|Year : 2016 | Volume
| Issue : 1 | Page : 34-38
Effect of periodontal therapy on type 2 diabetes mellitus patients with chronic periodontitis with the evaluation of HbA1c
Manvi Chandra Agarwal, Krishna Kumar Chaubey, Ellora Madan, Swati Agarwal
Department of Periodontics, Kothiwal Dental College and Research Centre, Moradabad, Uttar Pradesh, India
|Date of Web Publication||12-Feb-2016|
Dr. Manvi Chandra Agarwal
AM-9, DeenDayal Nagar, Moradabad, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Context: In the recent years, a two-way correlation has been postulated between periodontitis and systemic conditions. One such condition is diabetes mellitus (DM). Several studies have demonstrated a close relationship between DM and chronic periodontitis. Aims: To assess the effect of periodontal therapy and scaling and root planing (SRP) on the metabolic control in type 2 DM patients with chronic periodontitis based on the estimation of glycated hemoglobin (HbA1c). Settings and Design: A prospective, comparative, clinical study was performed on 50 patients suffering from type 2 DM with moderate, generalized chronic periodontitis. The study period was 6 months. Type 2 moderately controlled diabetic patients with glycated hemoglobin values within the range of 6-8% were selected. Patients with major diabetic complications, history of any antibiotic intake or periodontal treatment within the last 4 months, and smoking habits were excluded. Materials and Methods: The parameters recorded were gingival index (GI), plaque index (PI), sulcus bleeding index (SBI), probing pocket depth (PPD), clinical attachment level (CAL), and glycated hemoglobin. The recordings were done at baseline and 6 months after scaling and root planing procedures. HbA1c was measured by NycoCard Reader. Statistical Analysis Used: Karl-Pearson coefficient test, Z-test, and paired t-test. Results: Reductions in all the clinical parameters were observed and were found to be statistically significant (P < 0.005). Conclusions: Scaling and root planing resulted in a statistically significant reduction in the clinical parameters and HbA1c. So, periodontal treatment should be included in the management of diabetic patients.
Keywords: Advanced glycation end-products (AGEs), diabetes mellitus (DM), glycated hemoglobin, inflammatory mediators, nonsurgical periodontal therapy
|How to cite this article:|
Agarwal MC, Chaubey KK, Madan E, Agarwal S. Effect of periodontal therapy on type 2 diabetes mellitus patients with chronic periodontitis with the evaluation of HbA1c. J Int Clin Dent Res Organ 2016;8:34-8
|How to cite this URL:|
Agarwal MC, Chaubey KK, Madan E, Agarwal S. Effect of periodontal therapy on type 2 diabetes mellitus patients with chronic periodontitis with the evaluation of HbA1c. J Int Clin Dent Res Organ [serial online] 2016 [cited 2019 Oct 22];8:34-8. Available from: http://www.jicdro.org/text.asp?2016/8/1/34/176248
| Introduction|| |
Periodontitis is a bacterial infection associated with Gram-negative anaerobes. Diabetes mellitus (DM) is a clinically and genetically heterogeneous group of metabolic disorders manifested by abnormally high levels of glucose in the blood due to a deficiency of insulin secretion or resistance to insulin action.  In the recent years, there has been an emerging interest in the link between the periodontitis and systemic conditions. ,
Studies have also suggested that periodontal disease could also induce insulin resistance and a worsening of metabolic control in diabetic patients.  Further, several biomarkers evaluate the development of diabetic periodontitis, i.e., HbA1c, tumor necrosis factor (TNF)-α, interleukin (IL)-1 β and IL-6. ,,,
So, in the present article the effect of periodontal treatment on type 2 diabetic patients was evaluated by the improvement in HbA1c.
| Materials and Methods|| |
A prospective, interventional, comparative, clinicobiochemical study was planned. Medical records that preoperative and postoperative to periodontal treatment were reviewed and data regarding HbA1c level, type of medications, and changes in medication or dosages were taken care of.
