Heterogeneity of collagen secreting cells in gingival fibrosis--an immunohistochemical assessment and a review of the literature.

AIM

In this work, we compared the histological features of the gingival lesions clinically diagnosed as fibrotic overgrowths due to various etiologic factors as well as an immunohistochemical assessment of fibroblasts phenotypic heterogeneity using the specific labeling for vimentin, α-smooth muscle actin (α-SMA) and fibroblast specific protein-1 (FSP1).

MATERIALS AND METHODS

Tissue samples were obtained from 12 patients clinically diagnosed with fibrotic gingival overgrowth, divided in four groups. Fragments of gingiva were processed for paraffin embedding. Serial sections were used for routine staining Hematoxylin-Eosin, trichromic Masson and Goldner-Szekely, and for immunohistochemical reactions to label vimentin, α-SMA and FSP1 using for signal amplification several techniques (EnVision, LSAB, ABC).

RESULTS

Storage of collagen fibers, increase of fibroblast number and frequent presence of inflammatory infiltrate are histological issues of all fibrotic gingival overgrowth. The incidence of granulation tissue varies but the frequency of its presence point the attention to the involvement in collagen metabolism imbalance. Immunostaining for vimentin showed a difference between its expression in samples from different groups. Except the cases of fibrosis induced by orthodontic devices, cells positive for α-SMA were rare. FSP1-positive fibroblasts were the most frequent in all cases from all the groups selected for this study.

CONCLUSIONS

The phenotype of fibroblasts is different in gingival fibrosis in relation to the risk factor, at present the most common being vimentin-positive and FSP1-positive fibroblasts. Myofibroblasts are rare in gingival fibrosis, the most numerous being in local lesions caused by wearing orthodontic devices and in syndromic fibromatosis. Further studies are required to elucidate the manner in which the active fibroblasts are recruited in relation to the etiologic factor of gingival overgrowth.