|Year : 2014 | Volume
| Issue : 5 | Page : 37-42
Periodontal health in type 2 diabetics
T Radhika1, K Ranganathan2
1 Faculty of Dental Sciences, Sri Ramachandra University and Hospital, Porur, Chennai, Tamil Nadu, India
2 Department of Oral and Maxillofacial Pathology, Ragas Dental College, Uthandi, Chennai, Tamil Nadu, India
|Date of Web Publication||10-Mar-2014|
Department of Oral and Maxillofacial Pathology, Faculty of Dental Sciences, Sri Ramachandra University and Hospital, Porur, Chennai - 600 116, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Background: Periodontitis has been reported as the sixth complication of diabetes in addition to other microvascular and macrovascular complications. Prevention and management of periodontitis is an important component in the management of diabetes mellitus (DM) and physicians treating patients with DM should be alert to recognize the signs of severe periodontitis and refer patients for appropriate management. The aim of this study was to estimate and to compare the periodontal status in diabetics and non-diabetics.
Materials and Methods: A total of 150 adults, 100 with type 2 diabetes and 50 without diabetes (control subjects), aged 40-60 years, participated in the study. Diabetic status was determined by estimation of random non-fasting plasma glucose levels and glycosylated hemoglobin levels. Periodontal health was assessed by simplified-oral hygiene index (OHI-S), Loe and Silness gingival index (GI) and community periodontal index (CPI). The data were analyzed using Chi-square, Fisher exact test, analysis of variance and Kruskal-Wallis test.
Results: The mean GI, mean OHI and mean CPI score were significantly higher in diabetics than non-diabetics. However, mean OHI was similar in controlled diabetics and non-diabetics. Mean CPI score was significantly increased in controlled diabetics compared to uncontrolled diabetics.
Conclusion: Gingivitis, poor oral hygiene and periodontitis were more prevalent in diabetics compared to non-diabetics. Presence of poor periodontal health in diabetics, in spite of similar oral hygiene measures suggest the possibility of altered host response in periodontal tissues in these patients.
Keywords: Gingivitis, oral, periodontal disease, type 2 diabetes
|How to cite this article:|
Radhika T, Ranganathan K. Periodontal health in type 2 diabetics. J NTR Univ Health Sci 2014;3, Suppl S1:37-42
| Introduction|| |
"Diabetes mellitus (DM) is a complex syndrome of abnormal carbohydrate, fat and protein metabolism that results in acute and chronic complications due to the absolute or relative lack of insulin."  It is one of a number of highly prevalent metabolic disorders, that is predicted to afflict 300 million people globally by 2025 and at least 366 million people by 2030.  Diabetes, particularly type 2 diabetes, is a looming health issue constituting a huge global public health burden. 
The oral cavity harbors many infectious agents and also reflects the presence of systemic disease. Historically, many oral infections were thought to have effects limited to tissues of the oral cavity only. A change in paradigm has led to the view that the oral health significantly impacts systemic health in metabolic diseases such as DM. 
DM alters the cellular microenvironment in tissues that lead to a cascade of untoward effects collectively referred to as "diabetic complications" such as retinopathy, neuropathy, nephropathy and micro and macrovascular diseases.  Periodontal disease has been reported as the sixth most common systemic complication of diabetes.  Other oral complications include xerostomia, dental caries, candidal infection, burning mouth syndrome, lichen planus, odontogenic abscesses and impaired wound healing. 
When compared with healthy subjects, gingival and periodontal diseases are often reported to be more prevalent in both insulin and non-insulin dependent diabetic individuals. Periodontal disease and subsequent tooth loss not only affect the quality-of-life of a diabetic patient, but may have a significant impact on overall health by compromising a patient's ability to maintain a healthy diet and proper glycemic control.
