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Cover page of the Journal of Health Sciences

 Table of Contents  
Year : 2014  |  Volume : 7  |  Issue : 1  |  Page : 6-11

Diabetes mellitus and periodontal disease

Department of Periodontics, KLEU's VK Institute of Dental Sciences, Belgaum, Karnataka, India

Date of Web Publication2-Jul-2014

Correspondence Address:
Renuka Metgud
Department of Periodontics, KLEU's VK Institute of Dental Sciences, Belgaum, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2349-5006.135022

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Diabetes mellitus, caused by the malfunction of insulin - dependent glucose and lipid metabolism, presents with the classic triad of symptoms: Polydipsia, polyuria, and polyphagia. Complications include retinopathy, nephropathy, neuropathy, and cardiovascular disease. Periodontal diseases are infections affecting the periodontium and resulting in the loss of tooth support. There exists a bidirectional relationship between diabetes and periodontal disease as well as its complications. This article reviews the pathophysiology, the possible mechanisms that increase the severity of periodontal disease in diabetes and the periodontal management of diabetic patients.

Keywords: Advanced glycation end products, diabetes mellitus, periodontitis

How to cite this article:
Metgud R, Kore S. Diabetes mellitus and periodontal disease. Indian J Health Sci Biomed Res 2014;7:6-11

How to cite this URL:
Metgud R, Kore S. Diabetes mellitus and periodontal disease. Indian J Health Sci Biomed Res [serial online] 2014 [cited 2022 May 17];7:6-11. Available from: https://www.ijournalhs.org/text.asp?2014/7/1/6/135022

  Introduction Top

Diabetes mellitus is a clinically and genetically heterogeneous group of metabolic disorders manifested by abnormally high levels of glucose in the blood. The hyperglycemia is the result of a deficiency of insulin secretion caused by pancreatic β-cell dysfunction or of resistance to the action of insulin in liver and muscle, or a combination of these. [1] Periodontal disease has been recognized as not merely a local infectious disease, but as chronic, subclinical, inflammatory disease for the host. [2]

Diabetic subjects appear to respond to bacterial challenge in an exaggerated manner as compared with nondiabetic subjects through several possible mechanisms, and develop more severe forms of inflammatory periodontal disease. Severe periodontal disease in such subjects, in turn, acts to reduce insulin sensitivity known as insulin resistance, thereby contributing to the induction of hyperglycemia as well as hyperinsulinemia, which are the important risk factors for diabetic vascular complications. [2]

There exists a bidirectional relationship between diabetes and periodontal disease as well as its complications. Future strategies for prevention and treatment of periodontal disease in diabetic subjects needs to be considered. [2]

  Classification of Diabetes Mellitus Top

According to American Diabetes Association 1997 [3]

  • Type 1 diabetes (formerly, insulin-dependent diabetes)
  • Type 2 diabetes (formerly, non-insulin-dependent diabetes)
  • Gestational diabetes
  • Other types of diabetes
    • Genetic defects in β-cell function
    • Genetic defects in insulin action
    • Pancreatic diseases or injuries. e.g., Pancreatitis, neoplasia, cystic fibrosis, trauma, pancreatectomy
  • Infections
    • Cytomegalovirus, congenital rubella
  • Drug-induced or chemical-induced diabetes
    • Glucocorticoids, thyroid hormone
  • Endocrinopathies
    • Acromegaly, pheochromocytoma, glucagonoma, hyperthyroidism, Cushing's syndrome
  • Other genetic syndromes with associated diabetes.

  Pathophysiology of Diabetes Top

During digestion, foods are broken down into glucose, which then enters the circulatory system and is subsequently used by tissue cells for energy and growth. Most cells, excluding those in the brain and central nervous system require the presence of insulin to allow glucose entry. Insulin is produced by β-cell of the pancreas, and increased insulin secretion occurs in response to increased blood glucose concentrations. Excess glucose is stored in the liver in the form of glycogen. When required the liver breaks down glycogen and releases glucose by the process of glycogenolysis. Liver also produces glucose through the process of gluoneogenesis (i.e. from the noncarbohydrate sources such as amino acids and fatty acids). [4]

  Hormonal Control of Glycemia Top

Insulin is the primary hormone that reduces the blood glucose levels. A group of counter regulatory hormones serve to balance hyperglycemia. [4]

Hormones that raise the blood glucose level:

  • Glucagon
  • Catecholamine (epinephrine)
  • Growth hormone
  • Thyroid hormone
  • Glucocorticoids (cortisol).

Hormone that lowers the blood glucose level:

  • Insulin.

