|Year : 2021 | Volume
| Issue : 4 | Page : 111-115
Evaluation of periodontal health among tobacco chewers, smokers and non-tobacco users: A case–control study
Anuja Kashyapbhai Dave1, Bela Dave1, Viral Thakker1, Nancy Joshi1, Mahendrakumar Katariya1, Harsh Patel2
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 Submission||25-Dec-2020|
|Date of Decision||25-Feb-2021|
|Date of Acceptance||13-Apr-2021|
|Date of Web Publication||16-Oct-2021|
Anuja Kashyapbhai Dave
B/301, Jeevandham Towers, Bimanagar Sec-2, Opp. BSNL Office, Satellite Road, Ahmedabad - 380 015, Gujarat
Source of Support: None, Conflict of Interest: None
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|| |
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.
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.
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.
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. There is also a link between smokeless tobacco with leucoplakia and oral carcinomas.
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.
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. 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.
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.
| Materials and Methods|| |
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.
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|| |
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].
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 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].
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].
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].
| Discussion|| |
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.,,, 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., 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.
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.
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. 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.
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. Smokeless tobacco is likely to be a major source of chemical injury to thin areas of gingiva chronically exposed to the quid. 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.
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.
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., 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.
| Conclusion|| |
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.
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]