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A histochemical study of glycosidases in hydantoin induced hyperplastic, healthy and inflamed human gingiva
Author(s) -
Larmas Liisi
Publication year - 1974
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.1600-0765.1974.tb00693.x
Subject(s) - stratum spinosum , chemistry , epithelium , glucuronidase , stratum corneum , hyperplasia , enzyme , inflammation , enzyme assay , pathology , biology , biochemistry , medicine , immunology
Fresh samples of hydantoin induced hyperplastic, healthy and inflamed human gingiva were studied histochemically using various azo dyes for β‐glucuronidase (EC 3.2.1.31), for β‐ and β‐glucosidase (EC 3.2.1.20 and 3.2.1.21) as well as β‐galactosidase (EC 3.2.1.23) and for N‐acetylglucosaminidase (EC 3.2.1.30), in order to add support to the hypothesis that hydantoin induced hyperplasia is always connected with inflammation. Moderate β‐glucuronidase activity was observed in healthy, inflamed and hydantoinhyperplastic gingiva. The distribution of the enzyme activity was similar in all types of the tissue except the stratum corneum. The healthy gingiva did not reveal this activity whereas the inflamed and hydantoinhyperplastic gingiva did. The stratum basale and spinosum of the epithelium, the fibroblasts and the inflammatory cells, especially the macrophages, revealed enzyme activity in all types of tissues. In the healthy tissue only a few inflammatory cells were seen and thus the β‐glucuronidase activity was low when compared to inflamed or hyperplastic gingiva. Weak β‐galactosidase, N‐asetylglucosaminidase and β‐glucosidase activity was seen in all types of gingival samples. Enzyme activity was observed in the same structures as β‐glucuronidase with the exception of the stratum corneum, which revealed no activity. The relatively strong β‐glucuronidase activity in the keratinized cell layer of the epithelium of inflamed and hydantoinhyperplastic tissue may be due to the microbial enzyme diffusion into the keratinized cell layer of the injured tissue.

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