Pseudophakic Bullous Keratopathy

Purpose. The cornea is protected by apical hydrophilic transmembrane mucins and tears. In pathologic states the mucin barrier is disrupted, creating potential for meibomian lipids to adhere more strongly. Undisplaced lipids create an unwettable surface. The hypothesis that pathologic ocular surfaces alter lipid binding and the ability of tear proteins to remove lipids was tested. Methods. Corneas with pathologic surfaces were studied for lipid adhesion and removal by tears. Capture of fluorescence-labeled phospholipids by human tears was assessed by steady state fluorometry. Tear proteins were separated by gel filtration chromatography and analyzed for bound lipids. Results. Contact angle measurements revealed strong lipid adherence to corneas submerged in buffer. Lower contact angles are observed for lipids on completely de-epithelialized corneas compared with intact corneas (P = 0.04). Lipid removal from these surfaces is greater with whole tears than with tears depleted of tear lipocalin (P < 0.0005). Significantly fewer lipids are captured by tears from Bowman's layer than from epithelial-bearing surfaces (P < 0.025). The only tear component to bind the fluorescence-tagged lipid is tear lipocalin. The histology of a rare case of dry eye disease demonstrates the dominant features of contemporaneous bullous keratopathy. Lipid sequestration from this cornea by tear lipocalin was robust. Conclusions. Lipid is captured by tear lipocalin from corneas with bullous keratopathy and dry eye. Lipid removal is slightly abrogated by greater lipid adhesion to Bowman's layer. Reduced secretion of tear lipocalin documented in dry eye disease could hamper lipid removal and exacerbate ocular surface pathology.

Section: Discussionmentioning

confidence: 99%

Tear Lipocalin Captures Exogenous Lipid from Abnormal Corneal Surfaces

Glasgow

Gasymov²,

Abduragimov

et al. 2010

“…24 In contrast, pseudophakic bullous keratopathy (PBK) is an acquired corneal endothelial disorder that may occur following intraocular cataract extraction surgery. 25 Various causative factors such as excessive phacoemulsification energy 26 and mechanical trauma 27 to the corneal endothelium during cataract extraction surgery have been implicated in causing stress-induced apoptosis of CECs. 28 Although PBK is characterized by diffuse damage to the corneal endothelial layer, 29 a peripheral rim of healthy CECs and DM is usually retained in corneas affected by FED.…”

mentioning

confidence: 99%

Predicative Factors for Corneal Endothelial Cell Migration

Soh

Peh

George

et al. 2016

PURPOSE.To characterize the effects of Descemet's stripping, Rho-associated protein kinase inhibitor Y-27632, and donor age on endothelial migration in human corneas maintained in ex vivo culture.METHODS. Twenty-eight cadaveric human corneas underwent ex vivo culture in either standard or Y-27632-supplemented culture medium for 14 days. The posterior surface of each cornea was manipulated to create two types of wounds: scratched wound-corneal endothelial cells (CECs) were denuded from the Descemet's membrane (DM) to leave behind a bare but intact DM; and peeled wound-both the DM and overlying CECs were stripped to leave behind bare corneal stroma. Endothelial migration was assessed via Trypan blue staining. Morphologic traits of CECs were assessed via Alizarin red microscopy and scanning electron microscopy.RESULTS. The CECs migrated preferentially over scratched wounds compared with peeled wounds. Y-27632 supplementation accelerated endothelial migration over scratched wounds. Endothelial migration decreased with advanced donor age for both wound types, regardless of exposure to Y-27632. Y-27632 supplementation resulted in a less rapid decline in endothelial migration for donors older than 50 years of age for scratched surfaces. Greater cell density and hexagonality was observed over scratched wounds compared with peeled wounds, regardless of Y-27632 supplementation.CONCLUSIONS. The presence of an intact DM, Y-27632 supplementation, and young donor age are factors that promote endothelial migration in an ex vivo human cornea culture model. The negative effect of age on endothelial migration can be mitigated by the presence of an intact DM and Y-27632 supplementation.

“…However, patients with bullous keratopathy are known to have painful surface epithelial defects, subepithelial bullae, and punctate staining. Bullous keratopathy may be accompanied clinically by superficial epithelial keratopathy 6. Eagle et al7 noted that bullous keratopathy may manifest findings similar to map dot finger print dystrophy.…”

mentioning

confidence: 99%

Exfoliative Epitheliopathy of Bullous Keratopathy with Breaches in the MUC16 Glyocalyx

Glasgow

Gasymov²,

Casey

2009

Purpose Expression of cellular adhesion molecules is altered in bullous keratopathy. The hypothesis that epithelial alterations in bullous keratopathy compromise the surface of the cornea and its glycocalyx was tested. Methods Studies were performed on eight cases each of pseudophakic bullous keratopathy and healthy corneas. The number of epithelial cell layers was determined with a stereological method of point counting. The minimum distance between points was established by estimates of cell size with variable pressure scanning electron microscopy performed in backscatter mode. The mean number of cell layers with mucin expression was identified by immunohistochemistry with mouse monoclonal antibodies for MUC1 and MUC16. Data were analyzed by Student's t-test if values showed a normal distribution or, alternatively, by the Wilcoxon rank-sum test. Results Mean numbers of wing cell and superficial cell layers were lower in bullous keratopathy specimens (1.6 vs. 2.0; P < 0.0001) than in controls (1.1 vs. 1.8; P < 0.000001). The number of exfoliated cell layers evident in sections was increased in the bullous keratopathy specimens compared with controls (0.36 vs. 0.03; P < 0.0001). The number of cell layers decorated with antibodies to MUC16 was lower in bullous keratopathy specimens than in controls (0.5 vs. 1.2; P < 0.025). The reduction of layers expressing MUC1 in bullous keratopathy was not statistically significant. Conclusions Pseudophakic bullous keratopathy manifests an abnormal corneal ocular surface in which superficial cell layers are exfoliated, leaving breaches in the protective MUC16 glycocalyx. The results provide a morphologic correlate for the surface epithelial abnormalities noted clinically in these patients.