The objective of the current study was to estimate and to compare the periodontal status in diabetics and non-diabetics.
| Materials and Methods|| |
Subjects and study design
The study population included diabetic patients (n = 100) attending the Department of Diabetology in a Voluntary Health Service center. 50 age-matched non-diabetics who attended a private hospital for routine dental treatment like oral prophylaxis and restorations, constituted the controls. Verbal consent was obtained from every individual participating in the study. Our study was approved by the Institutional Review Board.
The subjects were divided into three groups: Group I (controlled diabetics, n = 50) comprised of patients 40-60 years of age who were being treated for diabetes and had random non-fasting plasma glucose (RNFPG) values >120 mg/dL and ≤200 mg/dL, Group II (uncontrolled diabetics, n = 50) comprised of patients 40-60 years of age who were being treated for diabetes and had RNFPG values >200 mg/dL and Group III (non-diabetics, n = 50) comprised of non-diabetic patients, who were age-matched with Group I and II, with RNFPG ≥80 mg/dL and ≤120 mg/dL. Plasma glucose levels were performed twice: Once as a part of their routine follow-up and 1 week later.
Diagnostic criteria for diabetes
All the diabetic subjects in this study had been diagnosed and were being managed for diabetes at the Voluntary Health Service using established criteria.  For this study; 2 mL of peripheral venous blood was collected from every patient. RNFPG levels were measured using the glucose-oxidase method. Subjects with RNFPG ≥200 mg/dL were diagnosed as diabetics. Glycosylated hemoglobin (HbA 1 c) was also measured using the ion-exchange resin method, which further confirmed the level of glycemic control in the diabetic patients.
Oral examination protocol
The oral examination included the following: (1) Dental examination: recording of missing teeth, existing carious lesions and dental restorations, based on clinical observation using a dental mirror and explorer. (2) Periodontal examination was done using the simplified-oral hygiene index (OHI-S), Loe and Sillness gingival index (GI)  and community periodontal index (CPI).  Clinical history and all measurements were done by the first author.
In the simplified OHI, buccal surfaces of 16, 11, 26, 31 and lingual surfaces of 36 and 46 were examined using a dental explorer following which debris index and calculus index scores were determined. In GI, distal-facial papilla, mesial-facial papilla and the entire lingual gingival margin of 16, 12, 24, 36, 32 and 44 were examined using a periodontal pocket probe to assess the bleeding potential of the tissues. CPI was assessed using a specially designed lightweight CPI probe with a 0.5 mm ball tip with a black band between 3.5 and 5.5 mm and rings at 8.5 and 11.5 mm from the ball tip. Three indicators of periodontal status were used for this assessment namely gingival bleeding, calculus and periodontal pockets and the teeth examined were 17, 16, 11, 26, 27, 31, 36, 37, 46 and 47. The probe was used as a sensing instrument to determine the pocket depth and to detect sub gingival calculus and bleeding response. The highest score was recorded in the appropriate box. The extent of loss of attachment was also recorded.
Attachment loss was recorded on six surfaces of the index teeth namely mesiobuccal, mid-buccal, distobuccal, mesiolingual, mid-lingual, distolingual. The level of attachment was calculated as the distance between the base of pocket and the cemento-enamel junction.
Data entry, database management and all statistical calculations were performed with the aid of the Statistical Package for the Social Sciences (SPSS™ , version 11) software. Descriptive statistics were calculated for all variables. Differences in proportions were assessed using the Chi-square test or Fisher exact test. Differences in means between more than two groups were assessed using the analysis of variance and the Kruskal-Wallis test when the data was not normal by distribution. P ≤ 0.05 was considered to be statistically significant.
| Results|| |
The mean GI in Group I, Group II and Group III were 1.09 (±0.35), 1.91 (±0.66) and 0.73 (±0.29) respectively with a significant difference between the groups (P < 0.05 between I and II, I and III and II and III) indicating that gingivitis was more prevalent in diabetics compared with non-diabetics [Table 1], [Figure 1]. The mean OHI index in Group I, Group II and Group III were 1.47 (±0.73), 2.47 (±0.77) and 1.34 (±0.52) respectively with a significant difference between the groups (P < 0.05 between I and II, II and III and I and III) [Table 1], [Figure 2]. The mean CPI score in diabetics (Group I + Group II) and non-diabetics (Group III) were 1.19 (±0.67) and 0.22 (±0.22) respectively with a significant difference between the groups (P < 0.05) indicating that periodontitis was more prevalent in diabetics than non-diabetics [Table 1], [Figure 3]. However, mean CPI index was significantly higher in controlled diabetics than uncontrolled indicating that there was no relationship between the control of DM and periodontal disease.
