Objectives Studies have suggested contradictory results on the relationship between chronic obstructive pulmonary disease (COPD) and periodontal disease (PD). The aim of this study was to determine whether PD increased the risk of COPD and COPD-related clinical events. Design A systematic review and meta-analysis. Data sources PubMed, Ovid EMBASE and Ovid CENTRAL were searched from inception to 22 February 2023. Eligibility criteria for studies We included trials and observational studies evaluating association of PD with the risk of COPD or COPD-related events (exacerbation and mortality), with statistical adjustment for smoking. Data extraction and synthesis Two investigators independently extracted data from selected studies using a standardised Excel file. Quality of studies was evaluated using the Newcastle-Ottawa Scale. OR with 95% CI was pooled in a random-effect model with inverse variance method. Results 22 observational studies with 51 704 participants were included. Pooled analysis of 18 studies suggested that PD was weakly associated with the risk of COPD (OR: 1.20, 95% CI 1.09 to 1.32). However, in stratified and subgroup analyses, with strict adjustment for smoking, PD no longer related to the risk of COPD (adjusting for smoking intensity: OR: 1.14, 95% CI 0.86 to 1.51; smokers only: OR: 1.46, 95% CI 0.92 to 2.31; never smokers only: OR: 0.93, 95% CI 0.72 to 1.21). Moreover, PD did not increase the risk of COPD-related exacerbation or mortality (OR: 1.18, 95% CI 0.71 to 1.97) in the pooled result of four studies. Conclusions This study demonstrates PD confers no risk for COPD and COPD-related events when strictly adjusted by smoking. Large-scale prospective cohort studies with control of potential confounding factors are warranted to validate the present findings.

Objectives: Diagnosis and assessment of chronic obstructive pulmonary disease (COPD) rely extensively on spirometry, which necessitates patient cooperation. The clinical value of impulse oscillometry (IOS) as a non-volitional method in patients with COPD remains uncertain.Design: This retrospective observational study was conducted using patient data from between January 2014 and December 2015.Setting: Five public hospitals in China: West China Hospital, Nuclear Industry 416 Hospital, Suining Central Hospital, Affiliated Hospital, Medical College of Chengdu University and 363 Hospital.Participants: The study included 6307 participants aged>40 years, comprising 2109 COPD patients and 4198 general non-COPD individuals, according to the Global Initiative for Obstructive Lung Disease (GOLD) spirometry standard. Participants with lung cancer, pulmonary tuberculosis, pneumonia or those who underwent lung resection were excluded from the study.Outcome measures and analysis: Demographic data, spirometry results and IOS results were collected. Spearman’s correlation analysis was used to examine the correlation between the IOS and spirometry parameters. Receiver operating characteristic curve analysis was used to evaluate the IOS performance in COPD diagnosis and severity staging.Results: Patients with COPD exhibited significant increases in Z5, R5, R20, R5−R20, Fres and Rp, but a decrease in X5 compared with non-COPD subjects (p<0.0001). IOS parameters, including Z5, R5−R20, Fres, Rp and X5, varied with the GOLD stages, with mild-to-moderate correlations with MMEF_25%–75%, forced expiratory volume in one second (FEV₁)/forced vital capacity and FEV_1%, respectively. However, the combination of these five IOS parameters did not exhibit ideal performance in diagnosing COPD (area under the curve (AUC) 0.78; sensitivity 63.68%; specificity 80.09%), differentiating GOLD stage 1 patients from the general non-COPD population (AUC 0.71; sensitivity 54.71%; specificity 77.49%) or identifying GOLD stages 3 and 4 patients among those with COPD (AUC 0.75; sensitivity 69.51%; specificity 70.32%).Conclusion: IOS parameters, while showing good correlation with spirometry in patients with COPD, did not perfectly substitute for spirometry in diagnosing COPD, especially in the early and advanced stages of the disease.

