Understanding the Pathogenesis of Neurotrophic Keratitis: The Role of Corneal Nerves

Neurotrophic keratitis (NK) is a rare degenerative disease of the cornea caused by trigeminal nerve damage, which leads to loss of corneal sensitivity, corneal epithelium breakdown, and poor healing. Though extremely uncommon, NK is increasingly recognized for its characteristics as a distinct and w...

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Veröffentlicht in:Journal of cellular physiology 2017-04, Vol.232 (4), p.717-724
Hauptverfasser: Mastropasqua, Leonardo, Massaro‐Giordano, Giacomina, Nubile, Mario, Sacchetti, Marta
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Sprache:eng
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Zusammenfassung:Neurotrophic keratitis (NK) is a rare degenerative disease of the cornea caused by trigeminal nerve damage, which leads to loss of corneal sensitivity, corneal epithelium breakdown, and poor healing. Though extremely uncommon, NK is increasingly recognized for its characteristics as a distinct and well‐defined clinical entity rather than a rare complication of various diseases that can disrupt trigeminal innervation. Indeed, the defining feature of NK is loss of corneal sensitivity, and its clinical findings do not correlate with the wide range of systemic or ocular conditions that underlie trigeminal nerve damage. Despite increasing awareness of NK as a distinct condition, its management continues to be challenged by the lack of treatments that target nerve regeneration. This review focuses on the role of corneal nerves in maintaining ocular surface homeostasis, the consequences (such as alterations in neuromediators and corneal cell morphology/function) of impaired innervation, and advances in NK diagnosis and management. Novel therapeutic strategies should aim to improve corneal innervation in order support corneal renewal and healing. J. Cell. Physiol. 232: 717–724, 2017. © 2016 Wiley Periodicals, Inc. This review focuses on the role of corneal nerves in maintaining ocular surface homeostasis, and on the consequences (such as alterations in neuromediators and corneal cell morphology/function) of impaired innervation.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.25623