|Table 1: Gingival index, ohi index and cpi score in the study population (n=150)|
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|Figure 1: Comparison of mean gingival index in the study population (N = 150) (CI: Confidence interval)|
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|Figure 2: Comparison of mean oral hygiene index in the study population (N = 150) (CI: Confidence interval)|
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|Figure 3: Comparison of mean community periodontal index score in the study population (N = 150). CI: Confidence interval, DM: Diabetes mellitus|
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Gingival condition of every patient was graded as mild, moderate and severe gingivitis based on the mean GI scores. In Group I, 56% (n = 28) had mild gingivitis, 44% (n = 22) had moderate gingivitis and none had severe gingivitis. In Group II, 12% (n = 6) had mild gingivitis, 54% (n = 27) had moderate gingivitis and 34% (n = 17) had severe gingivitis. In Group III 84, % (n = 42) had mild gingivitis, 16% (n = 8) had moderate gingivitis and none had severe gingivitis. There was a significant difference in the severity of gingivitis between the groups (P < 0.05 between I and II, I and III and II and III). Level of hygiene was assessed in each patient based on the mean OHI scores. Good hygiene was observed in 52% (n = 26), 45% (n = 2) and 54% (n = 27) in Group I, II and III respectively. Fair hygiene was observed in 44% (n = 22), 68% (n = 34) and 46% (n = 23) in Group I, II and III respectively whereas poor hygiene was observed in 4% (n = 2) and 28% (n = 14) in Groups I and II, whereas none had poor hygiene in Group III. There was a significant difference in the level of hygiene between the groups (P < 0.05) I and II, I and III and II and III. Presence of poor oral hygiene in diabetics compared to non-diabetics may be the cause of increased periodontitis as the individuals had similar oral hygiene habits. Percentage of people showing attachment loss ≥3 mm in one or more sites were 98 (n = 49), 92 (n = 46) and 70 (n = 35) in Group I, II and III respectively. There was a significant difference observed between Groups I and III and II and III (P < 0.05) but there was no significant difference between Groups I and II [P = 0.539; [Table 2], indicating similarity between controlled and uncontrolled DM.
|Table 2: Gingival condition, level of hygiene and % of people showing attachment loss ≥3 mm in 1 or more sites (n=150)|
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| Discussion|| |
DM and periodontitis are two distinct disease process, the pathogenesis of which involves both environmental and genetic factors. The biological association between these two diseases have been discussed in various studies and the various hypothesis include: (1) Microvascular alterations, (2) changes in components of gingival crevicular fluid, (3) changes in collagen metabolism, (4) altered host response, (5) altered subgingival flora, (6) genetic predisposition and (7) non-enzymatic glycation.  Hyperglycemia causes deposition of advanced glycation end products in the tissues, which transforms the macrophages into a destructive phenotype leading to uncontrolled release of pro-inflammatory cytokines. 
