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Expression of metalloproteinases and their tissue inhibitors in gingiva affected by hereditary gingival fibromatosis: analysis of three cases within a family
Background and Objective: Hereditary gingival fibromatosis (HGF) is a benign disorder manifested by fibrous enlargement of keratinized gingiva. Evidence exists concerning the role of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in mediating normal and pathological processes,...
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Published in: | Journal of periodontal research 2009-12, Vol.44 (6), p.714-717 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background and Objective: Hereditary gingival fibromatosis (HGF) is a benign disorder manifested by fibrous enlargement of keratinized gingiva. Evidence exists concerning the role of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in mediating normal and pathological processes, including HGF. Nevertheless, there are few and contradictory results on the analysis of MMPs and TIMPs transcripts in this pathology.
Material and Methods: We studied the expression of the transcripts encoding MMP‐1, ‐2 and ‐9 and TIMP‐1 and ‐2 in gingival biopsies, obtained from three cases of HGF within a family, by semi‐quantitative reverse transcriptase‐polymerase chain reaction analysis. Samples were also processed for gelatin zymography.
Results: Except for MMP‐9, most transcripts presented a higher level of expression in biopsies from HGF patients compared with control subjects. Accordingly, MMP‐9 gelatinase activity was detected at low and similar levels among samples. Moreover, MMP‐2 enzymatic activity was not detected at all.
Conclusion: The mRNA expression of MMP‐1 and ‐2 and TIMP‐1 and ‐2 does not explain the gingival overgrowth presented in these cases. In addition, it is suggested that the gene expression of those molecules in the course of HGF is regulated at the translational or post‐translational level. |
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ISSN: | 0022-3484 1600-0765 |
DOI: | 10.1111/j.1600-0765.2008.01180.x |