Fifty subjects with type 2 DM (HbA1c values 6-8%) within a period of 7 years with moderate generalized chronic periodontitis were recruited with their informed consent from the Outpatient Department of Periodontics. Approval was obtained from the Institutional Ethics and Review Board (IERB). Out of the 50 subjects, there were 31 (62%) males and 19 (38%) females. The ages of the subjects ranged from 40 years to 70 years. Males were within the range of 40-70 years with a mean age of 50.9 ± 0.94 years. Females were within the range of 46-61 years with a mean age of 51.9 ± 6.7 years. Among the males, the mean duration of diabetes was 3.3 ± 1.6 years and among females, it was 0.16 ± 1.74 years. Clinical diagnosis of moderate, generalized chronic periodontitis was made on the basis of ≤5 mm probing pocket depth in a minimum five teeth and clinical attachment loss of 3-4 mm in a minimum of eight teeth. The exclusion criteria included radiographic evidence of periapical pathology, current smokers, those who were on antibiotics for the last 4 months, physically or mentally disabled, pregnant, and patients with major diabetic complications such as retinopathy, nephropathy, cardiopathy, and cerebrovascular changes or who had undergone any periodontal treatment 4 months prior to the study.
Glucose control was determined by HbA1c, measured by NycoCard Reader (Axis-Shield, Norton, Massachusetts, USA) expressed in percentage. The patients underwent an initial examination: general medical history, radiographic examination, determinations of HbA1c and glucose in blood, periodontal examination, provision of information on periodontal disease and oral hygiene, and supragingival prophylaxis.
The clinical and biochemical parameters were recorded at the baseline (day 0) and 6 months after the periodontal therapy. To minimize the interexaminer and intraexaminer variability, calibration and standardization of the examiner were done. This was evaluated and calculated statistically till more than 90% similarity in their observations was achieved. The participants were instructed to continue with their medical management of DM without any modification during the study period.
Plaque index (PI) (Silness P and Loe H 1967) 
Gingival index (GI) (Loe H and Silness J 1963) 
Sulcus bleeding index (SBI) (Muhlemann HR and Son S 1971) 
Probing pocket depth (PPD) - The recordings were done on all the four sites (buccal, lingual, mesial, and distal) of each tooth. It was measured from the gingival margin to the base of the pocket using University of North Carolina (UNC)-15 probe. 
Clinical attachment level (CAL) - The recordings were done on all the four sites (buccal, lingual, mesial, and distal) of each tooth. It was measured from the cementoenamel junction (CEJ) to the base of the pocket using UNC-15 probe. 
For the metabolic assessment, 3-4 mL of venous blood sample was withdrawn and analyzed for: 
- Fasting blood glucose.
- Postprandial blood glucose.
- High density lipoproteins (HDLs) and low density lipoproteins (LDLs).
- Serum cholesterol.
- Serum triglyceride.
- Serum glutamate pyruvate transaminase (SGPT).
- Serum creatinine.
Test kit for the measurement of glycated hemoglobin (HbA1c) contains:
- Test device (TD): It is a plastic device containing a membrane filter.
- R 1 (Reagent 1): It is a glycinamide buffer containing zinc ions, dye bound boronic acid and detergents.
- R 2 (Reagent 2: washing solution)--It contains morpholine buffered sodium chloride (NaCl) solution and detergents.
The procedure for HbA1c measurement consisted of the following steps:
- 5 μl of whole blood was added to the test tube prefilled with R 1 . It was shaken well and left for a minimum of 2-3 min.
- The test tube was reshaken to obtain a homogeneous suspension and 25 ul of it was applied to a TD by holding the pipette approximately 0.5 cm above the TD and the mixture was allowed to soak completely into its membrane (approximately 10 s).
- 25 μl of R 2 was applied to the TD and it was allowed to soak completely into the membrane and left for minimum of 10 s.
- The calibration of the NycoCard Reader was done by placing its pen over the lid.
- The pen of the calibrated NycoCard Reader was finally placed over the TD to estimate its HbA1c.
All the participants received oral hygiene instructions before the first session of full-mouth scaling and root planing (SRP).  Bass method of brushing was instituted. The subjects were asked to repeat the procedure. Interdental brushing [Thermoseal Proxa brush, - International Compliance Professionals Association (ICPA), India] was also introduced and monitored. Required corrections were made till a satisfactory result was not observed.
The treatment period for scaling and root planing session was 1 week. There were four sessions and each session lasted for 1 h. The sessions were performed by the same investigator using an ultrasonic device (Satellec, Satellec Acteon Group, Gustave, Eiffel, France). Root planing was performed with Gracey curettes (Hu- Friedy Mfg. Co. LLC. 3232N, Rockwell St., Chicago, IL 60618, USA) using 12-14 strokes per site until a smooth, hard, and polished surface was obtained. These subjects were asked to visit at a 1-month interval to assess the efficiency of their oral hygiene methods and reinstructed, if required, during the follow-up of 6 months.
