Messmer E M, Heidenkummer H P, Kampik A
Universitäts-Augenklinik, Munich, Germany.
Graefes Arch Clin Exp Ophthalmol. 1998 Apr;236(4):248-54. doi: 10.1007/s004170050072.
The role of tangential traction exerted by epiretinal membranes in the pathogenesis of macular holes is not fully understood. Furthermore, the role of glial cells in the formation and/or closure of macular holes remains to be elucidated.
To better understand the pathogenesis of macular hole formation and to compare the ultrastructural features of epiretinal membranes associated with macular holes of primary and secondary etiology, we harvested 23 translucent epiretinal membranes associated with macular holes stages III-IV at the time of pars plana vitrectomy and examined them electron microscopically. Eighteen membranes were obtained from patients with idiopathic macular holes. 3 membranes from patients with myopic macular holes and 2 epiretinal membranes were associated with macular holes which had developed after retinal detachment surgery.
Eighteen membranes contained a continuous undulating piece of inner limiting lamina (ILL). Sixteen of 18 epiretinal membranes at the margins of idiopathic macular holes, 2 of 3 membranes in myopic macular holes and both membranes associated with a macular hole after retinal detachment surgery demonstrated mono- or multilayers of fibrous astrocytes with single macrophage- or fibrocyte-like cells. Vitreous and newly formed collagen occupied the space between the ILL and the glial cells. Three macular holes were surrounded by rather firmly attached acellular ILL.
Glial cells and newly formed collagen may play an important role in macular hole formation by exerting tangential traction regardless of the underlying disease process. Glial cells, however, may also be involved in healing of the retinal defect and pars plana vitrectomy with peeling of an epiretinal membrane, and/or the ILL may induce directed glial cell proliferation and migration. The similar ultrastructure of epiretinal membranes associated with macular holes and "simple epiretinal membranes" as described by Foos [8] suggests a common pathogenesis for macular holes and macular pucker.
视网膜前膜施加的切线牵引力在黄斑裂孔发病机制中的作用尚未完全明确。此外,神经胶质细胞在黄斑裂孔形成和/或闭合中的作用仍有待阐明。
为了更好地理解黄斑裂孔形成的发病机制,并比较原发性和继发性病因导致的黄斑裂孔相关视网膜前膜的超微结构特征,我们在玻璃体切割术时收集了23例与Ⅲ - Ⅳ期黄斑裂孔相关的半透明视网膜前膜,并进行电子显微镜检查。18例膜取自特发性黄斑裂孔患者。3例膜取自近视性黄斑裂孔患者,2例视网膜前膜与视网膜脱离手术后出现的黄斑裂孔相关。
18例膜中含有一片连续起伏的内界膜(ILL)。特发性黄斑裂孔边缘的18例视网膜前膜中的16例、近视性黄斑裂孔的3例膜中的2例以及与视网膜脱离手术后黄斑裂孔相关的2例膜均显示有单层或多层纤维星形胶质细胞以及单个巨噬细胞样或成纤维细胞样细胞。玻璃体和新形成的胶原占据了ILL与神经胶质细胞之间的空间。3个黄斑裂孔被附着相当牢固的无细胞ILL所环绕。
无论潜在的疾病过程如何,神经胶质细胞和新形成的胶原可能通过施加切线牵引力在黄斑裂孔形成中起重要作用。然而,神经胶质细胞也可能参与视网膜缺损的愈合以及视网膜前膜和/或ILL剥离的玻璃体切割术,并且/或者ILL可能诱导定向的神经胶质细胞增殖和迁移。与黄斑裂孔相关的视网膜前膜和Foos [8]所描述的“单纯视网膜前膜”的相似超微结构提示黄斑裂孔和黄斑皱襞有共同的发病机制。