| Evaluation of clinical and metabolic changes after non surgical periodontal treatment of type 2 diabetes mellitus patients: A clinico biochemical study. | |
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PMID: 21731253 Owner: NLM Status: PubMed-not-MEDLINE |
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AIM: To evaluate the clinical and metabolic changes following nonsurgical periodontal therapy of type-2 diabetic patients and nondiabetic patients. MATERIALS AND METHODS: Fifteen nondiabetics and fifteen type-2 diabetics with moderate to severe periodontitis were selected after meeting inclusion and exclusion criteria. Periodontal pocket probing was performed using a Williams graduated periodontal probe and comparisons of the clinical and biochemical parameters like plaque index, gingival index, probing depth, glycated hemoglobin, and lipid profile (total cholesterol, high density lipoprotein, low density lipoprotein, triglycerides and very low density lipoprotein) were done between and within two groups at baseline and 3 month. RESULTS: A correlation was observed between clinical and biochemical parameters between and within two groups at baseline and 3 month. The P value of diabetic group was<0.001 in all clinical parameters (plaque index PI, Gingival index GI, and Probing Pocket Depth PPD) in diabetic and nondiabetic group, showed statistically highly significant difference in GI, PI, PPD, <.01 in Glycated Hemoglobulin (HbAlc1) in test group and<0.05 in control group showed statistically significant difference. The P value of test group was >0.05 in Lipid profile (total cholesterol, low density lipoprotein, high density lipoprotein, serum triglyceride, very low density lipoprotein) that showed no significant difference and in control group<0.05 in total Cholesterol, high density lipoprotein and <0.01 in Low density lipoprotein, Very Low Density Lipoprotein, and Serum Triglyceride, respectively, showed statistically significant in Total cholesterol, Low density lipoprotein, Very Low Density Lipoprotein, and Serum Triglyceride, not significant in high density lipoprotein. The P value >0.05 showed no statistical significance of correlation between the test and control groups. CONCLUSION: Both groups of patients showed an improvement in clinical and metabolic parameters assessed at 3 months after nonsurgical periodontal therapy. |
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Authors:
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Praveen Kudva; Syeda Tawkhira Tabasum; Nidhi Garg |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of Indian Society of Periodontology Volume: 14 ISSN: 0975-1580 ISO Abbreviation: J Indian Soc Periodontol Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2011-07-06 Completed Date: 2011-07-14 Revised Date: 2011-08-01 |
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Nlm Unique ID: 101499342 Medline TA: J Indian Soc Periodontol Country: India |
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Languages: eng Pagination: 257-62 Citation Subset: - |
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Department of Periodontics, Jaipur Dental College, Dhand, Tehsil-Amer, Jaipur - 303 101, India. |
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Journal Information Journal ID (nlm-ta): J Indian Soc Periodontol Journal ID (publisher-id): JISP ISSN: 0972-124X ISSN: 0975-1580 Publisher: Medknow Publications & Media Pvt Ltd, India |
Article Information Copyright: © Journal of Indian Society of Periodontology open-access: Received Day: 04 Month: 6 Year: 2010 Accepted Day: 13 Month: 8 Year: 2010 Print publication date: Season: Oct-Dec Year: 2010 Volume: 14 Issue: 4 First Page: 257 Last Page: 262 ID: 3118078 PubMed Id: 21731253 Publisher Id: JISP-14-257 DOI: 10.4103/0972-124X.76933 |
| Evaluation of clinical and metabolic changes after non surgical periodontal treatment of type 2 diabetes mellitus patients: A clinico biochemical study | |
| Praveen Kudvaaff1 | |
| Syeda Tawkhira Tabasumaff1 | |
| Nidhi Gargaff1 | |
| Department of Periodontics, Jaipur Dental College, Dhand, Tehsil-Amer, Jaipur - 303 101, India |
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| Correspondence: Address for correspondence: Dr. Praveen Kudva, Department of Periodontics, Jaipur Dental College, Dhand, Tehsil -Amer, Jaipur - 303101, India hemprakudva@yahoo.com |
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Diabetes Mellitus, the most widespread infection of mankind, is a syndrome characterized by chronic hyperglycemia and disturbance of carbohydrate, fat, and protein metabolism associated with absolute or relative deficiencies in insulin secretion and/or insulin action.[1] Once regarded as a heterogenous group of disease characterized by a state of chronic hyperglycemia resulting from a diversity of environmental and genetics factors acting jointly. The underlying cause of diabetes mellitus is the defective production or action of insulin, a hormone that controls glucose, fat, and amino acid metabolism. Recent estimates indicate that there were 171 million people in the world with diabetes in the year 2000 and this number is projected to increase to reach 366 million by 2030.
