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ORIGINAL RESEARCH Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 4  |  Page : 466-470
Periodontitis as a potential risk factor for chronic obstructive pulmonary disease: A retrospective study


Department of Periodontics and Implantology, Sharad Pawar Dental College, Sawangi (Meghe), Wardha, Maharashtra, India

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Date of Submission26-Mar-2009
Date of Decision03-May-2009
Date of Acceptance10-Jun-2009
Date of Web Publication29-Jan-2010
 

   Abstract 

Aims and Objectives : A relationship between poor periodontal health and respiratory disease has been suggested by a number of recent studies. The present study was undertaken to evaluate potential association between respiratory diseases and periodontal health status and to co-relate the severity of periodontal disease with that of chronic obstructive pulmonary disease (COPD).
Materials and Methods : 150 patients of COPD (test group) and 50 Patients without COPD (control group) were recruited for the study. Information regarding patient's demographic and socioeconomic status and lifestyle (history of smoking) were considered in the study. Patients with COPD were grouped into mild, moderate and severe category on the basis of Spirometry. Periodontal health was assessed by measuring probing pocket depth, Clinical Attachment Loss (CAL) and Oral Hygiene Index (OHI).
Results : The results showed that the subjects with COPD had significantly more mean CAL) and a higher mean OHI than those without COPD. The risk for COPD appeared to be significantly elevated when attachment loss was found to be severe. A trend was noted in that lung function appeared to diminish as the amount of attachment loss increased.
Conclusion : On the basis of the observed results of the study it can be concluded that the risk for COPD appeared to be significantly elevated when attachment loss was found to be severe. It is conceivable that oral interventions that improve oral health status may prove to lower the severity of lung infection in susceptible populations.

Keywords: Periodontal disease, chronic obstructive pulmonary disease, lung function

How to cite this article:
Deo V, Bhongade ML, Ansari S, Chavan RS. Periodontitis as a potential risk factor for chronic obstructive pulmonary disease: A retrospective study. Indian J Dent Res 2009;20:466-70

How to cite this URL:
Deo V, Bhongade ML, Ansari S, Chavan RS. Periodontitis as a potential risk factor for chronic obstructive pulmonary disease: A retrospective study. Indian J Dent Res [serial online] 2009 [cited 2019 Sep 16];20:466-70. Available from: http://www.ijdr.in/text.asp?2009/20/4/466/59456
Over the past decade, increasing attention has been given to understand the relationship of periodontal disease to a number of systemic health outcomes including chronic obstructive pulmonary disease (COPD). [1],[2] COPD is a condition in which chronic obstruction to airflow occurs, with excess production of sputum as a result of chronic bronchitis and/or emphysema. The most important established risk factor for COPD is a history of prolonged cigarette smoking. [2]

A relationship between poor periodontal health and respiratory disease, especially in high-risk subjects, has been suggested by a number of recent microbiologic and epidemiologic studies. Several reports suggested that potential respiratory pathogens, which cause COPD, colonize the mouth of high-risk subjects; for example, those in intensive care unit [3] and nursing home residents. [4] Significantly, results from preliminary trials demonstrated that alteration to oral hygiene significantly reduces the rate of lower respiratory tract infection in institutionalized subjects. These studies suggest that mouth may serve as an important reservoir of lower respiratory tract infection. Studies by Scannapieco et al. (1998) [1] and Scannapieco et al. (2001) [5] have also suggested an association between poor oral health and COPD, after controlling for other confounding variables such as smoking, gender, age and sex.

Exacerbation and progression of COPD depend on the initial colonization of microbial pathogens to oral/pharyngeal surfaces. The pathogens are subsequently shed into the salivary secretions, together with oral bacteria and proinflammatory enzymes. Thus, the contents of this secretion may contaminate and induce alterations of the respiratory epithelium. [4] Oral bacteria may alter the environment of the upper airway to enhance the potential for respiratory pathogens colonization of the lower respiratory tract. [6] Enzymes within the aspirate may destroy macromolecules on the mucosal surface to expose receptors that permit adhesion and colonization of respiratory pathogens. Also, bacterial products in the aspirate may induce cytokine production from respiratory epithelial cells, resulting in recruitment of inflammatory cells. The resulting inflamed mucosal epithelium may be more susceptible to infection by respiratory pathogens. [7],[8]

Periodontal disease may alter environmental conditions to permit mucosal colonization and infection by respiratory pathogens. [6],[9] Oral conditions likely work in concert with other factors (continued smoking, environmental pollutants, allergy, genetic factors, etc.) to contribute to progression of COPD.

