Purpose: To investigate the relationship between meibomian gland dysfunction (MGD) and incomplete blinking caused by cranial nerve seven (CN VII) palsy. Methods: A prospective case series of 60 consecutive patients with unilateral CN VII palsy was evaluated for MGD. According to the House–Brackmann scale, patients were divided into complete or incomplete blinking group, with the incomplete group further subdivided to early, middle or late stage according to the paralysis duration. Schirmer’s I test, tear break-up time (BUT), superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression were evaluated. Unaffected contralateral eyes were used as control for comparison. Results: A paired sample t-test between affected and unaffected eyes demonstrated a significant difference for BUT, superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression in the incomplete blinking group. However, only BUT showed significant difference between affected and unaffected eyes in complete blinking group. Furthermore, we showed that paralysis duration was related to the incidence of MGD. Significant difference was demonstrated between the affected and unaffected eyes for superficial punctate keratopathy, eyelid abnormality, ability and quality of meibum expression in the middle and late stage, but not early stage. Conclusions: These findings suggest that the inability to blink completely induced by CN VII palsy for more than one week might contribute to the development of MGD. Clinical optimization of blinking may ameliorate MGD symptom and benefit CN VII palsy patients.

Dry eye-related ocular surface examination is very important in the diagnosis and treatment of dry eye disease. With the recent advances in science and technology, dry eye examination techniques have progressed rapidly, which has greatly improved dry eye diagnoses and treatment. However, clinically, confusion remains about which examination to choose, how to ensure the repeatability of the examination, and how to accurately interpret the examination results. In this review, we systematically evaluate previous examinations of dry eye, analyze the latest views and research hotspots, and provide a reference for the diagnosis and management of dry eye.

Neutrophils release neutrophil extracellular traps (NETs) in a pathogen-killing process called NETosis. Excessive NET formation, however, is implicated in disease pathogenesis. Therefore, to understand how NETosis is regulated, we examined the effect of dexamethasone (DXM), an anti-inflammatory drug, on this process and the role of toll-like receptors (TLRs). We stimulated human neutrophils with phorbol 12-myristate 13-acetate (PMA) or Staphylococcus aureus and quantified NET formation. We also examined the effect of DXM on the bactericidal effect of NETs and the role of reactive oxygen species (ROS) and nuclear factor (NF)-κB in DXM-regulated NETosis. DXM significantly inhibited S. aureus-induced NETosis and extracellular bacterial killing. ROS production and NF-κB activation were not involved in DXM-regulated NETosis. TLR2 and TLR4, but not TLR5 or TLR6, modified S. aureus-induced NET formation. Neither DXM nor TLRs were involved in PMA-induced NETosis. Furthermore, TLR2 and TLR4 agonists rescued DXM-inhibited NETosis, and neither TLR2 nor TLR4 antagonists could further inhibit NETosis reduction induced by DXM, indicating that DXM may inhibit NETosis by regulating TLR2 and TLR4. In conclusion, the mechanisms of S. aureus- and PMA-induced NETosis are different. DXM decreases NET formation independently of oxidant production and NF-κB phosphorylation and possibly via a TLR-dependent mechanism.