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ORIGINAL RESEARCH Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 1  |  Page : 20-22
The effect of smoking on gingival crevicular fluid levels of myeloperoxidase


1 Medical Imaging and Forensic Odontology Section, School of Dentistry, Rohtak, Haryana, India
2 Oral Pathology and Maxillofacial Surgery, KU, Rohtak, Haryana, India
3 Ex. Principal, PGIMS, Rohtak, Haryana, India
4 Sham Lal Cardiology Centre, PGIMS, Rohtak, Haryana, India

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Date of Submission15-May-2008
Date of Decision28-Jan-2009
Date of Acceptance26-Jun-2009
Date of Web Publication27-Apr-2010
 

   Abstract 

Objectives : To compare the gingival crevicular fluid (GCF) myeloperoxidase (GM) levels in smokers and non-smokers.
Materials and methods : This study comprised 45 subjects: (a) 12 smokers with periodontitis, (b) 10 non-smokers with periodontitis, (c) 11 smokers with healthy periodontium, and (d) 12 non-smokers with healthy periodontium were recruited for the study and their GM levels were analyzed.
Results and conclusion : GM levels were significantly higher in smokers with periodontitis compared with others. Hence, more incidence of mutagenesis and cytotoxicity were noted at sites of inflammation mediated by GM in smokers compared with non-smokers.

Keywords: Non smoker, periodontitis, gingival crevicular fluid, myeloperoxidase

How to cite this article:
Rai B, Kaur J, Anand S C, Laller K. The effect of smoking on gingival crevicular fluid levels of myeloperoxidase. Indian J Dent Res 2010;21:20-2

How to cite this URL:
Rai B, Kaur J, Anand S C, Laller K. The effect of smoking on gingival crevicular fluid levels of myeloperoxidase. Indian J Dent Res [serial online] 2010 [cited 2014 Oct 31];21:20-2. Available from: http://www.ijdr.in/text.asp?2010/21/1/20/62803
Periodontitis is an infectious bacterial disease in which loss of attachment and bone of the tooth occurs. It has been reported that the pathogenesis of disease is mediated by the host response. [1] Biomarkers of periodontal activity may be obtained from potential proteolytic and hydrolytic enzymes of inflammatory cell origin. [2] It has also been observed that increased myeloperoxidase (MPO) activity that is present in azurophilic granules of polymorphonuclear neutrophils, in periodontitis as compared with controls. [3] Myeloperoxidase is considered a promising marker of periodontal inflammation. [4],[5] It was reported that MPO levels were higher as compared with normal healthy periodontal patients. [1],[2],[3],[4],[5],[6],[7],[8] The function to combat pathogenic oral bacteria may protect from infection; on the other hand, activated neutrophils promote cell destruction and MPO activity measurements have been used as predictors of periodontal disease severity. [3],[4] Apart from this dual role in the pathogenesis of periodontitis, MPO-generated oxidants are capable of oxidising a wide variety of compounds, among these are also products of tobacco smoke. Leukocytes are recruited in immune response, and therefore reactive intermediates from xenobiotics generated by leukocyte metabolism may play a role in idiosyncratic drug reactions. [5],[6] Various drugs, also arylamines and benz[a]pyrene from tobacco smoke are converted to cytotoxic products. The degranulation of these cells and also their hyperactive state in the presence of chronic antigenic stimulation may transform environmental precarcinogens to highly reactive intermediates, [7] as was shown for heterocyclic amine activation by MPO in fibroblasts and epithelial cells. [8] Moreover, MPO provides one pathway for mutagenesis and cytotoxicity at sites of inflammation. Thus, MPO activity may contribute to the smoke-related risk of periodontitis. Most of the increased MPO activity in periodontally diseased patients can be attributed to the increased number of neutrophils. [9] It has been reported that the correlations between calprotectin and gingival crevicular fluid (GCF) myeloperoxidase (GM) indicate that polymorphonuclear neutrophils are a major contributor to the calprotectin content in gingival crevicular fluid of severely affected sites by periodontal disease. [9] The levels of GM had positive correlation with the periodontal parameters and the similarity of the inflammatory response of tissues surrounding implants and natural teeth, and suggested that MPO could be promising marker of inflammation around dental implants. [10] Hence, the present study was planned to investigate effect of smoking on gingival crevicular fluid MPO.


   Materials and Methods Top


A total of 45 patients comprising 12 smokers with periodontitis, 10 non-smokers with periodontitis, 11 smokers and 12 non-smokers with healthy periodontium, without any systemic disease, aged 22-40 years attending Bhagwan Dental clinic, Jind and Jain Dental Clinic, New Delhi (India), were selected for study. This was a double-blind randomized study.

