title: Bronchial cartilage atrophy in chronic bronchitis: observations on chondrolytic processes.
abstract: The status of bronchial cartilage degeneration in chronic bronchitis is unclear, and little is known about the chondrolytic mechanisms involved. The potential contributions of various inflammatory cells, chondrocytes and cartilage-degrading enzymes to cartilage atrophy have been examined. Bronchial cartilage specimens were obtained at autopsy from lobar secondary bronchi from chronic bronchitics and age-matched controls; each was examined by light microscopy and immunohistology for the distributions of mast cells, macrophages, eosinophils, collagenase 1, collagenase 3, and degradation products of cartilage collagen. Most bronchitic specimens showed hypertrophic chondrocytes, some of which were immunostained for collagenase 3, and occasionally for collagenase 1. Evidence for collagen degradation products was demonstrated around the lacunae of a proportion of chondrocytes, and both collagenases were also observed in the soft inflammatory tissues in close association with the cartilage surface, together with variable distributions of mast cells and macrophages. Such observations were generally absent or very much reduced in the control, non-bronchitic specimens. Degenerative changes, atrophy and loss of bronchial cartilage were common features of most chronic bronchitic specimens, this usually being related to intrinsic changes in the chondrocyte phenotype, including proliferative and matrix-degrading properties. Mast cells and macrophages were often observed in close association with the bronchial cartilage, suggesting that inflammatory cells may also contribute to the mechanisms of bronchial cartilage degradation and loss. These observations of bronchial cartilage degeneration were generally lacking in age-matched non-bronchitic control specimens.
authors.affiliation: University Department of Medicine, Manchester Royal Infirmary, Manchester, UK. lynne.c.tetlow@man.ac.uk
authors.forename: L C
authors.initials: LC
authors.lastname: Tetlow
authors.forename: A J
authors.initials: AJ
authors.lastname: Freemont
authors.forename: D E
authors.initials: DE
authors.lastname: Woolley
mesh_terms: D001284:Atrophy; D001980:Bronchi / Q000201:enzymology / Q000473:pathology*; D001991:Bronchitis / Q000150:complications / Q000201:enzymology / Q000473:pathology*; D002102:Cadaver; D002356:Cartilage / Q000201:enzymology / Q000473:pathology*; D002357:Cartilage Diseases / Q000201:enzymology / Q000209:etiology / Q000473:pathology*; D002455:Cell Division; D019902:Chondrocytes / Q000201:enzymology / Q000473:pathology*; D002908:Chronic Disease; D053818:Chymases; D017364:Collagenases / Q000378:metabolism; D004804:Eosinophils / Q000201:enzymology / Q000473:pathology; D006801:Humans; D008264:Macrophages / Q000201:enzymology / Q000473:pathology; D008407:Mast Cells / Q000201:enzymology / Q000473:pathology; D012697:Serine Endopeptidases / Q000378:metabolism; D053802:Tryptases
chemical_list: D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases; D017364:Collagenases