|Year : 2016 | Volume
| Issue : 2 | Page : 95-98
Effect of Non-surgical Periodontal Therapy on Glycosylated Haemoglobin Levels in Diabetics and Non-diabetic Healthy Controls with Periodontitis
Harnil Vaghani, Rupal Mehta, Khushboo Desai, Shilpa Duseja, Tanvi Mehta
Department of Periodontology, Karnavati School of Dentistry, Gandhinagar, Gujarat, India
|Date of Web Publication||12-Sep-2016|
Department of Periodontology, Karnavati School of Dentistry, Gandhinagar, Gujarat
Source of Support: None, Conflict of Interest: None
Aim: The aim of this study was to compare the glycosylated haemoglobin (HbA1c) levels in healthy patients and patients with periodontitis, before and after non-surgical periodontal therapy. Materials and Methods: A total of sixty patients were selected and divided into two groups. Group A included thirty patients without periodontitis and Group B included thirty patients with periodontitis. Body mass index and clinical parameters, including oral hygiene index-simplified (OHI-S), gingival index (GI), probing pocket depth (PPD), clinical attachment level and HbA1c levels, of all patients were recorded at baseline. Both group patients received non-surgical, periodontal therapy (scaling and root planing). After 3 months, all the patients were re-examined for clinical parameters, and HbA1c levels were evaluated and compared with the baseline values. Results: There were no significant differences in clinical parameters after 3 months when compared to baseline levels of OHI-S, GI, PPD and HbA1c in Group A. There was no clinical attachment loss in Group A, either at the baseline or after 3 months. At the end of 3 months, Group B showed improvement in all the clinical parameters, and their HbA1c levels also significantly decreased although the values never reached those of the healthy controls. Conclusion: The HbA1c levels of patients with periodontitis (Group B) were significantly reduced after 3 months of non-surgical periodontal therapy, although they never reached the same level as that of the patients without periodontitis (Group A).
Keywords: Diabetes, haemoglobin, periodontal therapy
|How to cite this article:|
Vaghani H, Mehta R, Desai K, Duseja S, Mehta T. Effect of Non-surgical Periodontal Therapy on Glycosylated Haemoglobin Levels in Diabetics and Non-diabetic Healthy Controls with Periodontitis. Adv Hum Biol 2016;6:95-8
|How to cite this URL:|
Vaghani H, Mehta R, Desai K, Duseja S, Mehta T. Effect of Non-surgical Periodontal Therapy on Glycosylated Haemoglobin Levels in Diabetics and Non-diabetic Healthy Controls with Periodontitis. Adv Hum Biol [serial online] 2016 [cited 2020 Feb 26];6:95-8. Available from: http://www.aihbonline.com/text.asp?2016/6/2/95/190313
| Introduction|| |
Diabetes mellitus is a highly prevalent chronic disease affecting approximately 4% of the population, almost half of those being unaware of the condition. Diabetes has widely described oral complications and also increased incidence and severity of periodontitis. In India, there are 62.4 million people with type 2 diabetes and 77 million people with pre-diabetes. Periodontal diseases are one of the most prevalent oral diseases, affecting more than 50% of the Indian population.
Periodontitis is the inflammation of the periodontium resulting in clinical attachment loss, alveolar bone loss and periodontal pockets. Chronic periodontitis is a slowly progressing disease process that may occur continuously or in bursts of activity. Histological features of periodontitis are the junctional epithelium more apical to the cementoenamel junction, loss of collagen fibres subjacent to the pocket epithelium, bone loss, numerous neutrophils (polymorphonuclear cells and dense inflammatory cell infiltrate with plasma cells, lymphocytes and macrophages. Tissue damage in chronic periodontitis is the result of major inflammatory and immunopathologic components activated by the host response.
Löe in 1993 described periodontal disease as the sixth complication of diabetes, after diabetic nephropathy, neuropathy, retinopathy, vascular disease and delayed healing. Research has been conducted on the relationship between diabetes and periodontal disease since the 1960s; these studies reported that there was at least 2-fold increase in the risk of periodontal disease in diabetics, when compared with healthy controls.,,
In periodontitis, the production of pro-inflammatory mediators such as tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1 β, interferon gamma (IF-γ) and C-reactive protein (CRP) is increased. All these mediators can cause insulin resistance and also alter the lipid and glucose metabolism. Thus, periodontal infection can adversely affect glycaemic control in diabetics.
Glycosylated haemoglobin (HbA1c) forms by irreversible binding of glucose to haemoglobin through non-enzymatic reaction. HbA1c levels reflect glycaemic control over the previous 1–3 months because it is based on the average life span of an erythrocyte. Wolff et al. found an association between periodontitis and HbA1c in non-diabetic adults, although a clear-cut association could not be established. We include non-diabetic patients with periodontitis and healthy controls without periodontitis, and evaluate the effects of non-surgical, periodontal therapy on HbA1c levels.
