Background To evaluate the effects of lid debris debridement and meibomian gland expression (MGX) on extracellular matrix metalloproteinase-9 (MMP-9) levels and clinical outcomes of moderate and severe MGD. Methods In this retrospective case series study, a total 48 eyes of 24 patients with moderate and severe MGD underwent one session of lid debris debridement using the BlephEx combined with MGX. We evaluated the tear film break-up time (TBUT), corneal and conjunctival fluorescein staining scores, Schirmer 1 test, biomicroscopic examination of lid margins and meibomian gland (MG), ocular surface disease index (OSDI) questionnaire score, and extracellular MMP-9 levels using a point-of-care MMP-9 immunoassay device before and 4 weeks after lid debris debridement and MGX. Linear mixed model and generalized estimating equations model were used to evaluate possible differences. Results There were significant improvements in the TBUT (P = 0.002), SICCA and Oxford staining scores (all P < 0.001), lid margin telangiectasia (P < 0.001 for upper and lower eyelids), lid thickness (P < 0.001 for upper and lower eyelids), MG orifice plugging (P < 0.001 for upper and lower eyelids), meibum color (P = 0.026 for upper eyelid, P < 0.001 for lower eyelid), meibum consistency (P < 0.001 for upper and lower eyelids), meibum grade (P < 0.001), MGD stage (P < 0.001), and OSDI score (P = 0.002). MMP-9 immunoassay positivity rate significantly decreased from 83.3 to 50.0% 4 weeks after treatment (P = 0.014). Conclusions In patients with moderate to severe MGD, lid debris debridement using the BlephEx combined with MGX improved clinical findings, subjective symptoms, meibomian gland function, along with ocular surface MMP-9 level. We hereby suggest lid debris debridement using BlephEx combined with MGX as an effective clinical strategy for treatment of moderate to severe MGD.

S1P has an important role in the pathological inflammatory process of GO, which is mediated through the SphK1-S1P- S1P receptor pathway. SphK1 inhibitors and S1P receptors or antagonists could be potential approaches for controlling the inflammatory process of GO.

This population-based, retrospective cohort study aimed to evaluate the association between glaucoma surgery and all-cause and cause-specific mortality among Korean elderly patients with glaucoma. A total of 16210 elderly patients (aged ≥ 60 years) diagnosed with glaucoma between 2003 and 2012 were included, and their insurance data were analyzed. The participants were categorized into a glaucoma surgery cohort (n = 487), which included individuals who had diagnostic codes for open angle glaucoma (OAG) or angle closure glaucoma (ACG) and codes for glaucoma surgery, and a glaucoma diagnosis cohort (n = 15,723), which included patients who had codes for OAG and ACG but not for glaucoma surgery. Sociodemographic factors, Charlson Comorbidity Index score, and ocular comorbidities were included as covariates. Cox regression models were used to assess the association between glaucoma surgery and mortality. The incidence of all-cause mortality was 34.76/1,000 person-years and 27.88/1,000 person-years in the glaucoma surgery and diagnosis groups, respectively. The adjusted hazard ratio (HR) for all-cause mortality associated with glaucoma surgery was 1.31 (95% confidence interval [CI], 1.05–1.62, P = 0.014). The adjusted HR for mortality due to a neurologic cause was significant (HR = 2.66, 95% CI 1.18–6.00, P = 0.018). The adjusted HRs for mortality due to cancer (HR = 2.03, 95% CI 1.07–3.83, P = 0.029) and accident or trauma (HR = 4.00, 95% CI 1.55–10.34, P = 0.004) associated with glaucoma surgery for ACG were significant as well. Glaucoma surgery was associated with an increase of mortality in elderly patients with glaucoma. In particular, the risk of mortality associated with glaucoma surgery due to neurologic causes was significant.