FACTA UNIVERSITATIS

Series: Medicine and Biology Vol.14, No 1, 2007, pp. 6 - 9 UC 616.379:616.31

DIABETES AND PERIODONTAL DISEASE: A BIDIRECTIONAL RELATIONSHIP

Rosa María Díaz-Romero, Rubén Ovadía

Subdirection of Public Health Research at the National Institute of Perinatology (Instituto Nacional de Perinatología)
Mexico City, Mexico
E-mail: dra_diazromero@yahoo.com.mx

Summary. Periodontal disease (PD) and diabetes mellitus (DM) hold a consistent relationship. DM not only
increases the risk of having PD and with that its prevalence, but it also augments the progression of more aggressive
and quickly defining signs. There is a bidirectional relationship between DM and PD. The treatment of periodontitis
in diabetic patients favors a reduction in mediators responsible for the destruction of periodontal tissue and decreases
with it, a resistance to insulin. PD is characterized by low grade chronic inflammation that may remain silent in
diabetics causing damage that is not locally limited but may extend systemically.
Key words: Periodontal disease, loss of glycemic control, low grade chronic inflammation

Introduction PD conditions the loss of dental organs, making

chewing food difficult, causing pain and as a result,
Periodontal disease is chronic inflammatory disease inadequate nutrition (7). In addition, frequently persons
of the tissues that support and attach the teeth to the with DM have a much more difficult time in tolerating
jaws (1). They are caused by gram-negative bacterial false dentures due to total bone loss and the sensitivity
infections and are, for the most part, asymptomatic, al- of the alveolar mucosa.
though much of the actual destructive tissue changes The participation of a physician is relevant in the
observed clinically are result of the inflamatory host opportune detection of PD as a health provider for dia-
response. betics and whom a patient comes into more contact
Periodontal disease (PD) is the second main cause of with.
oral cavity disorders affecting the population due to its This article reviews the literature analyzing the bidi-
high prevalence (2). It is more frequent in adults in rectional relationship between diabetes mellitus and
contrast to cavities which are more common and much periodontal disease, as well as the effects of periodontal
more frequent in children. treatment on glycemic control with the aim of providing
As per Socransky's (3) definition, PD is a mixed en- physicians and health personnel the basic elements sup-
dogenous infection caused by microorganisms that porting this relationship and which contribute to their
colonize the sub-gingival dental-bacterial plaque, in a active participation in the diagnosis and opportune re-
structure known as a biofilm. Biofilms are bacterial ferral (8).
communities that adhere to oral surfaces. Until now,
700 bacterial species capable of colonizing the mouth
have been described. This number competes only with Effects of Diabetes Mellitus
the flora found in the colon. A person may store over on the Periodontal State
150 different species.
Diverse studies carried out by the WHO confirm that The function of immune cells, including neutrophils,
the prevalence and severity of PD tends to be on the rise monocytes and macrophages is often altered in cases of
in the adult population compared to younger groups (4). diabetes. Neutrophilic adherence, chemotaxis and
Persons with diabetes mellitus (DM) are at greater phagocytosis are changed, inhibiting an adequate de-
risk of developing PD. PD is now considered the sixth fense against bacteria in the periodontal pouch and sig-
complication of DM (5). Not only is it more prevalent in nificantly increasing the destruction of the periodontal
this population, but also the progression of symptoms, membrane (9). Although neutrophil function is de-
in a more aggressive and more rapidly setting mode. creased in diabetics, the monocyte/macrophage cell line
The main reasons for this situation are the scarce infor- may be hyper-responding when faced with the bacterial
mation on the importance of oral hygiene, poor meta- antigenic contact. This hyper-response results in a
bolic control and the irregularity in visiting dentists, greater production of pro-inflammatory cytokines (10).
among others (6). Peripheral monocytes in diabetic patients produce
high levels of the tumor necrosis factor-α (TNF- α) in
DIABETES AND PERIODONTAL DISEASE: A BIDIRECTIONAL RELATIONSHIP 7

response to the Porphyromonas gingivalis antigens The above explains why periodontitis can increase
compared to the monocytes of non-diabetic patients the risk of poor glycemic control and how this improves
(11). The level of inflammatory cytokines in the crevi- with periodontal treatment (24).
cular fluid is also related to glycemic control. Egebret-
son (12) reported that diabetic patients with periodoni-
tis, whose HbA1c levels were over 8%, had approxi-
mately twice the amount of interleukin-1β (IL-1β) in
their crevicular fluid in comparison to patients with in-
dexes below 8%. The net effect of these changes in the
immune response of diabetics is an increase in perio-
dontal inflammation, a loss of epithelial insertion and
alveolar bone.
The gingival sulcus (13) is a labile site for the body to
present a hermetic closure to the external environment. In
this space, the crevicular fluid increases in the presence of
inflammation. The increase in the loss of periodontal in-
sertion and the alveolar bone (14) in diabetic patients is
associated with changes in the metabolism of connective
tissue where there is a lack of response in resorption and
formation. The effect of the hyperglycemic state includes
the inhibition of osteoblastic proliferation (15) and colla-
gen production resulting in a reduction in the formation
and decrease in mechanical properties of the newly
formed bone (16-17).
The changes mentioned above may contribute to the
pathogenicity of periodontal disease and changes in
healing since collagen is the predominating structural
protein in the gums. In addition, collagen is susceptible
to degradation due to the action of MMPs as colla-
genases found to be in high amounts in tissues of dia-
betics, including the periodontal tissue.

