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   Table of Contents    
ORIGINAL ARTICLE
Year : 2021  |  Volume : 25  |  Issue : 5  |  Page : 405-410  

Comparative evaluation of serum cotinine levels in chronic periodontitis and chronic obstructive pulmonary disease


1 Department of Periodontology, Manipal College of Dental Sciences, Manipal, Manipal Academy of Higher Education, Manipal, India
2 Department of Periodontics, A B Shetty Memorial Institute of Dental Sciences, Nitte deemed to be University, Mangalore, Karnataka, India
3 Department of Pulmonary Medicine, K S Hegde Medical Academy, Nitte (Deemed to be University), Mangalore, Karnataka, India
4 Consultant Periodontist, Thiruvananthapuram, Kerala, India

Date of Submission25-Jul-2020
Date of Decision14-Mar-2021
Date of Acceptance08-May-2021
Date of Web Publication01-Sep-2021

Correspondence Address:
Amitha Ramesh
Department of Periodontics, A.B Shetty Memorial institute of Dental Sciences, Nitte Deemed to be University, Deralakatte, Mangalore, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jisp.jisp_546_20

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   Abstract 


Context: Periodontitis and chronic obstructive pulmonary disease (COPD) are chronic progressive inflammatory conditions. Smoking has been associated with both chronic periodontitis and COPD. Hence, the present study was designed to correlate serum levels of cotinine with the severity of periodontal disease with or without COPD. Settings and Design: A total of eighty patients, twenty healthy individuals, twenty patients with chronic generalized periodontitis without smoking and without COPD, twenty patients who are smokers with chronic periodontitis without COPD and twenty patients who are smokers with chronic periodontitis and COPD in the age range of 43–65 years were selected for the study. Subjects and Methods: Serum cotinine level assessment, smoking history, and periodontal examination were done in all the patients and the data obtained were statistically analyzed. Results: The mean serum cotinine level was highest in smokers with chronic periodontitis and COPD (93.642 ± 14.727) and it differed significantly between the four groups (P < 0.001). There is a significant positive correlation between the number of cigarettes and serum cotinine levels in both groups involving smoking. There was no significant correlation between serum cotinine level and clinical attachment loss in chronic periodontitis smokers with or without COPD. Conclusions: The result of this study indicates that increased smoking with COPD causes a higher chance of progression of periodontal destruction but it is not statistically significant. Furthermore, this study indicates that the assessment of serum cotinine levels is a reliable method to evaluate smoking exposure.

Keywords: Chronic obstructive pulmonary disease, cigarette smoking, periodontitis, serum cotinine


How to cite this article:
Kedlaya MN, Ramesh A, Hosmane GB, Bhandary R, Sajna HR, Thomas B. Comparative evaluation of serum cotinine levels in chronic periodontitis and chronic obstructive pulmonary disease. J Indian Soc Periodontol 2021;25:405-10

How to cite this URL:
Kedlaya MN, Ramesh A, Hosmane GB, Bhandary R, Sajna HR, Thomas B. Comparative evaluation of serum cotinine levels in chronic periodontitis and chronic obstructive pulmonary disease. J Indian Soc Periodontol [serial online] 2021 [cited 2021 Nov 27];25:405-10. Available from: https://www.jisponline.com/text.asp?2021/25/5/405/325005




   Introduction Top


Periodontitis is an infectious disease that results from the inflammation within the supporting tissues of the teeth, leading to progressive attachment loss and bone loss.[1] In recent years, there has been increasing evidence suggesting an association between oral infections and systemic disease. An area of particular interest is the link between chronic obstructive pulmonary disease (COPD) with periodontitis. COPD is a common preventable and treatable disease.

Periodontitis and respiratory disease share a common risk factor, i.e. smoking.[2] It is a potent risk factor for the development of both COPD and periodontitis.[3] It affects body responses such as neutrophil/monocyte activities, vascular function, antibody production, expression of adhesion molecule, and the release of the inflammatory mediator such as strong cytokines and chemokines, which contribute to the development of the periodontal disease [Figure 1].[4] Several proinflammatory mediators are increased due to smoking and a significant relationship between Interleukin (IL)-12 levels and chronic periodontitis severity and smoking has been established.[5] The periodontal parameters such as mean pocket depth and gingival recession in smokers are greater than in nonsmokers.[6]
Figure 1: The link between chronic obstructive pulmonary disease (COPD) and chronic periodontitis: (1) The plaque accumulation around the tooth leads to the biofilm formation and growth of bacteria. (2) Particulate matter from the cigarette smoke is released. (3) Both lead to cytokine expression and accumulation of activated neutrophils. (4) Oxidative stress to the local tissue. (5) Release of various chemoattractants, protease, elastase, Cathepsin G and reactive oxygen species. (6) These amplify the inflammatory process whilst causing connective tissue damage which in turn leads to periodontitis and chronic obstructive pulmonary disease