Thus, any form of diabetes mellitus results from impaired insulin secretion or action leading to hyperglycemia.

The etiology of type 1 diabetes mellitus is the autoimmune destruction of β-cell of pancreas, while that of type 2 diabetes mellitus is insulin resistance, impaired insulin secretion and increased liver glucose production.

  Clinical Presentation Top

Type 1 diabetes mellitus is usually quite sudden, while type 2 diabetes mellitus may be present for years before the patient develops symptoms.

The classic signs and symptoms of DM include the following: [4]

  • Polyuria (excessive urination)
  • Polydipsia (excessive thirst)
  • Polyphagia (excessive hunger)
  • Unexplained weight loss

The other signs and symptoms include weakness, malaise, irritability, blurriness, nausea.

  Oral Manifestations Top

Cheilosis, mucosal drying and cracking, burning mouth and tongue, diminished salivary flow, alteration in the flora of oral cavity, with greater predominance of Candida albicans, hemolytic streptococci and staphylococci. [5]

  Periodontal Findings Top

Enlarged gingival, sessile or pedunculated gingival polyps, polypoid gingival proliferations, multiple abscess formation, periodontitis, and loosened teeth.

The most striking changes in uncontrolled diabetes are the reduction in defense mechanism and the increased susceptibility to infection, leading to destructive periodontal disease. [5]

  Diagnosis Top

The diagnosis of diabetes mellitus is established through the recognition of its signs and symptoms and by laboratory investigations. In 1998, the World Health Organization adopted the diagnostic parameters for diabetes established by the American Diabetes Association. [6]

  1. Symptoms of diabetes plus casual plasma glucose concentration >200 mg/dl. Casual glucose may be drawn at any time of day without regard to time since the last meal.
  2. Fasting plasma glucose >126 mg/dl. Fasting is defined as no caloric intake for at least 8-h
  3. 2-h postload glucose >200 mg/dl during an oral glucose tolerance test. The test should be performed using a glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water [Table 1].
Table 1: American diabetes association criteria for diagnosis of diabetes mellitus

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The fasting and casual plasma glucose tests and the oral glucose tolerance test do not evaluate glycemic control over a more extended period. The primary test for this purpose is glycosylated hemoglobin assay (glycohemoglobin test) [Table 2].
Table 2: Co-relation between glycosylated haemoglobin and mean plasma glucose levels

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The American Diabetes Association recommends that the diabetic patients try to achieve a target HbA1c of <7%.

  Classic Complications of Diabetes Mellitus  Top

  • Retinopathy
  • Nephropathy
  • Neuropathy
  • Macrovascular disease
  • Altered wound healing [4]
  • Periodontitis - sixth complication of diabetes. [7]

Two possible mechanisms for the complications have been proposed.

The first is the polyol pathway where glucose is reduced to sorbitol by the enzyme aldol reductase. Sorbitol is considered a tissue toxin and has been implicated in most of the complications of diabetes. [8]

The second mechanism is the production of advanced glycation end products (AGEs) due to the nonenzymatic addition of hexoses to proteins. This alteration of many of the body proteins, which include collagen, hemoglobin, plasma albumin, lens proteins, and lipoproteins, alters their function. [8]

The carbohydrate containing proteins, which accumulate in patients with sustained hyperglycemia are known as AGEs. Formation of AGEs begins with the attachment of glucose to the amino groups on proteins to form an unstable Schiff base adduct. Through a slow chemical rearrangement, these are converted to a more stable but still reversible glucose-protein adducts known as Amadori product. If hyperglycemia is sustained, the Amadori products become irreversible, once formed, they remain attached to proteins for lifetime of those proteins. [4]

  Mechanism of Diabetic Influence on Periodontium Top

Effect of diabetes on periodontal flora

Periodontal diseases are a heterogeneous group of diseases resulting from infections with Gram-negative bacteria. If left untreated, the inflammatory response of the periodontium to dental plaque can lead to destruction of connective tissue attachment, bone, and eventually tooth loss. [9] Mandell et al. [10] studied the microorganisms associated with diseased sites in a group of poorly controlled diabetics. They found bacterial patterns in the diseased sites of diabetics similar to those of healthy adults with periodontal disease. These sites commonly harbored Porphyromonas gingivalis and Prevotella intermedia in similar proportions to those in nondiabetic adult periodontitis patients. Other authors have reported higher levels of specific microorganisms such as Actinobacillus actinomycetemcomitans and Capnocytophaga.[11] However, most studies seem to indicate that the microorganisms associated with diabetic periodontitis are no different than those seen in healthy patients with periodontitis. The proportion of P. gingivalis was reported to be higher in noninsulin-dependent diabetes mellitus patients with periodontitis. It is possible that, in the diabetic patient, the abnormal host defense mechanisms in addition to hyperglycemic state can lead to the growth of particular fastidious organisms. [12]

