Chronic diseases generally involve two fundamental pathogenic aspects: present disease activity and cumulative damage from past disease progression. COPD, as a chronic disease, encompasses both aspects (Table 1) [6,7]. The concept of disease activity encompasses the ongoing disease processes (e.g., inflammation) that can lead to structural destruction and functional impairment in patients with chronic diseases. Disease activity in COPD manifests as airway inflammation or mucus hypersecretion, while cumulative damage presents as small airway obstruction or emphysema [8,9]. Methods for assessing disease activity in COPD include evaluating exacerbation history, symptom progression, deterioration in quality of life, and decline in lung function, alongside biomarker analysis [5]. However, COPD currently lacks ideal biomarkers; thus, disease activity is often assessed retrospectively, based on evidence of disease progression [10].

In contrast, cumulative damage in COPD can be assessed using quantitative chest computed tomography, pulmonary function tests, and impulse oscillometry [11,12]. In patients of COPD, the emphysematous damaged lung is observed as the cumulative result of disease activity with inflammation. The same applies to small airway obstruction. The term, ‘cumulative damage,’ incorporates the dimension of time, reflecting the long-term and repetitive nature of injury. The ideal treatment goal for COPD would be to completely halt disease activity and fully reverse cumulative damage to a normal state. However, given current medical advancements, a more practical approach is to aim for reducing disease activity and partially reversing cumulative damage. At present, several effective treatment strategies exist to reduce disease activity in COPD, including: (1) anti-inflammatory therapy; (2) anti-mucus treatment; (3) avoidance of exposure to cigarette smoke and air pollution; and (4) infection prevention through vaccination. Despite these advancements, no effective treatment currently exists to reverse cumulative damage, even partially.

Singh et al.’s concept [5] of disease stability refers to stopping or minimizing disease activity to prevent further progression or worsening of COPD. This approach does not include the reversal of cumulative damage, such as restoring small airway obstruction or emphysema to a normal state. Given that no effective methods currently exist to reverse cumulative damage, even partially, Singh et al.’s proposal [5] appears to be a pragmatic one. He defines disease stability in COPD based on three key components: exacerbation frequency, health status (measured by Saint George’s Respiratory Questionnaire [SGRQ] or COPD assessment test), and lung function (forced expiratory volume in 1 second) [5]. Thresholds for these components were also proposed, with a recommended assessment period of 6 to 12 months: (1) no exacerbations; (2) no worsening in SGRQ or CAT scores (or no clinically significant deterioration); and (3) no decline in lung function, accounting for age-related physiological decline. Singh et al.’s proposal [5] represents a step forward compared to the current GOLD treatment goals, as it introduces a more structured and measurable approach to COPD management (Table 2) [4].

In summary, a comprehensive approach targeting both disease activity and cumulative damage is essential for advancing COPD management. While disease stability offers a pragmatic interim target, future research should focus on developing therapies that target both disease activity and cumulative damage, alongside the development of an ideal biomarker to detect disease activity.