|
 
 |
| ORIGINAL ARTICLE |
|
| Year : 2021 | Volume
: 6
| Issue : 2 | Page : 72-76 |
|
Smoking and periodontal disease severity, probing pocket depth and bleeding on probing
J Suresh Babu1, C Swarnalatha1, Ritu Mathur2, Tayf Naif Radhi Alshammari1, Archana Meenakshi3, Asma Alavi4, Nashwa Alzaki Ali Bushara5, Yasser Riaz Malik5, Abhishek Singh Nayyar6
1 Division of Periodontology, Department of Preventive Dental Sciences, College of Dentistry, University of Ha'il, Ha'il, Kingdom of Saudi Arabia
2 Department of Periodontology and Implantology, Pacific Dental College and Research Center, Udaipur, Rajasthan, India
3 Department of Periodontology and Implantology, Ragas Dental College and Hospital, Chennai, Tamil Nadu, India
4 Consultant Daental Surgeon, Dammam, Kingdom of Saudi Arabia
5 Division of Dental Public Health, Department of Preventive Dental Sciences, College of Dentistry, University of Ha'il, Ha'il, Kingdom of Saudi Arabia
6 Department of Oral Medicine and Radiology, Saraswati Dhanwantari Dental College and Hospital and Post-graduate Research Institute, Parbhani, Maharashtra, India
| Date of Submission | 25-Apr-2021 |
| Date of Decision | 14-May-2021 |
| Date of Acceptance | 17-May-2021 |
| Date of Web Publication | 16-Jul-2021 |
Correspondence Address:
Dr. Abhishek Singh Nayyar
SD Dental College, NH 222, Pathri Road, Parbhani, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jncd.jncd_23_21
Background and Objective: The purpose of the present study was to investigate whether severity of disease process differed between smokers and nonsmokers and to study characteristic differences in pattern of periodontal disease in smokers in a group of known chronic periodontitis patients.
Materials and Methods: The study included 150 individuals in an age range of 35–60 years wherein periodontal evaluation including probing pocket depth (PPD) and bleeding on probing (BOP) was performed using Williams's periodontal probe. For both the parameters (PPD and BOP), mean scores were calculated from different quadrants of the oral cavity while the results obtained were subjected to statistical analysis.
Results: The mean percentage of sites that presented with BOP was higher for nonsmokers compared with smokers. Furthermore, smokers had more number of pockets and pockets with increased PPD. On analysis of buccal and lingual sides, also, it was observed that smokers had more number of sites with PPD of ≥5 mm than nonsmokers.
Conclusion: From the results, it could be concluded that smoking is associated with more severe periodontal attachment and bone loss and deeper periodontal pockets.
Keywords: Bleeding on probing, periodontal disease, probing pocket depth, smoking
How to cite this article:
Babu J S, Swarnalatha C, Mathur R, Radhi Alshammari TN, Meenakshi A, Alavi A, Ali Bushara NA, Malik YR, Nayyar AS. Smoking and periodontal disease severity, probing pocket depth and bleeding on probing. Int J Non-Commun Dis 2021;6:72-6 |
How to cite this URL:
Babu J S, Swarnalatha C, Mathur R, Radhi Alshammari TN, Meenakshi A, Alavi A, Ali Bushara NA, Malik YR, Nayyar AS. Smoking and periodontal disease severity, probing pocket depth and bleeding on probing. Int J Non-Commun Dis [serial online] 2021 [cited 2023 Mar 26];6:72-6. Available from: https://www.ijncd.org/text.asp?2021/6/2/72/321620 |
| Introduction | |  |
Periodontitis is the result of complex interrelationships between host factors and causative microorganisms with a plethora of risk factors modifying the expression of disease process.[1],[2],[3],[4] Among proposed risk factors, smoking has been found to be associated with an increased prevalence and severity of periodontal disease.[5],[6],[7],[8] There is, also, evidence in the literature that a disproportionately high number of people with severe periodontal disease were found to be chronic smokers, thus, implying a strong association between smoking and periodontal disease.[9],[10],[11] Furthermore, greater levels of alveolar bone loss, probing pocket depth (PPD), tooth mobility, and tooth loss have been seen in smokers than in nonsmokers.[12],[13],[14],[15] Several studies have, also, proposed a common observation that smokers, in general, have proportionately more periodontal pockets in anterior than posterior regions than nonsmokers.[16],[17],[18] The purpose of the present study was to investigate whether severity of disease process differed between smokers and nonsmokers and to study characteristic differences in pattern of periodontal disease in smokers in a group of known chronic periodontitis patients.
