Histopathologic and immunohistochemical features of capsular tissue around failed Ahmed glaucoma valves.

Impervious encapsulation around Ahmed glaucoma valve (AGV) results in surgical failure raising intraocular pressure (IOP). Dysregulation of extracellular matrix (ECM) molecules and cellular factors might contribute to increased hydraulic resistance to aqueous drainage. Therefore, we examined these molecules in failed AGV capsular tissue. Immunostaining for ECM molecules (collagen I, collagen III, decorin, lumican, chondroitin sulfate, aggrecan and keratan sulfate) and cellular factors (αSMA and TGFß) was performed on excised capsules from failed AGVs and control tenon's tissue. Staining intensity of ECM molecules was assessed using Image J. Cellular factors were assessed based on positive cell counts. Histopathologically two distinct layers were visible in capsules. The inner layer (proximal to the AGV) showed significant decrease in most ECM molecules compared to outer layer. Furthermore, collagen III (p = 0.004), decorin (p = 0.02), lumican (p = 0.01) and chondroitin sulfate (p = 0.02) was significantly less in inner layer compared to tenon's tissue. Outer layer labelling however was similar to control tenon's for most ECM molecules. Significantly increased cellular expression of αSMA (p = 0.02) and TGFß (p = 0.008) was detected within capsular tissue compared to controls. Our results suggest profibrotic activity indicated by increased αSMA and TGFß expression and decreased expression of proteoglycan (decorin and lumican) and glycosaminoglycans (chondroitin sulfate). Additionally, we observed decreased collagen III which might reflect increased myofibroblast contractility when coupled with increased TGFß and αSMA expression. Together these events lead to tissue dysfunction potentially resulting in hydraulic resistance that may affect aqueous flow through the capsular wall.

Pathological and Immunohistochemical Alterations of the Cornea in Congenital Corneal Opacification Secondary to Primary Congenital Glaucoma and Peters Anomaly.

PURPOSE: To examine the immunohistochemical alterations in the corneal stroma in Peters anomaly (PA) and congenital glaucoma (CG) compared with age-matched normals and acquired adult corneal scarring (AACS). METHODS: The clinical features of PA and CG patients who underwent penetrating keratoplasty were recorded. Immunohistochemistry of cornea and control tissue (normal and acquired corneal scars) was performed with antibodies against collagen types I, III, keratan sulfate, lumican, decorin, and smooth muscle actin followed by semiquantitative analysis of immunolabeling. RESULTS: Clinical features in 2 groups were consistent with PA and CG. Microscopy showed thickened stromal collagen bundles in PA (n = 15), CG (n = 11), and AACS (n = 20) compared with normals (n = 18). PA and CG had distinct immunophenotypes compared with controls. Type I collagen labeling was more intense in CG compared with PA (intensity grading (IG) 2.73 vs. 2.07; P < 0.001). Decorin, lumican, and keratan sulfate labeling was significantly less intense in PA versus AACS (IG; 1.91, 0.38, 1.75 in PA and 2.7, 1.11, 2.61 in AACS. respectively; P = 0.002, P = 0.001 and P = 0.004) and normals (IG 1.92, 1.06, 2.59 respectively; P < 0.001, P < 0.001 and P = 0.005). Collagen I labeling was less intense in CG versus AACS (IG 2.73 vs. 3.09) (P = 0.007). Collagen III labeling was more intense in PA/CG than in normals (IG 0.9, 0.64, 0.62 retrospectively) (P < 0.001 in both). CONCLUSIONS: The immunophenotype of the corneal scar in PA and CG differs from normal corneas and so does PA from AACS. The similarities between CG and AACS suggest that CG scarring has an acquired component.