The anatomical reattachment of the retina has always been a focal point of research. Many studies have focused on observing structures such as spontaneous retinal displacement under fundus autofluorescence, continuity of the ellipsoid zone and external limiting membrane (ELM) under OCT, secondary epiretinal membrane, and cystoid macular edema [1-3]. However, changes in the ORC structure during retinal detachment have received little attention. Ooto et al. [4]first summarized the structure known as "ORC," finding that in AMD patients, high-reflective corrugations on the outer retina over areas of RPE/Bruch’s membrane atrophy, possibly related to subretinal fluid and compensatory CNV formation, were visible only in regions associated with CNV or GA.
Other studies have found similar deposits in patients with late-onset RP and Sorsby's fundus dystrophy, where the deposition band is believed to impair nutrient transport to the inner retina [5,6]. The pathophysiology of ORC involves the loss of RPE regulation over subretinal fluid and retinal homeostasis. Some researchers have suggested that this might be due to differences in the physicochemical properties of the exudate [6]. In our observations, no ORC-like changes were found in exudative diseases such as VKH and CSC.
Previous theories have suggested that the longer the duration of retinal detachment, the poorer the visual function recovery after reattachment. However, summarizing the recovery mechanism of ORC, when the retinal tear is closed, the function of the RPE improves to balance the exchange of nutrients between the outer retina and the subretinal fluid (SRF). Through the RPE's promotion of SRF absorption, the recovery of the outer structure and the smooth reattachment of the detached retina are more likely to meet the requirements for anatomical reattachment. The more accepted mechanism of ORF is the misaligned healing between the retinal photoreceptors and the RPE. Observing different degrees of ORF cases, some cases, despite showing ORC, have good alignment during recovery or retain small retinal folds, with only high-reflective points on the RPE later on (considered to be local outer segment photoreceptor adhesion followed by subretinal fibrosis and RPE proliferation).
Additionally, an important change we observed is that in the case of retinal detachment, there are more noticeable adhesions between some wave-like structures in the ORC. The formation mechanism is similar to the connections between photoreceptors and the inner and outer segments of surrounding photoreceptors, mainly involving the myoid zone, ellipsoid zone, and inner segments of the photoreceptors [7]. According to OCT observations, such structures are difficult to restore during PPV or SB surgery, eventually forming typical ORF. This retinal structure misalignment ultimately leads to pigment migration, proliferation, or atrophy. It is unclear whether this structure is highly correlated with subretinal proliferative changes. Preoperative and postoperative OCT comparisons of this structure are important, but it is unknown whether RPE regulation can improve such adhesions.
Moreover, in PPV patients, such structural changes need to be differentiated from subretinal heavy droplet residues, which appear as a vertical elliptical subretinal cyst-like change with smooth boundaries and long-term structural stability. It is also necessary to distinguish this from full-thickness retinal folds, which result from the passive compression of the originally curved retina in the vitreous cavity after detachment, essentially a compression change in the tissue [8].
Based on our case observations, Type I ORC has a better prognosis compared to Types II and III. In Type I, some reattachment morphology can normalize during recovery. It is unclear whether this correction of simple point-to-point misalignment between the retina and RPE is regulated by RPE or corrected by the recovery of the elastic modulus of the outer retina. This aligns with the findings of Muni RH et al. [9], who concluded that during reattachment, ORC at the edge of the attachment has a tendency to gradually flatten. Types II and III ORC are considered to involve varying degrees of outer segment photoreceptor adhesion, which affects postoperative retinal flattening and reattachment.
Regarding the course of retinal detachment, patients with a duration of ≤4 days did not exhibit ORC, which might be a conditional factor for ORC formation. This change does not occur immediately after detachment, suggesting that early changes in the subretinal fluid environment might have a time constraint on the formation of ORC in the outer retinal layers. Among patients with a course of >4 days, 87% exhibited ORC. In a small subset of patients without ORC, this indicates that under natural conditions, some ORC structures may spontaneously recover or may not develop ORC changes at all. Even some patients with calcification-like changes in the outer segments or stable outer structures (without ORC) before surgery can achieve good structural recovery post-repair.
Evaluating the reasons for structural recovery in these patients could provide guidance for treating retinal detachment patients with ORC. Further research is needed to summarize the recovery time and conditions for Type I ORC. It is important to note that excessively prolonging retinal reattachment time is also detrimental to anatomical recovery, potentially leading to atrophy of the photoreceptor outer segments and RPE. Providing the outer retinal layer with time for physiological morphological recovery and balance with the RPE might be more beneficial for anatomical reattachment.
Preoperatively significant ORC, subretinal fluid drainage, and assisted reattachment techniques might prevent timely recovery of ORC. In this scenario, the elastic modulus between the inner and outer retinal layers may differ, leading to potential reattachment outcomes: 1) point-to-point misalignment healing, resulting in retinal folds; or 2) inability to smooth out the outer retinal folds, resulting in long-term local irreversible damage to the ellipsoid zone, IS/OS, and RPE [10].
Based on Dalvin's theory of hydration in ORC formation [11], subretinal fluid in rhegmatogenous retinal detachment (RRD) is essentially liquefied vitreous. The structural basis of the wavy outer plexiform layer lies in the differential hydration effects on the interstitial matrix of outer retinal photoreceptors compared to the inner retina, leading to the folding of the outer retina and potentially resulting in compensatory ORC formation. However, we propose that the occurrence of structural factors causing differences in the elastic modulus between the inner and outer retinal layers post-detachment fundamentally stems from the inherent structural differences between the inner and outer retinal tissues. These differences include variations in vascular density, cellular composition (e.g., retinal ganglion cells (RGC) vs. photoreceptors), and the asymmetric distribution of Müller cell endfeet [12-14].
Future research should employ elasticity models to analyze factors contributing to ORC structure recovery and summarize changes in the elastic modulus of ORC at different stages of the disease. This approach could provide better guidance for surgical interventions in retinal detachment. One limitation of this study is the constraint imposed by the use of SD-OCT. Ultra-widefield swept-source optical coherence tomography angiography (UWF SS-OCTA) could be more beneficial for in-depth observation and analysis of changes in the ORC recovery process. Moreover, extending the observation period for ORC and ORF is necessary to analyze their progression and structural changes comprehensively.