ABSTRACT
The lung’s response to injury is limited to a narrow range of histological reactions irrespective of etiology. Inflammatory tissue damage and repair pathways compete as they attempt to destroy or restore preexisting lung epithelium, microvasculature, and scaffolding. Normal architecture is restored when the connective tissue scaffolding is intact and the epithelial cells proliferate and reform on the underlying basement membrane (1). In cases of severe or prolonged inflammatory insult, repair by epithelial cells is not possible. Normal architecture is lost and replaced with disorganized connective tissue along distorted scaffolding resulting in pulmonary fibrosis and loss of gas exchange units.
