REVIEW  EMERGING ISSUES ON DIABETIC RETINOPATHY AND DIABETIC MACULAR EDEMA 

Minerva Oftalmologica 2018 June;60(2):26-35

DOI: 10.23736/S0026-4903.18.01791-9

Copyright © 2018 EDIZIONI MINERVA MEDICA

lingua: Inglese

Is diabetic retinopathy an inflammatory disease?

Elisabetta PILOTTO ¹ ✉, Silvia BINI ¹, Edoardo MIDENA ^{1, 2}

¹ Department of Ophthalmology, University of Padua, Padua, Italy; ² GB Bietti Foundation, IRCCS, Rome, Italy

Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM). Persistent hyperglycemia leads to the activation of multiple cellular pathways involved in the pathogenesis of DR, resulting in increased inflammation, oxidative stress and vascular dysfunction. For many years, DR has been considered a pure microvascular disease. An increasing body of evidence is conversely suggesting that both inflammation and neurodegeneration occur even before the development of clinical signs of DR in diabetic patients. The activation of retinal glia cells (RGC) is one of the first signs of inflammation in DM. RGC include macroglia (Müller cells and astrocytes) and microglia. Müller cells have relevant effect on retinal capillaries and control the retinal water content (edema). Activated RGC, increase the release of cytotoxic molecules responsible for recruitment of leukocytes, blood-retinal barrier breakdown of retinal capillaries, direct glial dysfunction, and neuronal cell death. Many studies, in the last years, investigated the inflammatory mediators in human vitreous and aqueous humor samples. These studies are tenting to clarify the multiple pathways leading to DR and diabetic macular edema (DME), to offer the opportunity for more targeted treatment. Moreover, non-invasive techniques, namely optical coherence tomography (OCT), have allowed the detection of new retinal biomarkers of both neurodegeneration and inflammation. In particular, the hyperreflective intraretinal spots (HRS), detectable in the retinal layers at the OCT, have been hypothesized as in vivo marker of microglial activation. The increase in thickness of the inner nuclear layer (INL), where the Müller cells are located, is a sign of Müller cells activation. These new emerging insights are fostering a better understanding of the pathogenesis of DR, which can no longer be considered as a pure retinal vascular complication of DM.

KEY WORDS: Diabetic retinopathy - Inflammation - Ependymoglial cells - Microglia - Macular edema