The Future of Dry Eye Treatments

Patients with ocular pain or ocular discomfort, with a symptoms ranging from mild irritation, foreign body sensation to severe pain,  often have an underlying meibomian gland, goblet cell, or lacrimal gland abnormality, which leads to a component of dry eye. 

Since the corneal nerves are so sensitive to changes in their microenvironment, even minor changes in surrounding molecules can set off chronic ocular pain. 

This paper below discusses such small molecules. 
It is the basis of another line of dry eye drops & drugs likely and explains why Cord Blood Serum and Amniotic Membrane work so well for these patients. 
 2012 Nov;119(11):2211-9. doi: 10.1016/j.ophtha.2012.05.038. Epub 2012 Aug 1.

Change in prostaglandin expression levels and synthesizing activities in dry eye disease.



To investigate the expression level of prostaglandins (PGs) and their de novo synthesis in dry eye (DE) disease.


Cross-sectional case-control study and in vivo mouse experimental study.


Forty-six eyes from 23 DE patients and 33 eyes from 17 age- and sex-matched controls were studied. Also, DE-induced murine eyes were compared with control eyes.


Patients completed a symptom questionnaire using a 100-mm visual analog scale (VAS). Nano-liquid chromatography tandem mass spectrometry was used for the quantification of PGE2 and PGD2. A DE disease environmental chamber was used to induce DE in mice. One week after induction, enzyme expressions of cyclooxygenase-1, cyclooxygenase-2 (COX-2), PG E synthase (PGES), and PG D synthase (PGDS) in the lacrimal glands, meibomian glands, and corneas were examined using immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR).


The mean PGE2 and PGD2 levels in the tears of DE patients were measured and compared with symptom severity scores. Immunohistochemistry staining patterns and qRT-PCR data of DE mice were quantified.


The mean PGE2 level in the tears of DE patients (2.72 ±3 .42 ng/ml) was significantly higher than that in the control group (0.88 ± 0.83 ng/ml; P = 0.003). However, the mean PGD2 level in the tears of DE patients (0.11 ± 0.22 ng/ml) was significantly lower (0.91 ± 3.28 ng/ml; P = 0.028). The mean PGE2-to-PGD2 ratio correlated strongly with VAS scoring (P = 0.008). In DE mice, COX-2 mRNA was significantly higher in ocular surface tissue and lacrimal glands. Furthermore, PGES mRNA was significantly higher in ocular surface tissue, whereas PGDS mRNA was decreased. Immunohistochemistry staining showed elevated COX-2 expression in the lacrimal glands, meibomian glands, corneas, and conjunctivas. Furthermore, PGES expression was found in periductal infiltrated cells of the lacrimal glands and conjunctival epithelium. Also, PGDS expression was decreased in meibomian glands and increased focally in the conjunctival epithelium.


A reciprocal change in PGE2 and PGD2 levels was found in the tears of DE patients, which correlated with patients’ symptom scores. These clinical results were supported by increased COX-2 and PGES expression levels found in tear-producing tissues of DE mice.
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