Histone deacetylase inhibitor reduces hypertrophic scarring in a rabbit ear model.

BACKGROUND: Hypertrophic scars result from excessive collagen deposition at sites of healing dermal wounds and could be functionally and cosmetically problematic. The authors tested the ability of the histone deacetylase inhibitor trichostatin A to reduce hypertrophic scar formation in a rabbit ear model. METHODS: The authors have developed a reliable rabbit model that results in hypertrophic scarring. Four 1-cm, full-thickness, circular wounds were made on each ear. After the wounds reepithelialized, 0.02% trichostatin A was injected intradermally into the wounds in the treatment group. Expression of collagen I and fibronectin was detected by reverse transcription polymerase chain reaction and Western blot analysis at postoperative day 23. Scar hypertrophy was quantified by measurement of the scar elevation index at postoperative day 45. RESULTS: Compared with the control group, injection of trichostatin A led to much more normal-appearing scars in the rabbit ear. The scar elevation index at postoperative day 45 was significantly decreased after injection of trichostatin A compared with untreated scars. Furthermore, the authors confirmed the decreased expression of collagen I and fibronectin at postoperative day 23 (after the rabbits had been treated with trichostatin A for 1 week) in the treated scars compared with the control scars according to reverse transcription polymerase chain reaction and Western blot analysis. CONCLUSIONS: The introduction of trichostatin A can result in the decreased formation of hypertrophic scars in a rabbit ear model, which is corroborated by evidence of decreased collagen I and fibronectin synthesis.

Clinical application of full-face, whole, full-thickness skin grafting: a case report.

A considerable portion of burn patients suffers severe full-face burns. Even after they were treated, some severe abnormalities still stay with them such as upper- and lower-eyelid ectropions, upper- and lower-lip ectropions, microstomia and extensive facial scar hyperplasia accompanied with pruritus. Patients suffer a great deal physically, emotionally and socially. Here we conclude our treatment experience of full-face burns with the full-face, whole, full-thickness skin grafting, which has not yet reported in the literature. We transplanted a whole, full-thickness skin graft to cover the wound in the primary operation and then remedied eyelid ectropions and microstomia in the operation that followed. The results of a 4-year-follow-up suggest that the patient has recovered part of facial expression and sensation without any geographic scars. Full-face, whole, full-thickness skin grafting appears to be an effective and relatively simple method for full-face burns that do not respond well to facial composite tissue allotransplantation (CTA).

Trichostatin A inhibits collagen synthesis and induces apoptosis in keloid fibroblasts.

Keloid, a fibro-proliferative benign tumor of skin, is characterized by an enriched milieu of growth factors and an abundant accumulation of extracellular matrix (ECM). Transforming growth factor (TGF)-ß1 is well known as the crucial fibrogenic cytokine promoting ECM production and tissue fibrosis in keloid forming. Epigenetic modifications have been shown to play a role in the pathogenesis of cancer as well as autoimmune and inflammatory disorders. Recent publication reports epigenetic modifications in keloid fibroblasts that include an altered pattern of DNA methylation and histone acetylation. Therefore, the field of epigenetics may provide a new therapeutic idea for keloid treatment strategies. Currently, there is some evidence from experimental studies that histone deacetylase (HDAC) inhibitor Trichostatin A (TSA) causes abrogation of TGF-ß1 induced collagen synthesis in skin fibroblasts. Furthermore, TSA could suppress proliferation and induce apoptosis in a broad spectrum of tumor cells both in vitro and in vivo. These findings suggest that TSA could also cause abrogation of TGF-ß1 induced collagen synthesis and induce apoptosis of proliferating keloid fibroblasts.

Rolling autogenetic dermis up to form a tube may be used as scaffold in tissue-engineered blood vessels.

Coronary and peripheral artery bypass grafting are widely being used to deal with vascular deficiencies currently, and a man-made synthetic tube or autogenous arteries or veins are needed a lot. But one's autogenous arteries or veins are limited, and artificial graft substitute isn't yet available in clinical applications because of many disadvantages. Various polymeric materials have been used as scaffolds, but without satisfying results due to intimal hyperplasia and the rate of degradation. Autogenetic dermis, which has the advantages of resistance to immunogenicity, good biocompatibility, and appropriate mechanical and physiological properties, has gained our attention to use it as a scaffold for tissue-engineered blood vessels. What is more, autogenetic dermis can be harvested easily. So we postulate that autogenetic dermis rolled up to form a tube may be an ideal scaffold for tissue-engineered blood vessels.

Aberrant Notch signaling: a potential pathomechanism of vitiligo.

Vitiligo is characterized by a localized and progressive loss of melanocytes which are pigment cells responsible for the pigmentation of human. The etiopathogenetic mechanisms leading to melanocytes loss in vitiligo lesions are not yet fully understood and no effective treatment or cure exists. Notch signaling has been shown to control many cellular functions of melanocytes. Activation of Notch signaling occurs during the formation of melanocytic tumors and inactivation of Notch signaling causes a dramatic elimination of melanocytes precursors. So we postulate that inactivation of Notch signaling in the melanocytes may be a potential pathomechanism of vitiligo. If the hypothesis was proved to be practical, we could provide new understanding of the etiology of vitiligo and produce new therapeutic avenues.

[Repair of facial and cervical scars with expanded deltopectoral flaps].

OBJECTIVE: To explore the methods for repair of facial and cervical scars after burn. METHODS: One hundred and two patients with facial and cervical scars as a result of burn injury were repaired by unilateral or bilateral deltopectoral flaps after expansion with pedicles. First, facial scars were excised and contractures were released to restore eye, mouth and nose to normal anatomical position. The facial scar flaps were overturned to join with the pedicles of deltopectoral flap for closing the wounds. The residual wounds were repaired by delayed flaps without pedicles 3 weeks later. RESULTS: Among 102 patients, the flaps survived well in 94 cases, and blood supply insufficiency was found in distal end of unilateral flap in 7 cases (depigmentation after primary healing ). Necrosis of unilateral flap occurred in one patient, and it healed after skin grafting. CONCLUSION: Expanded deltopectoral flap is efficacious procedure for repair of massive cervical and facial scars.

[Expanded skin flaps for the treatment of large scalp and face scar].

OBJECTIVE: To explore the method to repair large scalp and face scars. METHODS: 1-3 expanders under the scalp were needed for repair the scalp scar. The expanded deltopectoral flaps were transferred to repair the face scar. RESULTS: 12 cases were treated with satisfactory results. All the flaps survived and the donor sites were closed primarily. 2 cases had expander exposure which didn't affect the treatment results. Atrophic cutaneous striae was occurred because of overexpansion. CONCLUSIONS: Skin expansion is a good method for large scalp and face scar.