Impaired neutrophil function

Neutrophil impairment usually leads to increased susceptibility to periodontitis. Defects in chemotaxis, phagocytosis and killing have all been reported in diabetics. McMullen et al. [13] studied neutrophil chemotaxis in individuals with advanced periodontal disease and a genetic predisposition to diabetes. They reported that subjects with both conditions have significantly more depressed chemotactic function than those without a genetic predisposition to diabetes. Thus, altered neutrophil chemotaxis may contribute to the severity of periodontitis in diabetics, or it may be a marker of a more fundamental defect in neutrophil function, as has been shown in chemotactically impaired neutrophils from early-onset periodontitis patients. In addition to chemotactic impairments, other investigators have reported impairments in neutrophil phagocytosis in poorly controlled diabetics. Hyperglycemia or hyperlipidemia may be responsible for some of the impairments in neutrophil function. There are also reports of impaired in vivo inflammatory cell recruitment in diabetics. [12]

Excessive inflammatory response

The monocyte/macrophage cell line is critical to cell mediated host defense in periodontal disease. Many diabetic patients possesss a hyper responsive monocyte/macrophage phenotype in which stimulation by bacterial antigens such as lipopolysaccharide results in dramatically increased proinflammatory cytokine production. [14] Diabetic monocytes produce 24-32 times the level of tumor necrosis factor α, 4 times the level of prostaglandin E2 and interleukin-1β resulting in higher periodontal destruction. [15] The formation of AGEs also plays an important role in the upregulation of monocyte/macrophage cell line. Accumulation of AGEs in the periodontium stimulates influx of monocytes. Once in the tissues, AGEs interact with receptor for advanced glycation end products (RAGE) on monocyte cell surfaces. This halts the monocytes, fixing them at the local site. The AGE-RAGE interaction then induces changes in the monocyte cell phenotype, upregulating the cell and significantly increasing the production of proinflammatory cytokines. [16]

Collagen turnover defects

Collagen is the primary constituent of gingival connective tissue and the organic matrix of alveolar bone. Changes in collagen metabolism contribute to alterations in wound healing and to periodontal disease initiation and progression. [4] Increased collagen breakdown through stimulation of collagenase activity is observed in the periodontium of the diabetic patients. [17] Collagenase primarily degrade more newly formed and therefore more soluble collagen macromolecules. Sustained hyperglycemia results in AGE modification of existing collagen, with increased cross linking. The net effect of these alterations in collagen metabolism is a rapid degradation of recently synthesized collagen by host collagenases and a predominance of highly cross linked, AGE modified collagen. Change in collagen metabolism result in altered wound healing. Impaired wound healing is a well-recognized complication of diabetes and may affect any site, including the periodontium. [4]

  Effects of Diabetic Control on Periodontal Status Top

The issue of whether diabetic control is a factor in reversing the defects and complications that accompany diabetes is controversial. Most of the studies seem to indicate that poorly controlled diabetics suffer from more frequent and severe complications. Certain granulocyte abnormalities, such as impaired phagocytosis and killing, do seem to improve with better diabetic control. This has led some authors to hypothesize that functional disturbances in granulocytes may be due to a reduced oxidative burst as a result of hyperglycemia or hyperlipidemia. This reduction in oxidative metabolism can lead to a decreased phagocytic and killing efficiency. [12]

It has also been reported that, during infection, the insulin supplement needs to be increased to maintain glycemic control in the diabetic. As a corollary, with the resolution of infection, the amount of insulin required also decreases. Therefore, hyperglycemia associated with poor control of diabetes seems to set off a series of events leading to a higher risk of infection and periodontal literature deals with the effect of diabetic control on periodontal status and the effects of periodontal therapy on glycemic levels. [18]

Control of diabetes affects the host response and the environment for the growth of certain microorganisms and can thus affect the severity of periodontal disease as well. Most of the literature on diabetes indicates that acute infections and inflammatory conditions increase glucose and insulin utilization and therefore complicate the metabolic control of diabetes. The studies that attempt to correlate the incidence and severity of periodontal disease and the level of diabetic metabolic control also need to be evaluated based on the type of diabetes studied. Periods of hyperglycemia associated with poor diabetic metabolic control and the effect of adjustment of this hyperglycemic state on the progression and severity of infections (such as periodontal disease) may be more significant in type II versus type I diabetes. This can be attributed to the fact that type I diabetes has been associated with certain genetic factors that lead to monocytic hyperresponsiveness and the increased production of inflammatory mediators. Thus, hyperglycemia and hyperlipidemia may only play a minor role in exacerbating the underlying genetic and immune dysregulation. Type II diabetics, on the other hand, do not seem to have the same autoimmune factors associated with their systemic condition. Therefore, in this group of patients, the effects of metabolic control may have a more significant contribution to increasing susceptibility to infections, including periodontal diseases. [12]