Any alteration in diabetes control or antibiotic use was recorded during their visits.
The comparison between values of all the clinical and metabolic parameters at the baseline and 6 months was done by Z-test.
The correlation between the mean values of all the clinical parameters PI, GI, SBI, PPD, and CAL with HbA1c at the baseline and 6 months was done by Karl Pearson coefficient test.
The correlation between the differences in mean values of PI, GI, SBI, PPD, and CAL with HbA1c from the baseline to 6 months was done by paired t-test.
| Results|| |
The result was as following:
- Changes of glycemic control associated with periodontal therapy: The mean HbA1c value at the baseline was 7.764 ± 0.9, which reduced to 7.032 ± 0.68 at 6 months. The difference in the mean values was 0.732. The mean percentage reduction in HbA1c values was 0.94%, which was statistically significant (P < 0.05).
- Changes in periodontal parameters and their correlation to changes in glycemic control following periodontal therapy.
Plaque index (PI): The mean plaque index was 1.8620 ± 0.3785 at the baseline, which declined to 1.2726 ± 0.2928 6 months after the periodontal therapy. The mean difference was 0.5894. The mean percentage reduction in PI was 31.65%, which was statistically significant (P < 0.05) [Table 1].
|Table 1: The comparison of different parameters between baseline and six months and their significance level |
Click here to view
The correlation between PI and HbA1c was r = 0.4101 at the baseline and it was statistically significant (P < 0.05) but it became statistically insignificant at the sixth month r = 0.3121; P > 0.05. The correlation between the differences in mean values of PI and HbA1c from the baseline to 6 months was statistically significant r = 0.6951, P < 0.05 [Table 2].
|Table 2: The correlation between differences in the mean values of different periodontal parameters with HbA1c (baseline and 6 months) |
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GI: Following the treatment, the GI dropped from 1.7628 ± 0.3050 at the baseline to 1.2364 ± 0.3731 after 6 months. The mean difference was 0.5264. The mean percentage reduction in the GI was 29.86%, which was statistically significant (P < 0.05) [Table 1]. There was a statistically insignificant correlation (P > 0.05) between GI and HbA1c both at the baseline r = 0.3927 and after 6 months, r = 0.2910. The correlation between the differences in mean value of GI and HbA1c from the baseline to 6 months was statistically significant [Table 2].
SBI: The mean percentage reduction was 66.65% at 6 months following the periodontal therapy, which was statistically significant (P < 0.05) [Table 1]. The correlation between the differences in mean values of SBI and HbA1c from the baseline to 6 months was statistically significant, r = 0.4722, P < 0.05 [Table 2].
PPD: The mean percentage reduction in PPD was 25.83% at 6 months after periodontal therapy, which was statistically significant (P < 0.05) [Table 1].
The correlation between differences in the mean values of PPD and HbA1c from the baseline to 6 months was statistically significant r = 0.6783; P < 0.05 [Table 2].
CAL: The significant (P < 0.05) mean percentage reduction in the CAL after 6 months of the periodontal therapy was 21.56% [Table 1]. The correlation between differences in mean values of CAL and HbA1c from the baseline to 6 months was statistically significant (P < 0.05) [Table 2].
| Discussion|| |
The intention of the study was to evaluate the effect of periodontal therapy on the metabolic control in patients with type 2 DM without any diabetic complications. To rule out such subjects, the parameters, i.e., serum creatinine, cholesterol, triglyceride, HDL, LDL, and SGPT were assessed.
The results of this study suggest that following periodontal therapy, there is a marked improvement in glycemic control in individuals with type 2 DM when the baseline and 6-month readings are compared.
The influence of diabetes on periodontal health and vice versa has been discussed widely in the dental literature. ,,,
Many biologically plausible mechanisms have been identified and reviewed to explain the pathobiology of the interactions between diabetes and periodontal disease.  In a sustained hyperglycemic state, proteins become irreversibly glycated to form advanced glycation end-products (AGEs). AGEs form on collagen, increasing collagen cross-linking, and result in the formation of highly stable collagen macromolecules. These products accumulate in the tissues due to their resistance to normal enzymatic degradation and tissue turnover. They activate a receptor known as "receptor for AGEs" (RAGE), which is found in the periodontium. The AGE-RAGE interaction on monocytes increases cellular oxidant stress and activates the transcription factor, nuclear factor kappa β, which alters the phenotype of the monocyte/macrophage and results in the increased production of proinflammatory cytokines such as IL-1 β and TNF-α. These proinflammatory cytokines contribute to the pathogenesis of periodontal diseases and probably play a major role in patients with diabetes, especially when the glycemic control is poor. ,,
The authors proposed that chronic Gram-negative infections of periodontal origin alter the endocrinologic-metabolic status, leading to difficulty in controlling blood sugar and increased insulin resistance, hence complicating the metabolic control of diabetes. ,
A more direct influence regarding the effects of periodontal infection on glycemic control in diabetes comes from the treatment studies. There is evidence to support that periodontal infection has an adverse effect on glycemic control as assessed with the periodontal treatment. ,
After treatment, there were improvements in all of the monitored clinical parameters. These improvements were reflected at the systemic level by alterations in serum inflammatory markers and as verified in previous studies, a reduction in HbA1c.
