Inflammation and its effect on the vitreous.

The role of the vitreous in inflammatory diseases of the eye is now more clearly defined because of improved methods of examination and surgery. Inflammatory diseases of various aetiology produce opacification, liquefaction, and shrinkage. Additional changes include cellular proliferation and transformation leading to fibrosis in cases of prolonged inflammation. In some eyes the fibrosis is primarily cortical while in others it is extensive. Those inflammations with outpouring of a fluid exudate lead to detachment of the vitreous from the posterior eye and extensive shrinkage. In such eyes the vitreous becomes heavily organized and opaque in the central eye behind the lens, obscuring the view of the posterior fundus. In young eyes vitreo-retinal adhesions often form at the sites of inflammation, leading to traction on the retina and ciliary body; retinal tears may result from the traction. Exudate in many inflammatory vitreal inflammations tends to collect at the vitreous base where it organizes into scar tissue. The scar is formed by the retina and ciliary body, but there are also fibrosis-produced monocytes that become transformed into fibroblasts. Shrinkage of the new-formed scar can lead to disinsertion or peripheral tears of the retina. Specific inflammations such as chronic cyclitis and toxoplasmosis produce characteristic changes in the vitreous that can be recognized on clinical examination. Melanomas and reticulum cell sarcomas also produce a characteristic vitreous opacification.