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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 11  |  Issue : 4  |  Page : 111-115

Evaluation of periodontal health among tobacco chewers, smokers and non-tobacco users: A case–control study


1 Department of Periodontology, AMC Dental College and Hospital, Ahmedabad, India
2 Department of Medicine, Dr. N. D. Desai Medical College and Hospital, Nadiad, Gujarat, India

Date of Submission25-Dec-2020
Date of Decision25-Feb-2021
Date of Acceptance13-Apr-2021
Date of Web Publication16-Oct-2021

Correspondence Address:
Anuja Kashyapbhai Dave
B/301, Jeevandham Towers, Bimanagar Sec-2, Opp. BSNL Office, Satellite Road, Ahmedabad - 380 015, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aihb.aihb_160_20

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  Abstract 


Introduction: Periodontal disease is a multifactorial disease and one of the most common chronic diseases of the oral cavity. Smoking has a long-term chronic effect on many important aspects of the inflammatory and immune responses. Tobacco smoke has been found to affect both cell-mediated immunity and humoral immunity. Oral smokeless tobacco consumption has been considered a major risk factor for oral cancer. Its role as a risk factor for periodontal disease is less well-documented when compared to that of the relationship between smoking and periodontal disease. Materials and Methods: One hundred and eighty participants willing to sign informed consent were selected randomly with no gender bias, and the purpose of the study was explained. The periodontal examination was conducted, and the oral hygiene index-simplified (OHI-S), community periodontal index (CPI) score and loss of attachment (LOA) score were recorded. The collected data were analysed using SPSS 20 software. Results: Sixty participants in each group were examined. OHI-S mean score in Group 1 was 1.77 ± 0.43, in Group 2, it was 1.70 ± 0.65 and in Group 3, it was 1.73 ± 0.55. The mean value of CPI was 3.32 ± 0.47 in Group 1, 2.17 ± 0.46 in Group 2 and 2.67 ± 0.54 in Group 3. In comparison, the mean value of CPI-LOA was 1.35 ± 0.48 in Group 1, 1.65 ± 0.5 in Group 2 and 1.18 ± 0.65 in Group 3. Conclusion: The present survey concluded that tobacco consumption in both the forms caused poor periodontal status, with smokers having more pocket depth than tobacco chewers and non-tobacco users and tobacco chewers having more LOA than smokers and non-tobacco users.

Keywords: Attachment loss, clinical survey, tobacco chewers, tobacco smokers


How to cite this article:
Dave AK, Dave B, Thakker V, Joshi N, Katariya M, Patel H. Evaluation of periodontal health among tobacco chewers, smokers and non-tobacco users: A case–control study. Adv Hum Biol 2021;11:111-5

How to cite this URL:
Dave AK, Dave B, Thakker V, Joshi N, Katariya M, Patel H. Evaluation of periodontal health among tobacco chewers, smokers and non-tobacco users: A case–control study. Adv Hum Biol [serial online] 2021 [cited 2021 Dec 4];11:111-5. Available from: https://www.aihbonline.com/text.asp?2021/11/4/111/328390




  Introduction Top


Periodontal disease is one of the most common chronic diseases in adults. Tobacco smoking, mostly in the form of cigarette smoking, is recognised as the most important environmental risk factor in periodontitis.[1]

Periodontitis is an inflammatory disease of the supporting tissues of the teeth which is caused by specific microorganisms. It is characterised by progressive destruction of the periodontal ligament, destruction of alveolar bone, pocket formation and recession. Environmental, acquired and genetic risk factors may affect the onset or progression of periodontitis by modifying the expression of periodontal disease. There are several reports that among the environmental risk factors, tobacco smoking has been found to be associated with an increased prevalence and severity of the periodontal disease.[2]

Smoking has a long-term chronic effect on many important aspects of the inflammatory and immune responses. Histological studies have shown alterations in the vasculature of the periodontal tissues in smokers. Smoking induces a significant systemic neutrophilia, but neutrophil transmigration across the periodontal microvasculature is impeded. The suppression of neutrophil cell spreading, chemokinesis, chemotaxis and phagocytosis has been described. Protease release from neutrophils may be an important mechanism in tissue destruction. Tobacco smoke has been found to affect both cell-mediated immunity and humoral immunity. Research on gingival crevicular fluid has demonstrated that there are lower levels of cytokines, enzymes and possibly polymorphonuclear cells in smokers. In vitro studies have shown detrimental effects of nicotine and some other tobacco compounds on fibroblast function, including fibroblast proliferation, adhesion to root surfaces and cytotoxicity.[3]