| Materials and Methods | | |
The present study was designed as a cross-sectional, hospital-based study to assess association between smoking and periodontal disease severity and to investigate whether disease severity differed between smokers and nonsmokers in a group of chronic periodontitis patients by assessing PPD and bleeding on probing (BOP). The study included 150 individuals, 75 smokers, and 75 nonsmokers, in an age range of 35–60 years while individuals recruited in smoker group included individuals who smoked ≥10 cigarettes a day for ≥10 years. Inclusion criteria for the study included patients who were in good systemic health with chronic generalized periodontitis characterized by ≥5 mm pocket depth while patients having past dental history of oral prophylaxis in the past 6 months, patients who had taken antibiotics in the past 3 months, patients with a history of any form of systemic disease including cardiovascular diseases, diabetes mellitus, blood disorders, renal and hepatic disorders, and pregnant and lactating females were excluded from the study. The individuals were recruited based on the simple randomization process while the need for the study was explained to all the participants and a written, informed consent was obtained before their inclusion into the study. Furthermore, approval was obtained from Institutional Ethics Committee before the start of the study through letter approval no. SDDC/IEC/07-37-2018. A detailed history was taken for each participant followed by clinical examination performed as per protocol of Universal Precautions with the help of diagnostic instruments under artificial illumination. The findings were recorded in a specially designed proforma while periodontal evaluation including PPD and BOP was performed on all four quadrants and at six sites per tooth using Williams's periodontal probe. The PPD was measured from the gingival margin to the base of the pocket and BOP recorded as either present or, absent when provocation with the probe was done.[19],[20] For both the parameters (PPD and BOP), mean scores were calculated from different quadrants of the oral cavity while the results obtained were subjected to statistical analysis.
Statistical analysis
Statistical analysis was done using SPSS version 18.0 (SPSS Inc., Chicago, IL, USA). For both the parameters (PPD and BOP), mean scores were calculated considering distribution in relation to the upper and lower jaw, and buccal and lingual sites in anterior, premolar, and molar regions while comparisons were made using z-test (two-tailed test). P <0.05 was considered statistically significant.
| Results | | |
[Table 1] reveals comparison of nonsmokers and smokers in relation to mean age, number of teeth and sites affected, and at different levels of PPD wherein it was observed that mean age, mean number of teeth, and mean percentage of sites affected did not differ significantly between the smokers and nonsmokers, though, mean percentage of sites that presented with BOP was higher for nonsmokers compared with smokers. Furthermore, smokers had more number of pockets and pockets with increased PPD of 4–7 mm than nonsmokers. No significant difference, though, was detected in the prevalence of pockets with ≥8 mm PPD. [Table 2] reveals comparison of nonsmokers and smokers in relation to different levels of PPD in anterior, premolar, and molar regions wherein it was observed that at all sites, pockets with PPD of 6–7 mm were significantly more in smokers than nonsmokers. Overall, differences in the prevalence of pockets at PPD of ≥5 mm at all sites including anterior, premolar, and molar regions between smokers and nonsmokers were found to be statistically significant (P < 0.05) [Table 3]. Similarly, [Table 4] reveals comparison of nonsmokers and smokers at PPD of ≥5 mm in relation to the upper and lower jaw, and buccal and lingual sites in anterior, premolar, and molar regions while [Table 5] reveals comparison of nonsmokers and smokers at PPD of ≥5 mm in relation to the upper and lower jaw in terms of involvement of buccal and lingual sites in anterior, premolar and molar regions wherein statistically significant differences were observed at various sites in relation to both upper and lower jaw, and buccal and lingual sites in anterior, premolar and molar regions (P < 0.05). In relation to the upper jaw, 48% of sites in smokers while only 37% of sites in nonsmokers exhibited pockets with PPD of ≥5 mm. On analysis of buccal and lingual sides, also, it was observed that smokers had more number of sites with PPD of ≥5 mm than nonsmokers. The data, also, revealed that largest difference was found in relation to the upper jaw in anterior and premolar regions between smokers and nonsmokers with smokers, in particular, having more number of pockets with PPD of ≥5 mm on palatal and lingual sites in upper and lower jaw, respectively. | Table 1: Comparison of nonsmokers and smokers in relation to mean age, number of teeth and sites affected, and at different levels of probing pocket depth
