In order to study whether hyperplasia or hypertrophy of cells is responsible for the thickening of airway muscles, 3-D morphometry of airway muscle cells was performed on resin-embedded semithin serial sections of autopsied lungs from 10 asthmatics and five control subjects. There were five Type I and five Type II asthmatic lungs, as defined in an earlier study, thickened muscles being found only in the central bronchi in Type I and distributed over the whole airway tree in Type II. The analysis was based on" unbiased" 3-D morphometry to obtain the numerical density Nv of muscle cells using a" oisector" a spatial probe introduced by Sterio in 1984, which we modified into a stack of serial sections. The mean number NL of cells per unit airway length and the mean volume Vc of a single muscle cell were also determined. In Type I asthmatics, the number of cells increased in the larger bronchi unaccompanied by cellular hypertrophy at any level of the airway tree. In contrast, in Type II asthmatics, hypertrophy was shown to prevail over the whole airway, but it was most remarkable in the bronchioles, whereas hyperplasia was mild and localized only in the bronchi. The two types of asthmatic lungs may therefore result from different pathogeneses. Ebina M, Takahashi T, Chiba T, Motomiya M. Cellular hypertrophy and hyperplasia of airway smooth muscles underlying bronchial asthma: a 3-D morphometric study. Am Rev Respir Dis 1993; 148: 720-6.

Although many factors are known to be involved in defining the asthmatic status, pathologic findings in the airways do not always correlate with the clinical aspects of this disease. In a previous morphometric study on lungs of asthmatic patients (1, 2), we demonstrated that the airway muscles are more or less thickened, but at the same time we noticed that the sites of muscular thickening in the airway tree were not the same. In that study, the radius (R) and the muscular thickness (D) of the airways were defined at a standardized state where the epithelial basement membrane was stretched into a circle, and the distribution of muscles was analyzed by the pattern of log D-Iog R regression. This demonstrated that the patients were classifiable into two types: Type I, with hypertrophic muscles only in the larger bronchi, and Type II, where thickening was distributed uniformly over the whole airway, including the bronchiolar segments. So far, however, no clinical or pathologic factor has been found underlying the difference between the two types of asthma. The behavior of airway muscles in asthma arouses our interest in the mechanism of muscular thickening, ie, hyperplasia (increased number) or hypertrophy (increased volume) of muscle cells. In hypertension research, hypertrophy (3) and hyperplasia (4) of arterial smooth muscle have both been claimed to explain