Vitreous Liquefaction and Posterior Vitreous Detachment
The human vitreous gel undergoes progressive liquefaction beginning around 40 years of age, so that typically by age 80–90 years, more than half of the vitreous is liquid. A crucial step in the process of vitreous liquefaction is the breakdown of the thin (12–15-nm) collagen fibrils into smaller fragments. Implicated in this process is reduced shielding of type II collagen fibrils due to the age-related exponential loss of type IX collagen. Some proteolytic enzymes, such as plasminogen, may have elevated vitreous concentrations with increasing age, but others, such as MMP-2 (matrix metalloproteinase-2), do not.
The fragments aggregate into thicker fibers, or fibrillar opacities, which are visible with low-power slit-lamp microscopy. As liquefaction proceeds, the collagen fibers become condensed into the residual gel phase and are absent from (or in low concentration in) the liquid phase. In terms of hyaluronan concentration or molecular weight, there are no differences between the gel and liquid phases. With increasing age, a weakening of adhesion occurs at the vitreoretinal interface, which lies between the cortical vitreous gel and the ILM. These combined processes eventually result in posterior vitreous detachment (PVD) in approximately 50% of individuals after 50 years of age.
PVD is a separation of the cortical vitreous gel from the ILM as far anteriorly as the posterior border of the vitreous base; the separation does not extend into the vitreous base owing to the unbreakable adhesion between the vitreous and retina in that zone (Fig 11-5). PVD is often a sudden event, during which liquefied vitreous from the center of the vitreous body passes through a hole in the posterior vitreous cortex, at its attachment to the optic nerve, and then dissects the residual cortical vitreous away from the ILM. As the residual vitreous gel collapses anteriorly within the vitreous cavity, retinal tears sometimes occur in areas where the retina is more strongly attached to the vitreous than the surrounding retina can withstand, which subsequently can result in rhegmatogenous retinal detachment. Anomalous PVD can lead to the formation of epiretinal membranes and macular holes (see BCSC Section 12, Retina and Vitreous).
Bishop PN, Holmes DF, Kadler KE, McLeod D, Bos KJ. Age-related changes on the surface of vitreous collagen fibrils. Invest Ophthalmol Vis Sci. 2004;45(4):1041–1046.
Fincham GS, James S, Spickett C, et al. Posterior vitreous detachment and the posterior hyaloid membrane. Ophthalmology. 2018;125(2):227–236.
Figure 11-5 Posterior vitreous detachment (PVD). Gross photo graph of an eye with PVD. The vitreous gel remains anchored anteriorly at the vitreous base, having separated from the posterior pole.
(Courtesy of Hans E. Grossniklaus, MD.)
Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.