Diabetes Mmellitus manifests in two forms- Diabetes mellitus type 1 and type 2. Predominant form of diabetes is type 2 accounting for 90% of all cases worldwide.
Type-1 (Insulin-dependent diabetes mellitus) is caused by a cell-mediated autoimmune destruction of the insulin-producing beta cells of the Islets of Langerhans in the pancreas, which results in insulin deficiency. Type 1 diabetes accounts for 5% to 10% of all cases of diabetes, and most often occurs in children and young adults. Type 2 (Noninsulin-dependent diabetes mellitus) is a complex disorder characterized by an increased resistance to insulin and /or impaired secretion of insulin.[2] Type 2 diabetes occurs with an equal frequency in men and women and most commonly in over weight individuals older than 40 years of age.[2]
Periodontal disease is an infection that affects the periodontium, the tissues that support the teeth. It is a bacterial infection caused by gram negative anaerobes, which populate the sub gingival plaque. These putative pathogens include Aggregatibacter actinomycetecomitans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus and Spirochetes. Gram-negative organisms specifically of the Bacteroides species may affect the endocrine metabolic status of the diabetic patient.[3]
Diabetes mellitus is characterized by clinical signs such as retinopathy, neuropathy, nephropathy, cardiovascular, and peripheral vascular disease. According to American Diabetes Association, in 1993, periodontal disease was the sixth complication of diabetes mellitus.[4] Prevalence of periodontal disease among individuals with inadequately controlled type-2 diabetes mellitus is generally higher than that of people free of systemic disorder. Scientific evidence of the effects of periodontal disease and diabetes has emerged lately. Various studies have correlated response to periodontal treatment in diabetic patients and its influence on their metabolic control.[5] The treatment of periodontitis or other infections of the oral cavity can improve glycemic control in diabetic patients.[5]
The present study aims to research the impact of improved periodontal health on the glycemic status of type 2 diabetic patients.
Patients reporting to OPD of Diabetic Care and Research Centre, Bikaner, were screened using biochemical investigation for their glycemic status. Out of 75 patients, 15 diabetic (type 2, diabetes) and 15 nondiabetic patients, age range between 40 and 60 years, with untreated moderate to severe periodontitis were selected for the study. The periodontal status was assessed having chronic generalized periodontitis with periodontal pockets of 5-7 mm.
Patients with any of the following conditions were excluded from the study:
- Patient requiring premedication
- Prophylactic drug regime
- Patient having systemic infection/diseases
- Patients with chronic smoking, alcoholism
- Pregnant or lactating women
The biochemical values for glycated hemoglobulin of selected patients were taken as baseline values.
Clinical parameters were recorded prior to the commencement of the study.
Clinical parameters assessed were:
- Plaque Index: by Silness and Loe., 1967
- Gingival Index: by Loe and Silness, 1963
- Probing Depth: measured by Williams graduated periodontal probe [Figure 1]
All clinical parameters were recorded in both groups: Test group (chronic generalized periodontitis and diabetic patients) and control group (chronic generalized periodontitis and systemically healthy). These values were taken as baseline values.
Full mouth scaling using ultrasonics followed by root planning using Gracey curettes was done for the test and control group in a single sitting. Patients were directed to report to OPD Diabetic Care and Research Centre, Bikaner after an interval of 3 months. Patient were re-evaluated for clinical parameters like Plaque Index, Gingival Index, Probing depth, and Biochemical investigation namely glycated hemoglobulin and Lipid profile [Figures 2 and 3].
Venous blood was collected from each subject in EDTA contained tubes. One tube was analyzed in a clinical chemical laboratory for Glycated hemoglobulin [Figure 4]. From another tube, plasma was prepared for Lipid profile (cholesterol, High density lipoprotein, Low density lipoprotein, triglycerides)[Figure 5].
NycoCard Reader II (For assessing Glycated Hemoglobin) [Figure 6] and Complete Chemistry Autoanalyzer (ChemWell 2910) were used for analyzing the Lipid Profile [Figure 7].
