Superficial and Deep Capillary Plexuses: Potential Biomarkers of Focal Retinal Defects in Eyes Affected by Macular Idiopatic Epiretinal Membranes? A Pilot Study.

Inner macular layers are the most involved in the retinal distortion caused by idiopathic epiretinal membrane (iERM). They represent the anatomical structures in which the superficial (SCP) and deep (DCP) capillary plexus are embedded. We quantified flow signal (FS) in these capillary plexuses using Swept Source OCT angiography to identify possible markers for postoperative outcome. The software ImageJ was used to quantify the FS in a 150 µm radius area around each point analyzed by MAIA microperimeter. In 16 patients with unilateral iERM, focal light sensitivity (FLS) in the para- and perimacular areas was measured to evaluate macular function in 24 points overlapping macular plexuses and compared with normal fellow eyes (FEs). t-Test for independent samples iERM eyes (iERMEs) vs. fellow eyes (FEs) and Pearson correlation coefficient of FS vs. FLS in each point were calculated. A level of p < 0.05 was accepted as statistically significant. As a whole, FLS was significantly higher in FEs vs. ERMEs (p < 0.001); FS in both SCP and DCP was not significantly different between ERMEs and FEs (p = 0.827, p = 0.791). Correlation in focal retinal areas between FLS and FS in ERMEs was significant in SCP (p = 0.002) and not significant in DCP (p = 0.205); in FEs was significant in both SCP (p < 0.001) and DCP (p = 0.022). As previously described, these defective areas were located mainly in sites of distortion of retinal layers; therefore, it can be hypothesized that a focal change in FS, occurring mostly in SCP, could be involved in the onset of the functional defect.

Inner Macular Changes in Fellow Eye of Patients With Unilateral Idiopathic Epiretinal Membrane.

Purpose: We evaluated a series of fellow eyes (FEs) in patients affected by unilateral idiopathic epiretinal membrane (IERM) with spectral-domain optical coherence tomography (SD-OCT) and OCT angiography (OCT-A) to determine if a previous defect in the inner retina is present before the mechanical damage to the inner limiting membrane (ILM) caused by posterior vitreous detachment. Methods: In patients with IERM (N = 39), ganglion cell layer (GCL) thickness in FEs was assessed with SD-OCT; in a subgroup (N = 25) the vessel density (VD) at the superficial (SCP) and deep capillary plexus (DCP) was assessed with swept-source OCT-A (SS-OCT-A). These values were then compared with 30 age-matched healthy control eyes (CEs). The statistical analyses used SPSS software version 15.0 (SPSS, Inc., Chicago, IL, USA). Data collected underwent 1-way ANOVA. A level of P < 0.05 was accepted as statistically significant. Results: The GCL thickness in the FEs was significantly lower than in CEs, with a significant thinning in all sectors except temporal ones (mean P < 0.001, superior P = 0.0002, superonasal P < 0.001, inferonasal P < 0.001, and inferior P = 0.002). The VD was significantly lower in the FEs in all sectors of SCP (mean P = 0.009, inner ring P = 0.028, and outer ring P = 0.007). Conclusions: GCL and SCP are significantly reduced in the FEs. These data suggest that a vascular defect in the SCP could cause a cellular loss in the inner retina that may determine the cascade events leading to the IERM proliferation; the diagnosis in a preclinical phase could provide a treatment strategy to prevent the progression of the disease.

ALTERATIONS OF MACULAR BLOOD FLOW IN SUPERFICIAL AND DEEP CAPILLARY PLEXUSES IN THE FELLOW AND AFFECTED EYES OF PATIENTS WITH UNILATERAL IDIOPATHIC EPIRETINAL MEMBRANE.

