Thalidomide prevents donor corneal graft neovascularization in an alkali burn model of corneal angiogenesis

Abstract

Objective: Thalidomide is a potent inhibitor of angiogenesis. We evaluated the effects of Thalidomide on corneal angiogenesis and on tissue survival of grafts in rabbit eyes with pre-existing neovascularization secondary to alkali burn.

Methods: Sixteen rabbits received alkali burns to one cornea. One month post-injury, assessments of corneal neovascularization were performed followed by corneal transplantation. Four rabbits received oral Thalidomide and ten got placebo (powdered sugar) for thirty days. Total corneal neovascularization (NV), clock hours (CH) involved in (NV), longest (NV) pedicle length (NVP) and the duration of time required for NV to develop were assessed.

Results: Thalidomide significantly decreased the total neovascularization (p<0.0072), the number of (CH) involved (p<0.0002) and the longest (NVP) length (p<0.0001). There was also a significant delay in the earliest development of NV in the test group (p<0.0064). The test group retained corneal clarity significantly longer than the control group (p<0.0008).

Conclusion: Thalidomide is an effective inhibitor of corneal angiogenesis and prolongs graft survival as measured by graft clarity in donor corneas in eyes with previous neovascularization secondary to alkali injury.

Clinical relevance: Thalidomide may be used as a modulator of corneal angiogenesis to prolong graft survival in eyes with pre-existing corneal neovascularization.