The frequency of lung fibrotic disorders is much lower in children than in adults. Some clinical situations have features certainly unique to children, but many of these diseases overlap their adult counterparts with the primary event being injury and damage of the alveolar epithelium [11, 13] . Yet, the overall outcome and prognosis of the diseases in children are thought to be less severe than in adult patients. In addition, pediatric ILD is more responsive to therapeutic strategies than adult ILD [9] . These differences may be explained by the types of initial injury, which may not be similar due to changes in the host environment. Another explanation is the modifications of the process of wound healing with age. Comparison of the response to injury in foetal and adult skin shows clear differences [53] . Skin wound healing in the foetus is characterized by complete regeneration of the skin and the absence of scar formation. Progressively with age, the skin looses the capacity to regenerate the original tissue architecture with the result being scar formation that extends outside the wound bed. The process of healing involves the coordinated regulation of cell proliferation and migration and tissue remodeling, predominantly by polypeptide growth factors [54] . The slowing of wound healing that occurs in the aged may be related to changes in the activity of these various regulatory factors. In a study on the role of aging in the development of cardiac fibrosis in the rabbit, differences in the cascade of events leading to myocardial remodeling were observed, with mainly the presence of more myofibroblasts synthesising collagen and expressing high levels of TGF-β in older animals [55] . A study of growth factors involved in skin wound healing in young and aged mice also showed age-dependent changes. Expression of all the fibroblast growth factors was diminished in aged mice, even in healthy skin. In addition, the post-wound regulation of expression of these factors and of TGF-β was less pronounced and slower than in young mice. These findings are in agreement with data observed in muscle that indicated significant alterations in the TGF-β production with age [56, 57] . Other potential mechanism is linked to the observation that injury in adult tissues does in certain circumstances stimulate tissue regeneration, depending on the presence of small subsets of primitive stem cells. Stem cells are the self-renewing, primitive, undifferentiated, multipotent source of multiple cell lineages [49] . While such cells are critical for development and growth through childhood, residual pools of adult stem cells are hypothesized to be the source of the frequently limited tissue regeneration and repair that occurs in adults [58] . Unlike embryonic stem cells, adult stem cells are not immortal, and show decreasing telomere length with increasing age. The naturally limited replacement capacity of such endogenous stem cell pools may occur via exhaustion of the stem cell pool or arise as a consequence of inherited or acquired mutations that alter proper stem cell function [59] . The limited life span of cells may result from replicative senescence in response to various stresses including DNA damage, oxidants, and telomere erosion [52] . All these forms of injury have been documented in the lung from adult patients with ILD.