Dissolution of type I collagen fibrils by gingival fibroblasts isolated from patients of various periodontitis categories.
The classification of periodontitis in various disease categories, including juvenile periodontitis, rapidly progressive adult periodontitis and slowly progressive adult periodontitis 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 periodontitis (n = 14)). Both interleukin-1 beta 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.
Department of Periodontology, School of Dentistry, Faculty of Health Sciences, University of Copenhagen, Denmark. annehavemosepoulsen@odont.ku.dk
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Havemose-Poulsen
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Holmstrup
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Stoltze
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Birkedal-Hansen
D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D010520:Aggressive Periodontitis / Q000378:metabolism* / Q000473:pathology; D000704:Analysis of Variance; D002273:Carcinogens / Q000494:pharmacology; D002478:Cells, Cultured; D002648:Child; D003094:Collagen / Q000378:metabolism*; D017364:Collagenases / Q000378:metabolism; D018450:Disease Progression; D004198:Disease Susceptibility; D005260:Female; D005347:Fibroblasts / Q000378:metabolism*; D005881:Gingiva / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D008297:Male; D008666:Metalloendopeptidases / Q000187:drug effects / Q000378:metabolism; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000378:metabolism / Q000473:pathology; D010518:Periodontitis / Q000145:classification / Q000378:metabolism* / Q000473:pathology; D012044:Regression Analysis; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013997:Time Factors
D002273:Carcinogens; D007375:Interleukin-1; D003094:Collagen; D017364:Collagenases; D008666:Metalloendopeptidases; D013755:Tetradecanoylphorbol Acetate