Thus, the aim of this study was to compare HbA1c levels in non-diabetic, healthy controls and patients with periodontitis, before and after non-surgical periodontal therapy and to assess the relationship between periodontitis and HbA1c levels in non-diabetic patients.
| Materials and Methods|| |
The study was conducted in the Department of Periodontics, Karnavati School of Dentistry, Gujarat, India. The study was approved by the Ethical Committee of the Karnavati School of Dentistry, India. All participants were between ≥35- and ≤65-year-old and had not been diagnosed with diabetes. They should have at least a presence of twenty natural teeth. Patients with a history of diabetes mellitus or other systemic illness, pregnancy, lactation; history of antibiotic use or periodontal treatment within the past 6 months; patients with haemolytic anaemia and recent significant blood loss, smokers and alcoholics were excluded from the study. Patients who fulfilled the inclusion/exclusion criteria were invited to participate in the study.
They were divided into two groups. Group A consisted of thirty patients without periodontitis and Group B consisted of thirty patients with periodontitis. Group A patients had no bleeding upon probing, no probing pocket depth (PPD) >3 mm and no clinical attachment loss whereas Group B patients had PPD ≥5 mm and clinical attachment loss >3 mm in five or more teeth.
Body mass indexes (BMIs) and clinical parameters, including oral hygiene index-simplified (OHI-S), gingival index (GI), PPD, clinical attachment level (CAL) and HbA1c levels, of all the patients were recorded. All the patients received non-surgical, periodontal therapy (scaling and root planing). After the scaling and root planing (SRP) sessions, all the patients received oral hygiene instructions for home care (tooth brushing technique and interdental cleaning). After 3 months, all the patients were re-examined, and clinical parameters and HbA1c levels were evaluated and compared with the baseline values.
Mean BMI, PPD, CAL, GI, OHI-S and HbA1c were calculated per group. The ANOVA test was used to test correlations of BMI with HbA1c levels. Intra-group comparisons of parameters at the baseline and at the end of 3 months were performed using paired t-tests. The results were considered statistically significant at P < 0.05.
| Results|| |
Group A comprised thirty patients with a mean BMI of 20.24 ± 3.1 kg/m 2. Group B comprised thirty patients with a mean BMI of 26.59 ± 1.7 kg/m 2. There was no correlation between BMI with HbA1c levels.
In Group A, at the end of 3 months after SRP, there was no statistically significant difference in OHI-S, GI, PPD and HbA1c levels. Group A had no clinical attachment loss at the end of 3 months after SRP [Table 1].
In Group B, at the end of 3 months after SRP, there were statistically significant reductions in OHI-S, GI, PPD, CAL and HbA1c levels. Group A had no clinical attachment loss at the end of 3 months after SRP. The CAL of Group B decreased to 5.90 ± 1.45 mm at the end of 3 months after SRP [Table 2].
The HbA1c level of Group A at baseline was 5.62 ± 0.24% which reduced to 5.54 ± 0.25% at the end of 3 months after SRP, while that of Group B was 6.17 ± 0.22 at baseline, which reduced to 5.64 ± 0.05%. As compared to baseline, the difference in the HbA1c levels was less after 3 months, but it was statistically significant [Figure 1]. This indicated that even though there was a significant decrease in HbA1c levels in patients with periodontitis after SRP, the values never reached those of the healthy controls.
|Figure 1: Comparison of glycosylated haemoglobin (%) between Group A and Group B at baseline and 3 months.|
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| Discussion|| |
Periodontitis is a complex multi-factorial disease, and diabetes mellitus is a complex metabolic syndrome. Periodontal disease is considered as a sixth complication that seems to be a risk factor for incident diabetes.
The present study compares the levels of HbA1c in healthy patients and patients with periodontitis, before and after non-surgical periodontal therapy. Chronic exposure of haemoglobin to blood glucose is reflected by HbA1c, and it is not affected by any fluctuation of blood glucose on the day of assay. Therefore, in this study, it was decided to measure HbA1c levels. It reflects data on glucose in the blood over a period of time, ranging from 30 to 90 days. Hence, to detect any change in HbA1c level, re-examination was performed after 3 months of SRP.
There was no correlation of age and BMI with HbA1c levels indicated by the results. Therefore, the possibility of difference in the HbA1c levels of the two groups could be due to the difference in their periodontal status.
Wolff et al. showed that in non-diabetic patients, periodontitis is associated with a slight elevation in HbA1c. In their study, sample size was higher (59 cases and 53 controls) with age limit ≥18 years. The present study contained patients with age limit of ≥35 and ≤65 years, which was more appropriate because the prevalence of chronic periodontitis is more in patients >35 years of age. In the present study, the non-diabetic status of the participants was determined based on their clinical history and also on their fasting blood sugar (FBS) levels. Patients with a FBS level <110 mg/dl were included in the study. The limitation of measurement of FBS alone cannot be useful to rule out diabetes, as well-controlled diabetics can also have normal FBS levels. Ion-exchange, high-performance liquid chromatography was used to measure HbA1c levels in laboratory. HbA1c levels were measured at baseline and after non-surgical periodontal therapy. Smokers were excluded from the study.
