Dick G F, Ashe B M, Rodgers E G, Diercks R C, Goltz R W
Acta Derm Venereol. 1976;56(4):279-82.
Histopathological sections of anetoderma-like scars from 10 patients with acne vulgaris showed a selective absence of elastic fibers around pilosebaceous follicles. This finding is similar to the histologic changes of "perifollicular elastolysis" reported by Varadi. Bacteria isolated by anaerobic and aerobic cultures of swabs of the skin surface and pus of these 10 patients, 12 others with active acne vulgaris and 8 normal subjects were studied with particular attention to Staphylococcus epidermis and Propionibacterium acnes. These organisms were analysed for production of an elastolytic enzyme which might play a role in the observed selective loss of elastic fibers. No elastolytic activity was produced by S. epidermidis or P. acnes isolated from any of these individuals. Thus, we cannot attribute the perifollicular loss of elastic fibers in acne scarring to an elastase produced by organisms. The observed absence of elastic fibers might result from tissue necrosis produced by leukocytes during the inflammatory phase, followed by collagenous scar formation without regeneration of elastic fibers.
对10例寻常痤疮患者的类皮肤松弛症瘢痕进行组织病理学切片检查，结果显示毛囊皮脂腺周围的弹性纤维选择性缺失。这一发现与瓦拉迪报道的“毛囊周围弹性组织溶解”的组织学变化相似。对这10例患者、另外12例活动性寻常痤疮患者以及8名正常受试者的皮肤表面拭子和脓液进行厌氧及需氧培养，分离出的细菌进行了研究，特别关注表皮葡萄球菌和痤疮丙酸杆菌。对这些微生物进行分析，以确定其是否产生可能在观察到的弹性纤维选择性缺失中起作用的弹性溶解酶。从这些个体中分离出的表皮葡萄球菌或痤疮丙酸杆菌均未产生弹性溶解活性。因此，我们不能将痤疮瘢痕中毛囊周围弹性纤维的缺失归因于微生物产生的弹性蛋白酶。观察到的弹性纤维缺失可能是由于炎症期白细胞产生的组织坏死，随后形成胶原瘢痕，而弹性纤维未再生。
