This is the first study to evaluate vitreous liquefaction at the light and electron microscopic level. A breakdown of collagen fibrils into smaller fragments seems to be crucial to the pathogenesis of age-related liquefaction of the human vitreous body. The mechanism inducing fragmentation of vitreous fibrils has yet to be elucidated. From the absence of cells and cellular remnants in all specimens, it is tentatively concluded that an extracellular process is involved.

Staining patterns of collagen types I to V, IX, XI, and XVIII confirmed previous observations. Important new findings include the presence of type VI in the ILM and type VII in several layers of the retina. Both collagens can anchor matrix components, and type VI could be involved in vitreoretinal attachment. Furthermore, the presence of collagen mRNA in human retinectomy samples may be an indication of postnatal collagen production by retinal cells.

Type VI collagen and activated retinal Müller cells are present in iERM. Transforming growth factor-β1 induces an up-regulation of α-SMA stress fibers in retinal Müller cells and fibroblasts and appears to have a cell-specific effect on intracellular collagen expression.