Smokeless tobacco forms contain areca nut, catechu and lime, which are harmful to the oral structures. Smokeless tobacco use has been associated with several oral manifestations such as mucosal lesions and gingival–periodontal effects, such as gingival recession, gingival inflammation, changes in gingival blood flow and interproximal periodontal attachment loss.[2] There is also a link between smokeless tobacco with leucoplakia and oral carcinomas.[4]

Oral smokeless tobacco consumption has been considered a major risk factor for oral cancer. Its role as a risk factor for periodontal disease is less well-documented when compared to that of the relationship between smoking and periodontal disease.[5]

Nicotine and various compounds in tobacco may impose detrimental effects on vascular, inflammatory, immunological and healing cells, thereby affecting the vasculature and revascularisation, the inflammatory response and fibroblast function.[6] Nicotine, the principal alkaloid in tobacco, may play an important role in periodontal tissue destruction. Nicotine exposure has been shown to result in vasoconstriction and impaired angiogenesis.[7]

The habit of tobacco smoking and chewing is highly prevalent among the population these days. Studies have shown the deleterious effects of tobacco use on periodontal health. However, our literature survey did not find any documented study which compares the effect of smoking and tobacco chewing on periodontal health to the individuals with no habit. Hence, there is a genuine need for such studies.[8]


  Materials and Methods Top


In this cross-sectional study, 180 patients without gender bias aged between 18 and 65 years, having more than ten natural teeth and with and without the habit of tobacco consumption (either smoking or chewing) attending the outpatient department of periodontology were selected. The study protocol was approved by the Institutional Review Board, and informed consent was obtained from all the patients who were willing to participate in the study.

Patients who were suffering from chronic systemic pathologies, such as diabetes, other endocrine pathologies, haematological pathologies, periodontal health, with no clinical signs of periodontal inflammation community periodontal index (CPI = 0) and past periodontal treatment within 6 months before examination were excluded from the study.

The patients were divided into three groups based on the form of tobacco usage:

Group 1 – Tobacco smokers

Group 2 – Tobacco chewers

Group 3 – Non-tobacco users.

Clinical examination was carried to assess periodontal status by measuring oral hygiene index-simplified (OHI-S) and CPI, which includes assessment of probing depth (PD) and clinical attachment loss (CAL). Scaling, root planning and other necessary treatment were provided to each participant. Oral hygiene instructions were given.

Statistical method

The collected data were analysed using SPSS (V20, IBM. USA) software. Statistical analysis was analysed using the Chi-square test for categorical data and ANOVA test for quantitative data. For all statistical analyses, probability levels of P < 0.05 were considered statistically significant.


  Results Top


A total of 180 subjects, 60 in each group based on the form of tobacco usage consumption, were examined. The mean age of subjects in all three groups was similar, and no statistical difference was noticed [Table 1].
Table 1: Patient demographics

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The percentage of OHI-S scores under category 2 was 76.7% in Group 1, 50.0% in Group 2 and 63.3% in Group 3. Scores under category 1 were 23.3% in Group 1, 40.0% in Group 2 and 31.7% in Group 3 [Table 2]. The difference between the groups was not statistically significant [Table 3].
Table 2: Oral hygiene index simplified score in different groups

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Table 3: Mean values of oral hygiene index-simplified, community periodontal index and loss of attachment

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CPI score of PD (CPI-PD) was more underscore 2 in Group II (86.7%), more underscore 3 in Group I (68.3%) and Group III (60.6%) and more underscore 4 in Group I (31.7%) [Table 4]. The difference between the groups was statistically significant [Table 3].
Table 4: Community periodontal index score for pocket depth

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CPI score for the loss of attachment (LOA) (CPI-AL) in all the three groups under 1 was 65.0% in Group I, 36.7% in Group II and 60.0% in Group III; CPI score for the LOA (CPI-AL) in all the three groups under 2 was 35.0% in Group I, 61.7% in Group II and 26.7% in Group III and CPI score for the LOA (CPI-AL) in all the three groups under 3 was 1.7% in both Groups II and III [Table 5]. The difference between the groups was statistically significant [Table 3].
Table 5: Community periodontal index score for loss of attachment

