Second leading cause of blindness worldwide, glaucoma is an optic neuropathy related mainly but not exclusively to an increase of intraocular pressure. Angle closure glaucoma is related to a blockade of aqueous humor to the trabecular meshwork, whereas open-angle glaucoma is a degeneration of the trabecular meshwork, the filter that allows aqueous outflow from the eye. Many improvements have been made in terms of diagnosis, follow-up and treatments, although the treatment of glaucoma is restricted to control intraocular pressure, in order to prevent optic nerve degeneration or to stop the progression of the disease toward blindness. The first line therapy is based on topical medications that are administered for the whole life span. Although globally efficient, these treatments, and most likely the preservative included in the excipient to prevent bottle contamination, induce side effects in the long-term that may impair the quality of life, patient compliance or directly induce ocular surface changes like inflammatory cytokine release, or tear film destruction, with further dry eye disease and chronic inflammation. A large body of evidence has been accumulated, showing that benzalkonium chloride, the preservative mainly used, is toxic over the long run and plays a role in such ocular surface impairment. Therefore efforts have been made in the last decade to eliminate or replace this compound, providing safer therapies to the patients. Furthermore, the identification of chemokines as playing a role in the trabecular degeneration has open new directions for treating glaucoma. The blockade of one receptor of CXCL12 has been experimentally shown not only to decrease intraocular pressure but also to prevent trabecular cell degeneration. This is an innovative concept that could allow development of new treatments, more specifically targeting the disease at its onset, rather than attempting to reduce its progression in its later stages.
© Société de Biologie, 2013.