Shahida Maqsood*, Masood Anwar Qureshi**, Maqsood Ahmed Soomro***
How to CITE:
J Pak Dent Assoc 2010;19(4): 203-207.
OBJECTIVE:
The aim of this study was to determine the relationship between periodontal pocket depth (PD) and status of diabetes mellitus (DM) in type 2 diabetic patient.
METHODOLOGY:
The periodontal status was measured by using the Community Periodontal Index of Treatment Needs (CPITN) and condition of diabetes mellitus status was measured by determining glycated haemoglobin (HbA1c), fasting blood glucose level (FBGL) at the base line before giving any treatment and after three months of receiving periodontal therapy .
RESULT:
The results showed that the periodontal disease severity was high among diabetic subjects. The mean CPITN score was compared with mean blood glucose level and the severity of periodontal disease. There was a steady increase in blood glucose level with increase in CPITN scores, corresponded with HbA1c and FBGL among diabetic subjects.
CONCLUSION:
Poor glycemic control is a major risk factor related with periodontal disease, non surgical periodontal treatment shows improved glycemic control in type 2 diabetes.
KEYWORDS:
Periodontal disease, diabetes mellitus, blood glucose level, glycated haemoglobin (HbA1c), oral hygiene.
Introduction
It is necessary to improve the quality of life of diabetic patients and to prevent or minimize the complications such as retinopathy, nephropathy, neuropathy, fatigue, weakness, memory loss, cardiovascular disease, and need for amputations, tooth loss and periodontal infection.1There is a strong link between the overgrowth of mostly anaerobic bacterial group and continuous destruction of periodontal tissues that occur as a result of the host inflammatory response against these bacteria and from the release of toxic products from the pathogenic plaque bacteria.2 together with the Inflammation which has proved a critical player in the association of Diabetes Mellitus DM and periodontitis 3Periodontitis regarded as a chronic localized oral infection that triggers a systemic as well as local host immune-inflammatory response and that can be a source of bacteraemia, because of the large epithelial surface with ulcerated periodontal pockets 4The mechanisms of the interaction between DM and periodontitis comprise strong inflammatory response characterized by a large secretion ofinflammatiatory mediators, mainly pro-inflammatory cytokines, which can have both local (periodontal destruction) and systemic (impaired glycaemic control) effects. 5
Process of destruction leading to the change of the gingival sulcus into an infected periodontal pocket play a very important role in the progression of periodontal disease, but the exact mechanisms in this degeneration process has not been recognized up till now.6 A pocket depth of 6 mm might be an indicator for destructive periodontal disease. Increased risk for tooth loss is related with pocket depth values of 6 mm or higher.7 Scaling in periodontal pockets less than 3 mm was reported to result in attachment loss, whereas the same treatment in pockets deeper than 4 mm resulted in attachment gain. The inadequacy of this therapeutic definition of destructive periodontal disease is that no evidence exists about the short-term changes in the attachment level related to clinically relevant outcomes such as tooth loss8. The Laminins represent large molecular glycoprotein’s a major mechanism of the basement membrane having multiple functional and structural roles including cell migration, adhesion and proliferation.7 Cell migration is an important part of several physiological and pathogenic processes including chronic inflammatory conditions, tumor invasion, and wound healing.9 Recent evidence suggests that chronic sub clinical inflammation plays an intermediary role in the pathogenesis of type 2 diabetes10 , 11.High levels of inflammatory markers, such as C-reactive protein (CRP) and interleukin-6 (IL-6), have been reported as important risk indicators of type 2 diabetes11. Many studies show that the periodontitis is common among diabetic patients and becomes worse with the progression of diabetes. Type 2 patients are more likely to have deep periodontal pockets and loss of teeth than non-diabetic controlled group 12 receiving periodontal treatment with doxycycline has reduced the depth of periodontal pocket with the reduction of P. gingivalis, present in the pockets and also reduces hemoglobin A1C (HbA1c) after 3 months. 13 As the HbA1C test provides an estimate of the average glucose level over the 30-90 days , it does not account for short-term fluctuations in plasma glucose levels.14 These Studies have indicated that treating periodontitis in diabetic patients has a beneficial effect on their glucose control 15 Current research is paying attention on best possible ways of delivering non-surgical periodontal therapy but comparatively very little is known about patient factors that affect the variability in outcome of this important treatment modality16.