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The mean value for the OHI-S score in Group I was 1.77 ± 0.43, in Group II, it was 1.70 ± 0.65 and in Group III, it was 1.73 ± 0.55. When OHI-S scores were compared between the groups, there was no statistically significant difference (P > 0.05). The mean values of the CPI-PD score were 3.32 ± 0.47 in Group I, 2.17 ± 0.46 in Group II and 2.67 ± 0.54 in Group III, with a statistically significant difference between the groups (P < 0.05). The mean values of the LOA score were 1.35 ± 0.48 in Group I, 1.65 ± 0.51 in Group II and 1.18 ± 0.65 in Group III, with a statistically significant difference when compared between the groups (P < 0.05) [Table 3].

When pairwise comparisons of OHI-S in between the groups were assessed, no statistically significant difference with P values was seen among Group I versus Group II (0.100), Group I versus Group III (0.100) and Group II versus Group III (0.100). No statistically significant difference was seen when P values of CPI-PD were compared between Group I versus Group II (0.000), Group I versus Group III (0.000) and Group II versus Group III (0.000). A statistically significant difference with P values for LOA was seen between Group I versus Group II (0.010) and Group I versus Group III (0.228). No statistically significant difference was observed between Group II versus Group III (0.000), suggesting that smokeless tobacco usage causes a greater amount of attachment loss than tobacco smoking [Table 6].
Table 6: Pairwise comparison

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  Discussion Top


The present study was designed to evaluate the effect of tobacco consumption, i.e., smoking and smokeless tobacco consumption, on the periodontal status. Numerous studies have identified tobacco smoking as a significant risk factor for periodontal disease and increased tooth loss.[9],[10],[11],[12] In the present study, the OHI-S scores were almost similar in all the groups, though smokers had higher scores of category two than non-users and tobacco chewers; the difference between the groups was not statistically significant. According to Sreedevi et al.,[13] OHI-S scores were similar in smokers and non-smokers, with less clinical gingival inflammation being observed in smokers.

CPI-PD score was similar in all the groups, with a maximum number of subjects exhibiting a score of 2 in Group II and a score of 3 in Group I and III, which was statistically significant. A score of 4 was obtained in another study by Gautam et al. where CPI-PD was compared between current smokers and non-smokers.[1]

According to Mittal et al., tobacco consumption in both the forms, i.e., smoking and chewing, affects the severity of the periodontal disease. With respect to the comparison between smokers and tobacco chewers, smokers had significantly greater PD at baseline examination, while tobacco chewers had a more gingival recession.[2]

Multiple cross-sectional and longitudinal studies regarding the association between smoking and periodontal disease had stated that increased pocket depth measurements, attachment loss and alveolar bone loss are more prevalent in smokers than non-smokers.[9] A severe rate of periodontal disease might be due to greater amounts of plaque accumulation in smokers when compared to non-smokers. A high prevalence of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia was reported in subgingival plaque of smokers than non-smokers.[3]

LOA scores were high in Group I when compared between the three groups, and the difference was statistically significant (P < 0.05). The increased LOA observed among smokeless tobacco users in the present study may be due to the placement of tobacco adjacent to the site. While comparing loss of attachment scores between group i and ii, statastically significant difference (P <0.05) Were noted, with group ii showing increased score for loss of attachment. When compared between Group I and Group III, the subjects in Group I had high LOA scores, which were not statistically significant (P > 0.05). Statistical significance was seen with LOA scores when compared between Group II and Group III (P < 0.05), suggesting that subjects with a habit of chewing tobacco have a greater amount of attachment loss than non-users.

According to Katuri KK et al., tobacco consumption in both the forms caused poor periodontal status, with smokeless tobacco users having more amount of attachment loss than smokers.[5] Smokeless tobacco is likely to be a major source of chemical injury to thin areas of gingiva chronically exposed to the quid.[14] The recession presumably results from localised damage to gingival tissue by-products of the smokeless tobacco quid, particularly in areas with a thin-to-absent alveolar housing.[15]

According to Haffajee and Socransky, an increased amount of CAL was observed in current smokers at maxillary lingual sites and lower anterior teeth than past and never smokers.[16]

In contrast to the present findings, the use of Swedish moist snuff is shown to cause less attachment loss and bone loss. This is due to the presence of fermentable carbohydrates, high pH and low levels of tobacco-related nitrosamines.[17],[18] A study by Monten et al., in the Swedish adult population, has found similar results with the presence of periodontal disease and significantly high prevalence of gingival recessions in moist snuff users than non-users.[19]


