The purpose of this study was to evaluate the distribution of type I and type III collagen in drug-induced gingival hyperplasia, and then to prove differences in normal gingiva and drug-induced gingival hyperplasia.
2 cases of normal gingiva and fibroma as controls, 4 cases of dilantin gingival hyperplasia and nifedipine gingival hyperplasia from files of Dept. of Oral Pathology, School of Dentistry, Kyung Hee University were stained with H--E, Masson´s trichrome for collagen, Verhoeff for elastic fiber, Toluidine blue for mast cells, andimmunostained with rabbit anti-human type I and type III collagen antibody using labeled streptavidin-biotin complex peroxidase method.
The results were as follows ;
1. Age distribution showed that dilantin gingival hyperplasia and nifedipine gingival hyperplasia occurred in range of age from 13 to 39 years(mean age : 26.5 years) and from 33 to 57 years(mean age : 45.5 years), respectively. And sex distribution showed mastly more predilection for male.
2. The cases of dilantin gingival hyperplasia were weak positive immunoreactivity to anti-type I collagen antibody in covering epithelium and lamina propria, and strong positive immunoreactivity to anti-type III collagen antibody in lamina propria, perivascularand hyperplastic collagen bundles.
3. The cases of nifedipine gingival hyperplasia were moderate or strong positive immunoreactivity in hyperplastic covering epithelium to anti-type I collagen antibody, and strong positive immunoreactivity in subepithelial connective tissue, perivascular and hyperplastic collagen bundles to anti-type III collagen antibody but weak positive immunoreactivity in inflammatory region.
4. The elastic fibers were distributed in the area of hyperplastic collagen bundles and wall of blood vessels.
5. The mast cells were distributed in the subepithehal connective tissue, perivascular region and loose connective tissue.
6. The immunoreactivity to anti-type I , III collagen antibody were reduced in the inflammatory area withy prominent plasma cells.
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