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Cheng-Jong Chang, MD, PhD; Wico W. Lai; Deepak P. Edward, MD; Mark O. M. Tso, MD, DSc

Arch Ophthalmol. 1995;113(7):880-886.

Abstract
Objective
To determine the mechanism of photoreceptor cell death after traumatic retinal detachment in humans.

Design
Clinical records from 1975 to 1993 of 75 patients, whose eyes were enucleated after traumatic retinal detachment, were reviewed for age, sex, previous ocular or systemic medical history, interval from initial trauma to enucleation, visual acuity, and types of trauma. The patients were divided into five groups of 15 cases each, based on the interval from initial trauma to enucleation. The retinal tissue was examined for two markers of apoptosis: (1) nicked nuclear DNA in situ by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) technique and (2) apoptotic bodies by light and electron microscopy.

Results
Of the 75 cases of ruptured globe and traumatic retinal detachment that were evaluated, 19 eyes (25.3%) showed TUNEL-positive labeling of photoreceptor cells. Nicked nuclear DNA was detected in photoreceptor cells of detached retinas as early as 8 hours after trauma. The detached retinas in seven of 15 eyes enucleated within 2 days after ocular trauma showed TUNEL-positive photoreceptor nuclei. The number of cases showing TUNEL-positive photoreceptor nuclei decreased as the interval between initial trauma and enucleation increased. The TUNEL-positive photoreceptor cells could still be seen in the detached retinas of two eyes enucleated 22 days after trauma. Light microscopy disclosed condensation and fragmentation of photoreceptor nuclei in the detached retinas. Electron microscopy showed structures resembling apoptotic bodies phagocytosed by neighboring cells in the TUNEL-positive retinas.

Conclusions
Apoptosis is an important mechanism of photoreceptor cell degeneration in the early stage after traumatic retinal detachment in humans.

Author Affiliations
From the Department of Ophthalmology, Tri-service General Hospital and National Defense Medical Center, Taipei, Taiwan, Republic of China (Dr Chang); Georgiana Dvorak Theobald Ophthalmic Pathology Laboratory, Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago (Drs Chang, Edward, and Tso and Mr Lai); and Department of Ophthalmology and Visual Sciences, Chinese University of Hong Kong (Dr Tso). The authors have no proprietary interest in the companies or products mentioned in this study.

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