|Year : 2013 | Volume
| Issue : 2 | Page : 109-114
Reduction of HbA1c levels following nonsurgical treatment of periodontal disease in Type 2 diabetics
Sweatha Gurrala, Rameshbabu Mutthineni, Srikanth Chintala, Chandramohan Pabolu
Department of Periodontics, Mamata Dental College and Hospital, Khammam, Andhra Pradesh, India
|Date of Web Publication||21-May-2013|
Department of Periodontics, Mamata Dental College and Hospital, Giriprasad Nagar, Khammam - 507 002, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Objectives: A study was made of the effect of nonsurgical periodontal treatment upon blood glucose control in Type 2 diabetics with periodontal disease.
Materials and Methods: The study sample consisted of 20 patients who were diagnosed to have diabetes with an age range of 42 to 81 years. In all cases, non- surgical periodontal treatment was carried out and was completed in several sessions. Approximately, 30 days after the last session the clinical examination was carried out using a pre-post repeated measures analytical design.
Results: The improvement in glycosylated hemoglobin (HbA1c) after nonsurgical periodontal treatment on comparing the baseline (9.490 ± 0.491) and final values (8.990 ± 0.442) was 0.500 ± 0.066, and proved statistically significant ( P≤ 0.0001).
Conclusions: A decrease in HbA1c was observed after treatment, thus indicating improved blood glucose control in Type 2 diabetics with periodontal disease.
Keywords: HbA1c, periodontal disease, periodontitis, Type 2 diabetes
|How to cite this article:|
Gurrala S, Mutthineni R, Chintala S, Pabolu C. Reduction of HbA1c levels following nonsurgical treatment of periodontal disease in Type 2 diabetics. J NTR Univ Health Sci 2013;2:109-14
|How to cite this URL:|
Gurrala S, Mutthineni R, Chintala S, Pabolu C. Reduction of HbA1c levels following nonsurgical treatment of periodontal disease in Type 2 diabetics. J NTR Univ Health Sci [serial online] 2013 [cited 2020 Oct 1];2:109-14. Available from: http://www.jdrntruhs.org/text.asp?2013/2/2/109/112335
| Introduction|| |
Diabetes mellitus is clinically and genetically heterogeneous group of disorders affecting the metabolism of carbohydrates, lipids, and proteins, in which hyperglycemia is the main feature. These disorders are due to deficiency in insulin secretion caused by pancreatic β-cell dysfunction and or insulin resistance in liver and muscle.  It is the triad of symptoms including polydypsia, polyuria, and polyphagia. The classification of diabetes recognizes different forms of disease and they are divided into Type 1 diabetes results from cell-mediated autoimmune destruction of pancreatic β-cells, which usually leads to total loss of insulin secretion; in contrast, Type 2 diabetes is caused by resistance to insulin combined with a failure to produce enough additional insulin to compensate for the resistance. Type 2 diabetes is commonly linked to obesity, which contributes to insulin resistance through elevation of circulating levels of free fatty acids derived from the adipocytes; these free fatty acids inhibit glucose uptake, glycogen synthesis, and glycolysis.  The two possible mechanisms for complications have been proposed. The first is polyol pathway where glucose is reduced to sorbitol by enzyme aldol reductase. Sorbitol is considered as tissue toxin and has been implicated in most complications of diabetes. The second mechanism is production of advanced glycation end products (AGEs) due to the non enzymatic addition of hexoses to proteins.  The mechanisms responsible for infections, impairment of synthesis of collagen and glycosaminoglycan by gingival fibroblasts and increased crevicular fluid collagenolytic activity.  Alteration of many body proteins, which include collagen, hemoglobin, plasma albumin, lens proteins, and lipoproteins, alter their function. The control of diabetes is, therefore, directed at controlling the blood glucose levels within normal limits. Monitoring the effectiveness of this control is done by measuring the levels of glycated serum proteins, especially glycated α hemoglobin (HbA1c), which, because of its incorporation into red blood cells, gives an indication of serum glucose levels over preceding to 3 months. 
In a patient with diagnosed diabetes, the hemoglobin A1c test (HbA1c) is used to monitor the patient's overall glycemic control. It is not recommended for diagnosis because there is not a gold standard assay for the HbA1c and because many countries do not have ready access to the test. Glycohemoglobin is formed continuously in erythrocytes as the product of a non-enzymatic reaction between glucose and the hemoglobin protein, which carries oxygen. The binding of glucose to hemoglobin is highly stable; therefore, hemoglobin remains glycated for the life span of the erythrocyte; 123 ± 23 days. The HbA1c test is used to measure glycohemoglobin levels and provides an estimate of the average blood glucose level over the preceding 30 to 90-day period. Higher average blood glucose levels are reflected in higher HbA1c values. The normal HbA1c is <6%. HbA1c levels correlate well with the development of diabetic complications and may become established as a test for the diagnosis of diabetes at some time in the future. 
