Histopathology of rhinophyma - a clinical-histopathologic correlation.

BACKGROUND: Whereas early rhinophyma is histopathologically thought to resemble fully developed rosacea, a fibromatous variant has previously been described for severe rhinophyma. In terms of clinical characteristics, recently a new Rhinophyma Severity Index (RHISI) was introduced. METHODS: We studied 24 patients who had been treated with wide shave excisions for rhinophyma. Specimens were stained with hematoxylin-eosin, periodic acid-Schiff reaction and a panel of immunohistochemical stains and observed for any correlation between clinical severity and histopathologic features as well as for predictive markers of clinical recurrence. RESULTS: There were no significant histopathologic differences between the groups reflecting the different clinical expressions. From a histopathologic perspective, clinically severe forms did not show with exclusive fibrotic changes. Further, there was no histopathologic marker predicting the clinical course or possible recurrence of the disease after surgical treatment. Only the clinical pre-operative RHISI score correlated with the postoperative outcome, with a high pre-operative RHISI being a risk factor for recurrence. CONCLUSION: Histopathologic features do not correlate with the clinical expression of rhinophyma. An exclusively 'fibrotic' rhinophyma form does not appear to exist and could possibly be the result of sampling error based on small biopsies studied.

Further evidence for the role of fibrosis in the pathobiology of rhinophyma.

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.

Overexpression of transforming growth factor beta-2 and its receptor in rhinophyma: an alternative mechanism of pathobiology.

Proliferative scarring is one of the clinical features of rhinophyma. The following study was undertaken to test the authors' hypothesis that fibrosis might also play an important role in the pathobiology of rhinophyma. The rhinophyma specimens were obtained from 5 white men (mean age, 67.8 years). Normal skin biopsies near benign facial lesions from 5 additional white men of similar age were obtained to serve as controls. Peroxidase-labeled immunohistochemical staining was performed in the rhinophyma and normal skin specimens for the presence of transforming growth factor (TGF) beta-2 and/or TGF-beta II receptor. Histological slides were then measured for the intensity of staining for TGF-beta2 and TGF-beta II receptor using a computer-aided imaging system. The dermis of the rhinophyma tissue displayed stronger immunoreactivity of TGF-beta2 (p = 0.014) and TGF-beta II receptor (p = 0.006) compared with the normal skin. The results of this study demonstrate the overexpression of the fibrogenic protein TGF-beta 2 and TGF-beta II receptor in rhinophyma tissues. These findings support the authors' hypothesis that fibrosis may also play an important role in the pathobiology of rhinophyma.

Rhinophyma--unusual expression of simple-type keratins and S100A in sebocytes and abundance of VIP receptor-positive dermal cells.

Rhinophyma represents a severe variant of rosacea, a common mid-facial erythematous dermatosis. Increased blood flow and pooling in skin are thought to be involved in its pathogenesis. Since neuropeptides and their receptors are responsible for local blood flow regulation, immunolocalization for the vasoactive intestinal peptide (VIP)-receptor(R) was performed in slice biopsies taken from five patients with glandular rhinophyma. Additional immunostainings included intermediate filaments (keratin, vimentin) and neuroglandular antigen (NGA). In contrast to controls, rhinophyma disclosed not only a more dense distribution of VIP-R positive cells within the endothelium but immunoreactive perivascular large cells. The immature sebocytes stained positive with monoclonal antibody Cam5.2 against glandular antigens and polyclonal anti-S100A. Elastotic connective tissue in the dermis showed a strong immunoreactivity for vimentin and NGA. From these results we suggest that, (a) ligands of the VIP-R may contribute to vascular and dermal alterations in rosacea and (b) immature sebocytes show an unusual antigen expression of S100A and glandular keratin.