  Influence of Periodontal Therapy on Diabetic Control Top

Although it has been generally recognized that systemic infection increases the need for insulin in the diabetic patient, relatively few studies have investigated whether the metabolic control of diabetes improves after periodontal therapy. Two studies [18],[19] are in agreement that the frequency of recurrent diabetic complications and the insulin requirement in diabetics were reduced after periodontal treatment. Miller et al. [18] compared glycosylated hemoglobin levels before and after periodontal treatment in nine patients. There was a reduction in the percentage of hemoglobin A, after periodontal treatment (including scaling and root planning and 2 weeks of doxycycline and chlorhexidine rinses). These investigators concluded that metabolic control of diabetes can be altered by controlling periodontal inflammation. Glycosylated hemoglobin or hemoglobin A, measures the percentage of hemoglobin A, and gives an excellent indication of diabetic control over the previous 3 months. [12] It is generally a better indication of diabetic control than self-monitoring. The glycosylated hemoglobin values can be used to determine the level of diabetic control and alter the course of periodontal therapy by using adjuncts to conventional therapy such as antibiotics or antimicrobial rinses. [20]

  Prevention Top

In general, all diabetes mellitus patients should be encouraged to maintain meticulous oral hygiene and to receive supportive periodontal therapy at intervals necessary to sustain a high level of periodontal health. Patients should be carefully monitored for dental caries and home and office use of fluoride caries preventive agents is recommended. [21]

  Dental Management of The Diabetic Patient Top

Periodontal therapy

The well-controlled diabetes mellitus patient with periodontal disease is often an acceptable candidate for complete periodontal therapy, including surgical procedures when indicated. However, the presence of medical complications associated with diabetes mellitus should be carefully evaluated and considered in any periodontal therapeutic decision. Most authorities recommend that periodontal surgery be scheduled in the morning after breakfast and medication administration.

Treatment procedures should be short (2 h or less), as atraumatic as possible and should not significantly interfere with the patient's normal dietary intake. Patient anxiety should be managed to minimize endogenous epinephrine release, because epinephrine may increase insulin utilization and deplete insulin levels more quickly. In most instances preoperative oral sedation is suitable for this purpose.

In the event that general anesthesia or intravenous conscious sedation techniques are necessary or if extensive surgical procedures are likely to alter the patient's dietary intake, then changes in the type 1 patient's insulin intake may be necessary under the guidance of the patient's physician. Decisions regarding the prophylactic use of antibiotics in conjunction with periodontal surgery are best made on a case by- case basis since there is no evidence-based information to indicate that antibiotic premedication is necessary.

The poorly controlled type 1 patient is not a good candidate for periodontal therapy other than necessary emergency services. Medical coordination is probably indicated for any type of periodontal therapy and hospitalization may be required for emergency care. If time permits, microbiological testing is desirable to identify putative periodontal pathogens prior to antibiotic therapy. If stable metabolic control is achieved, routine periodontal therapy may be considered with close medical monitoring. [21]

Diabetes mellitus-related xerostomia

In general, diabetic patients should be encouraged to adhere to strict diabetes mellitus metabolic control and to avoid smoking or the use of alcohol (including mouthrinses with high alcohol content) and caffeine-containing beverages. Artificial saliva substitutes and frequent ingestion of water may be of benefit.

There is some evidence to suggest that oral hygiene products containing the detergent sodium lauryl sulfate may be irritating to the mucous membranes of xerostomic patients, and this agent should be avoided if xerostomia is a problem for the diabetes mellitus patient. Patients should be encouraged to stimulate salivary flow by the use of sugarless gum or natural salivary stimulants such as chewing raw carrots and celery. [21]

Fungal infections

Frequent monitoring for the overgrowth of oral fungal organisms such as C. albicans is indicated, and on occasion the prophylactic use of topical antifungal agents may be necessary. Most topical oral antifungal products contain sucrose and may be contraindicated for caries-susceptible diabetes mellitus patients. The topical agent, nystatin, however, can be obtained in a powder form which is sucrose-free, but it must be mixed with water for each use. More recently, an oral antifungal rinse containing itraconazole has become available that uses saccharin in place of sucrose. [21]

Improvement in burning mouth and altered taste sensation may occur when diabetes mellitus metabolic control is established or when xerostomia and associated candidiasis are controlled.