Diabetis mellitus and Periodontitis are polygenic disorders with some degree of immuno-regulatory dysfunction. Most of the connective tissue destruction-taking place in periodontal disease results from the interaction of bacteria and their products with mononuclear cells. One possible mechanism to explain as to why diabetics have more severe periodontal disease is that glucose-mediated advanced glycation end products (AGE) accumulation would affect migration and phagocytic activity of mononuclear and polymorphonuclear phagocytic cells resulting in establishment of more pathogenic sub-gingival flora. This triggers an infection-mediated pathway of cytokine regulation, especially with secretion of TNF-α and IL-l and a state of insulin resistance, affecting glucose utilizing pathways. Excessive local secretion of TNF-α and IL-l also mediates tissue destruction of connective tissue and alveolar bone evident in periodontal disease. 
Periodontitis may initiate or propagate insulin resistance in a manner similar to that of obesity, by enhancing activation of the overall systemic immune response initiated by cytokines. Proposed mechanism by which periodontal inflammatory mediators may contribute to the development of insulin resistance in individuals with both Type 2 diabetes and periodontitis.  The inflammatory mediators originating from periodontal sources can interact systemically with lipids, free fatty acids, and advanced glycation end products (AGES), all of which are characteristic of diabetes. 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, all of which are associated with insulin resistance. 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 periodontitis.  The pathogenesis of the 2 diseases is reviewed with an emphasis on common genetic and immune mechanisms. On the basis of overview, 2 hypotheses for testing the relationship in which the hyperglycemia and hyperlipidemia of diabetes result in metabolic alterations that may then exacerbate bacteria induced inflammatory periodontitis. The second hypothesis proposes that fortuitous combination of genes (gene sets) could result in a host who under the influence of a variety of environmental stressors, could develop either periodontitis or diabetes or both. 
Diabetes treatment aims to keep blood glucose within the recommended limits, and in this sense the presence of periodontitis affects blood glucose control.  The present study was carried out to evaluate the effect of nonsurgical periodontal treatment upon blood glucose control in Type 2 diabetics with periodontal disease.
| Materials and Methods|| |
The present study comprised a pre-post repeated measures analytical design. The study sample consisted of 20 patients: 12 males and eight females, with an age range of 42-81 years.
The inclusion criteria were: Type 2 diabetes mellitus, age over 18 years, the absence of cognitive impairment and previous periodontal treatment, willingness to undergo exploration and the required complementary tests, and the signing of informed consent.
We excluded patients receiving antibiotic treatment or who had received such treatment in the previous month, pregnant women, fully edentulous patients and Type 1 diabetics. Data collection and exploration of the oral cavity were carried out by the same dentist. In all cases a detailed case history was compiled, including patient age, sex, disease antecedents, type of diabetes, current treatment, duration of the disease in years, and associated systemic disorders. A clinical examination of the oral cavity was carried out, evaluating the condition of the oral mucosa, the Silness and Löe plaque index, and the community periodontal index (CPI). All patients were subjected for determination of glycosylated hemoglobin levels (HbA1c).
All 20 patients presented periodontal pockets in some of the explored sextants. In all cases nonsurgical periodontal treatment was carried out, with the extraction of those teeth showing excessive mobility or caries-induced destruction not amenable to conservative dental management.
Treatment was completed in several sessions, according to the needs of each individual patient, with an interval of 7 days between sessions. Calculus removal was carried out in a first session, and instructions were provided on correct tooth brushing and the use of interproximal brushes (Interprox; , Dentaid, Spain) and dental floss. In addition, 0.12% chlorhexidine digluconate rinses were prescribed (every 12 hours for 15 days).
Seven days after calculus removal, the scaling and root planing sessions were started in combination with ultrasound under local anesthesia (0.2% articaine), for a total of 1-4 sessions, depending on the number of affected quadrants. Whenever possible, 2 quadrants per session were completed. Following scaling and root planning, the periodontal pouches were irrigated with 0.12% clorhexidine digluconate using a fine-needled syringe.
Approximately 30 days after the last periodontal treatment session, clinical examination of the oral cavity was again carried out, evaluating the condition of the oral mucosa, the Silness and Lφe plaque index [Figure 1], CPI [Figure 2], and HbA1c [Figure 3] and [Figure 4].
|Figure 4: Samples ready for determination of glycosylated hemoglobin levels|
Click here to view
| Results|| |
Pre- and post-treatment comparisons of means were made with the Student t-test for paired data. All the patients who were diagnosed to have diabetes showed decrease in all the clinical findings. A statistically significant correlation P ≤ 0.0001) was found between HbA1c levels both at start and end of study.
