Recent evidence suggests that
fibrosis may play an important role in the pathobiology of
rhinophyma. The fibrogenic
cytokine transforming growth factor (TGF)-beta2 has been reported to be up-regulated in
rhinophyma tissue. Of the three common
isoforms of
TGF-beta,
TGF-beta1 and
TGF-beta2 are considered fibrogenic, whereas
TGF-beta3 has antiscarring properties. To provide further evidence for the role of
fibrosis in the pathobiology of
rhinophyma, specimens from 8 patients with
rhinophyma were compared with nine specimens of normal nasal skin. Immunohistochemistry was used to compare intensity levels of TGFbeta1 and TGFbeta3
proteins, and quantitative reverse transcription-polymerase chain reaction was used to determine messenger
ribonucleic acid (
mRNA) expression levels of TGFbeta1 and TGFbeta3.
TGF-beta1 was elevated significantly in
rhinophyma tissue (p < 0.001), whereas
TGF-beta3 was no different in the
rhinophyma specimens compared with normal nasal skin (p = 0.06). TGFbeta1
mRNA expression was five-fold higher in
rhinophyma tissue compared with normal skin (p < 0.001). The
mRNA expression of
TGF-beta3 was the same for both pathological and normal tissue (p < 0.09). These data, together with previously published observations, present further evidence that
fibrosis mediated by the fibrogenic
cytokines TGFbeta1 and TGFbeta2 play a role in the pathobiology of
rhinophyma and suggest a means of treatment by neutralizing or down-regulating these
cytokines.