Inflammation in Glaucoma: From the back to the front of the eye, and beyond

• Published in: Progress in retinal and eye research Vol. 83; p. 100916
• Main Authors: Baudouin, Christophe, Kolko, Miriam, Melik-Parsadaniantz, Stéphane, Messmer, Elisabeth M.
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.07.2021; Elsevier
• Subjects: Benzalkonium chloride; Human health and pathology; Inflammation; IOP-Lowering drugs; Life Sciences; Neuroinflammation; Ocular surface; Optic-nerve head degeneration; Oxidative stress; Para-inflammation; Preservatives; Primary open-angle glaucoma; Sensory Organs; Trabecular meshwork; Treatment; Oxidative stress; Preservatives; Trabecular meshwork; Treatment; Primary open-angle glaucoma; Para-inflammation; Benzalkonium chloride; Neuroinflammation; Inflammation; IOP-Lowering drugs; Optic-nerve head degeneration; Ocular surface
• ISSN: 1350-9462; 1873-1635; 1873-1635
• DOI: 10.1016/j.preteyeres.2020.100916

The pathophysiology of glaucoma is complex, multifactorial and not completely understood. Elevated intraocular pressure (IOP) and/or impaired retinal blood flow may cause initial optic nerve damage. In addition, age-related oxidative stress in the retina concurrently with chronic mechanical and vascular stress is crucial for the initiation of retinal neurodegeneration. Oxidative stress is closely related to cell senescence, mitochondrial dysfunction, excitotoxicity, and neuroinflammation, which are involved in glaucoma progression. Accumulating evidence from animal glaucoma models and from human ocular samples suggests a dysfunction of the para-inflammation in the retinal ganglion cell layer and the optic nerve head. Moreover, quite similar mechanisms in the anterior chamber could explain the trabecular meshwork dysfunction and the elevated IOP in primary open-angle glaucoma. On the other hand, ocular surface disease due to topical interventions is the most prominent and visible consequence of inflammation in glaucoma, with a negative impact on filtering surgery failure, topical treatment efficacy, and possibly on inflammation in the anterior segment. Consequently, glaucoma appears as an outstanding eye disease where inflammatory changes may be present to various extents and consequences along the eye structure, from the ocular surface to the posterior segment, and the visual pathway. Here we reviewed the inflammatory processes in all ocular structures in glaucoma from the back to the front of the eye and beyond. Our approach was to explain how para-inflammation is necessary to maintain homoeostasis, and to describe abnormal inflammatory findings observed in glaucomatous patients or in animal glaucoma models, supporting the hypothesis of a dysregulation of the inflammatory balance toward a pro-inflammatory phenotype. Possible anti-inflammatory therapeutic approaches in glaucoma are also discussed. •Glaucoma is associated with toxic inflammatory factors leading to cell death and disease progression.•Oxidative stress and aging are important risk factors involved in para-inflammation dysregulation.•Trabecular meshwork dysfunction is likely mediated by oxidative stress and inflammatory responses.•Ocular surface inflammation may compromise the cornea, conjunctiva and possibly the trabecular meshwork.•Modulation of inflammation may be a valuable therapeutic strategy.