Therefore, the present study was undertaken to evaluate potential association between respiratory diseases and periodontal health status and to correlate the severity of periodontal disease with that of COPD.


   Materials and Methods Top


A total of 150 patients of COPD (test group) with mean age 41.43 years were recruited from Outdoor Patient Department of Medicine, Acharya Vinoba Bhave Rural Hospital, Sawangi (M), Wardha, and 50 patients without COPD (control group) with mean age 43.62 years were recruited from the Department of Periodontics, Sharad Pawar Dental College and Hospital Sawangi (M), Wardha. All patients included were at least 20 years old and had at least 6 natural teeth.

Information regarding patient's demographic (age and gender), socioeconomic status (education-categorized as illiterate or literate; household income-categorized as Rs. <50,000/annum or Rs. >50,000/annum) and lifestyle (history of smoking-number of cigarettes smoked/day) were considered in the study.

A history of COPD was recorded. Information of lung function in the test group was estimated by calculating the ratio of forced expiratory volume after 1 second (FeV 1 )/Forced Vital Capacity (FVC) × 100 by expert physician. Patients with COPD were grouped into Mild (FeV 1 ≤ 80%, FeV 1 /FVC ≥ 70%), Moderate (FeV 1 = 50%-80%; FeV 1 /FVC ≥ 70%) and Severe (FeV 1 ≤ 50% with respiratory failure/FeV 1 ≤ 30% and FeV 1 /FVC ≤ 60%) category on the basis of spirometry.

Periodontal health was assessed by measuring (a) probing pocket depth (PPD) from the crest of the gingival margin to the base of periodontal pocket; (b) Mean clinical attachment loss (CAL) from cements enamel junction to the base of the periodontal pocket using William's graduated periodontal probe; and (c) Oral hygiene index (OHI, Greene and Vermilion; 1964), [10] which comprises debris index and calculus index.

The scoring for debris index is as follows:

0 - No debris or stains present.

1 - Soft debris covering not more than the gingival third of the tooth surface, or the presence of extrinsic stains without debris regardless of the surface area covered.

2 - Soft debris covering more than one-third but not more than two-third of the exposed tooth surface.

3 - Soft debris covering more than two-third of the exposed tooth surface.

The debris score were totaled and divided by the number of surfaces covered to obtain the simplified debris index.

The calculus index was calculated by using an explorer to estimate surface area covered by supragingival calculus. The scoring was as follows­:

0 - No calculus present.

1 - Supragingival calculus covering not more than one-third of the exposed tooth surface.

2 - Supragingival calculus covering more than one-third but less than two-third of the exposed tooth surface and/or the presence of individual flecks of subgingival calculus around the cervical portion of the tooth.

3 - Supragingival calculus covering more than two-third of the exposed tooth surface and/or the presence of a continuous band of subgingival calculus around the cervical portion of the tooth.

The calculus scores were added and divided by the number of surfaces examined to obtain the simplified calculus index. The simplified oral hygiene index (OHI) was calculated by adding together the simplified debris index and the simplified calculus index.

The study protocol was approved by the research and ethical committee of Jawaharlal Nehru Medical College, Sawangi (Meghe), Wardha.

Statistical analysis

The mean and standard deviation values were calculated for all clinical parameters. Chi-square test was used to compare data among the groups. Cross product method (a × d/b × c) was used for the analysis of the odds ratio (OR). Adjustment for confounding variables was done using one-way analysis of variance (ANOVA) for regression analysis. Analysis was done by using SPSS (statistical package for social sciences) version 14.0.


   Results Top


Demographic data of the sample population are summarized in [Table 1]. The mean age of subjects with COPD was 41.43 years, while the mean age of controls was 43.62 years. Number of females was less than males both in test and control groups (6.67% and 24%, respectively). Also, the number of literates was less than illiterates both in test group (34.67%) and control group (44%). It was also noted that most subjects in both groups had a household income of less than Rs. 50,000/ annum (70% in test group, 60% in control group).