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Various studies show that the COPD patients, when compared to non COPD patients showed higher levels of circulating inflammatory cytokines and C-reactive proteins, IL-8, tumor necrosis factor-α, and matrix metalloproteinase.[7],[8] Similarly, studies have stated that periodontitis also has similar pathophysiology and the same inflammatory mediators have been seen to cause increased periodontal destruction.[9],[10]

An increased prevalence of periodontal disease among those with COPD compared to non-COPD is observed in a few studies.[11] Thus, the study aims to correlate the serum levels of cotinine which is a metabolite of nicotine with the severity of periodontal disease in smokers with or without COPD.


   Subjects and Methods Top


A total of eighty patients, twenty healthy individuals, twenty patients with chronic generalized periodontitis without smoking and without COPD, and twenty patients who are smokers with chronic periodontitis without COPD, and twenty patients who are smokers with chronic periodontitis and COPD were selected for the study. Written informed consent was obtained from all the participants before the start of the cross-sectional study. The ethical clearance from the institution was obtained for the same.

Patients with an age group between 43 and 65 years with a minimum complement of 20 teeth were included for the study. Patients with Gingival Index <1 were included in Group A and Gingival Index >1 were included in Group B C D. The clinical attachment loss (CAL) ≥3 mm were included in Group B C D. The smoking history of all patients was recorded and COPD patients with a FEV1/Forced vital capacity ratio of <0.7 were included in Group D.

Patients with any other systemic disease and with a history of periodontal treatment in the past 6 months were excluded from the study. Patients with the inability to perform a lung function test and with a history of primary diagnosis of asthma and a history of previous lung volume reduction surgery, lung transplantation, or pneumonectomy were also excluded from the study. Patients on medication such as Nonsteroidal anti-inflammatory drugs, antibiotics, or any drugs known to influence the periodontal tissues and pregnancy or lactation were not included in the study.

A standard performa consisting of name, gender, address, occupation, chief complaint, past medical and dental history, personal history, smoking status, and CAL was recorded for all patients. Each patient was examined using a mouth mirror, and Williams graduated probe under artificial light.

From each patient, 2 ml of the venous blood sample was collected from the antecubital fossa, centrifuged at 2500 rpm for 10 min. The serum was collected and stored at-20°C until analysis.

Assessment of cotinine was done by using the Cotinine kit manufactured by Calbiotech Company which comprises solid-phase competitive ELISA. The samples along with cotinine enzyme conjugate were added to the anti-cotinine antibody. Cotinine in the collected samples competed with a cotinine enzyme (horseradish peroxidase) conjugate for binding sites. Unbound cotinine and cotinine enzyme conjugates were washed off and later substrate reagent was mixed. The color intensity obtained was noted which is inversely proportional to the concentration of cotinine in the samples for which a standard curve was prepared.

Clinical attachment level was measured using the Williams graduated periodontal probe. Patients were categorized as per the International workshop for classification of periodontal diseases and conditions, that is the involvement of >30% sites with moderate-to-severe CAL >3 mm.[12]

A lung function test was performed for each patient in Group C and D. A detailed history of duration, exacerbations, hospitalizations, and symptoms of COPD were recorded. A trained professional (Pulmonologist) assessed the lung function by doing the spirometry test. Spirometry measures the volume of air that the patient can expel from the lungs after a maximal inspiration.

Participants of this study were categorized as smokers and nonsmokers based on self-reported history of cigarette smoking. The number of cigarettes smoked per day was noted. Pack year was calculated using the following formula. Number of pack-years = (packs smoked per day) × (years as a smoker) (National Cancer Institute).[13]

Descriptive statistics mean and standard deviation were calculated for continuous variables. One-way analysis of variance (ANOVA) test was used to compare the mean values of age, Gingival Index, CAL, and serum cotinine level in all four groups. Pearson correlation was used to find a correlation between the number of cigarettes smoked with serum cotinine levels and also CAL with serum cotinine. Value of P < 0.05 was considered to be statistically significant. Microsoft Excel and SPSS software version 22 was used for statistical analysis (IBM Corp. (2013) IBM SPSS Statistics for Windows, Version 22.0. IBM Corp., Armonk, NY).