The results are given as mean and standard deviation values. To compare the two groups, t paired and t unpaired test was used.
The mean plaque index, Gingival index, Probing pocket depth scores for the test group, at baseline values were 1.51±0.44, 1.38± 0.38, 3.31± 1.54 and after 3 months the values were 0.79 ± 0.33, 0.73± 0.32, 1.69± 1.06, respectively. The mean changes in plaque index, Gingival index, and Probing pocket depth in the test group were 0.72± 0.37, 0.65± 0.27, 1.62± 0.79, which are highly significant, i.e., (P< 0. 001) [Tables 1 and 2].
The mean plaque index, Gingival index and Probing pocket depth scores for the Control group at base line values were 1.63± 0.46, 1.32± 0.20, 3.63± 1.61 and after 3 months the values were 0.85± 0.20, 0.58± 0.14, 1.78± 1.06, respectively. The mean changes in Plaque index, Gingival index, and Probing pocket depth in the control group were 0.88± 0.56, 0.74± 0.28, 1.85± 0.81, which are highly significant, i.e., P< 0. 001).
The mean glycated hemoglobin score for the test group at baseline values was 9.05± 1.81 and after 3 months the value was 8.57± 1.74, respectively. The mean change in glycated hemoglobin in the test group was 0.49± 0.54, which is significant, i.e., (P<0.01) [Table 3].
The mean glycated hemoglobin scores for the Control group at base line values was 6.57± 0.25 and after 3 months the values was 6.39± 0.23, respectively. The mean change in glycated hemoglobin in the control group was 0.18± 0.32, which is significant, i.e., (P< 0.05).
The mean total cholesterol scores, Low density Lipoprotein, Serum triglyceride, very Low density Lipoprotein for the test group at baseline values were 202.27±32.33, 124.04±37.47, 195.41±70.17, 39.22±13.96 and after 3 months the values were 196.53±35.54, 119.44±22.30, 186.23±55.81, 37.24±11.16, respectively. The mean change in total cholesterol, Low density Lipoprotein, Serum triglyceride, very Low density Lipoprotein the test group were 5.74±32., 514.60±30.35, 9.18±57.30, 1.98±11.42, which are not significant, i.e., (P> 0.05) [Tables 4 and 5].
The mean total cholesterol, low density lipoprotein, Serum triglyceride, very Low density Lipoprotein scores for the Control group, at base line values were 229.99±79.55, 128.63±39.97, 134.50±24.77, 27.86±4.11, and after 3 months the values were 207.83±54.08, 112.24±33.58, 123.38±27.93, 25.45±5.38, respectively. The mean change in total cholesterol, low density lipoprotein, Serum triglyceride, very Low density Lipoprotein in the control group were 22.16± 36.07, 16.39±17.21, 11.12±13.41, 2.41±3.09, which were significant, i.e., (P<0.05) (P<0.01) (P<0.01) (P<0.01).
The mean high density lipoprotein scores for the test group, at baseline values was 43.27±8.73 and after 3 months the values was 42.97±5.81, respectively. The mean change in high density lipoprotein in the test group was 0.30±9.76, which is not significant, i.e., (P>0.05). The mean high density lipoprotein scores for the Control group, at base line values was 67.97±0.14 and after 3 months the values was 59.31±23.32, respectively. The mean change in high density lipoprotein in the control group was 8.66±18.77, which is not significant, i.e., (P>0.05) [Tables 4 and 5].
When test and control group were compared for mean changes in plaque index, Gingival index and Probing pocket depth, Glycated Hemoglobulin, total cholesterol, High density lipoprotein, Low density lipoprotein, very low density lipoprotein, serum triglyceride there were no statistically significant difference observed (P>0.05).
The American diabetes association (ADA) recommends that screening for diabetes should start at the age of 45 years and be repeated every 3 years in persons without risk factors, and earlier and more often in those with risk factor for diabetes.
Two hypotheses for determining the relationship between periodontitis and diabetes mellitus exist. The first proposes a direct causal or modifying relationship in which the hyperglycemia and hyperlipidemia of diabetes result in metabolic alterations that may then exacerbate bacteria-induced inflammatory periodontitis.
