Periodontal disease is a common, chronic, complex multifactorial disease characterized by destruction and loss of connective tissue attachment. The most prevalent form is chronic periodontitis. There is increasing evidence that microbial biofilm and host susceptibility plays an important role in initiation and progression of periodontitis¹. Recent studies have demonstrated that chronic periodontitis is a potential risk factor for systemic diseases like coronary heart diseases/atherosclerosis, worsening glycemic control in diabetes mellitus, adverse pregnancy outcome etc². Periodontal disease has now be recognized as the sixth complication of diabetes³. Diabetes mellitus is a common multifactorial disease process involving genetic, environmental and behavioral risk factors affecting up to 5% of the general population of world⁴. India leads the world with largest number of diabetic subjects to around 40.9 million⁵. In Kerala, Kutty et. al reported 16.3 percent crude prevalence of diabetes mellitus among adults aged 20 years or above in an urban settlement⁶.

 Numerous epidemiologic surveys demonstrated that there is an increased prevalence of periodontitis among patients with uncontrolled or poorly controlled diabetes mellitus⁷. Evidence has consistently indicated that diabetes is a risk factor for increased severity of gingivitis and periodontitis⁸. Conversely, periodontitis may be a risk factor for worsening glycemic control. Although the biologic mechanisms linking periodontitis to impaired glucose metabolism have not been fully elucidated.  Inflammatory mediators(particularly interleukin-1, interleukin-6 and tumor necrosis factor-alpha) generated within the inflamed periodontal tissues translocate into the systemic circulation and interfere with the actions of insulin receptors, thereby decreasing insulin sensitivity associated with degree of glycemic control of diabetes⁹. These  inflammatory mediators  (IL-1), IL-6,(TNF-α) and prostaglandin E₂ (PGE₂)  can interact systemically with lipids, free fatty acids and advanced glycation end products (AGES). This interaction induces or perpetuates activation of the intracellular pathways, such as the I-kappa-B (IκB), I-kappa-B kinase-β (IKKβ), nuclear factor-kappa B (NF-kβ) and the protein c-Jun N-terminal kinase (JNK) axes. The activation of these inflammatory pathways in immune cells (monocytes or macrophages), endothelium cells, adipocytes, hepatocytes and muscle cells promotes and contributes  to an increase in the overall insulin resistance, which makes it difficult to achieve metabolic control in patients with both type 2 diabetes and periodontitis¹⁰ .In 2010 American Diabetes Association Standards of Medical care in Diabetes added the A1c ≥ 48 mmol/mol (≥6.5%) as another criterion for the diagnosis of diabetes¹¹. People without diabetes usually have a level of 4.5% - 6%. So,in between....6.0-6.5...may be ’pre-diabetes’ or ’at risk of diabetes’. (WHO 2010)

                Although many studies reported more severe periodontal disease in subjects with diabetes than those without diabetes, relatively very few examined the association between periodontitis and glycemia or the level of glycosylated hemoglobinin in adults without diabetes¹².  Saito et al.¹³ found that alveolar bone loss was associated with impaired glucose tolerance in Japanese men without diabetes. Similarly Nibali et al.¹⁴ found slightly, but statistically significantly, higher non-fasting glucose levels in periodontitis cases compared to healthy controls. These studies suggest that periodontitis may affect glucose metabolism in the general population, albeit to a lesser extent than in adults with diabetes.            

                So we hypothesized that patients with periodontitis have higher HbA1c levels than healthy patients and the purpose of this study is to examine the association between periodontitis and HbA1c level in otherwise systemically healthy individuals.  

AIM

To identify a possible association between chronic periodontitis and glycosylated hemoglobin levels in otherwise systemically healthy individuals.

 OBJECTIVES

1.      To assess glycosylated hemoglobin levels in otherwise systemically healthy individuals with chronic periodontitis and compare it with a healthy control group.

2.      To correlate the level of inflammatory marker like serum albumin and CRP with periodontal parameters.

METHODOLOGY

Study design

Crossectional (observational) study

MATERIALS AND METHODS

Study population and sample size: Subjects in this study group to comprise of 100 patients.   These subjects will be divided in to two groups.

1.      Cases: (Group I) cases includes total of 50 subjects otherwise systemically healthy patients with chronic periodontitis reporting to the department of periodontics GOVT DENTAL COLLEGE CALICUT.

2.      Control: (Group II) includes 50 subjects otherwise systemically healthy without chronic periodontitis. Control should match for age, sex, and to cases. These subjects will undergo general, oral or periodontal examination and laboratory investigations.

Duration of the study

18 months.

 Study setting

Location This study is to be conducted by the department of Periodontics, GOVT. DENTAL COLLEGE CALICUT in collaboration with department of biochemistry GOVT MEDICAL COLLEGE CALICUT.

INCLUSION CRITERIA FOR CASE GROUP

 1.Patients with age group between 25 to 55.

 2.Minimum of 20 teeth present.

 3.Patients who were diagnosed with severe periodontitis chronic periodontitis (CDC criteria   moderate periodontitis is defind as ≥2 interproximal sites with  ≥ 4mm clinical attacment loss (CAL) not on same tooth,or ≥2 interproximal with probing depth (PD) ≥ 5mm not on same tooth severe periodontitis is defind as ≥2 teeth with clinical attachment loss  ≥6mm not on same tooth and  ≥1 interproximal site with probing depth  â‰¥ 5mm).

