Abstract
Asthma and chronic obstructive lung disease (COPD) are both inflammatory
conditions of the lung associated with structural ``remodeling''
inappropriate to the maintenance of normal lung function. The clinically
observed distinctions between asthma and COPD are reflected by
differences in the remodeling process, the patterns of inflammatory
cells and cytokines, and also the predominant anatomic site at which
these alterations occur. In asthma the epithelium appears to be more
fragile than that of COPD, the epithelial reticular basement membrane
(RBM) is significantly thicker, there is marked enlargement of the mass
of bronchial smooth muscle, and emphysema does not occur in the
asthmatic nonsmoker. In COPD, there is epithelial mucous metaplasia,
airway wall fibrosis, and inflammation associated with loss of
surrounding alveolar attachments to the outer wall of small airways:
bronchiolar smooth muscle is increased also. Emphysema is a feature of
severe COPD: in spite of the destructive process, alveolar wall
thickening and focal fibrosis may be detected. The hypertrophy of
submucosal mucus-secreting glands is similar in extent in asthma and
COPD. The number of bronchial vessels and the area of the wall occupied
by them increase in severe corticosteroid-dependent asthma: it is likely
that these increases also occur in severe COPD as they do in
bronchiectasis. Pulmonary vasculature is remodeled in COPD. In asthma
several of these structural alterations begin early in the disease
process, even in the child. In COPD the changes begin later in life and
the associated inflammatory response differs from that in asthma. The
following synopsis defines and compares the key remodeling processes and
proposes several hypotheses.
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