J Clin Periodontol 2014; 41: 564–572 doi: 10.1111/jcpe.12247
Effects of periodontal treatment on lung function and exacerbation frequency in patients with chronic obstructive pulmonary disease and chronic periodontitis: A 2-year pilot randomized controlled trial
Xuan Zhou1, Jing Han1, Zhiqiang Liu1, Yiqing Song2, Zuomin Wang1 and Zheng Sun3 1
Department of Stomatology, Beijing ChaoYang Hospital affiliated to Capital Medical University, Beijing, China; 2 Department of Epidemiology, Indiana University Richard M. Fairbanks School of Public Health, Indianapolis, IN, USA; 3 Department of Oral Medicine, Capital Medical University School of Stomatology, Beijing, China
Zhou X, Han J, Liu Z, Song Y, Wang Z, Sun Z. Effects of periodontal treatment on lung function and exacerbation frequency in patients with chronic obstructive pulmonary disease and chronic periodontitis: A 2-year pilot randomized controlled trial. J Clin Periodontol 2014; 41: 564–572. doi: 10.1111/jcpe.12247.
Abstract Aim: To evaluate the direct effects of periodontal therapy in Chronic Obstructive Pulmonary Disease (COPD) patients with chronic periodontitis (CP). Materials and Methods: In a pilot randomized controlled trial, 60 COPD patients with CP were randomly assigned to receive scaling and root planing (SRP) treatment, supragingival scaling treatment, or oral hygiene instructions only with no periodontal treatment. We evaluated their periodontal indexes, respiratory function, and COPD exacerbations at baseline, 6 months, 1, and 2 years. Results: Compared with the control group, measurements of periodontal indexes were significantly improved in patients in two treatment groups at 6-month, 1-year, and 2-year follow-up (all p < 0.05). Overall, the means of forced expiratory volume in the first second/forced vital capacity (FEV1/FVC) and FEV1 were significantly higher in the two therapy groups compared with the control group during the follow-up (p < 0.05). In addition, the frequencies of COPD exacerbation were significantly lower in the two therapy groups than in the control group at 2-year follow-up (p < 0.05). Conclusions: Our preliminary results from this pilot trial suggest that periodontal therapy in COPD patients with CP may improve lung function and decrease the frequency of COPD exacerbation.
View the pubcast on this paper at http://www.scivee.tv/journalnode/62178.
Key words: chronic obstructive pulmonary disease; chronic periodontitis; dental scaling; randomized controlled trial; root planing Accepted for publication 27 February 2014
Conflict of interest and source of funding statement This study was supported by the National Natural Science Foundation of China (No. 81271158 and No. 81000449) and Beijing Science and Technology Program Fund (Z101107050210031). The authors declare that they have no conflict of interests related to the study.
