Diabetes and Periodontitis
Diabetes and Periodontitis
Diabetes and Periodontitis
Names of authors:
Dr. Benazir Ghani Dr. G.S. Srikanth Dr. Preeti Bhattacharya Dr. Manvi Agarwal
INTRODUCTION
.Diabetes has emerged as a major health problem in India .According to International Diabetes Federation every fifth diabetic in world would be an Indian by year 2005. Further the Asian Indian phenotype commonly known as thirfty genotype predispose Indian population to risk of developing diabetes. The first 60 years of the 20th century could be
termed the "medical era," in which allopathic medicine emerged as the dominant approach to health care: this was based on mass vaccination and the extensive use of antibiotics and is still the main aproach in many parts of the world. Now, however, the industrialized parts of the world has entered a "post medical" era, in which physical well-being is undermined by certain types of individual behaviors (e.g., smoking), economic factors (e.g., poverty, overeating), and factors influencing the physical environment . The debate on lifestyle and their impact on health is an expression of search for the ways, meeting the new situations. The chronic conditions like cardiovascular disorders, cancer, and periodontal diseases which make up the bulk of morbidity and psychological disorders such as depression are becoming important. The first key to prevent many of these conditions was considered to be a change in the health behavior . The term "lifestyle" is taken to mean a general way of living based on the interplay between living conditions in the wide sense and individual patterns of behavior as determined by sociocultural factors and personal characteristics. The range of behavioral patterns may open limited or may extend by means of environmental factors. The way in which an individual lives may produce behavioral patterns that are either beneficial or detrimental to health. If health is to be improved, actions must be directed at both the individual and environmental factors affecting lifestyle. The concept of a healthy lifestyle being directly related to health was stressed upon by several authors in
the past and they found that people with an active lifestyle had fewer symptoms in teeth and gums than those with inactive ones. So the concept of lifestyle makes it possible to study behavior in a wider sense and it sheds more light on the personal characteristics of an individual. Our results showed a positive correlation between lifestyle and periodontal status. This is in accordance with Rajala who had shown a positive association between dental health behavior and lifestyle variablesPeople with an unhealthy lifestyle have a poor periodontal status because of their aberrant brushing habits and detrimental effects of smoking. According to Revicki, [7] smokers tend to have a more negative lifestyle in general. It means that the association of tobacco with periodontal health was linked not only to poor oral hygiene but also to poor general lifestyle. Studies in the past have shown that females have a better periodontal status and a more positive dental health behavior compared to males. The reasons attributed to this could be esthetics and social pressure on women to look physically attractive thus causing them to lead a healthier lifestyle than men. When the socioeconomic status was compare It is important to appreciate such disorders and
conditions do not initiate periodontitis, but they may predispose ,accelerate or otherwise increase its progression. to the periodontal status, our study showed a positive association between higher
socioeconomic groups and better periodontal status. This is in accordance with Neuman et al who identified a lower occupational status limiting the use of dental services. Dental visiting is still not considered a preventive dental behavior; at present it only depends on treatment needs. Thus people from the lower income group fail to make prophylactic visits to a dentist thus giving them poorer dental health behavior. When education levels were compared to periodontal status, our study showed a positive association between higher education levels and better periodontal status. This is in accordance with Richard et al. who identified education level also a strong indicator of periodontal status. With regard to self-awareness we found better awareness in three groups: in those with a healthy lifestyle, education, and in those of a higher socioeconomic status.
Diabetes mellitus is an extremely important disease from periodontal standpoint .It is a complex metabolic disorder characterized by chronic hyperglycemia,diminished insulin production,impaired insulin action or a combination of both.This results in inability of glucose to be transported from the bloodstream into the tissues,which in turn results in high blood glucose levels and excretion of sugar in urine. There are mainly two types of diabetes mellitus,TypeI and TypeII With several less common secondary types.Type I diabetes mellitus formerly known as insulin dependent diabetes mellitus (IDDM), is caused by a cell mediated auto immune destruction of the insulin producing beta cells of the islets of langerhans in the pancreas,which results in Insulin deficiency. It accounts for 5% to 10% for all cases of diabetes and most often occurs in children and young.
