membrane of the ﬂap tear (cf, ﬁgure 15 in Green et al).11 Although RPE proliferation might theoretically lead to a func- tional RPE layer, this proliferation is not directed.11 In our study, we found misdirected RPE migration into the retina, which possibly did not lead to a functional RPE layer supporting the photoreceptors. Intraretinal RPE cell migration has been described in various retinal diseases, for example, retinitis pigmentosa, congenital RPE hypertrophy12 or early to late dry age-related macular degeneration.13e16 In OCT images, migrating intraretinal RPE cells are hyper-reﬂective lesions with high backscattering and appear as hyperﬂuorescent areas in FAF. Other structures, such as hard exudates, may also appear as HRDs in SD-OCT,17 but appear as hypoﬂuorescent lesions in FAF (ﬁgure 3). The origin of migrated RPE cells seen in this study is unclear; there is a possibility also that these cells are remnants of RPE cells attached to the photoreceptors left from the traumatic event of the RPE tear. In course of time due to lack of suitable scaffolding structures, they migrate into the retina. Individual cells might also proliferate into clumps, which are then big enough to be detected using FAF. This mechanism is however speculative. RPE cells migrate towards various chemokines and cytokines, such as tumour necrosis factor a or interleukin 1.18e21 After the acute event of an RPE tear, it is likely that such chemo attrac- tants are secreted. Nevertheless, it is unclear why certain RPE cells remain in the level of Bruch’s membrane and why others migrate into the retina. One possible explanation might be the absence of scaffolding structures, which are important for RPE cells for proliferation. Some authors described small RPE tears where the RPE denuded area became covered by a layer of relatively normal- looking, hypopigmented RPE derived from cells from the margin of the defect.22 23 We also documented a case with a small RPE tear, where RPE cells migrated and covered the defect. This healing property might not be enough for large RPE tears. In 41.7% (15 eyes) of all cases, we identiﬁed a homogenous subretinal mass in the RPE denuded area. This substance may represent ﬁbrin or proliferated RPE cells. Nevertheless, this subretinal mass failed to build a single layer, which is a prereq- uisite for RPE cell function in terms of ion and ﬂuid transport.24 In our study, only in 2.8% of cases RPE cells could fully cover the defect. Animal studies of retinal pigment epithelial wound healing in rabbits25 and monkeys26 suggested that newly proliferated RPE cells are hypopigmented. In our study, we also saw a hypo- ﬂuorescent RPE layer in FAF. We hypothesise that these new RPE cells originate from old RPE cells from tear border. But since by means of mitosis cells also give about half of their cytoplasm to the new cells, they have only about half as many lipofuscin as their original cells. Therefore, they emit less FAF signal. Although not shown in this study, it is logical to assume these new RPE cells will also accumulate lipofuscin over time as well. There are some limitations in this study, such as the retro- spective nature of the study prone to bias of uncertain kind and a relatively small number of patients. However, giving the fact that RPE tears are rare, we presented a relatively large number of patients observed. Also by combining FAF and SD-OCT we are able to observe RPE tears more efﬁciently. We observed in this study 12 patients with RPE tear grade 1 or 2; however, only one patient showed self-healing mechanism. Although the exact reason is speculative, there are in vitro studies suggesting that RPE cells proliferation is dependant of age27 and health of the scaffolding structure (Bruch’s membrane).28 We hypothesise that the patient with a self- Br J Ophthalmol 2012;96:1211–1216. doi:10.1136/bjophthalmol-2012-301750 Clinical science healing RPE tear might have a relatively undamaged Bruch’s membrane after the traumatic event, allowing the RPE cells to repopulate the area. Using current in vivo technologies, however, the health of Bruch’s membrane