Methodology
An interventional non probability purposive study was performed on one hundred four patients of type 2 diabetes belonging to middle socio economic group. Both males and female, who agreed to be the part of study suffering from Type 2 diabetes were included in this study. This study was carried out in the outpatient department of Periodontology, Fatima Jinnah Dental College and Hospital Karachi from Feb 07-Feb 09; The examination / data collection was carried out by the first author herself. The age of patients ranged between 25 to 65 years. The subjects were informed about the study and consent was obtained from each patient before the start of clinical examination. A standardized evaluation form was used for all the patients recording personal data, medical history and oral history
Clinical parameters:
At base line and after three months blood sample was taken for assesing the blood glucose level by HbA1c (well controlled metabolism 4.5-7.0% ) usingFast ion-Exchange resin Separation Method and fasting blood sugar ( > 126 mg/dl. )17 screened using a glucometer (ACCU CHEK, Advantage system/Sensor Comfort Strips, Roche Diagnostics, Mannheim, Germany)18. Periodontal status was assessed using the Community Periodontal Index of Treatment Needs (CPITN) to measure the four units of the gingiva (mesial, buccal, distal and lingual) corresponding to each tooth present in the mouth. We measured the distance from the gingival margin to the base of the periodontal pocket on the four surfaces of each tooth19,20.
The periodontal conditions was scored as follows:
- Code 1 was given to a sextant with no pockets, calculus or overhangs of fillings but in which bleeding occured after gentle probing in one or several gingival units.
- Code 2 was assigned to a sextant if there were no pockets exceeding 3 mm, but in which dental calculus and plaque retaining factors were seen or recognized subgingivally.
- Code 3 was given to a sextant that harbors 4-5 mm deep pockets.
- Code 4 was given to a sextant that harbors pockets 6 mm deep or more.
After the clinical data was obtained, scaling was done with ultrasonic scaler in all the patients, and systemic doxycycline100mg/day for 14 days was prescribed. Moreover patients were taught the tooth brushing technique and they were told to use a chlorhexidine mouthwash for ten days along with oral hygiene instructions. The patient were advised to strictly control their diet and use their medication .The study was completed in three months/ pre and post treatment records were collected. For each patient the blood test were conducted in the same laboratory to standardize the results and minimize the errors in two measurements of pre and post records. Similarly the data collected on clinical examination was standardized by keeping the same operator. All the data collected was tabulated and analyzed using SPSS v 13. (paired test was used to determine the significance difference)
Results
The periodontal status, level of FBGL and HbA1c at base line and after three months is shown in the table1. The group statistics obtained for the entire variable (Table 1) indicates mean values with the Std. Deviation. The result were highly significant (P<.005) difference in Fasting Blood Sugar Levels, and significant results (P<.o5) of Gingival Pocket depth and HbA1c
Discussion
DM is a complex metabolic syndrome and in the same manner periodontitis is multifactorial disease which has long been identified as a complicating factor in the periodontal therapy by the periodontist. Current research is paying attention on best possible ways of delivering non-surgical periodontal therapy to improve the periodontal pocket depth as well as improves the glycemic level of type 2 diabetic patients . In our study the patient sample was relatively small.
The results of this study recommend that following periodontal therapy, there was a marked improvement in glycemic control in individuals with type 2 DM when compared to pre treatment results as compared to post treatment results of same patients .Our results clearly demonstrate that mechanical periodontal treatment combined with systemic doxycycline, 100 mg day) once for 14 days, improved periodontal status of uncontrolled type 2 diabetic patients. In the present study, periodontal treatment was accompanied by a significant reduction in HbA1C levels in the type 2 diabetic subjects after 3 months . The determination of glucose in plasma or urine shows the level at the specific time of the sampling but this value can change within a few minutes due to various factors, including diet, physical activity or because of medication.21 for the reason that this parameter is not an appropriate indicator of long term metabolic control and the HbA1C test provides an estimate of the average glucose level over the 30-90 days preceding the test. It does not account for short-term fluctuations in plasma glucose levels 22 . The main finding of this study was the improved periodontal status of type 2 diabetic subjects accompanied by a significant improvement in their metabolic control. Many studies performed in near past give support to our study as one study on type 2 diabetic patients with chronic periodontitis receiving mechanical debridement plus amoxicillin/clavulanic acid for two months, compared with a group receiving only mechanical debridement showed a marked improvement in all periodontal variables. A significant reduction in HbA1C was only (p 0.05) in the later group, indicating a less-favorable response in the group receiving adjunctive treatment with systemic antibiotic.23