Type II diabetes mellitus formerly known as non insulin dependent diabetes mellitus is caused by peripheral resistance to insulin action,impaired insulin secretion and increased glucose production in liver. This is most common type .Another category of diabetes is gestational diabetes.
Periodontitis is defined as inflammatory disease of supporting tissues of teeth caused by specific microorganism, resulting in progressive destruction of periodontal ligament and alveolar bone with pocket formation ,recession or both. In recent years a lot of emphasis has been laid on
multifactorial aspect of disease entity. Microbiological ,immunological, environmental, genetic and systemic factors ,all contributes in a way or other to the pathogenesis and \progression of periodontal disease. Various systemic diseases have been considered to play a major and crucial role in periodontal destruction by modulating the host side of disease interaction, of which one of the most common condition is diabetes mellitus . Persons with diabetes mellitus (DM) are at greater risk of developing PD. PD is now considered the sixth complication of DM . Not only is it more prevalent in this population, but also the progression of symptoms,in a more aggressive and more rapidly setting mode.The main reasons for this situation are the scarce information on the importance of oral hygiene, poor metabolic control and the irregularity in visiting dentists,among others . PD conditions the loss of dental organs, making chewing food difficult, causing pain and as a result,inadequate nutrition . In addition, frequently persons with DM have a much more difficult time in tolerating false dentures due to total bone loss and the sensitivity of the alveolar mucosa.The participation of a physician is relevant in the opportune detection of PD as a health provider for diabetics and whom a patient comes into more contact with. This article reviews the literature analyzing the bidirectional relationship between diabetes mellitus and periodontal disease, as well as the effects of periodontaltreatment on glycemic control with the aim of providing physicians and health personnel the basic elements supporting this relationship and which contribute to their active participation in the diagnosis and opportune referral.
The precise Etiology of most cases of diabetes is uncertain, although certain contributing factors are as follows:
Type 1 diabetes
Type 1 Diabetes is autoimmune disease that affects 0.3% on average. It is result of destruction of beta cells due to aggressive nature of cells present in the body. Researchers believe that some of the Etiology and Risk factors which may trigger type 1 diabetes may be genetic, poor diet (malnutrition) and environment (virus affecting pancreas). Secondly, in most of the cases, diabetes occurs because there is abnormal secretion of some hormones in blood which act as antagonists to insulin. Example- Adrenocortical hormone, Adrenaline hormone and Thyroid hormone.
Type 2 diabetes
Type 2 Diabetes is also called non insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. It occurs when the body produces enough insulin but cannot utilize it effectively. This type of diabetes usually develops in middle age. A general observation says that about 90-95 % of people suffering with diabetes are type 2; about 80 percent are overweight. It is more common among people who are older; obese; have a family history of diabetes; have had gestational diabetes. There are number of risk factors found to be responsible for type 2 diabetes like, the more the Etiology and Risk factors carried by an individual, the higher the risk for developing diabetes.
With type 1 diabetes, which starts in childhood, the pancreas stops producing insulin. Insulin is a hormone your body needs to be able to use the energy -- glucose -- found in food. The primary risk factor for type 1 diabetes is a family history of this lifelong, chronic disease
Diabetes management requires awareness. Know what makes your blood sugar level rise and fall and how to control these day-to-day factors.