[Table 1] shows mean values of CPI. On processing the scores of the CPI, a component of the community periodontal index of treatment needs (CPITN), as quantitative variables, a mean value of (2.0990 ± 0.1974) was obtained for maximum CPI (defined as the maximum CPI score obtained in any of the explored sextants in each case) at initial exploration. Following periodontal treatment, a significant decrease was observed (P ≤ 0.0001), since the mean maximum CPI after treatment was (1.4760 ± 0.1515).
[Table 2] shows mean values of PI. The initial mean plaque index was 1.9770 ± 0.1830, and was seen to decrease significantly to 1.3650 ± 0.1360 after periodontal treatment (P ≤ 0.0001).
[Table 3] shows mean values with reduction in HbA1c. The observed improvement from initial HbA1c (9.490 ± 0.491) to final HbA1c (8.990 ± 0.442) was 0.500 ± 0.066 and proved statistically significant (P ≤ 0.0001).
| Discussion|| |
Diabetes mellitus and periodontal disease are two highly prevalent chronic disorders. Although many studies have examined the bidirectional relationship between diabetes and oral disease, and the effects of periodontal treatment upon the metabolic control of diabetes, the great diversity of screening criteria, designs, durations of follow-up, types of patients or treatment protocols involved makes it difficult to establish comparisons. In effect, most studies show great variability in the duration of follow-up. HbA1c estimates the mean blood glucose levels in the previous 30-90 days. The period between initial HbA1c recorded on the first visit and final HbA1c recorded on the post-treatment control visit falls within this time interval, since according to the study protocol the first treatment varied between 3-5 weeks after the first visit, and 30 days after the last scaling and root planing session a control was programmed and the final HbA1c value was registered. Other authors such as Faria-Almeida, et al, Navarro, et al, and Grossi, et al, recorded final HbA1c 3 and 6 months after treatment, while Rodrigues, et al, Promsudthi, et al, and Cruz, et al, recorded this parameter 3 months after the initial HbA1c value. In turn, O΄Connell, et al, and Kiran, et al, obtained the value 3 months after treatment, while Al-Mubarak, et al, did so 2 months after therapy, Iwamoto, et al, one month after treatment, and Stewart, et al,  recorded final HbA1c 10 months after the initial or baseline HbA1c value. Grossi, et al, reported that effective control of periodontal infection in patients with diabetes may help reduce the level of advanced glycation in serum to normal levels.
As regards the observed significant differences in both the initial and final HbA1c values depending on the type of diabetes treatment received, we consider such differences to be logical, since patients, subjected only to dietary management and physical exercise, tend to be individuals that maintain good blood glucose control without the need for medication. In contrast, Type 2 diabetics treated with oral anti-diabetic drugs are not controlled or present HbA1c values that are not close to the levels indicating metabolic control of the disease, and moreover, tend to vary treatment and receive insulin therapy. However, the recorded improvement in HbA1c levels was independent of the type of treatment received for diabetes, and may be regarded as independent of the latter. The treatment provided in our patient series improved the clinical parameters, and thus also oral health. All the subjects had periodontitis at the start of the study.
The improvement between initial and final CPI score was statistically significant (P ≤ 0.0001), in the same way as the improvement between the initial and final plaque index value (P ≤ 0.0001). The hypothesis that HbA1c decreases after periodontal treatment in diabetic individuals with periodontitis has been the subject of many studies, with variable results.
In our series, there were statistically significant differences (P ≤ 0.0001) between the initial and final HbA1c values after the treatment was provided with a decrease in HbA1c level and thus improved metabolic control of blood glucose. Similar data in relation to reductions in HbA1c have been published by other authors, ,,,,,,,,, though many investigators have recorded no such differences in similar studies.
Among the trials reporting reductions in HbA1c, we have found studies that use antibiotics (fundamentally local minocycline or systemic doxycycline) together with periodontal treatment. ,,, Other authors such as Promsudthi, et al, who likewise used antibiotic treatment, failed to obtain satisfactory results.  In contrast, Rodrigues, et al, reported good results but in the group not administered antibiotics. The rest of the studies in the reviewed literature reporting such metabolic improvements did not use antibiotic treatment.
Thus, the role of antibiotics in reducing HbA1c does not seem quite clear, since similar results appear to be achieved with periodontal treatment in the absence of antibiotics. Nevertheless, most studies that use antibiotic treatment report significant results.
| Conclusions|| |
The following conclusions can be drawn from the present study:
- Following nonsurgical periodontal treatment, a decrease in HbA1c is observed, thus indicating improved blood glucose control in Type 2 diabetics.