Analysis of data showed the mean reduction in PI, GI, and SBI [Table 1], which was in accordance with the studies by Christgau, Patricia et al., Ricardo FA et al., and Kiran et al.,,, Rodrigues et al. and Kiran et al. , found in their studies PI reductions of 30-34%, GI reductions of 19-25% and BOP reductions of 63-65%.
In this study, 25.83% reduction in PPD was observed at 6 months following the periodontal therapy [Table 1], which corroborated with the findings of the study by Rodrigues et al.,
The mean percentage reduction in CAL was also statistically significant (P < 0.05). It was in conformity with the findings of studies by Ricardo et al. and Navarro-Sanchez et al. ,
This clinical trial provided evidence that elimination of periodontal infection and reduction of periodontal inflammation significantly (P < 0.05) reduced the HbA1c level, thus improving diabetic metabolic control.
The mean percentage reduction in HbA1c was statistically significant (P < 0.05) in the present study. Other studies by Navarro-Sanchez et al., Ricardo et al., Rodrigues et al., Patricia et al., Stewart et al., and Grossi et al. also reported a significant reduction in HbA1c level. ,,,
The tests for correlation between the clinical parameters and the HbA1c levels showed a positive correlation. At 6 months, there was an obvious reduction in the periodontal parameters and when correlation coefficient was evaluated, a significant correlation (P < 0.05) was observed with SBI [Table 2]. A strong significant correlation (P < 0.05) was found when differences in the mean values of periodontal parameters were correlated with HbA1c. This is in consistence with the study by Lim LP et al., who have also found a positive correlation between these periodontal parameters and HbA1c.
The periodontal tissues are highly vascular. During inflammation, this vascularity is further increased, the inflammatory cytokines such as TNF-α, IL-1, IL-6, and inflammatory mediators have been found to have important effects on glucose and lipid metabolism. ,, With the reduction in the severity of the periodontal parameters, there was a decrease in inflammation and hence, a reduction in the metabolic parameter (HbA1c) was also observed in the individuals.
- One of the limitations of the study was that it did not include a control group of diabetic subjects who were not given any periodontal treatment though this would have been unethical.
- Another limiting factor was the small sample size (n = 50).
| Conclusion|| |
The data in the current study have been interpreted to suggest that periodontal therapy is associated with improvement in the periodontal status simultaneously with the improvement in the glycemic control in persons with type 2 DM.
The clinical improvement obtained was accompanied by a significant reduction in HbA1c values in type 2 DM patients, confirming the existing interrelationship between DM and periodontal disease. Therefore, periodontal treatment should be included in diabetes preventive measures.
Because of the limitations of the study, further studies are warranted to demonstrate an association between the periodontal treatment of diabetic patients and improvement in their metabolic control.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Stewart JE, KA Wager, AH Friedlander, Zadeh HH. The effect of periodontal treatment on glycemic control in patients with type 2 diabetes mellitus. J ClinPeriodontol 2001;28:306-10.
Persson RE, Hollender LG, MacEntee MI, Wyatt CC, Kiyak HA, Persson GR. Assessment of periodontal conditions and systemic disease in older subjects. J ClinPeriodontol 2003;30:207-13.
MonnierVM, Mustata GT, Blemel KL, Reihl O, Lederer MO, Zhenyu D, et al
. Cross-linking of the extracellular matrix by the maillard reaction in aging and diabetes: An update on "a puzzle nearing resolution". Ann N Y AcadSci 2005;1043:533-44.
Takeda M, Ojima M, Yoshioka H, Inaba H, Kogo M, Shizukuishi S, et al
. Relationship of serum advanced glycation end products with deterioration of periodontitis in type 2 diabetes patients. J Periodontol 2006;77:15-20.