Effects of Periodontal Disease

on the State of Diabetes
Periodontal disease may have a significant impact on Fig. 1. Association of the HbA1c values with the severity
the metabolic state of diabetes. The presence of PD in- of periodontal disease in a group of type 2
creases the risk of worsening glycemic control in time. pre-gestational diabetics.
(0=Healthy gingival, 1=Early gingivitis,
Taylor (18), in a cohort study of patients with diabetes
2=Establisehed Gingivitis, 4=Periodontitis)
with severe PD for two years, found a relative risk six
times more the probability of worsening glycemic con-
trol in comparison to periodontally healthy diabetics. Periodontal Treatment
Our research group found an association in the increase on the State of Diabetes
of HbA1c values to the severity of periodontal disease in
pre-gestational type 2 diabetic women (19) (Fig. 1). Periodontal treatment decreases local inflammation
Periodontal disease may induce or perpetuate an ele- and as a consequence, decreases chemical mediators
vated inflammatory state not only locally (20), but has involved in inflammation, among them IL-6 and CRP,
also been associated to severe periodontitis with the risk positively contributing to proper glycemic control. It is
of mortality due to cardio-renal disease (21). evident that PD exceeds the local environment affecting
Several studies suggest that patients with periodontitis, the systemic one (25).
particularly those colonized with Gram negative bacteria D'Auito (26) points out that tissue insulin demand in
such as P. gingivalis, Tannerella forsynthesis, and type I diabetic patients decreases after periodontal
Prevotella intermedia, have greater inflammatory serum treatment including scraping and radicular smoothing,
markers such as C-reactive protein (CRP), IL-6, and fi- curettage, local gingivectomies and selective extrac-
brinogen than patients without periodontitis (22-23). tions, scaling and root planning in addition to the use of
Similarly, there is an increase in resistance to insulin antibiotics such as penicillin and streptomycin.
decreasing glycemic control. The most important concern for applying evidence
in the early diagnosis of PD is educating the patient.
8 R. María Díaz-Romero, R. Ovadía

Periodontal disease is a silent condition. Diabetics Table 1. Signs of Alarm related to Periodontal Disease
need to be aware of the signs of PD (Table 1). Bleeding
of the gums is the first sign of subgingival infection. • Gum bleeding
This is when all the personnel involved in the care of • Gingival inflammation
diabetic patients should take active participation and • Halitosis
therefore opportunely refer patients to the dentist. • Sensitive denture
• Dental movement