Periodontal health parameters between subjects with and without COPD are compared in [Table 2]. Subjects with COPD had significantly higher mean CAL (4.22 ± 0.56) and a higher mean OHI score (3.37 ± 0.48) than those without COPD (CAL-3.92 ± 0.53; OHI-2.878 ± 0.64). Also, the percentage of subjects with <20% bleeding sites was significantly greater in subjects without COPD (12% of subjects without COPD and 4% of subjects with COPD).

Calculated odds ratios for COPD in patients with various parameters are presented in [Table 3]. The risk for COPD appeared to be significantly elevated when attachment loss was found to be severe (CAL ≥ 3.5 mm) when compared to the healthy group (odds ratio 0.71,95% CI: 0.02-0.46). Furthermore, the odds ratio was highly significant, that is, 1.11 (95% CI: 0.79-1.34) for those who had CAL ≥ 4.5 mm.

The levels of lung function as related to periodontal status were also considered and are presented in [Table 4]. A trend toward diminishing lung function was noted with the increase in the amount of attachment loss. The data suggested that more subjects with chronic disease were males (11.50, P < 0.05) and smokers (P < 0.05) [Table 5].

After adjusting for confounding variables (smoking, gender and age), one-way ANOVA for regression analysis showed that mean CAL > 3.5 mm was significantly associated with increased risk of COPD with F value = 15.21 (P < 0.001), R 2 = 0.23 and R = 0.48. Similarly, one-way ANOVA for regression analysis showed that mean CAL > 4.5 mm was also significantly associated with increased risk of COPD with F value = 13.21 (P < 0.001), R 2 = 0.22 and R = 0.47 [Table 6].

Another interesting finding noted among the nonsmokers of both test and control groups was that the mean CAL was significantly greater in the test group (4.01 ± 0.36) than in the control group (3.77 ± 0.44) (P < 0.05). Also, the scores of mean OHI were significantly greater in the test group (3.21 ± 0.29) than in the control group (2.80 ± 0.22) (P < 0.05) [Table 7].


   Discussion Top


The findings of the present analysis, together with other recently published studies [5],[9] support an association between poor periodontal health and COPD. On the basis of the calculated odds ratio, the association of periodontal attachment loss with the prevalence of COPD appears moderate. However, a distinct trend was noted whereby the more severe the mean clinical attachment loss, the greater was the association with COPD. The analysis indicated that subjects with more clinical attachment loss had a higher prevalence of diminished lung function. This suggests the possibility that periodontitis may contribute to COPD. Periodic exacerbations of COPD are thought to be provoked by bacterial infection. [11],[12] Although the potential mechanism by which poor oral health may influence the course of COPD remain obscure, a number of mechanisms can be envisioned. The most direct means by which the oral cavity may influence the lung disease is by aspiration of indigenous oral bacteria in salivary secretions to the lower respiratory tract. Indeed, it is well known that anerobic lung infections occur following aspiration of salivary secretions, especially in patients with periodontal disease. [13],[14] Recently, it has been hypothesized that the oral cavity may also influence the oral-pharyngeal colonization by recognized pathogens, especially in high-risk patients with poor oral hygiene. Oral bacteria may stimulate periodontal tissues (epithelial cells, endothelial cells, fibroblasts, macrophages, white cells, peripheral mononuclear cells) to release cytokines such as IL-1a, IL-1b, IL-6, IL-8 and TNF-α. [15] A mechanism proposed for the gross airway epithelial damage observed in COPD involves cytokines, which recruit neutrophils to infiltrate airway parenchyma and to release proteolytic enzymes and toxic oxygen radicals. [16] The release of cytokines from the respiratory epithelium is followed by binding of respiratory pathogens or their products to the respiratory epithelial cells. Oral bacteria in the secretions that adhere to the mucosal surface may bind to mucosal epithelium to stimulate cytokine production. It is also possible that cytokines originating from the oral tissues, for example, from the gingival crevicular fluids, [16] enters the whole saliva, which then contaminates distal respiratory epithelium. The release of hydrolytic enzymes from these inflammatory cells may result in damage of the epithelium, making it more susceptible to infection by respiratory pathogens.