   Results Top


The result showed that the mean age in smokers with chronic periodontitis and COPD was highest (59.550 ± 4.7181), followed by smokers with chronic periodontitis without COPD and chronic periodontitis without smoking and without COPD. The mean age of healthy patients was the least. The mean age overall differed significantly between the four groups (P < 0.001) [Table 1].
Table 1: Comparison of mean age between four groups-One-way ANOVA AGE (years)

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The mean gingival index was highest in smokers with chronic periodontitis and with COPD (2.165 ± 0.458) followed by smokers with chronic periodontitis without COPD (1.870 ± 0.379) and chronic periodontitis without smoking and without COPD (1.865 ± 0.533). The mean gingival index was lowest in the healthy group (0.620 ± 0.158). The mean gingival index overall differed significantly between the four groups (P < 0.001) [Table 2].
Table 2: Comparison of Gingival index between four groups One-way ANOVA

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Mean CAL was highest in smokers with chronic periodontitis and with COPD (4.98 ± 0.86), followed by smokers with chronic periodontitis but without COPD (4.76 ± 0.82) and chronic periodontitis without smoking and without COPD (4.54 ± 1.023). CAL did not differ significantly between the three chronic periodontitis groups. One-way ANOVA = P = 0.33 [Table 3].
Table 3: Comparison of CAL between four groups-One-way ANOVA

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Mean serum cotinine level was highest in smokers with chronic periodontitis with COPD (93.642 ± 14.727), followed by smokers with chronic periodontitis without COPD (68.675 ± 19.667) and healthy group (9.720 ± 3.756). Mean serum cotinine level was least in chronic periodontitis without smoking and without COPD patients (7.862 ± 4.321). One-way ANOVA showed the mean serum cotinine level overall differed significantly between the four groups (P < 0.001) [Table 4].
Table 4: Comparison of Serum cotinine level between four groups-One-way ANOVA

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In smokers with chronic periodontitis without COPD, there is a mild positive correlation between serum cotinine and CAL but not significant [Table 5]. However, there is a significant positive correlation between the number of cigarettes smoked and serum cotinine (r = 0.740, P < 0.001) [Table 6].
Table 5: Chronic periodontitis smoker-Serum cotinine and CAL correlation

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Table 6: Correlations - Number of cigarettes, years, pack years with serum cotinine (Smokers with chronic periodontitis without COPD)

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In smokers with chronic periodontitis with COPD, there is a mild negative correlation between serum cotinine and CAL but not significant [Table 7]. However, there is a significant positive correlation between the number of cigarettes and serum cotinine (r = 0.573, P = 0.008.) [Table 8].
Table 7: Chronic Periodontitis COPD Smoker-Serum cotinine and CAL correlation

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Table 8: Correlations- Number of cigarettes, years, pack years with serum cotinine (Smokers with chronic periodontitis and with COPD)

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   Discussion Top


Periodontal disease is an inflammatory process, which is a chronic condition associated with various inflammatory mediators and inflammatory cells such neutrophils and monocytes. These mediators released into the saliva are carried into the respiratory epithelium leading to a pulmonary inflammatory condition.[14],[15]

Lower respiratory tract infection depends on the oral and oropharyngeal flora and dental plaque, which act as a reservoir for the lower respiratory tract pathogens. The majority of the pathogens in the lower respiratory tract are similar to the aerobic pathogens associated with oral disease. Hence, the distal contamination of the respiratory tract by the saliva containing these pathogens is the cause of a lower respiratory infection.[16] An association between chronic obstructive lung disease and poor oral hygiene was first reported by Scannapieco et al.[15] and Hayes et al. in 1998.[14]

There have been numerous mechanisms proposed to find a possible association between COPD and periodontal disease. The studies, to date, have directly or indirectly indicated that this could be due to the residual confounding factor-like tobacco smoking, age, and gender.[17],[18],[19]

Grossi et al. conducted a study and found a significant difference in CAL in smokers and nonsmokers, which was dose-dependent, where higher exposure to tobacco smoking led to an increase in periodontal destruction.[20] As stated by Horning et al. 1992, this strong association between smoking and cumulative periodontal destruction is consistent with the hypothesis that the more a person smokes greater is the degree of periodontal destruction.[21]

Another study conducted by Putri et al. also showed that there was an increase in mean pocket depth and gingival recession in smokers when compared to nonsmokers.[6]

Kenney et al. and Gala et al. stated that tobacco and its products alter the leukocyte chemotaxis, migration, and phagocytosis.[22],[23] There are various studies in vitro that have stated that tobacco metabolites lead to suppression of neutrophil functions which alter host response and inhibit the immune response.[24],[25] Similarly, the inflammatory response which is seen in the airway epithelium is mainly triggered by tobacco smoking.[26]

