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Ocular Surface Changes Differ Significantly Between Oxaliplatin- and Diabetes-Induced Polyneuropathy.

Martin Schicht¹, Marco Sisignano^2,3, Jessica Farger¹

¹Institute of Functional and Clinical Anatomy, Friedrich-Alexander University Erlangen-Nürnberg, 91054 Erlangen, Germany.

International Journal of Molecular Sciences

|March 13, 2025

Summary

Oxaliplatin-induced polyneuropathy (PN) causes dry eye disease (DED) through distinct mechanisms compared to diabetic polyneuropathy (DPN). Oxaliplatin-treated mice developed evaporative DED, unlike DPN mice which developed aqueous-deficient DED.

Keywords:

dry eye disease (DED)ocular surface oxaliplatin (Ox)polyneuropathies (PNs)tear film

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Area of Science:

Neuroscience
Ophthalmology
Pathology

Background:

Dry eye disease (DED) is frequently observed in patients with polyneuropathies (PNs).
The specific relationship between different types of PNs and DED remains unclear.
Investigating these connections can reveal novel therapeutic targets for DED.

Purpose of the Study:

To investigate the distinct mechanisms linking oxaliplatin-induced polyneuropathy (OPN) and diabetic polyneuropathy (DPN) to dry eye disease (DED).
To analyze morphological and molecular changes in ocular tissues and peripheral nerves in OPN.
To differentiate the types of DED caused by OPN versus DPN.

Main Methods:

Morphological analysis of sciatic nerve (SN), dorsal root ganglia (DRG), trigeminal ganglia (TG), and ocular tissues in oxaliplatin-treated mice.
Tear proteomics and gene expression analysis of ocular surface tissues.
Comparison of findings with previously studied DPN models.

Main Results:

Oxaliplatin-induced polyneuropathy (OPN) led to significant changes in six tear proteins and ocular tissue gene expression.
Morphological changes included decreased conjunctival goblet cells and altered Meibomian gland myofibroblasts.
OPN resulted in evaporative DED, contrasting with aqueous-deficient DED in DPN, with distinct trigeminal nerve findings.

Conclusions:

Oxaliplatin-induced polyneuropathy causes evaporative dry eye disease through mechanisms differing from diabetic polyneuropathy.
Peripheral nerve and ocular nerve damage patterns vary between OPN and DPN.
Understanding these differences is crucial for targeted DED treatment in specific polyneuropathy contexts.