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磨皮瘢痕修复。免疫组织化学和超微结构评估。

Dermabrasive scar revision. Immunohistochemical and ultrastructural evaluation.

作者信息

Harmon C B, Zelickson B D, Roenigk R K, Wayner E A, Hoffstrom B, Pittelkow M R, Brodland D G

机构信息

Department of Dermatology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA.

出版信息

Dermatol Surg. 1995 Jun;21(6):503-8.

PMID:7539704
Abstract

BACKGROUND

Dermabrasion of facial scars 4-8 weeks after injury frequently completely eliminates visible evidence of scar formation. However, efforts to define the cellular and structural mechanisms by which this phenomenon occurs have been limited in their success.

OBJECTIVE

We investigated wound healing after dermabrasive scar revision.

METHODS

The surgical scars of seven patients were abraded 6-8 weeks after injury. Comparative electron microscopic and immunohistochemical studies were performed on punch biopsy specimens taken before and after the dermabrasion. Ultrastructural changes in the basement membrane components and dermal structures were evaluated. Monoclonal antibody staining techniques were used to observe the presence, location, and temporal expression of tenascin, epiligrin, cadherins, and integrin subunits.

RESULTS

We observed: 1) an increase in collagen bundle density and size with a tendency toward unidirectional orientation of fibers parallel to the epidermal surface, 2) an upregulation of tenascin expression throughout the papillary dermis, and 3) expression of alpha-6/beta-4 integrin subunit on the keratinocytes throughout the stratum spinosum.

CONCLUSIONS

The mechanisms by which dermabrasive scar revision alters the events of primary cicatrix formation include modification of extracellular ligand expression, thereby influencing epithelial cell-cell interaction, and reorganization of connective tissue.

摘要

背景

损伤后4 - 8周对面部瘢痕进行磨皮术常常能完全消除瘢痕形成的可见痕迹。然而,确定这种现象发生的细胞和结构机制的努力成效有限。

目的

我们研究了磨皮瘢痕修复后的伤口愈合情况。

方法

7例患者的手术瘢痕在损伤后6 - 8周进行磨皮。对磨皮前后采集的打孔活检标本进行对比电子显微镜和免疫组织化学研究。评估基底膜成分和真皮结构的超微结构变化。使用单克隆抗体染色技术观察腱生蛋白、表皮整联配体蛋白、钙黏着蛋白和整合素亚基的存在、位置和时间表达。

结果

我们观察到:1)胶原束密度和大小增加,纤维有平行于表皮表面单向排列的趋势;2)整个乳头层真皮中腱生蛋白表达上调;3)整个棘层的角质形成细胞上α-6/β-4整合素亚基表达。

结论

磨皮瘢痕修复改变原发性瘢痕形成过程的机制包括细胞外配体表达的改变,从而影响上皮细胞间相互作用,以及结缔组织的重组。

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Dermabrasive scar revision. Immunohistochemical and ultrastructural evaluation.磨皮瘢痕修复。免疫组织化学和超微结构评估。
Dermatol Surg. 1995 Jun;21(6):503-8.
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