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The purpose of this contribution is to place a higher value on the existence of a turn-over of bronchial and pulmonary elastic fibers: the former would derive from the smooth muscle cells of the bronchial wall, the latter from the interstitial myofibroblasts of the alveolar septa. The reduction of the number of the elastic fibers in the bronchial wall during chronic atrophic bronchitis depend on the atrophy of the bronchial smooth muscle cells; in the alveolar septa the hyperplasia of the elastic fibers during pulmonary fibroses depend on the myofibroblastic proliferation, while the reduction of the elastic fibers number during pulmonary enphysema depend on the reduction in the number of myofibroblasts.

A new framework for pulmonary fibroses may be obtained by distinguishing the "true" forms (solely collagen hyperplasia) from the "false" forms or mesenchymal fibril lung diseases (collagen, reticular and elastic hyperplasia with neo-angiogenesis): the "true fibroses" are then divisible into those not causing architectural subversion of the lung and those which bring it about. Pulmonary architectural subversion is common to true granulomatous fibroses and mesenchymal fibril lung diseases: it is, in our opinion, the product of a combination of factors, including the hyperactivity of a fibroblast sub-population normally in the minority, stimulated by T lymphocytes which are activated by an autoimmune response to type I collagen produced in excess.