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. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Mech Res Commun. 2012 Jun;42:92–106. doi: 10.1016/j.mechrescom.2012.01.007

Fig. 8.

Fig. 8

G&R simulation of the LC thickening seen in early experimental glaucoma. The collagen fibril volume fraction in the neural canal tissues is shown for the initial configuration and the modeled homeostatic configuration at normal (15 mmHg) and elevated IOPs (25 mmHg). Neural canal tissues with a collagen fibril density of 10% or more were defined to represent the LC. The simulation starts with an initial homogeneous collagen fibril density (6%) throughout the neural canal tissues without presupposing the existence of a LC. After reaching model homeostasis at normal IOP (15 mmHg), the model predicted the existence of a LC-like structure spanning the scleral canal of similar dimensions, shape and location of the normal LC in vivo. To regain model homeostasis after IOP elevation to 25 mmHg, the model predicted the significant thickening of the LC due to local increase in collagen fibril density in the pre- and retrolaminar tissues and the recruitment of these tissues into the LC. The borders of the LC insertion into the surrounding sclera also migrated as the LC thickened (Grytz et al., 2011b).