Papillofoveal Traction in Macular Hole Formation

Abstract

THERE HAVE BEEN many theories on the pathogenesis of macular holes during the past 150 years.¹ The most widely held group of theories invokes tractional forces at the fovea that are exerted at points of vitreofoveal adhesion. In the normal eye, the adhesion at the vitreoretinal interface is thought to be greatest at the vitreous base, the margins of the optic disc, and the overlying major retinal vessels.² The anatomical basis of this adhesion consists of 2 junctional systems.² The first, and probably the weaker most commonly, is the widespread insertion of cortical vitreous collagen fibrils into the substance of the inner limiting membrane (ILM).³ The nature of these bonds is believed to be chemical, as electron microscopy reveals no junctional structures.² The second is stronger and consists of interspersed junctions between the ILM and Müller cells. At the fovea, the ILM is known to be thin, but the anatomy of the vitreous, and its attachment to the fovea, is somewhat controversial. In vitro studies have demonstrated the presence of a premacular bursa⁴ and discrete zones of vitreofoveal adhesion,^5,6 but these have been difficult to corroborate in vivo.^7,8