Saving nerves may be key to preserving eye health in RDEB: Study
Patients have nerve cell loss, increased inflammatory immune cell numbers
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People with recessive dystrophic epidermolysis bullosa (RDEB) often experience a profound loss of nerve cells in the front of the eye, accompanied by increased numbers of inflammatory immune cells, a study found, suggesting that treatments to promote the health of these nerve cells and reduce eye inflammation may be essential to helping RDEB patients maintain healthy eyes.
The study, “In vivo confocal microscopic evaluation of patients with epidermolysis bullosa demonstrates severe loss of corneal nerves,” was published in the American Journal of Ophthalmology Case Reports. The work was funded by Research to Prevent Blindness and the Massachusetts Lions Eye Research Fund, two organizations dedicated to improving the lives of people with eye diseases.Â
RDEB is a genetic disorder marked by fragile skin that’s prone to blistering and poorly healing wounds. People with RDEB also commonly experience damage to the surface of the eyes, which can lead to vision problems.
The transparent layer forming the front of the eye, called the cornea, houses many sensory nerve cells that help maintain the health of the eye surface and detect irritation or injury. These nerve cells also release signaling molecules that support tissue repair and help regulate inflammation.
Still, little is known about how these nerve cells are affected in people with RDEB.
Advanced imaging shows loss of corneal nerves
Scientists used advanced imaging tools to examine corneal nerve cells in five RDEB patients, aged 11 to 18. All five were experiencing eye-related pain or discomfort, which prompted detailed evaluations.
The researchers found substantial loss of corneal nerves across all 10 eyes of the five patients. In fact, in most eyes, the researchers could hardly see any nerves at all.
Because these nerve cells are crucial to eye health, the researchers called for greater efforts to better understand how these nerves are affected in RDEB. “Detecting early corneal nerve changes may ultimately inform approaches aimed at … preserving long-term visual function,” they said.
In tandem with the loss of corneal nerves, the researchers found, RDEB patients’ eyes showed increased levels of dendritic cells, a type of inflammatory immune cell.
Based on these data, they postulated that RDEB-related damage of the eye surface may trigger chronic inflammation that damages corneal nerves — which leads to a loss of corneal nerves, further worsening damage at the eye surface and triggering a self-perpetuating cycle of eye damage.
The researchers stressed that their observations were limited to a few patients, and further work is needed to understand exactly how corneal nerves become damaged in RDEB.
Still, they said, the study’s findings imply that combination treatments to simultaneously reduce inflammation and promote nerve regeneration may be a promising strategy to preserve eye health for people with RDEB.
“Given the concurrent findings of nerve loss and dendritic cell infiltration, a combined therapeutic approach targeting both inflammation and nerve regeneration may have potential to reduce [eye surface complications], though further studies are needed to confirm efficacy,” the researchers wrote.
