PDF(Sci-hub)
Abstract：
Tractional deformations of the fovea mainly arise from an anomalous posterior vitreous detachment and contraction of epiretinal membranes, and also occur in eyes with cystoid macular edema or high myopia. Traction to the fovea may cause partial- and full-thickness macular defects. Partial-thickness defects are foveal pseudocysts, macular pseudoholes, and tractional, degenerative, and outer lamellar holes. The morphology of the foveal defects can be partly explained by the shape of Müller cells and the location of tissue layer interfaces of low mechanical stability. Because Müller cells and astrocytes provide the structural scaffold of the fovea, they are active players in mediating tractional alterations of the fovea, in protecting the fovea from such alterations, and in the regeneration of the foveal structure. Tractional and degenerative lamellar holes are characterized by a disruption of the Müller cell cone in the foveola. After detachment or disruption of the cone, Müller cells of the foveal walls support the structural stability of the foveal center. After tractional elevation of the inner layers of the foveal walls, possibly resulting in foveoschisis, Müller cells transmit tractional forces from the inner to the outer retina leading to central photoreceptor layer defects and a detachment of the neuroretina from the retinal pigment epithelium. This mechanism plays a role in the widening of outer lameller and full-thickness macular holes, and contributes to visual impairment in eyes with macular disorders caused by conractile epiretinal membranes. Müller cells of the foveal walls may seal holes in the outer fovea and mediate the regeneration of the fovea after closure of full-thickness holes. The latter is mediated by the formation of temporary glial scars whereas persistent glial scars impede regular foveal regeneration. Further research is required to improve our understanding of the roles of glial cells in the pathogenesis and healing of tractional macular disorders.
摘要：
中央凹的牵引变形主要来自异常的后玻璃体脱离和视网膜前膜的收缩，并且也发生在黄斑囊样水肿或高度近视的眼睛中。牵引到中央凹可能会导致部分和全厚度黄斑缺损。部分厚度缺损是中央凹假性囊肿，黄斑假孔,和牵引，退化,和外部层状孔。中央凹缺损的形态可以部分通过Müller细胞的形状和低机械稳定性的组织层界面的位置来解释。因为Müller细胞和星形胶质细胞提供了中央凹的结构支架，他们是调解中央凹的牵引改变的积极参与者，为了保护中央凹免受这种改变，在中央凹结构的再生中。牵引性和退行性板层孔的特征是中央凹的Müller细胞锥破裂。在圆锥体脱离或破裂后，中央凹壁的Müller细胞支持中央凹中心的结构稳定性。在中央凹壁内层牵引抬高后，可能会导致中央凹，Müller细胞将牵引力从内部传递到外部视网膜，导致中央感光层缺陷和神经视网膜从视网膜色素上皮脱离。这种机制在外层和全厚度黄斑孔的加宽中起作用，并有助于由视网膜前膜引起的黄斑疾病的视力障碍。中央凹壁上的Müller细胞可以密封外部中央凹的孔，并在全厚度孔闭合后介导中央凹的再生。后者是由暂时性神经胶质疤痕的形成介导的，而持续性神经胶质疤痕会阻碍定期的中央凹再生。需要进一步的研究来提高我们对神经胶质细胞在牵引性黄斑疾病的发病机理和愈合中的作用的理解。
