Occupying 80% of the volume of the eye, the vitreous is a clear matrix composed of collagen, hyaluronic acid, and water. The vitreous body is composed of 2 main portions: the central, or core, vitreous and the cortical vitreous, the outer portion of the vitreous. The anterior bounding surface of the vitreous body is the anterior hyaloid membrane, a condensation of protein fibers that has a retrolental indentation called the patellar fossa. In the vitreous base, the collagen fibers are especially dense; they implant into an area that extends 2 mm anterior and 3 mm posterior to the ora serrata. These fibers are very difficult to disinsert during surgery. They extend radially in toward the vitreous gel for several millimeters. The vitreous gel contains collagen fibers that arch posteriorly. Between the collagen fibers are hyaluronate molecules, which bind water molecules. These hyaluronate molecules, with their associated water molecules, act as fillers and separators between the adjacent collagen fibers. The collagen fibers in the cortical vitreous are much more densely packed, in a feltlike network; these fibers course in a direction roughly parallel to the inner surface of the retina. Although the vitreous is most firmly attached to the vitreous base, it is also firmly attached to retinal vessels, the optic nerve, and the macula. The attachment of the vitreous to the macula is arranged in 3 circumferential zones centered on the foveola; this specific attachment configuration influences the morphology of tractional maculopathies. Liquefaction of the vitreous starts as early as age 2 in a zone above the posterior pole and produces a space known as the premacular bursa, or the precortical vitreous pocket (Fig 1-1). The anatomy of the vitreous is difficult to delineate in vivo, but the vitreous appears to contain interconnected smaller bursae as well.
Over time the vitreous cavity develops larger and more numerous pockets of liquefaction. Enzymatic and nonenzymatic cross-linking of collagen fibers, free-radical damage, and decreases in network density of collagen fibers lead to destabilization of the vitreous gel. Eventually the vitreous gel starts to shrink, putting various portions of the retina under tractional stress. Focal traction on the retina may produce retinal tears or holes. The vitreous may also place traction over a somewhat larger area of the retina; because the resultant tensile force is spread over this larger area, it may be below that required to cause tears. This force may instead distort the retina or cause tractional elevation of the retina. One example of this process is the vitreomacular traction syndrome, a condition where the patient develops blurring and distortion of the central vision because of traction on the macula by the vitreous. More focal traction on the fovea may produce foveal cavitation and macular holes. The force vectors on the macula from vitreous traction are probably modified by the presence of bursae. The posterior vitreous starts to detach from the retina in discrete zones but later may detach from wide areas of the posterior pole. This produces a posterior vitreous detachment, which happens to almost everyone who lives long enough.