Purpose: DNA methylation, a major epigenetic modification, has been documented to play an important role in chronic obstructive pulmonary disease (COPD). In this study, we aimed to profile the DNA methylation patterns in a mouse model of airway inflammation induced by cigarette smoke (CS), a foremost risk factor of COPD. Material and Methods: To establish a model of airway inflammation, wild-type mice were exposed to mainstream CS or room air for 2 hours twice daily, 6 days per week for consecutive 4 weeks. Lung tissues of the mice were collected for genome-wide DNA methylation analysis by liquid hybridization capture-based bisulfite sequencing, which were used for intersection analysis with gene expression by cDNA microarray to identify candidate methylated genes. Then, functional enrichment analyses with protein–protein interaction (PPI) network regarding these genes were conducted to explore the potential mechanisms. Results: After 4-week CS exposure, the level of DNA methylation accompanied by a subacute airway inflammation was markedly enhanced, and 2002 differentially methylated genes (DMGs) were annotated, including 565 DMGs contained methylations in gene promoters, which were used for intersection with the differentially expressed genes. Then, 135 candidate methylated genes were further selected by the intersection, among which 58 genes with functional methylated modification were finally identified. Further analyses revealed candidate methylated genes were significantly enriched in a complicated network of signals and processes, including interleukins, toll-like receptors, T-cells differentiation, oxidative stress, mast cells activation, stem cells proliferation, etc., as well as the 58 functional methylated genes were partially located at key positions in PPI network, especially CXCL1, DDX58 and JAK3. Conclusion: This study suggests CS exposure significantly enhances DNA methylated level, and the potential functional methylated genes are closely related to complicated inflammatory-immune responses, which may provide some new experimental evidence in understanding the epigenetic mechanisms of CS-induced airway inflammation in COPD.

Background: Pulmonary hypertension (PH) is a multi-causal disease and no satisfactory therapeutic strategies for it. Statins have been suggested as potential drugs in PH, whose effects in different clinic types of PH have not been conclusive. In this study, we included randomized controlled clinical trials (RCTs) evaluating the efficacy and safety of statins therapy in PH. Methods: We searched databases including Medline, Embase, Cochrane, PubMed and Web of science, with time up to January 1, 2019. With 95% confidence interval (CI), weighted mean difference (WMD) or standardized mean difference (SMD) was pooled and calculated in a random or fixed effect model according to I2 statistic. Results: A total of nine RCTs with 657 patients were included. Four types of statins (atorvastatin, pravastatin, rosuvastatin and simvastatin) were used at different doses (10–80 mg daily) for up to 6 months. In the pooled-data analysis, compared with placebo, there were significant improvements in pulmonary arterial pressure (PAP), in addition to low-density lipoprotein (LDL) in patients treated with statins, but not in 6-minute walking distance (6MWD), cardiac index (CDI). No more adverse events and all-cause mortality were revealed. Subgroup analysis indicated that statins could decrease PAP in the subtype of PH due to chronic obstructive pulmonary disease (COPD), but not pulmonary arterial hypertension (PAH). Conclusions: This study indicates that statins can efficiently and safely reduce PAP in PH, especially in the subtype due to COPD. Further RCTs are needed to focus on the efficacy and safety of statin therapy in different subtypes of PH.

Background: Current guideline conditionally recommends regular use of anti-reflux medication in idiopathic pulmonary fibrosis (IPF). However, the effect of anti-reflux therapy in this group remains controversial. We systematically reviewed literatures to evaluate whether anti-reflux therapy could ameliorate pulmonary function in IPF. Methods: We performed electronic search in PubMed, Embase and CENTRAL (Cochrane Central Register of Controlled Trials) to identify original articles published in English language. We included randomized controlled trials (RCTs) and observational studies regarding anti-reflux therapy on pulmonary function in IPF. Qualitative and quantitative analyses were conducted. In quantitative analysis, the inversevariance method with fixed-effect model was used to analyze pooled data. Results: Fifteen studies (2 RCTs and 13 observational studies) including 3,891 patients with IPF were included. Pooled analysis suggested that anti-reflux therapy did not improve forced vital capacity (FVC)% predicted [mean difference (MD) =0.88, 95% confidence interval (CI): -0.22 to 1.98, P=0.12, I-2 =0%, 8 studies, n=3,076], diffusing capacity of the lung for carbon monoxide (DLCO) % predicted (MD =0.75, 95% CI: -0.13 to 1.62, P=0.10, I-2 =0%, 8 studies, n=3,073), and FVC decline (MD =0.02, 95% CI: -0.01 to 0.04, P=0.29, I-2 =17%, 5 studies, n=1,586) in IPF. Discussion: Anti-reflux therapy may not ameliorate pulmonary function in IPF. However, adequately powered studies are warranted to validate the present findings.