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.

中央凹的牵引变形主要是由异常的玻璃体后脱离和视网膜前膜收缩引起的，也发生在黄斑囊样水肿或高度近视眼中。对中央凹的牵引可能导致部分和全层黄斑缺损。部分厚度缺损是中心凹假性囊肿、黄斑假孔以及牵引性、退行性和外板层孔。中心凹缺陷的形态可以部分解释为 Müller 细胞的形状和机械稳定性低的组织层界面的位置。由于 Müller 细胞和星形胶质细胞提供了中央凹的结构支架，它们在调节中央凹的牵引性改变、保护中央凹免受此类改变以及中央凹结构的再生方面发挥着积极作用。牵引性和退行性板层孔的特征在于中央凹中的 Müller 细胞锥体的破坏。在锥体分离或破坏后，中央凹壁的 Müller 细胞支持中央凹中心的结构稳定性。在中央凹壁内层的牵引抬高后，可能导致中央凹劈裂，Müller 细胞将牵引力从视网膜内部传递到外部，导致中央感光层缺陷和神经视网膜从视网膜色素上皮细胞脱离。这种机制在外层和全层黄斑裂孔的扩大中发挥作用，并导致由收缩性视网膜前膜引起的黄斑病变眼睛的视力障碍。中央凹壁的 Müller 细胞可以封闭外中央凹的孔，并在全层孔闭合后介导中央凹的再生。后者是由暂时性胶质瘢痕的形成介导的，而持续性胶质瘢痕阻碍了正常的中央凹再生。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制和愈合中的作用的理解。