PURPOSE: Previous research suggests that proliferation of the idiopathic epiretinal membrane (IERM) is related to microbreaks in the inner limiting membrane, which are caused by posterior vitreous detachment. In this study, we used optical coherence tomography angiography to determine whether a vascular defect in the inner retina is present before the mechanical damage caused by posterior vitreous detachment. METHODS: For patients with unilateral IERM (N = 23), optical coherence tomography angiography with blood flow measurement was performed in both eyes at the superficial capillary plexuses (SCP) and deep capillary plexuses (DCP) with 6 mm × 6-mm scans and ETDRS grids centered on the fixation point. These values were then compared with 45 healthy control eyes (CEs). RESULTS: The optical coherence tomography angiography data showed that blood flow was lower in the fellow eyes of IERM patients than in CEs when the whole enface macula (SCP: P = 0.031, DCP: P = 0.004) and extramacular area (SCP: P = 0.048, DCP: P = 0.026) were compared between groups. The blood flow was also lower in the affected eyes compared with CEs in both whole en face macula (SCP: P < 0.001, DCP: P < 0.001) and extramacular areas (SCP: P = 0.011, DCP: P < 0.001). CONCLUSION: Data from this study revealed that blood flow is significantly reduced in the fellow eyes of patients with unilateral IERM when compared with CEs. Overall, the data suggest that a vascular retinal defect could produce changes in the inner retina, preceding and influencing the formation of microbreaks occurring at the time of posterior vitreous detachment in the inner limiting membrane. Understanding the upstream mechanism of inner limiting membrane microbreaks may provide a therapeutic target aimed to ultimately prevent Mu[Combining Diaeresis]ller cells, astrocyte, and fibroblast migration, which cause IERM proliferation.

Posterior vitreous detachment and retinal detachment following cataract extraction.

PURPOSE OF THE REVIEW: Cataract surgery induces considerable vitreous modifications that can lead to posterior vitreous detachment. Studies indicate that these changes, whether combined or not with peripheral retinal degenerations such as lattice areas, carry risk for subsequent retinal breaks or detachment. RECENT FINDINGS: The incidence of retinal detachment increases after cataract extraction, but it decreases with improved surgical technique. Postoperative posterior vitreous detachment is a major promoter of retinal detachment after cataract surgery and is related to onset of most retinal tears leading to retinal detachment. Vitreous body destabilization increases the incidence of retinal detachment after surgery; this destabilization of the vitreous body can result from aggressive surgical technique, intraoperative or postoperative posterior capsule breaks, high myopia and retinal detachment in the fellow eye. These factors can act alone or together to determine the onset of anomalous forms of posterior vitreous detachment; in such cases, retinal breaks frequently develop and culminate in retinal detachment. SUMMARY: Vitreous modifications occurring after cataract extraction in patients without preoperative posterior vitreous detachment may be involved in the onset of postoperative retinal detachment. Careful postoperative follow-up is recommended in these patients to allow early detection of posterior vitreous detachment arising after surgery.

Conjunctival expression of thymosin-beta4 in vernal keratoconjunctivitis.

PURPOSE: Thymosin-beta4 (Tbeta4) is a small actin-sequestrating peptide that modulates inflammation and healing in different tissues. The aim of this study was to investigate the molecular and biochemical expression of Tbeta4 in the healthy conjunctiva and in the conjunctiva of patients with vernal keratoconjunctivitis (VKC), a severe allergic eye disease characterized by chronic inflammation and marked tissue remodeling. METHODS: Conjunctival tissues, obtained from seven VKC patients and five sex/age-matched healthy subjects, were evaluated for Tbeta4 expression by relative real time-PCR and light/confocal microscopy. The distribution patterns of Tbeta4 in conjunctival sections as well as Tbeta4 expression by mast cells (AA1), eosinophils (EG2), and fibroblast/myofibroblasts (Thy1/alpha-SMA) in VKC tissues was also evaluated by double immunofluorescence. RESULTS: Compared to healthy specimens, Tbeta4 mRNA appeared upregulated in VKC conjunctival biopsies as detected by real-time PCR. In the healthy conjunctiva, Tbeta4 protein expression was confined to the conjunctival epithelium, while a weak staining was observed in the stroma. In VKC conjunctival sections, Tbeta4 immunoreactivity was selectively increased in the stroma where, by confocal analysis of VKC papillary formations, Tbeta4 appeared to be mostly localized in eosinophils and activated fibroblasts/myofibroblasts. CONCLUSIONS: Our data provides the first evidence of Tbeta4 expression in the conjunctival tissues. The upregulation of both Tbeta4 mRNA and protein in the conjunctival stroma, and its peculiar localization in eosinophils and myofibroblasts populating VKC lesions, suggest a possible role for Tbeta4 in tissue inflammation and remodeling occurring in VKC.