Many studies found higher HbA1c levels in non-diabetics with periodontitis compared to periodontally healthy non-diabetics. However, these studies did not evaluate the effect of periodontal therapy on the HbA1c levels.,,
In the present study, there was no significant change in the GI, OHI-S, PPD and HbA1c levels of participants without periodontitis (Group A) after SRP. In contrast to this, there were significant reductions in the GI, OHI-S, PPD and CAL levels of patients with periodontitis (Group B) after SRP. These findings are similar to a study done by Obeid which showed the effectiveness of SRP in improving the periodontal status of patients with periodontitis. In non-diabetics with periodontitis (Group B), there was a significant reduction in HbA1c levels after SRP. These results suggested that the reduction in the HbA1c levels in Group B after 3 months could be due to an improvement in their periodontal status brought about by SRP.
The exact mechanism of association between periodontitis/periodontal inflammation and HbA1c levels is still not clearly known. Non-enzymatic glycosylation of haemoglobin results from hyperglycaemia which occurs due to insulin resistance or low insulin levels that induce inflammation and impede wound healing.
The pro-inflammatory cytokines such as TNF-α, IL1-β, IL-6 and IF-γ are produced by inflamed periodontium. The insulin resistance caused by these pro-inflammatory cytokines interferes with glucose and lipid metabolism, also resulting in decreased insulin production by causing apoptotic cell death of pancreatic β cells, thereby leading to a vicious cycle. Non-surgical, periodontal therapy decreases serum levels of these pro-inflammatory mediators. Thus, SRP will control the inflammation and also insulin resistance and thus, decrease the systemic level of sugar and the non-enzymatic glycosylation of haemoglobin. In our study, the significant reduction in all clinical parameters indicates that periodontal inflammation was reduced after SRP, and thus HbA1c levels were also reduced.
Aldridge et al. reported a significant improvement in periodontal parameters after SRP but did not found any improvement in HbA1c levels in 22 patients with type 1 diabetes and severe periodontitis.
Grossi et al. demonstrated that topical antimicrobial and systemic doxycycline along with mechanical therapy (100 mg/day for 14 days) resulted in a significant gain in attachment level and a reduction of almost 1% in the levels of HbAlc at 3 months after treatment. This may be due to their antimicrobial and host modulation effects, as well as their inhibition of non-enzymatic glycosylation. It suggests that once the diabetic state is established, the conventional periodontal therapy alone cannot achieve a significant improvement in glycaemic control. Because in this study only non-diabetic participants were included, SRP alone was able to produce a significant reduction in the HbA1c levels of patients with periodontitis, although the level could not be brought down to that of healthy controls.
Zhang et al. reported an association between HbA1c and subsequent diabetes risk. In patients with HbA1c values of 5.5 to <6.0% and 6.0 to <6.5%, the risk of developing diabetes was 21% and 44%, respectively. According to the American Diabetes Association, individuals with HbA1c levels ranging from 5.7% to 6.4% are pre-diabetic, with an increased risk for future diabetes  and should be informed about the risk of developing diabetes and counselled about effective strategies to lower their risks.
In this study, the mean HbA1c level of non-diabetic patients with periodontitis (Group B) at the baseline was 6.08 ± 0.23%, which was in the pre-diabetic range compared to non-diabetic participants without periodontitis (Group A), whose mean HbA1c level at the baseline was 5.38 ± 0.22%. Three months after SRP, the mean HbA1c level of non-diabetic patients with periodontitis (Group B) was 5.6 ± 0.33%, which indicated that periodontal therapy improved their glycaemic status.
The results of this study could improve the awareness among medical practitioners and the general public regarding the importance of maintaining good oral health for good systemic health. It can motivate other investigators to conduct studies with longer follow-up periods to evaluate the effect of other forms of periodontal therapy, such as local drug delivery and surgical periodontal therapy, on the HbA1c levels of non-diabetic patients with periodontitis.
The limitations of the study were small sample size and only FBS was measured to confirm the non-diabetic status of participants. In addition, serum and/or GCF levels of pro-inflammatory mediators such as TNF-α, IL-1 β, IL-6 and CRP were not measured. This study also failed to adjust for confounding factors such as race/ethnicity. Thus, there is a need for more randomised controlled clinical trials with larger sample sizes, long-term follow-ups and with strict adjustments for confounding factors, such as age, gender, BMI, race/ethnicity and smoking status to confirm the findings of this study and it should also correlate serum and/or GCF levels of various pro-inflammatory mediators with HbA1c levels.
| Conclusion|| |
The HbA1c levels of patients with periodontitis (Group B) were significantly reduced after 3 months of non-surgical periodontal therapy, although they never reached the same level as that of the patients without periodontitis (Group A). There is a need of more studies with larger sample size and long-term follow-up period.
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Conflicts of interest
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[Table 1], [Table 2]