Asthma is estimated to affect 15 million people in the United States. After declining in the 1970s, its prevalence, morbidity, and mortality have increased since the 1980s. It now affects 1 in 7 children in the United Kingdom, and is the most frequent reason for preventable childhood hospitalizations in the United States. In 1990, total asthma-related health care costs were estimated at 6.2 billion dollars in the United States. This figure exceeded 10 billion dollars by 1995.

Asthma used to be thought of as an entirely reversible disorder. As a consequence, our therapeutic approach to asthma has focused on symptomatic control through the alleviation of bronchospasm and the reduction of airway inflammation. It is now known, however, that this optimistic picture of the natural history of asthma is not entirely complete. A number of studies have demonstrated that asthmatics, as a group, experience an accelerated rate of respiratory functional deterioration (1, 2). This is nicely illustrated in a recent study of 17,506 people followed over a 15-year period in the Copenhagen Heart Study. In this population, the 1,095 patients with self-reported asthma experienced a greater decline in airway function (forced expiratory volume in 1 second [FEV1]) than did controls (38 mL per year vs. 22 mL per year), and the greatest rates of decline were experienced by smokers with asthma (1). Patient-to-patient variability has also been noted, with some patients acquiring a physiologic state characterized by irreversible or partially reversible airway obstruction, and others manifesting incomplete β-agonist responses and persistent airways hyperresponsiveness (AHR) even after prolonged corticosteroid therapy. The pathologic correlates and pathogenetic mechanisms responsible for these findings are incompletely understood. Recent attention has, however, been directed at the structural changes—collectively referred to as airway remodeling—in the asthmatic and normal airway. This is based on the belief that these changes are responsible, in a cause-and-effect fashion, for these adverse outcomes and for other manifestations of the asthmatic diathesis. The change that this represents in our concept of the pathogenesis of asthma and the features and pathogenesis of asthmatic airway remodeling is reviewed below.