Click here to view |
 | Table 2: Comparison of nonsmokers and smokers in relation to different levels of probing pocket depth in anterior, premolar, and molar regions
Click here to view |
 | Table 3: Comparison of nonsmokers and smokers at probing pocket depth of≥5 mm in anterior, premolar, and molar regions
Click here to view |
 | Table 4: Comparison of nonsmokers and smokers at probing pocket depth of≥5 mm in relation to the upper and lower jaw, and buccal and lingual sites in anterior, premolar, and molar regions
Click here to view |
 | Table 5: Comparison of nonsmokers and smokers at probing pocket depth of≥5 mm in relation to the upper and lower jaw in terms of involvement of buccal and lingual sites in anterior, premolar, and molar regions
Click here to view |
| Discussion | | |
The present study was planned to investigate whether the severity of periodontal disease process differed between smokers and nonsmokers in a group of known chronic periodontitis patients wherein the findings suggested that mean percentage of sites that presented with BOP was higher for nonsmokers compared with smokers. The findings of the present study were found to be in accordance with findings of other studies which concluded that smokers had less bleeding on provocation than nonsmokers. Decreased gingival BOP in smokers has been explained on the basis of vasoconstriction of peripheral blood vessels induced by cotinine, a by-product of nicotine metabolism that reduces clinical signs of inflammation including redness, edema, and gingival bleeding.[19],[21],[22] Furthermore, a plethora of studies have shown an association between smoking and in particular, the number of cigarettes smoked per day and prevalence and severity of periodontal disease with observation that individuals smoking >ten cigarettes per day and with a habit of longer duration were relatively more frequent in moderate to advanced periodontitis group with those smoking lesser number of cigarettes or, with shorter duration of habit having lesser severity of disease process.[8],[9] The present study was different from these studies on the basis of a detailed analysis of PPD and BOP assessment considering distribution in relation to the upper and lower jaw, and buccal and lingual sites in anterior, premolar and molar regions. The findings of the present study suggested that at all sites, pockets with PPD of 6–7 mm were significantly more in smokers than nonsmokers while differences in the prevalence of such pockets at PPD of ≥5 mm at all sites including anterior, premolar and molar regions were found to be statistically significant (P < 0.05) between smokers and nonsmokers. Furthermore, on further analysis, it was observed that smokers had more number of sites with PPD of ≥5 mm than nonsmokers. All these findings were found to be in accordance with finding of previous studies wherein it was observed that smokers had significantly more pronounced periodontitis characterized by a greater mean loss of attachment and teeth affected sites than nonsmokers.[23],[24],[25],[26],[27] The findings of the present study, also, revealed that largest difference was found in relation to the upper jaw, and in anterior and premolar regions, between smokers and nonsmokers, with smokers, in particular, having more number of pockets with PPD of ≥5 mm on palatal and lingual sites in the upper and lower jaw, respectively. All these observations were found to be in close accordance with findings of previous studies which suggested that periodontal microflora is modified by smoking which results in varying patterns of distribution of sites affected by periodontitis in smokers than nonsmokers. Various in vitro studies have, also, reported a shift in bacterial flora in smokers and that, in smokers, there is decreased oxygen tension in periodontal pockets that favors colonization, preferably, by anaerobic bacteria.[28],[29],[30],[31]
| Conclusion | | |
From the results, it could be concluded that smoking is associated with more severe periodontal attachment and bone loss and deeper periodontal pockets with a characteristic intraoral distribution that is suggestive of local effect.
Ethical approval statement
The ethical approval was obtained from Institutional Ethics Committee before the start of study via letter approval no. SDDC/IEC/07-37-2018.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Page RC, Schroeder HE. Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab Invest 1976;34:235-49.  |
| 2. | Socransky SS, Haffajee AD. The bacterial etiology of destructive periodontal disease: Current concepts. J Periodontol 1992;63:322-31. |
