Definitions for processes contributing to lung remodelling during pulmonary tuberculosis (TB) and pulmonary impairment after TB

Pulmonary cavitationProcess by which normal pulmonary tissue is obliterated, becoming gas-filled spaces or cavities in the lung. This process initially involves caseous necrosis of lipid pneumonia lesions, producing caseous pneumonia. During caseation, alveolar cells and septa are destroyed along with neighbouring vessels and bronchi. Cavities form when these regions of caseous pneumonia liquefy, fragment and are released upon coughing.
Pulmonary fibrosisResults from long-term lung tissue injury that is characterised by excessive extracellular matrix deposition in the lung. Replacement of normal lung parenchyma with collagenous tissue results in architectural changes in the lung, such as thickening and stiffening of the lung walls.
BronchiectasisManifests as irreversible bronchial dilatation and thickening of the bronchial wall. Elastic and muscular components of the bronchial wall are destroyed in bronchiectasis. Bronchial dilatation associated with bronchiectasis in TB may be due to multiple factors, including traction from surrounding tissue fibrosis, caseous necrosis that makes its way into the bronchi, and elevated luminal pressure due to coughing. Bronchiectasis can also predispose to recurrent exacerbations of purulent sputum production and possibly bacterial pneumonia in subsequent years.
Pulmonary impairment after TBA broad term we use in this review to refer to lung dysfunction that includes airflow obstruction, restrictive ventilatory defects and impaired gas exchange. Pulmonary impairment after TB is probably downstream of a wide variety of lung remodelling events, some of which are described above. Given the lung's considerable reserve, these structural changes may manifest as symptoms and pulmonary disability over a period of time.