Know your numbers. Talk to your doctor about what blood sugar levels are appropriate for you before you begin exercise.Check your blood sugar level. Check your blood sugar level before, during and after exercise, especially if you take insulin or medications that lower blood sugar. Be aware of warning signs of low blood sugar, such as feeling shaky, weak, confused, lightheaded, irritable, anxious, tired or hungry.Stay hydrated. Drink plenty of water while exercising because dehydration can affect blood sugar levels.Be prepared. Always have a small snack or glucose pill with you during exercise in case your blood sugar drops too low. Wear a medical identification bracelet when you're exercising.Adjust your diabetes treatment plan as needed. If you take insulin, you may need to adjust your insulin dose before exercising or wait a few hours to exercise after injecting insulin. Your doctor can advise you on appropriate changes in your medication. You may need to adjust treatment if you've increased your exercise routine. Medication Insulin and other diabetes medications are designed to lower your blood sugar level when diet and exercise alone aren't sufficient for managing diabetes. But the effectiveness of these medications depends on the timing and size of the dose. And any medications you take for conditions other than diabetes can affect your blood sugar level, too. What to do:
Store insulin properly. Insulin that's improperly stored or past its expiration date may not be effective.Report problems to your doctor. If your diabetes medications cause your blood sugar level to drop too low, the dosage or timing may need to be adjusted.Be cautious with new medications. If you're considering an over-the-counter medication or your doctor prescribes a new drug to treat another condition such as high blood pressure or high cholesterol ask your doctor or pharmacist if the medication may affect your blood sugar level. Sometimes an alternate medication may be recommended.
that diabetes is a risk factor for gingivitis and periodontitis The degree of glycemic control is an important variable in the relationship between diabetes and periodontal diseases, with a higher prevalence and severity of gingival inflammation and periodontal destruction being seen in those with poor control . Large epidemiological studies have shown that diabetes increases the risk of alveolar bone loss and attachment loss approximately three-fold when compared to nondiabetic individuals . These findings have been confirmed in meta-analyses of studies in various diabetic populations . In longitudinal analyses,diabetes increases the risk of progressive bone loss and attachment loss over time . The degree of glycemic control is likely to be a major factor in determining risk. For example, in a large epidemiological study in the U.S. (NHANES III), adults with poorly controlled diabetes had a 2.9-fold increased risk of having periodontitis compared to nondiabetic subjects; conversely, subjects with well-controlled diabetes had no significant increase in the risk for periodontitis. Similarly, poorly controlled type 2 diabetic subjects had an 11-fold increase in the risk for alveolar bone loss over a 2-year period compared to nondiabetic control subjects . On the other hand, well-controlled type 2 patients had no significant increase in risk for longitudinal bone loss compared to nondiabetic controls. Many of the mechanisms by which diabetes influences the periodontium are similar to the pathophysiology of the classic microvascular. Many of the mechanisms by which diabetes influences the periodontium are similar to the pathophysiology of the classic microvascular and macrovascular diabetic complications. There are few differences in the subgingival microbiota between diabetic and nondiabetic patients with periodontitis . This suggests that alterations in the host immunoinflammatory response to potential pathogens may play a predominant role. Diabetes may result in impairment of neutrophil adherence, chemotaxis,and phagocytosis, which may facilitate bacterial persistence in the periodontal pocket and significantly increase periodontal destruction . While neutrophils are often hypofunctional in diabetes, these patients may have a hyper-responsive monocyte/macrophage phenotype, resulting in significantly increased production of pro-inflammatory cytokines and mediators . This hyperinflammatory response results in elevated levels of pro-inflammatory cytokines in the gingival crevice fluid. Gingival crevice fluid is a serum transudate, thus, elevated serum levels of inflammatory mediators may be reflected in similarly elevated levels of these mediators in gingival crevice fluid. The level of cytokines in the gingival crevice fluid has been related to the level of glycemic control in diabetic patients. In one study of diabetic subjects with periodontitis, those with hemoglobin A1c levels >8% had gingival crevice fluid levels of interleukin-1b almost twice as high as subjects whose hemoglobin A1c levels were <8% . The net effect of these host defense alterations in diabetes is an increase in periodontal inflammation, attachment loss, and bone loss. Elevated pro-inflammatory cytokines in the periodontal environment may play a role in the increased periodontal destruction seen in many people with diabetes.Formation of advanced glycation end-products, a critical link in many diabetic complications, also occurs in the periodontium, and their deleterious effects on other organ systems may be reflected in periodontal tissues as well . Likewise, a 50% increase in messenger RNA for the receptor of advanced glycation end-products was recently identified in the gingival tissues of type 2 diabetic subjects compared to nondiabetic controls . Matrix metalloproteinases are critical components of tissue homeostasis and wound healing, and are produced by all of the major cell types in the periodontium. Production of matrix metalloproteinases such as collagenase increases in many diabetic patients, resulting in altered collagen homeostasis and wound healing within the periodontium
elevated interleukin-6 production in obesity results in higher circulating levels of both interleukin-6 and tumor necrosis factor-a. Periodontal infection can induce elevated serum interleukin-6 and tumor necrosis factor-a levels, and may play a similar role as obesity in inducing or exacerbating insulin resistance.