564
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Periodontal therapy on COPD with CP Periodontal diseases have been associated with a number of systemic diseases such as chronic respiratory diseases (Scannapieco et al. 2003, Sharma & Shamsuddin 2011, Si et al. 2012), cardiovascular disease (Seymour et al. 2007, Ouyang et al. 2011, Dietrich et al. 2013), and diabetes mellitus (Ryan et al. 2003, Taylor 2003, Taiyeb-Ali et al. 2011, Borgnakke et al. 2013). Chronic Obstructive Pulmonary Disease (COPD) is one of the most common and costly respiratory diseases. The high prevalence and mortality of COPD worldwide pose an immense public health and medical challenge for development and implementation of effective preventive and treatment strategies (Murray & Lopez 1997). It is the third leading cause of death in the United States, affecting as many as 24 million Americans, and resulting in 700,000 hospital admissions and 124,000 deaths annually (Corbridge et al. 2012). COPD is an inflammatory disease characterized by progressive deterioration of pulmonary function and increasing airway obstruction, including chronic bronchitis and emphysema. The association between periodontitis and COPD has been increasingly recognized over the last two decades. As reviewed by Azarpazhooh & Leake, four cross-sectional studies suggested an association between poor oral health (including alveolar bone loss, periodontal attachment loss, oral hygiene index, and oral plaque colonization) and chronic pulmonary disease (Hayes et al. 1998, Scannapieco et al. 1998, Russell et al. 1999, Scannapieco & Ho 2001, Azarpazhooh & Leake 2006). Garcia’s study found a consistent association between periodontitis and COPD even after stratification for smoking (Garcia et al. 2001). Katancik’s study of 860 elderly patients found that all periodontal measures among former smokers were associated with pulmonary disease status (Katancik et al. 2005). Another cross-sectional epidemiological study suggested that current smokers with ≥4 mm mean loss of attachment had a high risk of COPD (odds ratio: 3.71) (Hyman & Reid 2004). Three recent case–control studies also reported that poor periodontal health status, including
plaque index (PLI), alveolar bone loss, and dental care, was significantly associated with increased risk of COPD (Leuckfeld et al. 2008, Wang et al. 2009, Si et al. 2012). A meta-analysis of 14 observational studies suggested that periodontal disease is a significant and independent risk factor of COPD (Zeng et al. 2012). Several recent studies have reported the positive association between periodontitis and COPD exacerbations (Liu et al. 2012, Takahashi et al. 2012). However, these were all observational studies. Only Kucukcoskun’s trial suggested that initial periodontal therapy in patients with COPD and chronic periodontitis (CP) could decrease the exacerbation frequency (Kucukcoskun et al. 2013); however, the trial was not randomized. Adequately powered randomized clinical trials that test the efficacy of periodontal interventions on the progression of COPD are required (Linden & Herzberg 2013a). Several mechanisms have been proposed to explain the association of periodontal disease and COPD. As summarized by the European Federation of Periodontology and American Academy of Periodontology (EFP/ AAP), COPD inflammatory status may be modified either by aspiration of dental plaque and/or haematogenous dissemination of inflammatory mediators and plaque organisms from periodontal pockets (Linden et al. 2013b). Thus, we hypothesized that reducing periodontal inflammation by periodontal treatment may help to prevent the progressive deterioration of lung function and reduce the frequency of exacerbations in COPD patients with CP. Due to the lack of direct evidence from randomized trials, however, it remains unclear whether and to what extent conventional periodontal therapy would impact on COPD patients. Therefore, we conducted a pilot randomized controlled trial to evaluate the feasibility and potential clinical effects of periodontal therapy on lung function and exacerbation frequency in COPD patients with CP. Materials and Methods Sample size calculation
We assumed two-sided hypothesis testing with 5% type I error and 80%
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
565
statistical power to detect the differences between treatment groups. We estimated the sample size based on the primary outcome of forced expiratory volume in first second (FEV1), which represented the severity of COPD. According to previous published randomized controlled trials of COPD patients, the magnitude of clinically meaningful difference in FEV1 was 0.10–0.20. Based on the median values (to avoid unstable outliers), a SD of 0.15 in difference for the groups was chosen for our sample size and power calculation. Considering periodontal treatment was an adjunctive treatment for COPD patients, the change in FEV1 may be small. We designed this study to detect an absolute between-group difference in improvement in FEV1 of 0.10 with an expected within-group standard deviation (SD) of 0.15. For a two-sided test, 18 subjects were needed in each group. To allow for a dropout rate of 3 mm periodontal attachment loss. Accordingly, the gingival margin is at or apical to the cemento-enamel junction (CEJ) (Albandar et al. 1999). Exclusion criteria: (1) having fever, worsening of respiratory symptoms, or medication change in the 4-week period prior to baseline interview; (2) primary diagnosis of asthma; (3) history of lung volume reduction surgery, lung transplantation, or pneumonectomy; (4) history of any periodontal treatment in the last 6 months; (5) other inflammatory diseases except COPD and periodontitis; and (6) expected survival of
Effects of periodontal treatment on lung function and exacerbation frequency in patients with chronic obstructive pulmonary disease and chronic periodontitis: A 2-year pilot randomized controlled trial
Xuan Zhou1, Jing Han1, Zhiqiang Liu1, Yiqing Song2, Zuomin Wang1 and Zheng Sun3 1
Department of Stomatology, Beijing ChaoYang Hospital affiliated to Capital Medical University, Beijing, China; 2 Department of Epidemiology, Indiana University Richard M. Fairbanks School of Public Health, Indianapolis, IN, USA; 3 Department of Oral Medicine, Capital Medical University School of Stomatology, Beijing, China
Zhou X, Han J, Liu Z, Song Y, Wang Z, Sun Z. Effects of periodontal treatment on lung function and exacerbation frequency in patients with chronic obstructive pulmonary disease and chronic periodontitis: A 2-year pilot randomized controlled trial. J Clin Periodontol 2014; 41: 564–572. doi: 10.1111/jcpe.12247.
