Procollagen type I gene expression and cell proliferation are increased in lipodermatosclerosis

Abstract

These results suggest that enhanced cell proliferation and procollagen gene expression are both involved in LDS development. Furthermore, fibrotic changes may occur in the absence of, or subsequent to, any significant inflammatory response, indicating that additional profibrotic factors produced in the skin as a consequence of chronic venous insufficiency may play a role in LDS formation.

New insights into therapy by mathematical analysis: Recalcitrant granulated improved more than sclerotic venous leg ulcers with amelogenin treatment

“…This temporary matrix should provide growth structures for the fibroblasts, stimulate their migration and adhesion and finally lead to healing of the wound [6,7]. This supports the hypothesis that there may be a divergent result after treatment of granulated or sclerotic ulcerations and especially that sclerotic ulcerations may benefit more from the treatment because of their reduced potential to build up granulation tissue [8,9]. Additionally, we tried to analyse whether there is a correlation between pain intensity (measured via the visual analogue scale) and response to treatment.…”

Lipodermatosclerosis: A clinicopathological study of 25 cases

“…Histologically, an increase in dermal fibroblast proliferation and procollagen gene expression have been noted on biopsy specimens of patients with lipodermatosclerosis in comparison with control subjects, suggesting that those factors are both involved in the development of the disease. 8 A variety of medications and therapies have been tried, both singly and in differing combinations. These have included compression therapy with elastic bandages or stockings 9 ; anabolic steroids 9 ; topical, intralesional, and oral corticosteroids 5,10,11 ; nonsteroidal anti-inflammatory drugs 5 ; topical capsaicin 12 ; antibiotics 5 ; methotrexate 5 ; pentoxifylline 13 ; oral prostaglandin E 11 ; tocopherol nicotinate 11 ; ultrasound 14 ; and surgical intervention.…”

Ulcus cruris venosum auf dem Boden eines Adipositas-assoziierten Dependency-Syndroms

“…Eine Vielzahl von Studien untersucht die für das Entstehen der Lipodermatosklerose, der Atrophie blanche oder der Ulzeration verantwortlichen Faktoren. Diese reichen von einer erhöhten Prokollagen Typ I-Genexpression über Angiogeneseinhibition bis hin zu prokoagulativen-thrombogenen Effekten (23)(24)(25)(26)(27). Um den genauen Zusammenhang der venösen Hypertonie und anderer Adipositas-abhängiger Faktoren mit diesen Pathomechanismen zu klären, wird wohl eine Vielzahl an weiteren Studien benötigt.…”