Gandorfer A, Rohleder M, Kampik A
Department of Ophthalmology, Ludwig-Maximilians-University, Mathildenstrasse 8, D - 80336, München, Germany.
Br J Ophthalmol. 2002 Aug;86(8):902-9. doi: 10.1136/bjo.86.8.902.
To investigate the ultrastructure of the vitreoretinal interface in patients with vitreomacular traction syndrome.
14 patients with vitreomacular traction syndrome underwent standard pars plana vitrectomy. After induction of posterior vitreous detachment, epiretinal tissue and the inner limiting membrane (ILM) of the retina were removed, and processed for transmission electron microscopy.
Ultrastructural analysis revealed two basic patterns of vitreoretinal pathology in eyes with vitreomacular traction syndrome. Seven specimens showed mostly single cells or a cellular monolayer covering closely the vitreal side of the ILM, not resulting in a biomicroscopically detectable epiretinal fibrocellular proliferation. The other seven specimens revealed premacular fibrocellular tissue which was separated from the ILM by a layer of native collagen, resembling the clinical features of idiopathic epiretinal membranes. In both groups of eyes, the myofibroblast was the predominant cell type. Fibrous astrocytes and fibrocytes were less frequent. Retinal pigment epithelial cells and macrophages were absent. Deposits of newly formed collagen were present only adjacent to fibrocellular multilayers.
There are two distinct clinicopathological features of vitreomacular traction syndrome which suggest different forms of epiretinal fibrocellular proliferation: (1) epiretinal membranes interposed in native vitreous collagen and (2) single cells or a cellular monolayer proliferating directly on the ILM. The presence of remnants of the cortical vitreous which remain attached to the ILM following posterior vitreous separation may determine the clinicopathological feature of the disease. The predominance of myofibroblasts may help to explain the high prevalence of cystoid macular oedema and progressive vitreomacular traction characteristic for this disorder.
研究玻璃体黄斑牵引综合征患者玻璃体视网膜界面的超微结构。
14例玻璃体黄斑牵引综合征患者接受了标准的玻璃体切除术。在诱导玻璃体后脱离后,切除视网膜前组织和视网膜内界膜(ILM),并进行透射电子显微镜检查。
超微结构分析揭示了玻璃体黄斑牵引综合征患者玻璃体视网膜病变的两种基本模式。7个标本显示主要为单个细胞或细胞单层紧密覆盖ILM的玻璃体侧,未导致生物显微镜下可检测到的视网膜前纤维细胞增殖。另外7个标本显示黄斑前纤维细胞组织,其与ILM之间被一层天然胶原分隔,类似于特发性视网膜前膜的临床特征。在两组眼中,肌成纤维细胞是主要的细胞类型。纤维性星形胶质细胞和纤维细胞较少见。视网膜色素上皮细胞和巨噬细胞不存在。新形成的胶原沉积物仅存在于纤维细胞多层结构附近。
玻璃体黄斑牵引综合征有两种不同的临床病理特征,提示视网膜前纤维细胞增殖的不同形式:(1)插入天然玻璃体胶原中的视网膜前膜;(2)直接在ILM上增殖的单个细胞或细胞单层。玻璃体后脱离后仍附着于ILM的皮质玻璃体残余物的存在可能决定了该疾病的临床病理特征。肌成纤维细胞的优势可能有助于解释该疾病中黄斑囊样水肿的高发生率和进行性玻璃体黄斑牵引的特征。