Photoreceptor apoptosis is the basis for permanent visual loss in a number of retinal disorders including age-related macular degeneration (AMD) and retinal detachment (RD). Thus, despite tremendous advances in vitreoretinal surgery and management of rhegmatogenous RD leading to a primary reattachment rate over 95%, some patients show poor visual recovery because of photoreceptor apoptosis.

Physiologically, microglial cells (resident macrophages) are present only in the inner retina. The subretinal space, located between the retinal pigment epithelium (RPE) and the photoreceptor outer segments (POS), is devoid of all mononuclear phagocytes and form a zone of immune privilege. In AMD, several studies showed a strong association between subretinal mononuclear phagocytes infiltration and advanced forms of AMD. Experimental work in mice suggest that this infiltration plays an important role in the pathogenesis of this condition by producing inflammatory cytokines.

RD-induced photoreceptor apoptosis might result from similar mechanisms. The aim of this study is to determine the cytokine profile in vitreous samples from patients with RD and to compare it with those from control patients with macular hole.

Inclusion Criteria:

• Patients with primary retinal detachment requiring vitrectomy
• Patients with idiopathic macular hole requiring vitrectomy

Exclusion Criteria:

• History of retinal detachment or intraocular inflammatory diseases

Patients from the department of Ophthalmology (Nancy University Hospital)