  Conclusion Top


The present survey concluded that tobacco consumption in both the forms caused periodontal problems, with smokers having more tendency for the formation of periodontal pockets than tobacco chewers and non-tobacco users and tobacco chewers having more LOA than smokers and non-tobacco users.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Gautam DK, Jindal V, Gupta SC, Tuli A, Kotwal B, Thakur R. Effect of cigarette smoking on the periodontal health status: A comparative, cross sectional study. J Indian Soc Periodontol 2011;15:383-7.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Mittal S, Dani N, Abullais SS, Al-Qahtani NA, Shah K. Effect of smoking and tobacco chewing on periodontal disease and non-surgical treatment outcome: A clinical and biochemical study. J Int Acad Periodontol 2017;20:12-8.  Back to cited text no. 2
    
3.
Palmer RM, Wilson RF, Hasan AS, Scott DA. Mechanisms of action of environmental factors – tobacco smoking. J Clin Periodontol 2005;32 Suppl 6:180-95.  Back to cited text no. 3
    
4.
Lung ZH, Kelleher MG, Porter RW, Gonzalez J, Lung RF. Poor patient awareness of the relationship between smoking and periodontal diseases. Br Dent J 2005;199:731-7.  Back to cited text no. 4
    
5.
Katuri KK, Alluri JK, Chintagunta C, Tadiboina N, Borugadda R, Loya M, et al. Assessment of periodontal health status in smokers and smokeless tobacco users: A cross-sectional study. J Clin Diagn Res 2016;10:C143-6.  Back to cited text no. 5
    
6.
Zee KY. Smoking and periodontal disease. Aust Dent J. 2009 Sep;54 Suppl 1:S44-50.  Back to cited text no. 6
    
7.
Kamath KP, Mishra S, Anand PS. Smokeless tobacco use as a risk factor for periodontal disease. Front Public Health 2014;2:195.  Back to cited text no. 7
    
8.
Borojevic T. Smoking and periodontal disease. Mater Sociomed 2012;24:274-6.  Back to cited text no. 8
    
9.
Clarke NG, Hirsch RS. Personal risk factors for generalized periodontitis. J Clin Periodontol 1995;22:136-45.  Back to cited text no. 9
    
10.
Johnson GK, Hill M. Cigarette smoking and the periodontal patient. J Periodontol 2004;75:196-209.  Back to cited text no. 10
    
11.
Bergström J. Influence of tobacco smoking on periodontal bone height. Long-term observations and a hypothesis. J Clin Periodontol 2004;31:260-6.  Back to cited text no. 11
    
12.
Rosa GM, Lucas GQ, Lucas ON. Cigarette smoking and alveolar bone in young adults: A study using digitized radiographs. J Periodontol 2008;79:232-44.  Back to cited text no. 12
    
13.
Sreedevi M, Ramesh A, Dwarakanath C. Periodontal status in smokers and nonsmokers: a clinical, microbiological, and histopathological study. Int J Dent. 2012;2012:571590.  Back to cited text no. 13
    
14.
Robertson PB, Walsh M, Greene J, Ernster V, Grady D, Hauck W. Periodontal effects associated with the use of smokeless tobacco. J Periodontol 1990;61:438-43.  Back to cited text no. 14
    
15.
Robertson PB, Walsh MM, Greene JC. Oral effects of smokeless tobacco use by professional baseball players. Adv Dent Res 1997;11:307-12.  Back to cited text no. 15
    
16.
Haffajee AD, Socransky SS. Relationship of cigarette smoking to attachment level profiles. J Clin Periodontol 2001;28:283-95.  Back to cited text no. 16
    
17.
Hugoson A, Rolandsson M. Periodontal disease in relation to smoking and the use of Swedish snus: Epidemiological studies covering 20 years (1983-2003). J Clin Periodontol 2011;38:809-16.  Back to cited text no. 17
    
18.
Bergström J, Keilani H, Lundholm C, Rådestad U. Smokeless tobacco (snuff) use and periodontal bone loss. J Clin Periodontol 2006;33:549-54.  Back to cited text no. 18
    
19.
Monten U, Wennstrom J, Ramberg P. Smokeless tobacco (snuff) use and periodontal bone loss. J Clin Periodontol 2006;33:863-8.  Back to cited text no. 19
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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