Preliminary Results of Noninvasive Ocular Rigidity in Diabetic Retinopathy Using Optical Coherence Tomography

The pathologic mechanism of diabetic retinopathy is directly related to the underlying hyperglycemia associated with diabetes. Hyperglycemia causes non-enzymatic cross-linking of collagen fibrils which contributes mechanistically to tissue stiffening. However, investigations on diabetic retinopathy-associated alteration in ocular biomechanics remain scarce, especially in living human eyes. Ocular rigidity is classically defined as a measure of the change in intraocular pressure produced by a change in ocular volume. We recently implemented an approach for the direct in-vivo non-invasive estimate of ocular rigidity using optical coherence tomography, allowing for the evaluation of the biomechanical behavior in eyes with diabetic retinopathy. Our preliminary results showed that diabetic retinopathy exhibited higher ocular rigidity and higher scleral stiffness compared to normal controls, which may possibly be attributed to hyperglycemia-induced collagen cross-linking in the ocular tissues. Knowledge of diabetic retinopathy-associated biomechanical changes will equip us with new quantitative tools to identify diagnostic markers in diabetic retinopathy.

Automated summary

The pathologic mechanism of diabetic retinopathy is directly related to hyperglycemia, which causes non-enzymatic cross-linking of collagen fibrils and contributes to tissue stiffening. This study assessed the ocular biomechanical behavior in eyes with diabetic retinopathy using optical coherence tomography. The preliminary results showed higher ocular rigidity and scleral stiffness in diabetic retinopathy, possibly attributing to hyperglycemia-induced collagen cross-linking in ocular tissues.