Drachman RH, Root RK, Wood WB Jr. Studies on the effect of experimental nonketotic diabetes mellitus on antibacterial defense. I. Demonstration of a defect in phagocytosis. J Exp Med 1966;124:227-40.
Pickup JC, Crook MA. Is type II diabetes mellitus a disease of the innate immune system? Diabetologia 1998;41:1241-8.
Williams RC, Offenbacher S. Periodontal medicine: The emergence of a new branch of periodontology. Periodontol 2000 2000;23:9-12.
Genco RJ. Current view of risk factors for periodontal diseases. J Periodontol 1996;67(Suppl):1041-9.
Spolsky V. The epidemiology of gingival and periodontal disease.In: Carranza FA, editor. Glickman′s Clinical Periodontology. 7 th
ed. W.B.Saunders company, Harcourt Brace Jovanovich, Inc., The Curtis Centre, Independence Square West, Philadelphia, PA 19106:1990. p. 302-29.
Kiran M, Arpak N, Unsal E, Erdoğan MF. The effect of improved periodontal health on metabolic control in type 2 diabetes mellitus. J ClinPeriodontol 2005;32:266-72.
Emrich LJ, Shlossman M, Genco RJ. Periodontal disease in non-insulin dependent diabetes mellitus. J Periodontol1991;62:123-31.
Bridges RB, Anderson JW, Saxe SR, Gregory K, Bridges SR. Periodontal status of diabetic and non-diabetic men: Effects of smoking, glycemic control, and socioeconomic factors. J Periodontol 1996;67:1185-92.
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.
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-alphaand glycated hemoglobinlevel in patients with type2 diabetes. J Periodontol 2001;72:774-8.
Grover HS, Luthra S. Molecular mechanisms involved in the bidirectional relationship between diabetes mellitus and periodontal disease. J Indian SocPeriodontol 2013;17:292-301.
Mealey BL, Oates TW; American Academy of Periodontology. Diabetes mellitus and periodontal diseases. J Periodontol 2006;77:1289-303.
Oliver RC, Tervonen T. Diabetes - A risk factor for periodontitis in adults? J Periodontol 1994;65(Suppl):530-8.
Grossi SG, Genco RJ. Periodontal disease and diabetes mellitus: A two-way relationship. Ann Periodontol 1998;3:51-61.
Preshaw PM,Alba AL,Herrera D,Jepsen S,Konstantinidis A,Makrilakis K,et al
. Periodontitis and diabetes: A two-way relationship. Diabetologia 2012;55:21-31.
Smith GT, Greenbaum CJ, Johnson BD, Persson GR. Short-term responses to periodontal therapy in insulin-dependent diabetic patients. J Periodontol 1996;67:794-802.
Christgau M, Palitzsch KD, Schmalz G, Kreiner U, Frenzel S. Healing response to non-surgical periodontal therapy in patients with diabetes mellitus: Clinical, microbiological, and immunological results. J ClinPeriodontol 1998;25:112-24.
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.
Rodrigues DC, Taba MJ, Novaes AB, Souza SL, Grisi MF. Effects of non-surgical periodontal therapy on glycemic control in patients with type 2 diabetes mellitus. J Periodontol 2003;74:1361-7.
Quirynen M, Teughels W, Haake SK, Newman MG. Microbiology of periodontal diseases. In: Newman MG, Takei CH, Klokkevold PR, Carranza FA, editors. Clinical Periodontology. 10 th
ed. St. Louis, Missouri 63146:Elsevier; 2007. p. 134-69.
Lim LP, Tay FB, Sum CF, Thai AC. Relationship between markers of metabolic control and inflammation on severity of periodontal disease in patients with diabetes mellitus. J ClinPeriodontol 2007;34:118-23.
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.
Lösche W, Karapetow F, Pohl A, Pohl C, Kocher T. Plasma lipid and blood glucose levels in patients with destructive periodontal disease. J ClinPeriodontol 2000;27:537-41.
Grossi SG, Skrepcinski FB, DeCaro T, Robertson DC, Ho AW, Dunford RG, et al
. Treatment of periodontal disease in diabetics reduces glycatedhemoglobin. J Periodontol 1997;68:713-9.
Demmer RT, Desvarieux M, Holtfreter B, Jacobs DR Jr, Wallaschofski H, Nauck M, et al
. Periodontal status and A1C changes: Longitudinal results from the study of Health in Pomerania (SHIP). Diabetes Care 2010;33:1037-43.
[Table 1], [Table 2]