. A "syndemie" approaeh to treatment is 8. Obese patients have more than a (an)

required when: increased risk for developing type 2 diabetes.
a. 2 or more linked health problems act a. 4-fold

i
synergistically. b. 6-fold
b. the liver produces additional Interleukin (lL)-6. c. 8-fold
c. nutnerous cytokines are released into the d. 10-fold
systetnic circulation.
d. periodontal disease becomes chronic. 9. Oral health researchers recommend proactive
diabetic dental patieni management, such as:
4. Which of the following statements is true a. monitoring blood glucose levels.
regarding ohesity? b. comtnunication with the patient's physician.
a. Obese individuals arc unlikely to experience c. adjusting the frequency of dental visits.
periodontitis. d. all of the above
b. Obesity enhances the synthesis and release of
Tumor necrosis factor (TNF)-a and IL-6. 10. The combination of whicb ofthe following has
c. Distribution of adipose tissue is not a risk been reported lo improve periodonlitis and
factor for periodontitis. glycmie control?
d. Adipose tissue contains low concentrations of a. mechanical debridement atid systemic antibiotics
proinflammatory cytokines. b. mechanical debridement and increased
physical activity
5. Which of the following is an etiologic factor c. systemic antibiotics and increased physical
for periodontitis and also blocks the insulin activity
receptor, contributing to insulin resistance and d. mechanical debridement and chlorhexidine
type 2 diabetes? rinses
a. IL-6
b. IL-l
e. TNF-a
d. IL-4

Please see tester form on page 528.

This article provides 1 hour of CE credit from Ascend Dental Media, in association wiih ihe University of Southern
California School oi DeniLstry and the University of Pennsylvania School of Dental Medicine, representatives of which have
reviewed the articles in this issue for acceptance. Record your answers on the enciosed answer sheet or submit ihem on a
separate sheet of paper. You may also phone your answers in to (888) 5^6-4605 or fax them to (703) 404-1801. Be sure Ut
include your name, address, lelephone number, and last 4 digits of your Social Security number.

506 Compendium September 2007;28(9}:500-505