PURPOSE: To evaluate histopathological changes induced in keratoconic corneas after implantation of Intacs intracorneal ring segments (Addition Technology, Inc.). SETTING: Departments of Ophthalmology and Pathology, Hospital Pellegrin, Bordeaux, France. METHODS: This retrospective study included 8 keratoconic, contact-lens-intolerant eyes of 8 patients who had penetrating keratoplasty (PKP) after removal of Intacs inserts because of a poor refractive outcome or insert extrusion. Light microscopy was performed on all specimens after conventional staining. Immunohistochemistry was performed to identify cell types located next to the tunnel using AE1/AE3 cytokeratins, CD34, vimentin, collagen IV, and alpha-smooth muscle actin monoclonal antibodies. RESULTS: Conventional histology showed hypoplasia of the epithelium immediately surrounding the channel. There was no evidence of an inflammatory response or foreign-body granuloma. Keratocyte density was decreased above and below the tunnel, and collagen IV synthesis was seen in the scar area. All samples stained negatively with alpha-smooth muscle actin, indicating that myofibroblasts were not present. These changes were no longer visible when PKP was performed more than 6 months after Intacs explantation. CONCLUSIONS: Intacs induced keratocyte apoptosis, probably through a switch to a collagenous synthetic phenotype. Although histological changes seem to be entirely reversible after implant removal, longer follow-up is necessary to determine whether they accelerate corneal thinning and keratoconus progression via apoptosis and release of metalloprotease.
PURPOSE: To evaluate histopathological changes induced in keratoconic corneas after implantation of Intacs intracorneal ring segments (Addition Technology, Inc.). SETTING: Departments of Ophthalmology and Pathology, Hospital Pellegrin, Bordeaux, France. METHODS: This retrospective study included 8 keratoconic, contact-lens-intolerant eyes of 8 patients who had penetrating keratoplasty (PKP) after removal of Intacs inserts because of a poor refractive outcome or insert extrusion. Light microscopy was performed on all specimens after conventional staining. Immunohistochemistry was performed to identify cell types located next to the tunnel using AE1/AE3 cytokeratins, CD34, vimentin, collagen IV, and alpha-smooth muscle actin monoclonal antibodies. RESULTS: Conventional histology showed hypoplasia of the epithelium immediately surrounding the channel. There was no evidence of an inflammatory response or foreign-body granuloma. Keratocyte density was decreased above and below the tunnel, and collagen IV synthesis was seen in the scar area. All samples stained negatively with alpha-smooth muscle actin, indicating that myofibroblasts were not present. These changes were no longer visible when PKP was performed more than 6 months after Intacs explantation. CONCLUSIONS: Intacs induced keratocyte apoptosis, probably through a switch to a collagenous synthetic phenotype. Although histological changes seem to be entirely reversible after implant removal, longer follow-up is necessary to determine whether they accelerate corneal thinning and keratoconus progression via apoptosis and release of metalloprotease.
Authors: Hussain F Al-Habboubi; Hernan Martinez-Osorio; Azza M Y Maktabi; Abdulrahman H Badawi; Faisal N Aldosari; Rajiv Khandekar; Samar A Al-Swailem Journal: Saudi J Ophthalmol Date: 2022-07-11