[Vitreous and macular diseases]

Abstract

We investigated the vitreous in its origin, morphology, metabolism and regeneration, and its role in various vitreomacular diseases. Focal vitreous liquefaction developed anterior to a laser induced chorioretinal scar in rabbit eyes, which suggested that a normal retina is necessary to maintain the integrity of the vitreous. We measured levels of hyaluronic acid and of the precursor of type II collagen in vitreous samples obtained by vitrectomy. Those levels declined with age in women. The precursor of type II collagen was at the same level in the samples from vitrectomy and those obtained by fluid air exchange, which suggested a persistent secretion of type II collagen into the vitreous cavity even after vitrectomy. We found a posterior precortical vitreous pocket in human autopsied eyes whose vitreous was stained with fluorescein. Using the same methods, we confirmed the presence of intravitreal fibrous membranes in the "tractus" in the anterior vitreous. In clinical studies using biomicroscopy, observations during surgery, scanning laser ophthalmoscopy, and optical coherence tomography (OCT), we clarified the role of premacular vitreous cortex which forms the posterior wall of the "pocket" in the premacular membrane and macular hole. The premacular vitreous cortex seems to be the main structure of the premacular membrane and its contraction may cause macular hole. Ring-shaped proliferation tends to develop along the outer margin of the "pocket". OCT demonstrated that some diabetic macular edema is caused by traction of the premacular vitreous cortex. Vitrectomy appear to be effective for diabetic macular edema by eliminating vitreous traction and the accumulated cytokine in the "pocket". The retina appears to have a program for vitreous metabolism throughout life, including the premacular pocket formation.