Inclusion criteria

  • Periodontitis in patients was defined as at least seven teeth having a probing depth of >5 m and demonstrable radiographic bone loss of >30% of tooth sites, by a full-mouth intraoral radiographic series.
  • All participants had chronic periodontitis who had not received any previous surgical therapy.
  • All subjects were systemically healthy, with no medical conditions that would affect their participation in the study.
  • Patients were classified as current smoker; that is, regular daily smokers of 18-20 cigarettes (with and without periodontitis), non-smokers, that is, who had never smoked tobacco.
Exclusion criteria

The exclusion criteria was a course of anti-inflammatory or antimicrobial therapy within the previous 3 months, a history of regular use of mouth washes, use of any vitamin supplementation or mucosal lesions, chemotherapy, radiation therapy or medications that cause xerostomia. Informed consent was obtained from all subjects.

Clinical measures of the severity of periodontal disease, such as bleeding on probing (BP), probing depth (PD) and loss of clinical attachment level (CL) were determined using a conventional periodontal probe (Hu-Friedy Chicago, IL) at six sites around each tooth mesiobuccal, midbuccal, distobuccal, mesiolingual, midlingual and distolingual, excluding third molars. The bleeding on probing (BP) was measured as done in our previous study. [16] The probe was directed parallel to the long axis of the tooth. Clinical measurements for loss of attachment were done from the cemento-enamel junction to bottom of the sulcus. For GCF collection, 1-4 sites per patients were randomly selected. The respective tooth was isolated with cotton after removing the supragingival plaque with curettes (avoiding contact with the gingival margin), and the crevicular area was dried. GCF was collected by inserting Periopaper strips in gingival pocket for 45 seconds and the volume was measured with the Periotron 6000. The strips contaminated by blood or saliva were discarded as done in our previous study. [13] MPO activity was analyzed as previous studies. [12] Relationships between GM, probing depths and bleeding on probing, were analyzed using a performed during statistical package for the social sciences (SPSS) (version 11.0, Chicago, USA).


   Results Top


The mean GM levels in non-smokers (D) and smokers (C) without periodontitis were 0.68 0.32 U/μl and 0.84 0.32 U/μl, respectively (P < 0.05), while in non-smokers periodontitis (B) and smokers periodontitis (A) were 1.02 0.24 U/μl and 1.18 0.29 U/μl, respectively. The mean clinical loss of attachment were 4.82 0.28, 2.80 0.22, 1.28 0.14 and 0.72 0.13 mm in smokers with periodontitis, non-smokers with periodontitis, healthy smokers and healthy non-smokers, respectively (P < 0.05), [Table 1]. The mean data on probing depth and bleeding on probing are presented in [Table 1].


   Discussion Top


In the present study, high levels of GCF myeloperoxidase were observed in periodontitis patients and the levels were still higher in smokers as compared with non-smokers [Table 1], (P < 0.05). Previous reports have shown a direct relationship between GCF myeloperoxidase and gingival inflammation and plaque. [4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23] The levels of GCF myeloperoxidase in smokers were higher as compared to non-smokers. The GM levels may be increased in smokers as compared with non-smokers due to antibacterial activity of GM, that is, smokers give more favorable environments for accelerated growth of the periodontal bacterial as compared with non-smokers. A positive correlation was noted between GCF myeloperoxidase and percentage of BP, CL and PD [Table 1] as in previous study. [7],[8],[11],[13] In the present study, smoker subjects with chronic periodontitis, smokers exhibited greater BP, PD and CL as compared with non-smokers [Table 1], (P < 0.05), which supported previous studies. [17],[18],[19],[20],[21],[22],[23] Although MPO is involved in the pathogenesis of inflammatory periodontal diseases, it is also found in clinically healthy sites in lower levels than the periodontal diseases sites. [5],[6],[7] To the best of our knowledge, there is no published study determining the effects of smoking on GM levels. Therefore, we could not compare the results of present study with any other previous results. High levels of GCF myeloperoxidase were observed in patients with periodontitis and levels were still higher in smokers as compared with non-smokers. Arylamines and benz[a]pyrene from tobacco smoke are converted to cytotoxic products. The degranulation of these cells and also their hyperactive state in the presence of chronic antigenic stimulation may transform environmental precarcinogens to highly reactive intermediates as it was shown for heterocyclic amine activation by MPO in fibroblasts and epithelial cells. Moreover, MPO provides one pathway for mutagenesis and cytotoxicity at sites of inflammation. [5] Hence, higher incidences of mutagenesis and cytotoxicity are observed at sites of inflammation mediated by GM in smokers as compared with non-smokers. GCF myeloperoxidase can be easily measured and may prove to be useful in identifying patients at risk of tooth loss because it is easy to measure and cost-effective in contrast to other markers. Hence, GCF myeloperoxidase analysis for periodontal diagnosis may prove a cost-effective method for screening large populations.

