PT  - JOURNAL ARTICLE
AU  - K Petermeier
AU  - O Tatar
AU  - W Inhoffen
AU  - M Völker
AU  - B A Lafaut
AU  - S Henke-Fahle
AU  - F Gelisken
AU  - F Ziemssen
AU  - S Bopp
AU  - K U Bartz-Schmidt
AU  - S Grisanti
TI  - Verteporfin photodynamic therapy induced apoptosis in choroidal neovascular membranes
AID  - 10.1136/bjo.2006.090852
DP  - 2006 Aug 01
TA  - British Journal of Ophthalmology
PG  - 1034--1039
VI  - 90
IP  - 8
4099  - http://bjo.bmj.com/content/90/8/1034.short
4100  - http://bjo.bmj.com/content/90/8/1034.full
SO  - Br J Ophthalmol2006 Aug 01; 90
AB  - Aim: To evaluate the impact of verteporfin photodynamic therapy (PDT) on the induction of apoptosis in choroidal neovascular membranes (CNV) secondary to age related macular degeneration. Methods: Retrospective review of 22 surgically excised CNV. 12 of these patients had been treated with PDT 3–146 days previously. Apoptotic cells were detected with the TUNEL technique and compared to the expression of CD34 (endothelial cells, EC), CD105 (activated endothelial cells), Ki-67 (proliferation marker), and cytokeratin18 (retinal pigment epithelial cells, RPE). Results: CNV excised 3 days after PDT were characterised both by collapsed and patent vessels. The EC displayed a statistical significant positive TUNEL reaction when compared to the remaining treated CNV (p<0.001) and untreated CNV (P = 0.002). The proliferative activity was reduced. CNV excised 1–5 months after PDT displayed a patent vascularisation and high proliferative activity. All membranes either treated or untreated disclosed only sporadic TUNEL positive cells within the stroma and the RPE. Conclusions: Verteporfin PDT leads to selective and effective damage of EC within CNV. Both patent and occluded vessels were lined by apoptotic EC. This finding and the increased expression of proliferation marker at later time points suggest that revascularisation after PDT is caused by angiogenesis rather than recanalisation.