Lamina cribrosa in glaucoma

Abstract

Purpose of review: This article presents, summarizes, and interprets the most recent advances in the study and understanding of the lamina cribrosa in glaucoma, in the context of previous work.

Recent findings: The lamina is an active living structure that responds to strain by changing morphology at the micro-scale and macro-scale in glaucoma. Changes in lamina cribrosa morphology in glaucoma include posteriorization of the laminar insertion into the sclera, increased cupping or depth of the lamina cribrosa, and the development of focal lamina cribrosa defects. These lamina cribrosa changes are associated with disk hemorrhages and visual field damage, and are detectable with clinical imaging techniques such as optical coherence tomography. Glaucomatous changes in the lamina cribrosa are thought to be driven by cellular processes mediated by focal cyclical mechanical strain. Strain is eye specific and mediated by intraocular pressure, cerebrospinal fluid pressure, scleral and lamina cribrosa morphology, and structural stiffness; deleterious lamina cribrosa strains can occur at all levels of mean intraocular pressure.

Summary: Laminar morphology is ever changing in health and disease, and recent studies have identified several promising morphological changes that are indicative of glaucoma susceptibility, onset, and progression.

Figure 1

A high-resolution three-dimensional (3D) reconstruction of the lamina cribrosa from a human donor eye. The fluorescent histologic reconstruction was created using a custom, automated, microtome-based episcopic fluorescent image capture device that images the embedded ONH tissue block face after each thin section is cut away, thereby capturing the LC structure in an image volume at 1.5×1.5×1.5 micrometer voxel resolution. Regional differences in laminar density and beam orientation are evident. Callouts show the laminar microstructure (top), the typical mechanical strain in the laminar microstructure in response to an IOP elevation from 10 to 45 mmHg as estimated by a computational model (middle), and the F-actin (red) and αSMA (green) in activated fibroblastic cells that engender LC remodeling after cyclic strain is applied (bottom).