Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease of unknown etiology,

 characterized by inflammation and fibrosis of the lung parenchyma. No specific pathognomonic clinical or pathologic findings are associated with IPF, and diagnosis is made after excluding other causes of interstitial lung disease.IPF is thought to evolve from undefined alveolar injuries produced by infectious, oxidative, or immunologic agents in susceptible individuals, resulting in a recurring sequence of injury, repair, and subsequent fibrosis. Neutrophils, eosinophils, lymphocytes, and activated alveolar macrophages are the cells significant in the pathogenesis of chronic inflammation and ongoing damage to the lung parenchyma.

The HRCT pattern of IPF commonly shows patchy, predominantly peripheral, subpleural, bibasal reticular abnormalities. There may also be a variable amount of ground glass opacity that is usually limited in extent. In areas of more severe involvement there is often traction bronchiectasis and bronchiolectasis and/or subpleural honeycombing. Scleroderma ,rheumatoid arthritis and asbestosis are commonly similar in CT appearance to IPF, except for the presence of parenchymal bands of fibrosis and pleural plaques in patients with asbestosis. Patients with subacute or chronic hypersensitivity pneumonitis can havesimilar reticular opacity or honeycombing, but often lack the bibasilar predominance seen in IPF.

HRCT has been proposed as a technique for determining the "activity" of IPF. The ground glass opacity seen on HRCT in some patients with IPF can be associated with alveolar inflammation , but ispredominantly associated with patchy fibrotic thickening of alveolar septa, and intraalveolar granulation tissue.