 
   References Top

1.van Dyke TE, Serhan CN. Resolution of inflammation: A new paradigm for the pathogenesis of periodontal diseases. J Dent Res 2003;82:82-90.  Back to cited text no. 1      
2.Eley BM, Cox SW. Advances in periodontal diagnosis. 8. Commercial diagnostic kits based on GCF proteolytic and hydrolytic enzyme levels. Br Dent J 1998;184:373-8.  Back to cited text no. 2      
3.Altman LC, Baker C, Fleckman P, Luchtel D, Oda D. Neutrophil-mediated damage to human gingival epithelial cells. J Periodontal Res 1992;27:70-9.  Back to cited text no. 3      
4.Hofstra AH, Uetrecht JP. Myeloperoxidase-mediated activation of xenobiotics by human leukocytes. Toxicology 1993;82:221-42.  Back to cited text no. 4      
5.Uetrecht JP, Shear NH, Zahid N. N-chlorination of sulfamethoxazole and dapsone by the myeloperoxidase system. Drug Metab Dispos 1993;21:830-4.  Back to cited text no. 5      
6.Trush MA, Seed JL, Kensler TW. An overview of the relationship between oxidative stress and chemical carcinogenesis. Free Radic Biol Med 1991;10:201-9.  Back to cited text no. 6      
7.Williams JA, Stone EM, Millar BC, Hewer A, Phillips DH. Pathways of heterocyclic amine activation in the breast: DNA adducts of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) formed by peroxidases and in human mammary epithelial cells and fibroblasts. Mutagenesis 2000;15:149-54  Back to cited text no. 7      
8.Cao CF, Smith QT. Crevicular fluid myeloperoxidase at healthy, gingivitis and periodontitis sites. J Clin Periodontol 1989;16:17-20.  Back to cited text no. 8      
9.Yamalik N, Caglayan F, Kilinc K, Kilin CA, Tumer C. The importance of data presentation regarding gingival crevicular fluid myeloperoxidase and elastase like activity in periodontal disease and health status. J Periodontol 2000;71:460-7.  Back to cited text no. 9      
10.Kaner D, Bernimoulin JP, Kleber BM, Heizmann WR, Friedmann A. Gingival crevicular fluid levels of calprotectin and myeloperoxidase during therapy for generalized aggressive periodontitis. J Periodontal Res 2006;41:132-9.  Back to cited text no. 10      
11.Tervahartiala T, Konttinen YT, INgman T, Hδyrinen-Immonen R, Ding Y, Sorsa T. Cathepsin G in gingival tissue and crevicular fluid in adult periodontitis. J Clin Periodontol 1996;23:68-75.  Back to cited text no. 11      
12.Suzuki K, Ota H, Sasagawa S, Sakatani T, Fujikura T. Assay method for myeloperoxidase in human polymorphonuclear leukocytes. Anal Biochem 1983;132:345-52.  Back to cited text no. 12      
13.Rai B, Kharb S, Jain R, Anand SC. Biomarkers of periodontitis in oral fluids. J Oral Sci 2008;50:53-6.  Back to cited text no. 13      
14.Kaner D, Bernimoulin JP, Kleber BM, Heizmann WR, Friedmann A. Gingival crevicular fluid levels of calprotectin and myeloperoxidase during therapy for generalized aggressive periodontitis. J Periodontal Res 2006;41:132-9.  Back to cited text no. 14      
15.Liskmann S, Zilmer M, Vihalemm T, Salum O, Fischer K. Correlation of peri-implant health and myeloperoxidase levels: A cross-sectional clinical study. Clin Oral Implants Res 2004;15:546-52.  Back to cited text no. 15      
16.Rai B, Jain R, Anand SC, Kharb S. 8- hydroxydeoxyguanosine levels: Peridontitis in smoker and non-smoker: A pilot study. J Pak Dent Assoc 2006;15:89-90.  Back to cited text no. 16      
17.Salvi GE, Lawrence HP, Offenbacher S, Beck JD. Influence of risk factors on the pathogenesis of periodontitis. Periodontol 2000 1997;14:173-201.  Back to cited text no. 17      
18.Savage SM, Donaldson LA, Cherian S, Chilukuri R, White VA, Sopori ML. Effects of cigarette smoke on the immune response II. Chronic exposure to cigarette smoke inhibits surface immunoglobulin-mediated responses in B cells. Toxicol Appl Pharmacol 1991;111:523-9.  Back to cited text no. 18      
19.Schenkein HA. Host responses in maintaining periodontal health and determining periodontal disease. Periodontol 2006;40:77-93.  Back to cited text no. 19      
20.Selby C, Drost E, Brown D, Howie S, MacNee W. Inhibition of neutrophil adherence and movement by acute cigarette smoke exposure. Exp Lung Res 1992;18:813-27.  Back to cited text no. 20      
21.Socransky SS, Haffajee AD. Periodontal microbial ecology. Periodontol 2005;38:135-87.  Back to cited text no. 21      
22.Sφder PO, Jin LJ, Sφder B, Wikner S. Periodontal status in an urban adult population in Sweden. Community Dent Oral Epidemiol 1994;22:106-11.  Back to cited text no. 22      
23.Solomon HA, Priore RL, Bross ID. Cigarette smoking and periodontal disease. J Am Dent Assoc 1968;77:1081-4.  Back to cited text no. 23      

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Correspondence Address:
Balwant Rai
Medical Imaging and Forensic Odontology Section, School of Dentistry, Rohtak, Haryana
India
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DOI: 10.4103/0970-9290.62803

PMID: 20427901

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