References
1. Offenbacher S. Periodontal disease patogénesis. Ann Periodon- factors that regulate osteoblast differentiation. Endocrinology
tol 1996; 1: 821−878. 2003; 144: 346−352.
2. Petersen PE. The World Oral Health Report 2003: Continuos 16. Beam HA, Parsons JR, Lin SS. The effects of blood glucose
improvement of oral health in the 21st century – The approach control upon fracture healing in the BB Wistar ratwith diabetes
of the WHO Global Oral Health Programme. Community Dent mellitus. J Orthop Res 2002; 20: 1210−1216.
Oral Epidemiol 2003; 31 (suppl 1): 3−24. 17. Gooch HL, Hale JE, Fujioka H, Balian G, Hurwitz SR. Alterations
3. Socransky S, Haffajee AD. Periodontal microbial ecology. of cartilage and collagen expression during fracture and healing in
Periodontol 2000. 2005; 38: 135−87. experimental diabetes. Connect Tissue Res 2000; 41: 81−85.
4. World Health Organization. The WHO Global Oral Health 18. Taylor GW, Burt BA, Becker MP. Severe periodontitis and risk
Data Bank. Geneva: World Health Organization 2003. for poor glycemic control in patients with non-insulin – de-
5. Loe H. Periodontal disease. The six complications of diabetes pendent diabetics. J Clin Periodontol 1996; 23: 194−202.
mellitus. Diabetes Care 1993; 16 (Suppl 1): 329−334. 19. Díaz RRM, Casanova RG, Belmont J, Ávila H. Oral Infections
6. Seppälä B, Ainamo J. A longitudinal study on insulin depend- and Glycemic Control. Archives of Medical Research. 2005; 36:
ent diabetes mellitus and periodontal disease. J Clin Periodontol 42−48.
1993; 20: 161−165. 20. Loos BG. Systemic markers of inflammation in periodontitis. J
7. Taylor GW. Bidirectional interrelationships between diabetes Periodontol 2005; 76: 2106−2115.
and periodontal diseases: An epidemiological perspective. Ann 21. Wu T, Trevisan M, Genco RJ, Falkner KL. Examination of the
Periodontol 2001; 6: 99−112. relation between periodontal health status and cardiovascular
8. Mealy LB, Oates WT. AAP- Commissioned review. Diabetes risk factors: Serum total and high density lipoprotein choles-
and periodontal disease. J Periodontol 2006; 77-8: 1289−1303. terol, C – reactive protein, and plasma fibrinogen. Am J Epi-
9. Manouchehr-Pour M, Spagnuolo PJ, Rodman HM, Bissada NF. demiol 2000; 151: 273−282.
Comparison of neutrophil chemotactic response in diabetic pa- 22. Noack B, Genco RJ, Trevisan M, Grossi S, Zambon JJ. Perio-
tients with mild and severe periodontal disease. J Periodontol dontal infections contribute to glycated systemic C- reactive
1981; 52: 410−415. protein level. J Periodontol 2001; 72: 1221−1227.
10. Salvi GE, Collins JG, Yalda B, Arnold RR, Lang NP, Offenbacher 23. Miller LS, Maxwell MA, Newbold D. The relationship between
S. Monocytic TNF-α secretion patterns in IDDM patients with reduction periodontal inflammation and diabetes control: A re-
periodontal diseases. J Clin Periodontol 1997; 24: 8−16. port of 9 cases. J Periodontol 1992, 63: 843−848.
11. Salvi GE, Collins JG, Yalda B, Offenbacher S. Monocytic 24. Stewart JE, pager KA, Friedlander AH, Zadeh HH. The effect
TNF- alpha secretion patterns in IDDM patients with perio- of periodontal treatment on glycemic control in type 2 diabetes
dontal diseases. J Clin Periodontol 1997; 24: 8−16. mellitus. J Clin Periodontol 2001; 28: 306−310.
12. Engebretson SP, Hey-Hadavi J, Ehrhardt FJ, et al. Gingival 25. Grossi SG, Skrepcinski FB, DeCaro T. Treatment of periodon-
crevicular fluid levels of interleukin-1β and glycemic control in tal disease in diabetics reduces glycated hemoglobin. J Perio-
patients with chronic periodontitis and type 2 diabetes. J Perio- dontal 1997; 68: 713−719.
dontol 2004; 75: 1203−1208. 26. D’ Aiuto F, Parker M, Andreou G. Periodontitis and systemic
13. Marshall RI. Gingival defensins. Linking the innate and adaptive inflammation: Control of the local infection is associated with a
immune responses to plaque. Periodontol 2000. 2004; 35: 14−20. reduction in serum inflammatory markers. J Dent Res 2004; 83:
14. Amir G, Rosenmann E, Sherman Y, Greenfeld Z, Ne'eman Z, 156−160.
Cohen AM. Osteoporosis in the Cohen diabetic rat: Correlation
between histomorphometric changes in bone and microan-
giopathy. Lab Invest 2002; 82: 1399−1405.
15. Lu H, Kraut D, Gerstenfeld LC, Graves DT. Diabetes interferes
with bone formation by affecting the expression of transcription
DIABETES AND PERIODONTAL DISEASE: A BIDIRECTIONAL RELATIONSHIP 9

DIJABETES I PERIODONTALNA BOLEST: UZAJAMNI ODNOS

Rosa María Díaz-Romero, Rubén Ovadía

Departman za istraživanje javnog zdravlja, Nacionalni institut za perinatologiju, Meksiko Siti, Meksiko
E-mail: dra_diazromero@yahoo.com.mx

Kratak sadržaj: Periodontalna bolest (PB) i diabetes mellitus (DM) su u doslednoj vezi. DM ne samo da povećava rizik od
pojave PB, a samim tim i njegovu učestalost, nego i povećava progresiju znakova koji su agresivniji i koji se brže određuju.
Postoji dvosmerna veza između DM i PB. Tretiranjem periodontitisa kod pacijenata sa dijabetesom, smanjuju se posrednici
odgovorni za razaranje periodontalnog tkiva a samim tim smanjuje se i rezistentnost na insulin. PB karakteriše hronična
upala niskog inteziteta koja može ostati prikrivena kod dijabetičara, uzrokujući štetu koja nije lokalno ograničena već može
sistematično da se širi.
Ključne reči: Periodontalna bolest, gubitak glikemičke kontrole, upala niskog inteziteta