J. Sebag, MD, FACS, FRCOphth., Professor of Clinical Ophthalmology, Doheny Eye Institute, University of Southern California Los Angeles, California, USA

Invisible by design1, 2, vitreous is a viscoelastic extracellular matrix that normally exists in a gel state as a result of the intricate organization of its macromolecular components3. Hyaluronan (HA) and collagen, primarily type II but also type IX, and a hybrid of types V/XI, are organized into a three-dimensional network that maintains media clarity and provides shock-absorption. The peripheral vitreous cortex consists of densely packed collagen fibrils and has a high concentration of HA. In youth the posterior vitreous cortex is firmly adherent to the internal limiting lamina (ILL) of the retina4. While the exact nature of vitreo-retinal adhesion is not known, it most probably results from the biophysical properties of the extracellular matrix molecules found at this interface5, 6.

Diabetes causes elevated levels of glucose and advanced glycation end-products in vitreous7, 8. These induce structural changes within the corpus vitreus9 and at the vitreo-retinal interface that promote the migration and proliferation of vasculogenic cells. Traction upon new vessels growing into the posterior vitreous cortex10 worsens the prognosis in these patients. Posterior vitreoschisis11 is another manifestation of diabetic vitreopathy that can cause vitreous hemorrhage. Diabetic vitreopathy12 is also important in macular edema refractory to laser therapy.

Prevention via improved glycemic control and adjunctive therapy to prevent non-enzymatic glycation may mitigate against the effects of diabetic vitreopathy. The induction of posterior vitreous detachment via pharmacologic vitreolysis13, 14 prior to onset of advanced disease may also greatly improve the prognosis.

1. Sebag J: The Vitreous – Structure, Function, and Pathobiology. Springer-Verlag, New York, 1989.
2. Sebag J: Guest editorial: Classifying Posterior Vitreous Detachment – a new way to look at the invisible. Brit J Ophthalmol 81:521-522, 1997.
3. Sebag J: Macromolecular structure of vitreous, In: Polymer Science and the Eye (TV Chirila, ed). Prog Polym Sci 23:415-446, 1998.
4. Sebag J: Age-related differences in the human vitreo-retinal interface. Arch Ophthalmol 109:966-971, 1991
5. Sebag J, Hageman GS: Interfaces. (Guest Editorial) Eur J Ophthalmol 10:1-3, 2000
6. Green WR, Sebag J: Vitreous and the vitreo-retinal interface. In: Retina (SJ Ryan, ed) Mosby, St. Louis, 2001; Vol III, pp 1882 – 1960
7. Sebag J, Buckingham B, Charles MA, Reiser K: Biochemical abnormalities in vitreous of humans with proliferative diabetic retinopathy. Arch Ophthalmol 110:1472-79, 1992..
8. Sebag J, Nie S, Reiser KA, Charles MA, Yu NT: Raman spectroscopy of human vitreous in proliferative diabetic retinopathy. Invest Ophthalmol Vis Sci 35:2976-2980, 1994.
9. Sebag J: Abnormalities of human vitreous structure in diabetes. Graef Arch Clin Exp Ophthalmol 231:257-260, 1993.
10. Faulborn J, Bowald S: Microproliferations in proliferative diabetic retinopathy and their relation to the vitreous – corresponding light and electron microscopic studies. Graef Arch Clin Exp Ophthalmol 223:130, 1985..
11. Chu T, Lopez PF, Cano MR, et al: Posterior vitreoschisis – an echographic finding in proliferative diabetic retinopathy. Ophthalmology 103:315-22, 1996
12.. Sebag J: Diabetic Vitreopathy (Guest Editorial). Ophthalmology 103:205-206, 1996.
13. Sebag J: Pharmacologic vitreolysis. Retina 18:1-3, 1998.
14. Sebag J: Is pharmacologic vitreolysis brewing? Retina 22:1-3, 2002.