- Improvement in the HbA1c levels is obtained regardless of the duration of the disease and the treatment provided for Type 2 diabetes mellitus.
- Improvement in the HbA1c levels of Type 2 diabetics after periodontal treatment is obtained regardless of the degree of periodontal involvement at baseline.
| References|| |
|1.||Santos Tunes R, Foss-Freitas MC, Nogueira-Filho Gda R. Impact of periodontitis on the diabetes-related inflammatory status. J Can Dent Assoc 2010;76:a35. |
|2.||Soskolne WA, Klinger A. The relationship between periodontal diseases and diabetes: An overview. Ann Periodontol 2001;6:91-8. |
|3.||Diaz RM. Diabetes and periodontal disease: A bidirectional relationship. Med Biol 2007;14:22-5. |
|4.||Li X, Kolltveit KM, Tronstad L, Olsen I. Systemic diseases caused by oral infection. Clin Microbiol Rev 2000;13:547-58. |
|5.||Malik. Periodontitis with diabetes mellitus. J Med Col Chandigarh 2011;1:11-8. |
|6.||Amar S, Han X. The impact of periodontal infection on systemic diseases. Med Sci Monit 2003;9:RA291-9. |
|7.||Teng YT, Taylor GW, Scannapieco F, Kinane DF, Curtis M, Beck JD, et al. Periodontal health and systemic disorders. J Can Dent Assoc 2002;68:188-92. |
|8.||Kinane D, Bouchard P; Group E of European Workshop on Periodontology. Periodontal diseases and health: Consensus Report of the Sixth European Workshop on Periodontology. J Clin Periodontol 2008;35(Suppl 8):333-7. |
|9.||Löe H. Periodontal disease. The sixth complication of diabetes mellitus. Diabetes Care 1993;16:329-34. |
|10.||Faria-Almeida R, Navarro A, Bascones A. Clinical and metabolic changes after conventional treatment of type 2 diabetic patients with chronic periodontitis. J Periodontol 2006;77:591-8. |
|11.||Navarro-Sanchez AB, Faria-Almeida R, Bascones-Martinez A. Effect of non-surgical periodontal therapy on clinical and immunological response and glycaemic control in type 2 diabetic patients with moderate periodontitis. J Clin Periodontol 2007;34:835-43. |
|12.||Grossi SG, Skrepcinski FB, DeCaro T, Robertson DC, Ho AW, Dunford RG, et al. Treatment of periodontal disease in diabetics reduces glycated hemoglobin. J Periodontol 1997;68:713-9. |
|13.||Rodrigues DC, Taba MJ, Novaes AB, Souza SL, Grisi MF. Effect of non-surgical periodontal therapy on glycemic control in patients with type 2 diabetes mellitus. J Periodontol 2003;74:1361-7. |
|14.||Promsudthi A, Pimapansri S, Deerochanawong C, Kanchanavasita W. The effect of periodontal therapy on uncontrolled type 2 diabetes mellitus in older subjects. Oral Dis 2005;11:293-8. |
|15.||da Cruz GA, de Toledo S, Sallum EA, Sallum AW, Ambrosano GM, de Cássia Orlandi Sardi J, et al. Clinical and laboratory evaluations of non-surgical periodontal treatment in subjects with diabetes mellitus. J Periodontol 2008;79:1150-7. |
|16.||O'Connell PA, Taba M, Nomizo A, Foss Freitas MC, Suaid FA, Uyemura SA, et al. Effects of periodontal therapy on glycemic control and inflammatory markers. J Periodontol 2008;79:774-83. |
|17.||Kiran M, Arpak N, Unsal E, Erdoðan MF. The effect of improved periodontal health on metabolic control in type 2 diabetes mellitus. J Clin Periodontol 2005;32:266-72. |
|18.||Al-Mubarak S, Ciancio S, Aljada A, Mohanty P, Ross C, Dandona P. Comparative evaluation of adjunctive oral irrigation in diabetics. J Clin Periodontol 2002;29:295-300. |
|19.||Iwamoto Y, Nishimura F, Nakagawa M, Sugimoto H, Shikata K, Makino H, et al. The effect of antimicrobial periodontal treatment on circulating tumor necrosis factor-alpha and glycated hemoglobin level in patients with type 2 diabetes. J Periodontol 2001;72:774-8. |
|20.||Stewart JE, Wager KA, Friedlander AH, Zadeh HH. The effect of periodontal treatment on glycemic control in patients with type 2 diabetes mellitus. J Clin Periodontol 2001;28:306-10. |
|21.||Schara R, Medvescek M, Skaleric U. Periodontal disease and diabetes metabolic control: A full-mouth disinfection approach. J Int Acad Periodontol 2006;8:61-6. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]