Organizing pneumonia (OP) is a histologic “pattern” that denotes a subacute phase of lung injury characterized by loose fibrosis that is reasonably discrete and circumscribed.¹ The term “BOOP” (bronchiolitis obliterans organizing pneumonia) is used by some² and discouraged by others.³ The true frequency of bronchiole-related OP may be underestimated due to sampling or sectioning artifact, but it seems fairly certain that a large proportion of OP occurs in the interstitium remote from the airways, favoring the term “OP” over “BOOP.” Idiopathic OP is termed “cryptogenic organizing pneumonia” or “idiopathic BOOP” and is discussed in Chapter 19. OP or BOOP should not be confused with obliterative bronchiolitis, bronchiolitis obliterans syndrome, or constrictive bronchiolitis (see Chapter 37), all of which are immunerelated airway destructive processes and histologically distinct from OP.

OP is characterized by nodules of myofibroblasts within a background of extracellular matrix and collagen (Fig. 5.1). These nodules are sometimes called “Masson bodies,” a term ascribed to Masson years after he published histologic findings of the lungs of patients with acute rheumatic fever.⁴ OP is either within the bronchioles (“polypoid bronchiolitis obliterans”) (Fig. 5.2), adjacent to the bronchioles (Fig. 5.3), or within the interstitium. If there is coalescence into a nodule, or if airways are not readily identified, relationship to airway is indeterminate (Fig. 5.4). There may be associated granulomas adjacent to or within the organizing pneumonia (Fig. 5.5). Fibrin is occasionally present, in which case, the term “acute and organizing pneumonia” may be used. Granulation tissue may occur, but usually, the lesion is often composed almost completely of fibroblasts, ground substance, and chronic inflammation, with little neovascularity. There may be focal reactive pneumocyte hyperplasia, but widespread pneumocyte changes with diffuse interstitial loose fibrosis are more typical of diffuse alveolar damage than OP (Fig. 5.6). There may be adjacent interstitial inflammation, especially in hypersensitivity pneumonitis, as well as adjacent fibrosis, with an NSIP-like pattern, especially in COP.