To Editor:
We have carefully reviewed the recent article “Association between oral microbiome diversity and chronic obstructive pulmonary disease in the US population” by Guo et al. [1]. This study investigates the potential impact of oral microbiome health on COPD risk, which holds significant implications and opens new avenues for further research into COPD pathogenesis and potential intervention strategies.
This study analyzed data from the NHANES 2009–2010 and 2011–2012 cycles, excluding participants under 20 years of age or those without complete oral microbiome and lung function measurements. The analysis also removed 1,116 asthma cases, though the specific exclusion criteria were not fully described in the Methods section. Although asthma and COPD demonstrate different inflammatory profiles, obstruction patterns, and clinical presentations, they can manifest similar symptoms such as airflow limitation [2]. This exclusion criterion potentially limits the broader applicability of the results.
The analysis of oral microbiome diversity and COPD risk appropriately accounted for key confounders, including age, sex, and smoking status. Although smoke remains the dominant environmental risk factor, airborne particulate matter, particularly PM2.5, contributes significantly to respiratory impairment through oxidative stress, inflammation, and potential microbiota disruption. Evidence suggests PM2.5 exposure may modify microbial community structure and pulmonary function [3]. Therefore, including this PM2.5 exposure as a covariate would strengthen the comprehensiveness and reliability of the study findings.
The study found that oral microbiome α-diversity (e.g., Simpson index) correlated with COPD risk in specific subgroups, particularly among older individuals with lower education levels, partnered status, alcohol consumption, and smoking history. While the periodontitis-COPD relationship showed some variability, epidemiological evidence from diverse populations consistently linked periodontitis prevalence and severity to COPD incidence and progression [4]. Severe periodontitis may damage lower airway epithelium, promoting periodontal pathogen dissemination, inflammatory cell recruitment, and MMP secretion, which collectively drive COPD advancement and acute exacerbations [5]. These observations highlight the need to investigate oral microbiota-periodontitis interactions in COPD populations to identify potential mechanistic differences.
The β-diversity analysis yielded a low PERMANOVA R²value (< 0.01), indicating limited explanatory power of oral microbiome diversity for COPD risk. These results imply that community structure differences explain only a minor fraction of disease variability, suggesting the involvement of unmeasured factors or mechanisms. Expanding the sample size would strengthen statistical power and clarify microbiome-COPD associations. Besides, stratifying COPD patients by clinical characteristics or disease stages could further minimize within-group heterogeneity and enhance detection sensitivity.
In summary, it is anticipated that the recommendations presented in this letter may serve as valuable references for researchers to enhance their understanding of the relationship between the oral microbiome and COPD. An in-depth exploration of oral microbiome alterations and their impact on COPD progression will not only provide novel perspectives for future research but also offer more precise guidance for clinical and community-based prevention and therapeutic strategies. Ultimately, these efforts may contribute to improving patients’ quality of life, particularly among populations with increasingly severe chronic respiratory diseases.
Acknowledgements
Not applicable.
Author contributions
Mingwu Luo contributed to the study design and manuscript review, Kai Xin interpreted the article and prepared the initial draft, and Tao Luo revised the manuscript.
Funding
No funding was received.
Data availability
Not applicable.
Declarations
Ethics approval and consent to participate
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Consent for publication
Not applicable.
Conflict of interest
The authors declare that there are no conflicts of interest.
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References
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Associated Data
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Data Availability Statement
Not applicable.