ABSTRACT

Airway wall thickening was first described in the 1920s and confirmed by several groups, most notably by Dunnill and colleagues (1). Recent studies have confirmed and extended these observations by demonstrating that both hypertrophy and hyperplasia contribute to the increase in volume of the airway wall occupied by airway smooth muscle (2). The notion that airway wall re­ modeling contributes significantly to airway hyperresponsiveness (AHR) in asthma and chronic obstructive pulmonary disease is largely based on the work of Hogg and colleagues, whose studies of postmortem material have shown that there is a severity-dependent increase in the overall dimensions of the airway. When modeled mathematically, the resulting airway wall thickening appears to be capable of accounting for much of the AHR in asthma (3).