   Conclusion Top


The results of this study indicate that poor periodontal health status is associated with an increased severity of COPD. It was found that patients with a history of COPD had more mean clinical attachment loss than those without COPD. The risk for COPD appeared to be significantly elevated when attachment loss was found to be severe. Also, lung function appeared to diminish as the amount of attachment loss increased. Also, the oral hygiene scores and percentage of gingival bleeding sites were found to be significantly associated with the severity of COPD.

It is conceivable that improved oral health may help prevent the progression of COPD. Oral interventions that improve oral health status may prove to lower the severity of lung infection in susceptible populations.

 
   References Top

1.Scannapieco FA, Wang B, Shiau HJ. Oral bacteria and respiratory infection: Effects on respiratory pathogen adhesion and epithelial cell proinflammatory cytokine production. Ann Periodontol 2001;6:78-86.   Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Scannapieco FA, Ho AW. Potential associations between chronic respiratory disease and periodontal disease: Analysis of National Health and Nutrition Examination Survey III. J Periodontol 2001;72:50-6.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Scannapieco FA, Stewart EM, Mylotte JM. Colonization of dental plaque by respiratory pathogens in medical intensive care patients. Crit Care Med 1992;20:740-5.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Russell SL, Boylan RJ, Kaslick RS, Scannapieco FA, Katz RV. Respiratory pathogen colonization of the dental plaque of institutionalized elders. Spec Care Dentist 1999;19:128-34.   Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Scannapieco FA, Papandonatos GD, Dunford RG. Associations between oral conditions and respiratory disease in a national sample survey population. Ann Periodontol 1998;3:251-6.  Back to cited text no. 5  [PUBMED]    
6.Scannapieco FA, Mylotte JM. Relationships between periodontal disease and bacterial pneumonia. J Periodontol 1996;67:1114-22.   Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Hedges SR, Agace WW, Svanborg C. Epithelial cytokine responses and mucosal cytokine networks. Trends Microbiol 1995;3:266-70.   Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Svanborg C, Hedlund M, Connell H, Agace W, Duan RD, Nilsson A, et al. Bacterial adherence and mucosal cytokine responses. Receptors and transmembrane signaling. Ann N Y Acad Sci 1996;797:177-90.   Back to cited text no. 8      
9.Hayes C, Sparrow D, Cohen M, Vokonas PS, Garcia RI. The association between alveolar bone loss and pulmonary function: The VA Dental Longitudinal Study. Ann Periodontol 1998;3:257-61.  Back to cited text no. 9  [PUBMED]    
10.Greene JC, Vermillion JR. The simplified oral hygiene index. J Am Dent Assoc 1964;68:7-13.   Back to cited text no. 10  [PUBMED]  [FULLTEXT]  
11.Murphy TF, Sethi S. Bacterial infection in chronic obstructive pulmonary disease. Am Rev Respir Dis 1992;146:1067-83.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  
12.Fagon JY, Chastre J. Severe exacerbations of COPD patients: The role of pulmonary infections. Semin Respir Infect 1996;11:109-18.   Back to cited text no. 12  [PUBMED]    
13.Finegold SM. Aspiration pneumonia. Rev Infect Dis. 1991.   Back to cited text no. 13      
14.Morris JF, Sewell DL. Necrotizing pneumonia caused by mixed infection with Actinobacillus actinomycetemcomitans and Actinomyces israelii: Case report and review. Clin Infect Dis 1994;18:450-2.   Back to cited text no. 14  [PUBMED]  [FULLTEXT]  
15.Wilson M, Reddi K, Henderson B. Cytokine-inducing components of periodontopathogenic bacteria. J Periodontal Res 1996;31:393-407.   Back to cited text no. 15  [PUBMED]  [FULLTEXT]  
16.Birkedal-Hansen H. Role of cytokines and inflammatory mediators in tissue destruction. J Periodontal Res 1993;28:500-10.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]  

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Correspondence Address:
Vikas Deo
Department of Periodontics and Implantology, Sharad Pawar Dental College, Sawangi (Meghe), Wardha, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0970-9290.59456

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]

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