  Conclusion Top

The dentists should have a thorough understanding of the diagnostic, therapeutic methodologies and the pharmacological agents commonly used in the diabetic patients. The physicians and the dentists together play an important role in the treatment of diabetic patients, as there is a bidirectional relationship between periodontitis and diabetes. Working with diabetic patients can be challenging and rewarding when open lines of communication are established and thorough patient education is attained.

  References Top

1.Mealey BL, Ocampo GL. Diabetes mellitus and periodontal disease. Periodontol 2000 2007;44:127-53.  Back to cited text no. 1
2.Nishimura F, Iwamoto Y, Soga Y. The periodontal host response with diabetes. Periodontol 2000 2007;43:245-53.  Back to cited text no. 2
3.Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 1997;20:1183-97.  Back to cited text no. 3
4.Rose L, Genco R, Cohen D, Mealey B. Periodontal Medicine. 1 st ed., Pmph Bc Decker; 1999.  Back to cited text no. 4
5.Newman M, Takei H, Klokkevold P, Carranza F. Clinical Periodontology 10 th ed. New Delhi: Elsevier Publisher; 2007  Back to cited text no. 5
6.Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: Diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med 1998;15:539-53.  Back to cited text no. 6
7.Löe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care 1993;16:329-34.  Back to cited text no. 7
8.Soskolne WA, Klinger A. The relationship between periodontal diseases and diabetes: An overview. Ann Periodontol 2001;6:91-8.  Back to cited text no. 8
9.Slots J. Bacterial specificity in adult periodontitis. A summary of recent work. J Clin Periodontol 1986;13:912-7.  Back to cited text no. 9
10.Mandell RL, Dirienzo J, Kent R, Joshipura K, Haber J. Microbiology of healthy and diseased periodontal sites in poorly controlled insulin dependent diabetics. J Periodontol 1992;63:274-9.  Back to cited text no. 10
11.Mashimo PA, Yamamoto Y, Slots J, Park BH, Genco RJ. The periodontal microflora of juvenile diabetics. Culture, immunofluorescence, and serum antibody studies. J Periodontol 1983;54:420-30.  Back to cited text no. 11
12.Yalda B, Offenbacher S, Collins JG. Diabetes as a modifier of periodontal disease expression. Periodontol 2000 1994;6:37-49.  Back to cited text no. 12
13.McMullen JA, Van Dyke TE, Horoszewicz HU, Genco RJ. Neutrophil chemotaxis in individuals with advanced periodontal disease and a genetic predisposition to diabetes mellitus. J Periodontol 1981;52:167-73.  Back to cited text no. 13
14.Offenbacher S. Periodontal diseases: Pathogenesis. Ann Periodontol 1996;1:821-78.  Back to cited text no. 14
15.Salvi GE, Yalda B, Collins JG, Jones BH, Smith FW, Arnold RR, et al. Inflammatory mediator response as a potential risk marker for periodontal diseases in insulin-dependent diabetes mellitus patients. J Periodontol 1997;68:127-35.  Back to cited text no. 15
16.Schmidt AM, Hori O, Cao R, Yan SD, Brett J, Wautier JL, et al. RAGE: A novel cellular receptor for advanced glycation end products. Diabetes 1996;45 Suppl 3:S77-80.  Back to cited text no. 16
17.Ramamurthy NS, Golub LM. Diabetes increases collagenase activity in extracts of rat gingiva and skin. J Periodontal Res 1983;18:23-30.  Back to cited text no. 17
18.Miller LS, Manwell MA, Newbold D, Reding ME, Rasheed A, Blodgett J, et al. The relationship between reduction in periodontal inflammation and diabetes control: A report of 9 cases. J Periodontol 1992;63:843-8.  Back to cited text no. 18
19.Sastrowijoto SH, Hillemans P, van Steenbergen TJ, Abraham-Inpijn L, de Graaff J. Periodontal condition and microbiology of healthy and diseased periodontal pockets in type 1 diabetes mellitus patients. J Clin Periodontol 1989;16:316-22.  Back to cited text no. 19
20.Seymour RA, Heasman PA. Systemic diseases and the periodontium. In: Drugs, Diseases and the Periodontium. Oxford: Oxford University Press; 1992. p. 20-2.  Back to cited text no. 20
21.Rees TD. Periodontal management of the patient with diabetes mellitus. Periodontol 2000 2000;23:63-72.  Back to cited text no. 21


  [Table 1], [Table 2]


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