Indian Journal of Dental Research

ORIGINAL RESEARCH
Year
: 2010  |  Volume : 21  |  Issue : 1  |  Page : 20--22

The effect of smoking on gingival crevicular fluid levels of myeloperoxidase


Balwant Rai1, Jasdeep Kaur2, SC Anand3, Kuldeep Laller4,  
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

Correspondence Address:
Balwant Rai
Medical Imaging and Forensic Odontology Section, School of Dentistry, Rohtak, Haryana
India

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.



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;21:20-22


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 2021 Mar 7 ];21:20-22
Available from: https://www.ijdr.in/text.asp?2010/21/1/20/62803


Full Text

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



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



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 [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 [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.

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