| 3. | Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: Summary of developments, clinical implications and future directions. Periodontol 2000 1997;14:216-48. |
| 4. | Burt B, Research, Science and Therapy Committee of the American Academy of Periodontology. Position paper: Epidemiology of periodontal diseases. J Periodontol 2005;76:1406-19. |
| 5. | Bergström J. Cigarette smoking as risk factor in chronic periodontal disease. Community Dent Oral Epidemiol 1989;17:245-7. |
| 6. | Haber J, Kent RL. Cigarette smoking in a periodontal practice. J Periodontol 1992;63:100-6. |
| 7. | Haber J, Wattles J, Crowley M, Mandell R, Joshipura K, Kent RL. Evidence for cigarette smoking as a major risk factor for periodontitis. J Periodontol 1993;64:16-23. |
| 8. | Martinez-Canut P, Lorca A, Magán R. Smoking and periodontal disease severity. J Clin Periodontol 1995;22:743-9. |
| 9. | Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: Findings from NHANES III. National Health and Nutrition Examination Survey. J Periodontol 2000;71:743-51. |
| 10. | Mullally BH. The influence of tobacco smoking on the onset of periodontitis in young persons. Tob Induc Dis 2004;2:53-65. |
| 11. | Van Dyke TE, Sheilesh D. Risk factors for periodontitis. J Int Acad Periodontol 2005;7:3-7. |
| 12. | Ahlqwist M, Bengtsson C, Hollender L, Lapidus L, Osterberg T. Smoking habits and tooth loss in Swedish women. Community Dent Oral Epidemiol 1989;17:144-7. |
| 13. | Krall EA, Dawson-Hughes B, Garvey AJ, Garcia RI. Smoking, smoking cessation, and tooth loss. J Dent Res 1997;76:1653-9. |
| 14. | Krall EA, Garvey AJ, Garcia RI. Alveolar bone loss and tooth loss in male cigar and pipe smokers. J Am Dent Assoc 1999;130:57-64. |
| 15. | Krall EA, Dawson-Hughes B, Garvey AJ, Garcia RI. Smoking, smoking cessation, and tooth loss. J Dent Res 1997;76:1653-9. |
| 16. | Grossi SG, Genco RJ, Machtei EE, Ho AW, Koch G, Dunford R, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 1995;66:23-9. |
| 17. | van der Weijden GA, de Slegte C, Timmerman MF, van der Velden U. Periodontitis in smokers and non-smokers: Intra-oral distribution of pockets. J Clin Periodontol 2001;28:955-60. |
| 18. | Lima FR, Cesar-Neto JB, Lima DR, Kerbauy WD, Nogueira-Filho GR. Smoking enhances bone loss in anterior teeth in a Brazilian population: A retrospective cross-sectional study. Braz Oral Res 2008;22:328-33. |
| 19. | Larson PS, Silvette H. Tobacco: Experimental and Clinical Studies (Supplement III). PS Larson, HB Haag, H Silvette (ed): Tobacco: Experimental and clinical studies; A comprehensive account of the world literature. The Williams & Wilkins Co, Baltimore, US; 1961. |
| 20. | Newbrun E. Indices to measure gingival bleeding. J Periodontol 1996;67:555-61. |
| 21. | Gelskey SC. Cigarette smoking and periodontitis: Methodology to assess the strength of evidence in support of a causal association. Community Dent Oral Epidemiol 1999;27:16-24. |
| 22. | Bagaitkar J, Demuth DR, Daep CA, Renaud DE, Pierce DL, Scott DA. Tobacco upregulates P. gingivalis fimbrial proteins which induce TLR2 hyposensitivity. PLoS One 2010;5:e9323. |
| 23. | Bergström J, Eliasson S, Dock J. A 10-year prospective study of tobacco smoking and periodontal health. J Periodontol 2000;71:1338-47. |
| 24. | Machuca G, Rosales I, Lacalle JR, Machuca C, Bullón P. Effect of cigarette smoking on periodontal status of healthy young adults. J Periodontol 2000;71:73-8. |
| 25. | Petropoulos G, McKay IJ, Hughes FJ. The association between neutrophil numbers and interleukin-1alpha concentrations in gingival crevicular fluid of smokers and non-smokers with periodontal disease. J Clin Periodontol 2004;31:390-5. |
| 26. | Jacob V, Vellappally S, Smejkalová J. The influence of cigarette smoking on various aspects of periodontal health. Acta Medica (Hradec Kralove) 2007;50:3-5. |
| 27. | Ojima M, Hanioka T. Destructive effects of smoking on molecular and genetic factors of periodontal disease. Tob Induc Dis 2010;8:4. |
| 28. | Bardell D. Viability of six species of normal oropharyngeal bacteria after exposure to cigarette smoke in vitro. Microbios 1981;32:7-13. |
| 29. | Zambon JJ, Grossi SG, Machtei EE, Ho AW, Dunford R, Genco RJ. Cigarette smoking increases the risk for subgingival infection with periodontal pathogens. J Periodontol 1996;67:1050-4. |
| 30. | Darby IB, Hodge PJ, Riggio MP, Kinane DF. Microbial comparison of smoker and non-smoker adult and early-onset periodontitis patients by polymerase chain reaction. J Clin Periodontol 2000;27:417-24. |
| 31. | Kubota M, Tanno-Nakanishi M, Yamada S, Okuda K, Ishihara K. Effect of smoking on subgingival microflora of patients with periodontitis in Japan. BMC Oral Health 2011;11:1. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
|
![JOURNAL_FULL_NAME]](images/logo.gif){kind=logo}
Search Pubmed for