Acquired subglottic stenosis - depth and not extent of the insult is key

In contrast to skin, mucosal wound healing has not been extensively studied . Subglottic stenosis (SGS) is an excellent model for such investigation. T he main objective of this pilot study was to develop a chronic model of SGS in a small animal (i.e. rabbit). In so doing, a serendipitous observation was made that the development of SGS is directly related to depth of the in jury and is independent of circumferential extent. Animals with deep injury (i.e. deep to the lamina propria, reaching the perichondrium), independent of age and circumferential extent, experienced respiratory obstruction res ulting from edema and granulation tissue formation and died or had to be sa crificed in the acute period. This was in contrast to no risk of mortality in the more superficially injured group. Histology was used to characterize this model of SGS. In the mucosal epithelium, or mucosa, changes of inflam mation, squamous metaplasia, basal cell hyperplasia, necrosis and ulceratio n were only seen acutely and total regeneration of the epithelium was achie ved by the end of the study period. In contrast, changes within the lamina propria, including chronic inflammatory cellular infiltrates and fibroplasi a, were lasting and resulted in fibrotic repair, not regeneration. These fi ndings are quite similar to the healing events in skin and suggest that SGS is the mucosal equivalent of a 'keloid or, perhaps more appropriately, a ' hypertrophic scar.' Likewise, cartilage degeneration and deformation were p ersistent markers of the chronic phase of healing. Like the lamina propria, the response to injury was reparative. Therefore, injury to the connective tissue is a critical component of development of SGS. (C) 1998 Published b y Elsevier Science Ireland Ltd. All rights reserved.