The self-reported smoking habits are unreliable.[27],[28] Various methods are used to validate self-reported smoking. There are mainly three biological measurements: carbon monoxide, thiocyanate, and cotinine.[29] Cotinine is a major metabolite of nicotine. It is present in the plasma with a half-life of about 16 h. Cotinine is generally further metabolized into water-soluble substances whereas a very minute fraction of it is excreted by the kidney.[30],[31] Cotinine may represent as an alternative measure to estimate tobacco exposure. It can be estimated in blood, saliva, or urine.[32] Hence, it is the most preferred biomarker for tobacco exposure.[33] According to CDC 2001, values <1 ng/ml are considered to be ideal for a nonsmoker who has not been exposed to passive smoking whereas in an active smoker it is higher than 15 ng/ml and can raise to 500 ng/ml. In the case of passive smoking, the cotinine value usually ranges from 1 to 15 ng/ml.[34]

In this study, serum cotinine level was used as a biomarker and correlated with the periodontal parameters in different study groups to estimate the level of smoking and to analyze their association. It represents a confirmative measure of tobacco exposure to the self-reported smoking status of a patient when long-term effects are needed to be studied.[32] However, the smoking pattern varies from patient to patient, individual metabolism, and its rate of absorption. This may explain the cotinine level difference.[35] It is also used to assess passive smoking as reported in a study by Hoffmann et al. 1984.[36]

In the present study, the mean cotinine value in the nonsmokers was 8.791 ng/ml, which was similar to a study conducted by González et al. where it was 10.56 ng/ml. However, in this study mean serum cotinine value of smokers (81.16 ng/ml) was much lower when compared to the value presented by the same authors (421.01 ng/ml).[37] The difference in the mean serum cotinine levels was statistically significant between the smokers and the nonsmokers. It was also statistically significant between smokers with chronic periodontitis with and without COPD. The higher exposure of smoking in COPD patients than non-COPD patients may be due to the increased age, duration of smoking, and pack-years.

In the present study, the mean age was highest in chronic periodontitis COPD patients (59.550 ± 4.7181) and least in healthy patients (49.700 ± 5.2825), and an overall significant difference in age between all the groups was seen. This is similar to the difference found in a study conducted by Peter et al. where the mean age of COPD patients was (59.48 ± 11.13) and non-COPD patients were (49.69 ± 10.16).[38]

The number of cigarettes smoked, and the serum cotinine levels were directly proportional to each other in chronic periodontitis smokers with or without COPD. This is similar to the result stated by González et al.[37]

The diagnosis of periodontitis is mainly done by assessing various periodontal parameters such as bleeding on probing, the assessment of CAL, pocket probing depth, and radiographic bone loss. In the present study, CAL was considered as a more appropriate periodontal parameter than pocket probing depth to assess the periodontal condition as there is gingival recession occurring in older individuals. Furthermore, pocket probing depth alone represents the current disease status, whereas CAL represents the long-term periodontal destruction with old age. Gingival recession, without measurable pockets, as frequently found in smokers was also taken as a sign of progression of periodontal disease.[39]

The result of the present study showed no significant difference in CAL among smokers and nonsmokers as seen in studies conducted by Feldman et al., 1983; Bergstrom, 1989; Robertson et al., 1990.[40] It differed from those presented in studies conducted by Sheiham, 1971, and Danielsen et al., 1990 where there was either a significant positive or negative association.[41]

Since smoking is a confounding factor for both COPD and chronic periodontitis, it is important to find the extent of severity of periodontal destruction caused by smoking in these patients. In our study, all the periodontal parameters were higher in smokers with chronic periodontitis and COPD than in smokers with chronic periodontitis without COPD. These results were not statistically significant which is similar to the study conducted by Hyman and Reid[17] This is different from the studies conducted by Si Y et al.; Deo et al.; where they found a significant increase in the attachment loss in COPD patients.[42] Hence, there is a need for further studies including all the known relevant confounding factors associated with chronic periodontitis and COPD in a larger population.


   Conclusions Top


Chronic periodontitis and COPD are common inflammatory conditions associated with smoking. Our study indicates that increased smoking along with COPD has a higher chance of progression of periodontal destruction although the effect is not statistically significant. Similarly, there was no statistically significant correlation between the serum cotinine levels and periodontal destruction in smokers with and without COPD. There is a need for future studies involving a larger sample size while taking into consideration of all the confounding factors. It also indicates that the assessment of serum cotinine level is a reliable method to evaluate smoking exposure as the number of cigarettes smoked significantly correlated with the serum cotinine level. This may act as a confirmative method in evaluating the role of smoking in chronic periodontitis and COPD.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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