Abstract Aim: To evaluate the direct effects of periodontal therapy in Chronic Obstructive Pulmonary Disease (COPD) patients with chronic periodontitis (CP). Materials and Methods: In a pilot randomized controlled trial, 60 COPD patients with CP were randomly assigned to receive scaling and root planing (SRP) treatment, supragingival scaling treatment, or oral hygiene instructions only with no periodontal treatment. We evaluated their periodontal indexes, respiratory function, and COPD exacerbations at baseline, 6 months, 1, and 2 years. Results: Compared with the control group, measurements of periodontal indexes were significantly improved in patients in two treatment groups at 6-month, 1-year, and 2-year follow-up (all p < 0.05). Overall, the means of forced expiratory volume in the first second/forced vital capacity (FEV1/FVC) and FEV1 were significantly higher in the two therapy groups compared with the control group during the follow-up (p < 0.05). In addition, the frequencies of COPD exacerbation were significantly lower in the two therapy groups than in the control group at 2-year follow-up (p < 0.05). Conclusions: Our preliminary results from this pilot trial suggest that periodontal therapy in COPD patients with CP may improve lung function and decrease the frequency of COPD exacerbation.
View the pubcast on this paper at http://www.scivee.tv/journalnode/62178.
Key words: chronic obstructive pulmonary disease; chronic periodontitis; dental scaling; randomized controlled trial; root planing Accepted for publication 27 February 2014
Conflict of interest and source of funding statement This study was supported by the National Natural Science Foundation of China (No. 81271158 and No. 81000449) and Beijing Science and Technology Program Fund (Z101107050210031). The authors declare that they have no conflict of interests related to the study.
564
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Periodontal therapy on COPD with CP Periodontal diseases have been associated with a number of systemic diseases such as chronic respiratory diseases (Scannapieco et al. 2003, Sharma & Shamsuddin 2011, Si et al. 2012), cardiovascular disease (Seymour et al. 2007, Ouyang et al. 2011, Dietrich et al. 2013), and diabetes mellitus (Ryan et al. 2003, Taylor 2003, Taiyeb-Ali et al. 2011, Borgnakke et al. 2013). Chronic Obstructive Pulmonary Disease (COPD) is one of the most common and costly respiratory diseases. The high prevalence and mortality of COPD worldwide pose an immense public health and medical challenge for development and implementation of effective preventive and treatment strategies (Murray & Lopez 1997). It is the third leading cause of death in the United States, affecting as many as 24 million Americans, and resulting in 700,000 hospital admissions and 124,000 deaths annually (Corbridge et al. 2012). COPD is an inflammatory disease characterized by progressive deterioration of pulmonary function and increasing airway obstruction, including chronic bronchitis and emphysema. The association between periodontitis and COPD has been increasingly recognized over the last two decades. As reviewed by Azarpazhooh & Leake, four cross-sectional studies suggested an association between poor oral health (including alveolar bone loss, periodontal attachment loss, oral hygiene index, and oral plaque colonization) and chronic pulmonary disease (Hayes et al. 1998, Scannapieco et al. 1998, Russell et al. 1999, Scannapieco & Ho 2001, Azarpazhooh & Leake 2006). Garcia’s study found a consistent association between periodontitis and COPD even after stratification for smoking (Garcia et al. 2001). Katancik’s study of 860 elderly patients found that all periodontal measures among former smokers were associated with pulmonary disease status (Katancik et al. 2005). Another cross-sectional epidemiological study suggested that current smokers with ≥4 mm mean loss of attachment had a high risk of COPD (odds ratio: 3.71) (Hyman & Reid 2004). Three recent case–control studies also reported that poor periodontal health status, including