Conclusions
Diabetic patients are commonly encountered in the dental office. Proper patient management requires close interaction between the dentist and physician.Dentists and other oral health care providers should understand the diagnostic and therapeutic methodologies used in diabetes care. They must be comfortable with the parameters of glycemia that are used to establish a diagnosis and an assessment of patients_ ongoing glycemic control. A thorough understanding of the pharmacological agents commonly encountered in this patient population is a must. The dentist should know how these agents can affect the risk for hypoglycemia, and should be able to manage such events should they occur in the office.Dentists must educate patients and their physicians about the interrelationships between periodontal health and glycemic control, with an emphasis on the inflammatory nature of periodontal diseases and the potential systemic effects of periodontal infection. Working with diabetic patients can be challenging and rewarding when open lines of communication are established and thorough patient education is attained.
References
1. Slade GD, Offenbacher S, Beck, JD, Heiss G, Pankow JS: Acute-phase inflammatory response to periodontal disease in the US population. J Dent Res 79: 49-57,2001 2. Brownlee M: The pathological implications of protein glycation. Clin Invest Med 18: 275-281,1995 3. Luger A, Schernthaner G, Urbanski A, Luger TA: Cytokine production in patients with newly diagnosed insulin-dependent (type I) diabetes mellitus. Eur J Clin Invest 18:233 -236, 1988 4. Nishimura F, Soga Y, Iwamoto Y, Kudo C, Murayama Y: Periodontal disease as part of the insulin resistance syndrome in diabetic patients. J Int Acad Periodontol 7:16 -20, 2005
5. Wautier, JL, Schmidt AM: Protein glycation: a firm link to endothelial cell dysfunction. Circ Res 95:233 -238, 2004
6. Basta G, Lazzerini G, Del Turco S, Ratto GM, Schmidt AM, De Caterina R: At least 2 distinct pathways generating reactive oxygen species mediate vascular cell adhesion molecule-1 induction by advanced glycation end products. Arterioscler Thromb Vasc Biol25 : 1401-1407,2000 7. Cutler CW, Machen RL, Jotwani R, Iacopino AM: Heightened gingival inflammation and attachment loss in type 2 diabetics with hyperlipidemia. J Periodontol 70:1313 -1321, 1999
8. Lamster IB, Lalla E: Periodontal disease and diabetes mellitus: discussion, conclusions, and recommendations. Ann Periodontol6 : 146-149,2001 9. Lovegrove JM: Dental plaque revisited: bacteria associated with periodontal disease. J N Z Soc Periodontol 87:7 -21, 2004 10. Lalla E, Lamster IB, Drury S, Fu C, Schmidt AM: Hyperglycemia, glycoxidation and receptor for advanced glycation endproducts: potential mechanisms underlying diabetic complications, including diabetes-associated periodontitis. Periodontol 23:50 -62, 2000
11. Salvi G E, Yalda, B, Collins JG, Jones BH, Smith FW, Arnold RR, Offenbacher S: Inflammatory mediator response as a potential risk marker for periodontal diseases in insulin-dependent diabetes mellitus patients. J Periodontol 68:127 -135, 1997
12. Miller LS, Manwell MA, Newbold D, Reding ME, Rasheed A, Blodgett J, Kornman KS: The relationship between reduction in periodontal inflammation and diabetes control: a report of 9 cases. J Periodontol 63:843 -848, 1992 13. Tsai C, Hayes C, Taylor GW: Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population. Community Dent Oral Epidemiol 30:182 -192, 2002