Department of Biomedical Engineering, Yale University, New Haven, CT 06520, USA.
Wilmer Ophthalmological Institute, School of Medicine, The Johns Hopkins University, Baltimore, MD 21287, USA.
Acta Biomater. 2020 Apr 1;106:225-241. doi: 10.1016/j.actbio.2020.01.049. Epub 2020 Feb 8.
This study investigated the inflation response of the lamina cribrosa (LC) and adjacent peripapillary sclera (PPS) in post-mortem human eyes with no history of glaucoma. The posterior sclera of 13 human eyes from 7 donors was subjected to controlled pressurization between 5-45 mmHg. A laser-scanning microscope (LSM) was used to image the second harmonic generation (SHG) response of collagen and the two-photon fluorescent (TPF) response of elastin within the volume of the LC and PPS at each pressure. Image volumes were analyzed using digital volume correlation (DVC) to calculate the three-dimensional (3D) deformation field between pressures. The LC exhibited larger radial strain, E, and maximum principal strain, E, (p < 0.0001) and greater posterior displacement (p=0.0007) compared to the PPS between 5-45 mmHg, but had similar average circumferential strain, E, and maximum shear strain, Γ. The E and Γ were highest near the LC-PPS interface and lowest in the nasal quadrant of both tissues. Larger LC area was associated with smaller E in the peripheral LC and larger E in the central LC (p ≤ 0.01). The E, Γ, and E in the inner PPS increased with increasing strain in adjacent LC regions (p ≤ 0.001). Smaller strains in the PPS were associated with a larger difference in the posterior displacement between the PPS and central LC (p < 0.0001 for E and E), indicating that a stiffer pressure-strain response of the PPS is associated with greater posterior bowing of the LC. STATEMENT OF SIGNIFICANCE: Glaucoma causes vision loss through progressive damage of the retinal ganglion axons at the lamina cribrosa (LC), a connective tissue structure that supports the axons as they pass through the eye wall. It is hypothesized that strains caused by intraocular pressure may initiate this damage and that these strains are modulated by the combined deformation of the LC and adjacent peripapillary sclera (PPS). In this study we present a method to measure the pressure-induced 3D displacement and strain field in the LC and PPS simultaneously. Regional strain variation in the LC and PPS was investigated and compared and strains were analyzed for associations with age, LC area, LC strain magnitude, and LC posterior motion relative to the PPS.
本研究旨在探究无青光眼病史的人眼死后,颅神经纤维层(LC)和其周围视乳头巩膜(PPS)的膨胀反应。通过对来自 7 位供体的 13 只人眼的后巩膜施加 5-45mmHg 的可控压力,使用激光扫描显微镜(LSM)来测量 LC 和 PPS 体积内的二次谐波产生(SHG)的胶原蛋白反应和双光子荧光(TPF)的弹性蛋白反应。通过数字体积相关(DVC)分析图像体积,以计算压力之间的三维(3D)变形场。与 PPS 相比,LC 在 5-45mmHg 之间表现出更大的径向应变(E)和最大主应变(E)(p<0.0001)以及更大的后向位移(p=0.0007),但平均周向应变(E)和最大剪切应变(Γ)相似。E 和 Γ 在 LC-PPS 界面附近最高,在两个组织的鼻象限最低。LC 面积越大,外周 LC 的 E 越小,中央 LC 的 E 越大(p≤0.01)。内 PPS 的 E、Γ 和 E 随着相邻 LC 区域应变的增加而增加(p≤0.001)。PPS 中的应变越小,PPS 和中央 LC 之间的后向位移差异越大(E 和 E 时 p<0.0001),这表明 PPS 的压力-应变响应越硬,LC 的后向弯曲越大。意义声明:青光眼通过在颅神经纤维层(LC)处的视网膜神经节轴突进行渐进性损伤导致视力丧失,LC 是一种结缔组织结构,作为轴突穿过眼球壁的支撑。假设眼压引起的应变可能会引发这种损伤,并且这些应变是由 LC 和相邻视乳头巩膜(PPS)的联合变形调节的。在这项研究中,我们提出了一种同时测量 LC 和 PPS 中压力诱导的 3D 位移和应变场的方法。研究了 LC 和 PPS 中的区域应变变化并进行了比较,并分析了应变与年龄、LC 面积、LC 应变幅度和 LC 相对于 PPS 的后向运动之间的关系。