Cystoid macular oedema (CMO) is a major cause of reduced vision following intraocular surgery. Although the aetiology of CMO is not completely clarified, intraocular inflammation is known to play a major role in its development. The macula may develop cytotoxic oedema when the primary lesion and fluid accumulation occur in the parenchymatous cells (intracellular oedema) or vasogenic oedema when the primary defect occurs in the blood-retinal barrier and leads to extracellular fluid accumulation (extracellular oedema). We report on the mechanisms of CMO formation after pars plana vitrectomy and associated surgical procedures and discuss possible therapeutic approaches.

Purpose To evaluate changes in macular morphology due to myopic choroidal neovascularization (CNV), using spectraldomain optical coherence tomography (SD-OCT). Methods In all, 22 eyes with recent-onset untreated CNV underwent 1 intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF), followed by a pro-re-nata regimen. SD-OCT was performed at baseline (before first administration of anti-VEGF treatment) and month 1, and 2; macular morphologic changes and outer retina characteristics (SD-OCT findings) associated with CNV activity were evaluated. Sensitivity and specificity were calculated for SD-OCT findings using fluorescein angiography (FA) as standard reference. Results Mean central retinal thickness (CRT) showed no significant reduction from baseline (284±98 mm) to month 1 (257±74 mm) and month 2 (263±72 mm). A hyper-reflective lesion with fuzzy borders (fuzzy area), and 'absent or altered' IS/OS junction were the only SD-OCT findings associated with CNV activity (Po0.0001). Both these SD-OCT findings showed good sensitivity and specificity (95.1 and 96.0% (95% CI: 0.87-0.89), respectively, for the fuzzy area; 87.9 and 66.7% (95% CI: 0.65-0.87), respectively, for 'absent or altered' IS/OS junction) when compared with FA leakage (standard reference). Conclusions Outer retina characteristics (ie, hyper-reflective lesion with fuzzy borders, and 'absent or altered' IS/OS junction) appear more meaningful than CRT in the evaluation of myopic CNV activity. These SD-OCT findings show overall good sensitivity and specificity when compared with FA leakage (standard reference), and could be considered as an alternative diagnostic tool to FA for myopic CNV monitoring.

Effective treatment for vascularized PED is still lacking. Until now, only stabilization of the disease has been achieved using anti-VEGF therapy, but the risk of RPE tear can further hamper our expectations. Baseline characteristics are helpful for prognosis, but patients must be informed of the uncertain response. New therapeutic strategies are needed.

Intravitreal bevacizumab is effective in producing juxtafoveal CNV stabilization and visual acuity improvement in a patient affected by RP, over a 12-month follow-up. Future studies are required to ascertain the best therapeutic approach for CNV complicating RP.

Matrix metalloproteinases (MMPs), myofibroblasts (MFs) and epithelial proliferation have key roles in neoplastic progression. In this study immunoexpression of MMP-1, MMP-2 and MMP-9, presence of MFs and the epithelial proliferation index were investigated in actinic cheilitis (AC), lip squamous cell carcinoma (LSCC) and mucocele (MUC). Thirty cases of AC, thirty cases of LSCC and twenty cases of MUC were selected for immunohistochemical investigation of the proteins MMP-1, MMP-2, MMP-9, α-smooth muscle actin (α-SMA) and Ki-67. The MMP-1 expression in the epithelial component was higher in the AC than the MUC and LSCC. In the connective tissue, the expression was higher in the LSCC. MMP-2 showed lower epithelial and stromal immunostaining in the LSCC when compared to the AC and MUC. The epithelial staining for MMP-9 was higher in the AC when compared to the LSCC. However, in the connective tissue, the expression was lower in the AC compared to other lesions. The cell proliferation rate was increased in proportion to the severity of dysplasia in the AC, while in the LSCC it was higher in well-differentiated lesions compared to moderately differentiated. There were no statistically significant differences in number of MFs present in the lesions studied. The results suggest that MMPs could affect the biological behaviour of ACs and LSCCs inasmuch as they could participate in the development and progression from premalignant lesions to malignant lesions.