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Dissolution of type I collagen fibrils by gingival fibroblasts isolated from patients of various periodontitis categories
Author(s) -
HavemosePoulsen Anne,
Holmstrup Palle,
Stoltze Kaj,
BirkedalHansen Henning
Publication year - 1998
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1998.tb02321.x
Subject(s) - periodontitis , fibril , fibroblast , collagen fibril , periodontal fiber , chemistry , type i collagen , cytokine , medicine , pathology , immunology , dentistry , in vitro , biochemistry , anatomy
The classification of periodontitis in various disease categories, including juvenile periodontitis, rapidly progressive adult periodontitis and slowly progressive adult periodontitits is based mainly on differences in disease progression and age group susceptibility. Because dissolution of collagen fibers is an integral part of periodontal attachment loss, we investigated whether the clinical differences among these periodontitis/control groups are reflected in the collagen‐degrading activity of gingival fibroblasts isolated from affected tissues. All fibroblast strains isolated from the 4 groups (n =48) displayed cell‐associated collagenolytic activity when seeded in contact with a reconstituted film of type I collagen fibrils. Cells from the control group (n = 14) dissolved the collagen fibril film twice as fast as those from each of the 3 disease groups (juvenile periodontitis (n = 13), rapidly progressive adult periodontitis (n = 7), and slowly progressive adult periodontitits (n = 14)). Both interleukin‐1β and phorbolester accelerated the rate of dissolution 2‐4‐fold, but even after cytokine or phorbolester stimulation control cells were still considerably more effective in dissolving the collagen fibrils than cells from the disease groups. The observation made in this study, that dissolution of collagen fibrils by gingival fibroblasts from periodontally diseased individuals is significantly slower than by cells from healthy control subjects, challenges disease paradigms based on a direct relationship between collagenolytic potential and disease activity.