Whereas in another study the effect of prophylaxis , localized scaling and root planning with systemic antibiotic therapy on periodontal health and glycemic controlled group of subjects with diabetes whose periodontal status was similar but received no treatment. After treatment the subjects experienced a 50% reduction in the prevalence of gingival bleeding. This was accompanied by a statistically significant improvement in glycemic control, with a reduction in the mean HbA1C value of 0.8% (baseline, 7.3%; follow-up, 6.5%). The untreated control group experienced no change in gingival bleeding or glycemic control.24 A controlled clinical trial performed consisting of thirteen Japanese patients with type 2 DM found a significant reduction in the plasma HbA1C levels (mean reduction of 0.8%)25. Recently a meta analysis of interventional studies may lead to conclude that periodontal therapy may improve glycemic control, their meta analysis provided a mean standard deviation for HbA1c of 1.71 in a poorly controlled diabetic patients they find a significant ( 0.79%) reduction in HbA1c values.26 Another study was performed in Thailand and they found PD reduction and clinical attachment gain of the treatment group were 29.19 and 11.17% respectively. The magnitude of pocket depth reduction and clinical attachment gain found in their study (0.94 and 0.45 mm,respectively). 27 where as our results showed paired mean 0.1850 with standard deviation of 0.78117. PD reduction, HbA1c and FBGL significantly improved within three months. The results of the present study suggested that, without periodontal treatment, uncontrolled older diabetics were at risk of rapidly losing their periodontally-affected teeth. At baseline, the subjects had higher mean pocket depth, HbA1c and FBGL. After three months of receiving periodontal therapy, it results with 0.279 mean difference of pocket depth. This high significance suggest that periodontal therapy, consisting of non-surgical mechanical therapy with accompanied by adjunctive systemic antibiotics in subjects, showed improvement of glycemic control, as determined by HbA1c levels .
As a result at the end of the study, some patients experienced little change in glycaemic control, whereas others experienced a major improvement. Thus, the variability in the HbA1C values observed at the end of the study, from little change to major improvement, may be attributable to differences in baseline HbA1C values.
Also meta-analysis of ten intervention trials in order to quantify the effects of periodontal treatment on HbA1C level among diabetic patients 28revealed possible causes for the discrepant reports and made recommendations for future studies.Recently a study shows an improvement in the clinical response was observed in both study groups at 3 and 6 months, with a reduction in the percentage of sites with plaque and bleeding, reduction in the percentage of periodontal pockets> 4 mm, reduction in probing depth and gain in clinical attachment level. with significant post-treatment reductions in all three biochemical variables( IL-1b, TNF and the volume of GCF ) studied. 29
Conclusion
Our results show that non-surgical periodontal treatment is associated with improved glycemic control in type 2 DM patients.
The result of present study verify that poor glycemic control is the most important risk factor related with periodontal health in conditions of increased Probing depths and more severe gingival inflammation in diabetic patients.
The findings emphasize a need to endorse oral health in patients with diabetes as an essential part of total patient care so prevention and control of periodontal disease must be considered an integral part of diabetes.
Considering our study population with moderate pocket depths, the effect on the metabolic control is a consequence of a decrease in gingivitis. This treatment could be undertaken along with the standard measures for the diabetic patient care.
Longitudinal studies are needed to assess the long-term treatment result in terms of oral health as well as the systemic implications
ACKNOWLEDGMENT:
We thanks to DR Asghar Mehdi, Dr Babur Ashraf and Dr Arsalah Raffat for their helpful advices and we are grateful to Dr Saima Ikram Butt, Dr Perveen Razaq for their enthusiastic participation in this study and their guidance for the subject.
References
1. Madden TE, Herriges B, Boyd L, Laughlin G, Chiodo GT, Rosenstein DI. Alterations in HbA1c following minimal or enhanced non-surgical, non-antibiotic treatment of gingivitis or mild periodontitis in type 2 diabetic patients: A pilot trial. J Contemp Dent Pract 2008; 5:9-16.
2. Krejci CB, Bissada NF. Periodontitis–the risks for its development. Gen Dent. 2000; 48:430-6; quiz 437-8 Review.
3. Mealy, b.L. & oates, T.w. Diabetes mellitus and periodontal diseases. J of Periodontol, 2006; 77, 1289-1303.
4. Ebersole, J. L. & Cappelli, D. Acute phase reactants in infections and inflammatory diseases. Periodontol ,2000; 23, 19-49.
5. Genco, R. J., Grossi, S. G., Ho, A., Nishimura, F. Murayama, Y. A proposed model linking inflammation to obesity, diabetes and periodontal infections. J of Periodontol, 2005;76, 20, 75-84.
6. Pöllänen MT, Salonen JI, Uitto VJ. Structure and function of the tooth-epithelial interface in health and disease. Periodontol 2003; 31:12-31.
7. Hujoel PP, Leroux BG, Selipsky H, White BA. Non-surgical periodontal therapy and tooth loss. A cohort study. J Periodontol 2000; 71: 736-742.