The second proposes that a 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.[6]
The study associated between periodontal disease and diabetes mellitus was published by Faria Almeida, Navarro in 2006 that two way interrelationship between diabetes mellitus and periodontitis, with the former producing a greater severity of periodontal disease and the latter compromising blood glucose control in diabetes patients. Treatment of periodontitis in diabetic patients would lead to a reduction in the soluble mediators responsible for periodontal tissue destruction and would lessen the insulin resistance of the tissues.[5]
The mechanism associated with periodontitis found in diabetic patients is the accumulation of advanced glycation end products (AGEs), which would affect the migration and phagocytosis of polymorphonuclear and mononuclear cells, producing a subgingival flora with a predominance of gram negative anaerobes according to Grossi et al.[7] This would trigger the secretion of soluble mediators that facilitate connective tissue destruction and bone resorption and produce a state of insulin resistance in the tissues at the same time, the periodontal infection would also induce resistance to insulin in the tissues, which would contribute in turn to the accumulation of AGEs.[5]
The 3-months interval was chosen because glucose in blood is irreversibly bound to hemoglobulin. The glycated hemoglobulin indicates the glucose status during atleast half of the life of Red blood cells that is 30 to 90 days because the half life of blood cells is 120 days.[5]
Highly significant reduction in the plaque index scores, Gingival index, and Probing pocket depth was seen in both the control and test groups from baseline to 3 months. [Figures 8–10] These findings are in accordance with the results obtained in studies conducted by Bridges R et al.,[8] Kiran M et al.,[9] Guglielmo Campus et al.,[10] Mattout C et al.,[11] and Patricia A.A. O’Connell et al.,[12] These reductions in the scores can be attributed to scaling and root planning accompanied by diminution of inflammatory infiltrate and laying down of new collagen.[9]
The relationship between gingival status and metabolic parameters have been studied by numerous authors. Karjalainen and Knuutila 1996 evaluated the relation of gingival status with metabolic parameters. The study concluded that high vascularity of the inflamed tissue may serve as an endocrine like source for tumor necrosis factor α (TNF-α) and other inflammatory mediators, which have been showed to have important effects on glucose and lipid metabolism.[9]
The relationship between gingival status and metabolic parameters showed significant relation in both the test and control groups, which were in accordance with the results obtained in studies conducted by Iacopina and Cutler 2000, Loeshe et al. 2000,[9] but De Pommereau et al. 1992 found a negative correlation.[9]
Pocket probing depth is considered to be of pathognomic significance of periodontal disease.Thetest group showed highly significant reduction in the probing pocket depth at the third month when compared with the test group.These findings are similar to those of Morton AA et al[13] ,Bridges R et al[8] , Grossi SG et al[14] , Debora C et al[15] , Kiran M et al[9] , Ricardo Faria Almeida et al[5]
The mean reduction in glycated hemoglobin values was 0.49±0.54 for test group and control group was 0.18±0.32, which was found to be statistically significant [Figure 11].
Kiran M et al. (2005) focused diabetes as a risk factor for periodontal health and also provided evidence that periodontal infection adversely effects glycaemic control in diabetes patients. This lead to a hypothesis that successful management of periodontal infection will lead to a reduction of the local symptoms of the disease and control the glucose metabolism.[9]
The improvement in the glycated hemoglobulin values was observed due to the reduction in the gingival index. This was in accordance with the results of studies conducted by Grossi et al.[14] and Bridges RB et al.,[8] which indicates that diabetes significantly affects all measured clinical parameters of periodontal status. This is contradictory to the result obtained in the study done by Alpagot T et al.,[16] who found no correlation between glycated hemoglobulin levels and clinical measurements. Hence, results of the present study indicate that the systemic disease like diabetes mellitus predisposes to oral infection and once the infection is established, it exacerbates the systemic disease. The results obtained in this study strongly recommend maintaining good oral hygiene as well as prevention and control of periodontal disease to be made mandatory as part of diabetes control.
Notes
Source of Support: Nil
Conflict of Interest: None declared.
This study was supported by the Department of Periodontics of Jaipur Dental College.
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Figures
Tables
Comparison of mean values of various parameters (PI, GI, and PD) at baseline and at 3 months in diabetic patients
Comparison of mean values of various parameters (PI, GI, and PD) at baseline and at 3 months in non diabetic patients
Mean change±SD of HbAlc1 from baseline value to at 3 months in diabetic and non-diabetic patients
Article Categories:
Keywords: Glycated hemoglobulin (HbAlC1), lipid profile and non surgical periodontal therapy, type 2 diabetes. |
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