Matrix metalloproteinase-1 gene polymorphism in renal transplant patients with and without gingival enlargement.
Аннотация
BACKGROUND
Gingival enlargement frequently occurs in transplant patients receiving immunosuppressive drugs. It was hypothesized that gingival enlargement associated with cyclosporin use results in a disturbance of the homeostatic balance, which is characterized by an increase in the number of fibroblasts and volume of the extracellular matrix. Matrix metalloproteinase (MMP) serves as an initiator of extracellular matrix destruction. The aim of this study was to determine whether there is an association between genotypes of the MMP-1 gene and gingival enlargement in kidney transplant patients.
METHODS
Sixty-one unrelated kidney transplant patients with gingival enlargement and 121 control transplant patients without enlargement were enrolled in the study. Six months after transplantation, all patients were given medication, which included cyclosporin A, and gingival enlargement was assessed. MMP-1 polymorphism was determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay.
RESULTS
In kidney transplant patients with gingival enlargement, the mean score of gingival enlargement was 1.42+/-0.63, whereas in control subjects, it was 0.0. There were no significant differences in the frequency of -1607 1G>2G alleles and genotypes between patients with and without gingival enlargement. In all subjects (N=182) and in patients without gingival enlargement, the genotype distribution met Hardy-Weinberg equilibrium criteria, whereas in patients with gingival enlargement, it was markedly different (P<0.06). There was a trend for carriers of at least the 1G allele to have an increased risk of gingival enlargement, but the trend was not statistically significant (odds ratio, 2.32; P<0.073).
CONCLUSION
No association between the MMP-1 gene polymorphism and gingival enlargement was revealed in kidney transplant patients who were administered cyclosporin A as a principal immunosuppressive agent.
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