DISSOLUTION OF TYPE-I COLLAGEN FIBRILS BY GINGIVAL FIBROBLASTS ISOLATED FROM PATIENTS OF VARIOUS PERIODONTITIS CATEGORIES

Citation
A. Havemosepoulsen et al., DISSOLUTION OF TYPE-I COLLAGEN FIBRILS BY GINGIVAL FIBROBLASTS ISOLATED FROM PATIENTS OF VARIOUS PERIODONTITIS CATEGORIES, Journal of periodontal research, 33(5), 1998, pp. 280-291
Citations number
38
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
ISSN journal
00223484
Volume
33
Issue
5
Year of publication
1998
Pages
280 - 291
Database
ISI
SICI code
0022-3484(1998)33:5<280:DOTCFB>2.0.ZU;2-A
Abstract
The classification of periodontitis in various disease categories, inc luding juvenile periodontitis, rapidly progressive adult periodontitis and slowly progressive adult periodontitits is based mainly on differ ences in disease progresssion and age group susceptibility. Because di ssolution of collagen fibers is an integral part of periodontal attach ment loss, we investigated whether the clinical differences among thes e 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-as sociated collagenolytic activity when seeded in contact with a reconst ituted film of type I collagen fibrils. Cells from the control group ( n=14) dissolved the collagen fibril film twice as fast as those from e ach of the 3 disease groups (juvenile periodontitis (n=13), rapidly pr ogressive adult periodontitis (n=7), and slowly progressive adult peri odontitits (n=14)). Both interleukin-lp and phorbolesler accelerated t he rate of dissolution 2-4-fold, but even after cytokine or phorbolest er stimulation control cells were still considerably more effective in dissolving the collagen fibrils than cells from the disease groups. T he observation made in this study, that dissolution of collagen fibril s by gingival fibroblasts from periodontally diseased individuals is s ignificantly slower than by cells from healthy control subjects, chall enges disease paradigms based on a direct relationship between collage nolytic potential and disease activity.