5.No family history of Diabetes,

INCLUSION CRITERIA FOR CONTROL GROUP

1.      Healthy individuals with age group between 25 to 55.

2.      Minimum of 20 teeth present.

3.      Subjects who do not fall within the diagnostic criteria for moderate or severe periodontitis (CDC criteria)

4.      No family history of Diabetes    

EXCLUSION CRITERIA

1.      Patients with known systemic disease and condition such as CVD, renal disease, RA, diabetes Mellitus, liver and pancreatic disease, nutritional deficiencies, pregnant and lactating mother.

        2.  Patients with conditions that shorten erythrocyte survival (e.g., hemolytic anemia, pregnancy, or recent  significant blood loss, or who are positive for rheumatoid factors.)

          3.  Patients with acute condition that contraindicate a periodontal examination.

          4.  Patients who received systemic antibiotic therapy within past 6 month.

          5.  Patients who received periodontal therapy (scaling and root planing or surgery) past 1 year.

          6.  Patients not willing to sign informed consent.

        ARMAMENTARIUM

1.      Mouth mirror

2.      Explorer

3.      Williams graduated periodontal probe

4.      Disclosing agents

5.      HbA1c assessment kit

6.      CRP assessment kit

 DATA COLLECTION

         Data Collection Tools

1.      Questionnaire

2.      Clinical examination

3.      Blood  investigation

        Periodontal Parameters

1.      Probing depth

2.      Clinical attachment level

3.      Gingival recession

4.      Simlified oral hygiene index

5.      Plaque index

6.      Modified gingival index

     Systemic Parameters

1.      TCH

2.      HDL

3.      LDL

4.       VLDL

5.      TRIGLYCERIDES

6.       BLOOD GLUCOSE (fasting and post prandial)

7.      BP

8.      BMI

9.      WHR

10.   GLYCOSYLATED HEMOGLOBIN

11.  CRP

12.  SERUM ALBUMIN

  INFORMED CONSENT

A written informed consent will be obtained from all participants in the study .Demographic data includes age, gender, weight, educational level, ethnicity, occupation, family income . Complete medical history includes diabetic history, history of CVD and hypertension, medication etc. The laboratory assays include, BMI, WHR, CRP, fasting blood sugar, total cholesterol, HDL, LDL, Triglycerides etc.

DATA ANALYSIS

 (α value will be set at 5% and β value will be set at 80%)

Qualitative Data by chi-square test

Quantitative Data by student ‘t’ test

Odds ratio & correlation coefficient

Multivariate linear regression

FUNDING      -Rs60000/-

ANNEXURE

1.      PROFORMA

2.      CONSENT

REFERENCES

1. Schenkein HA. Host responses in maintaining periodontal health and determining periodontal disease. Periodontol 2000 2006;40:77-93.

2. Lindhe J, Karring T, Lang NP. Clinical periodontology and implant dentistry. Oxford ; Malden, Mass.: Blackwell Munksgaard; 2003: xxiv, 1044 p.

3. Loe H. Periodontal disease the sixth complication of diabetes mellitus. Diabetes Care 1993;16:329-334.

4. King H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projections. Diabetes Care 1998;21:1414-1431

5. Mohan V, Sandeep S, Deepa R, Shah B, Varghese C. Epidemiology of type 2 diabetes: Indian scenario. Indian J Med Res 2007;125:217-230.

6.  Raman Kutty V, Joseph A, CR S. High prevalence of type 2 diabetes in an urban settlement in Kerala, India. Ethn Health 1999;4.

7. Taylor GW. Bidirectional interrelationships between diabetes and periodontal diseases: an                 epidemiologic perspective. Ann Periodontol 2001;6:99-112.

8.   Mealey BL, Oates TW. Diabetes mellitus and periodontal diseases. J Periodontol. 2006;77:1289-303.

 9. Mealey BL, Ocampo GL. Diabetes mellitus and periodontal disease. Periodontol 2000 2007;44:127-153.

10. Roberta Santos Tunes. Impact of Periodontitis on the Diabetes-Related Inflammatory Status. : J      Can Dent Assoc 2010;76:a35

11.Standards of medical care in diabetes Care 33(Suppl 1) S4– 10 January 2010.

12.  Ryan E. Wolff,* Larry F. Wolff,† and Bryan S. Michalowicz. Pilot Study of Glycosylated Hemoglobin Hemoglobin Levels in Periodontitis Cases and Healthy Controls( J Periodontol 2009;80:1057-1061)

13.  Saito T, Murakami M, Shimazaki Y, Matsumoto S, Yamashita Y. The extent of alveolar bone loss is associated with impaired glucose tolerance in Japanese men. J Periodontol 2006;77:392-397.

14.  Nibali L, D’Aiuto F, Griffiths G, Patel K, Suvan J,Tonetti MS. Severe periodontitis is associated    with systemic inflammation and a dysmetabolic status: A case-control study. J Clin Periodontol 2007;34:931-937.