Morphology of the Airway Wall in Asthma and in Chronic Obstructive Pulmonary Disease

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Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are complex conditions with imprecise definitions, which make definitive morphologic comparisons difficult. Broadly, the airways in asthma are occluded by tenacious plugs of exudate and mucus, and there is fragility of airway surface epithelium, thickening of the reticular layer beneath the epithelial basal lamina, and bronchial vessel congestion and edema. There is increased inflammatory infiltrate comprising "activated" lymphocytes and eosinophils with release of granular content in the latter, and there is enlargement of bronchial smooth muscle, particularly in medium-sized bronchi. Three conditions contribute to COPD. In chronic bronchitis there is mucous hypersecretion with enlargement of tracheobronchial submucosal glands and a disproportionate increase of mucous acini. In small or peripheral airways disease, there is inflammation of bronchioli and mucous metaplasia and hyperplasia, with increased intraluminal mucus, increased wall muscle, fibrosis, and airway stenoses. Respiratory bronchiolitis is a critically important early lesion that may predispose to the development of centrilobular emphysema. The severity of emphysema, rather than type, appears to be the most important determinant of chronic deterioration of airflow, and in this there may be significant loss of elastic recoil prior to the observed morphologic destruction of the acinus.