Graves et al. has suggested that dysregulation of tumor necrosis factor and the formation of advanced glycation products can potentiate inflammatory responses and induce apoptosis of fibroblasts and osteoblasts, which in turn contributes to limited repair of injured tissue, particularly when combined with other known defects in diabetic wound-healing.  Alterations in neutrophil function may also lead to an increased susceptibility to periodontal disease in diabetes.  The chronic inflammation in diabetes causes an elevation of serum proinflammatory cytokines (interleukin-1 β and tumor necrosis factor-α) and an acute phase proteins (C-reactive protein), which negatively influences the serum lipid profile by reducing high-density lipoprotein cholesterol and raising low-density lipoprotein cholesterol and triglycerides. This cascade of events reduces the capacity for tissue repair and thereby increases the susceptibility of periodontal tissues to break down in response to the biofilm plaque.  Furthermore, the increase in salivary glucose levels in diabetics as shown in studies by us and other investigators, ,, may predispose to altered oral flora thus aggravating the breakdown of periodontal tissues. Diabetes and periodontal disease are closely interrelated and represent a classic example for a systemic disease leading to oral infection and further exacerbation of the systemic disease once the oral infection is established. 
In the present study, the gingival condition, oral hygiene and periodontal condition were evaluated using GI, OHI and CPI respectively. In spite of similar oral hygiene habits, GI and OHI were significantly increased in diabetics compared to non-diabetics. This could be due to the fact that excess glucose enters into the oral cavity through saliva and gingival crevicular fluid in patients with marginal metabolic control and contributes to a sugar-rich biofilm, which enhances plaque growth in general as discussed above. Severe gingivitis was present only in uncontrolled diabetics and GI and OHI were significantly increased in Group II compared with Groups I and III, indicating that gingivitis and poor oral hygiene were more prevalent in uncontrolled diabetics.
The mean CPI score and percentage of people showing attachment loss greater than 3 mm in one or more sites were significantly increased in diabetics compared with non-diabetics indicating that periodontitis was more prevalent in diabetics than non-diabetics as reported in other studies. ,,,, A meta-analysis by Chαvarry et al. has proved that DM can be considered as a risk factor for periodontitis.  However, mean CPI score was significantly increased in controlled diabetics compared with non-diabetics indicating that there is no relationship between control of DM and periodontal disease as reported by Barnet et al.  Tervonen and Oliver have reported increased periodontal disease in poorly controlled diabetes over the long-term suggesting that destruction of periodontal tissues is more likely to occur during long periods of hyperglycemia.  Maintenance of good oral hygiene does ameliorate periodontal health in DM. However, it may not be sufficient by itself in averting gingivitis and periodontitis in uncontrolled DM.
Opinion is divided with respect to the role of periodontal infection on the glycemic control in DM. ,, Recent systematic reviews and meta-analyses have concluded that periodontal therapy aimed at promoting periodontal health improves glycemic control. Periodontal treatment seems to reduce glycated hemoglobin levels by about 0.4%.  Based on current literature it would be prudent to suggest that prevention and management of periodontitis may be the important component in the management of DM and that physicians treating patients with DM should be alert to recognize the signs of severe periodontitis and refer patients for appropriate management.
| Conclusion|| |
The findings of the present study, along with earlier studies associating periodontitis and diabetes suggest that periodontitis is a complication of type 2 DM. It is reasonable to suggest that an uncontrolled DM is a predictor of severe periodontal disease. Regular oral prophylaxis and/or antibiotic therapy with modification of oral hygiene practices including use of mouthwashes can reduce the severity of periodontal disease in diabetics. Patients who are unresponsive to traditional methods of mechanical debridement can be referred to medical professionals for assessment and management of diabetes as improper glycemic control may inhibit resolution of oral inflammation.
Therapeutic goals for management of periodontal disease and gingivitis in patients with diabetes must involve elimination of infection by appropriate periodontal therapy including regular oral prophylaxis, antibiotic therapy and maintenance of glycemic control.
| Acknowledgments|| |
The authors would like to thank all the staffs of Department of Oral and Maxillofacial Pathology, Ragas Dental College, Chennai for facilitating the study. I also thank Dr. N. Malathi, Professor and Head, Department of Oral and Maxillofacial Pathology, Sri Ramachandra Dental College, Chennai for encouraging me to publish my study. Manuscript was part of "First Euro-India International Conference" conducted by the Institute of Holistic Medical Sciences and Ayurveda- and Venen-Klinik, Austria at Kottayam, Kerala on 9-11 April, 2012.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2]