cannot be easily assessed. In conclusion, there is a chance that small RPE tears are populated by RPE cells, and so waiting might be appropriate. As shown previously, photoreceptors in the RPE denuded area are able to survive up to 325 days after the acute event;2 we propose therefore to continue anti-vascular endothelial growth factor therapy to slow down scar progression, to protect the photore- ceptors from further damage (unpublished data) and giving the chance of self-healing. In large RPE tears, however, RPE prolif- eration and migration might not happen in the right plain, which is under the photoreceptors. In these cases, therapies aiming at RPE layer replacement, such as in macular trans- location or autologous RPE and choroid transplantation can offer help. Although we are not able to predict which patient has the greatest chance of self-healing, because only one patient in this study showed self-healing, knowing the facts that photo- receptors will survive up to 325 days2 and there is a chance of self-healing of small RPE tears, we propose that therapies aiming at RPE layer replacement do not have to be performed as an emergency procedure. In fact, such risky procedures can be planned and offered, if after waiting the self-healing properties have been proven to be insufﬁcient. Contributors Conception, design and data acquisition: AC. Data analysis and interpretation: AC, SF, BK. Drafting and revising the article: AC, SF. BK. Final approval: AC, SF, BK. Competing interests None. Patient consent Obtained. Provenance and peer review Not commissioned; externally peer reviewed. REFERENCES 1. Caramoy A, Kirchhof B, Fauser S. Morphological versus functional photoreceptor viability of retinal pigment epithelium tears. Acta Ophthalmol 2012;90:e328e9. 2. Caramoy A, Kirchhof B, Fauser S. Retinal pigment epithelium tears secondary to age-related macular degeneration: a simultaneous confocal scanning laser ophthalmoscopy and spectral-domain optical coherence tomography study. Arch Ophthalmol 2011;129:575e9. 3. Gelisken F, Karim-Zoda K, Grisanti S, et al. Macular translocation with 360 degrees retinotomy for retinal pigment epithelial tear. Graefes Arch Clin Exp Ophthalmol 2005;243:619e21. 4. Polito A, Cereda M, Romanelli F, et al. Macular translocation with 360 degrees retinotomy for management of retinal pigment epithelial tear: long-term results. Br J Ophthalmol 2011;95:74e8. 5. Caramoy A, Fauser S, Kirchhof B. Retinal stimuli can be restored after autologous transplant of retinal pigment epithelium and choroid in pigment epithelium tears. Acta Ophthalmol 2011;89:e490e5. 6. Maaijwee K, Joussen AM, Kirchhof B, et al. Retinal pigment epithelium (RPE)- choroid graft translocation in the treatment of an RPE tear: preliminary results. Br J Ophthalmol 2008;92:526e9. 7. Pece A, Vitale L, Milani P, et al. Spontaneous reattachment of the margins of a macular retinal pigment epithelium tear: optical coherence tomography documentation of a case. Ophthalmologica 2010;224:159e61. 8. Peiretti E, Iranmanesh R, Lee JJ, et al. Repopulation of the retinal pigment epithelium after pigment epithelial rip. Retina 2006;26:1097e9. 9. Sarraf D, Reddy S, Chiang A, et al. A new grading system for retinal pigment epithelial tears. Retina 2010;30:1039e45. 10. Chuang EL, Bird AC. Repair after tears of the retinal pigment epithelium. Eye (Lond) 1988;2:106e13. 11. Green WR, McDonnell PJ, Yeo JH. Pathologic features of senile macular degeneration. Ophthalmology 1985;92:615e27. 12. Schneider S, Green WR. Congenital and Acquired Lesions of the Retinal Pigment Epithelium. Retinal Pigment Epithelium and Macular Diseases. Dordrecht, The Netherlands: Kluwer, 1998:69e80. 13. Ho J, Witkin AJ, Liu J, et al. Documentation of intraretinal retinal pigment epithelium migration via high-speed ultrahigh-resolution optical coherence tomography. Ophthalmology 2011;118:687e93. 14. Schuman SG, Koreishi AF, Farsiu S, et al. Photoreceptor layer thinning over drusen in eyes with age-related macular degeneration imaged in vivo with spectral-domain optical coherence tomography. Ophthalmology 2009;116:488e96.e2. 1215