plaque index (PLI), alveolar bone loss, and dental care, was significantly associated with increased risk of COPD (Leuckfeld et al. 2008, Wang et al. 2009, Si et al. 2012). A meta-analysis of 14 observational studies suggested that periodontal disease is a significant and independent risk factor of COPD (Zeng et al. 2012). Several recent studies have reported the positive association between periodontitis and COPD exacerbations (Liu et al. 2012, Takahashi et al. 2012). However, these were all observational studies. Only Kucukcoskun’s trial suggested that initial periodontal therapy in patients with COPD and chronic periodontitis (CP) could decrease the exacerbation frequency (Kucukcoskun et al. 2013); however, the trial was not randomized. Adequately powered randomized clinical trials that test the efficacy of periodontal interventions on the progression of COPD are required (Linden & Herzberg 2013a). Several mechanisms have been proposed to explain the association of periodontal disease and COPD. As summarized by the European Federation of Periodontology and American Academy of Periodontology (EFP/ AAP), COPD inflammatory status may be modified either by aspiration of dental plaque and/or haematogenous dissemination of inflammatory mediators and plaque organisms from periodontal pockets (Linden et al. 2013b). Thus, we hypothesized that reducing periodontal inflammation by periodontal treatment may help to prevent the progressive deterioration of lung function and reduce the frequency of exacerbations in COPD patients with CP. Due to the lack of direct evidence from randomized trials, however, it remains unclear whether and to what extent conventional periodontal therapy would impact on COPD patients. Therefore, we conducted a pilot randomized controlled trial to evaluate the feasibility and potential clinical effects of periodontal therapy on lung function and exacerbation frequency in COPD patients with CP. Materials and Methods Sample size calculation
We assumed two-sided hypothesis testing with 5% type I error and 80%
© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
565
statistical power to detect the differences between treatment groups. We estimated the sample size based on the primary outcome of forced expiratory volume in first second (FEV1), which represented the severity of COPD. According to previous published randomized controlled trials of COPD patients, the magnitude of clinically meaningful difference in FEV1 was 0.10–0.20. Based on the median values (to avoid unstable outliers), a SD of 0.15 in difference for the groups was chosen for our sample size and power calculation. Considering periodontal treatment was an adjunctive treatment for COPD patients, the change in FEV1 may be small. We designed this study to detect an absolute between-group difference in improvement in FEV1 of 0.10 with an expected within-group standard deviation (SD) of 0.15. For a two-sided test, 18 subjects were needed in each group. To allow for a dropout rate of 3 mm periodontal attachment loss. Accordingly, the gingival margin is at or apical to the cemento-enamel junction (CEJ) (Albandar et al. 1999). Exclusion criteria: (1) having fever, worsening of respiratory symptoms, or medication change in the 4-week period prior to baseline interview; (2) primary diagnosis of asthma; (3) history of lung volume reduction surgery, lung transplantation, or pneumonectomy; (4) history of any periodontal treatment in the last 6 months; (5) other inflammatory diseases except COPD and periodontitis; and (6) expected survival of