8. Hujoel PP. Endpoints in periodontal trials: the need for an evidence-based research approach. Periodontol 2004; 36: 196-204.
9. O’Toole EA. Extracellular matrix and keratinocyte migration. Clin Exp Dermatol 2001; 26: 525-30.
10. Festa A, D’Agostino R Jr, Howard G, Mykkänen L, Tracy RP, Haffner SM. Chronic sub clinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation 2000; 102: 42-47.
11. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. Creactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. J Am Med Assoc 2001; 286: 327-334.
12. Campus G, Salem A, Uzzau S, Baldoni E, Tonolo G. Diabetes and periodontal disease: a case-control study. J Periodontol 2005; 76: 418-425.
13. Grossi SG. Treatment of periodontal disease and control of diabetes: an assessment of the evidence and need for future research. Ann Periodontol 2001;
14. Rohlfing CL, Wiedmeyer HM, Little RR, England JD, Tennill A, Goldstein DE. Defining the relationship between plasma glucose and HbA1C: analysis of glucose profiles and HbA1C in the diabetes control and complications trial. Diabetes Care 2002; 25: 27578. 6: 138-145.
15. 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: 306-310.
16. Wennstro¨m JL, Tomasi C, Bertelle A, Dellasega E. Full-mouth ultrasonic debridement versus quadrant scaling and root planing as an initial approach in the treatment of chronic periodontitis. Journal of Clinical Periodontology 2005; 32: 851-859.
17. Kuzuya, T., Nakagawa, S., Satoh, J., Kanazawa, Y., Iwamoto, Y., Kobayashi, M., Nanjo, K., Sasaki, A., Seino, Y., Ito, c., shima, K., Nonaka, K., Kadowaki, T.; Committee of japan diabetes society on the diagnostic criyeria of diabetes mellitus. Report of the committee on the classification and diagnostic criteria of diabetes mellitus. Diabetes Re Clini Pract, (2002) 55, 65-85.
18. Pearson, S., Brolos, E.J., Herner, E.b., Hansen, B. olsen, B.S. Screening Copenhagen school children at risk of type 2 diabetes mellitus using random capillary blood glucose. Acta Paediatrica,(2008) 96, 885-889
19. Ainamo, J., Barmes, D., Beagrie, G., Cutress, T., Martin, J. & Sardo-Infirri, J. Development of the World Health Organization (WHO) community periodontal index of treatment needs (CPITN). Inte Dent J 1982, 32, 281-291
20. Benigeri, M., Brodeur, J.M., Payette, M., Charbonneau, A. Ismail, A.I. (2000). Community periodontal index of treatment needs and prevalence of periodontal conditions. Journal of Clinical Periodontology 2002. 27, 308-312.
21. Rees, T. D The diabetic dental patient. Dent Clini North Am 1994, 38, 447-463.)
22. (Rohlfing, Rohlfing, C. L., Wiedmeyer, H. M., Little, R. R., England, J. D., Tennill, A. & Goldstein, D. E. 2002
23. Rodrigues D, Taba M, Novaes A, Souza S, Grisi M. Effect of non-
surgical periodontal therapy on glycemic control in patients with type 2 diabetes mellitus. J of Periodontol 2003; 74: 1361-1367.
24. Kiran M, Arpak N, Unsal E, Erdogan MF. Effect of improved periodontal health on metabolic control in type 2 diabetes mellitus. J of Clini Periodontol 2005; 32: 266-272.
25. Iwamoto Y, Nishimura F, Nakagawa M et al. The effect of antimicrobial periodontal treatment on circulating TNF-a, and glycated hemoglobin level in patients with type 2 diabetes. Journal of Periodontology 2001; 72: 774-748.
26. L. Daree , J.-N. Vergnes ,P. Gourdy ,M . Sixou. Efficacy of periodontal treatment on glycemic control in diabetic patients: A meta analysis of interventional studies. J Sci direct. Diabetes & Metabolism 2008; 34 :497-506
27. A Promsudthi, S Pimapansri, C Deerochanawong, W Kanchanavasita The effect of periodontal therapy on uncontrolled type 2 diabetes mellitus in older subjects Oral Dis (2005) 11, 293-298
28. Janket SJ, Wightman A, Baird AE, Van Dyke TE, Jones JA. Does periodontal treatment improve glycemic control in diabetic patients? A meta-analysis of intervention studies. J Dent Res 2005; 84: 1154-1159.
29. Navarro-Sanchez AB, Faria-Almeida R, Bascones-Martinez A. Effect of non-surgical periodontal therapy on clinical and immunological response and glycaemic controlin type 2 diabetic patients with moderate periodontitis. J Clin Periodontol 2007; 34: 835-843.