Effects of daily and overnight wear of a novel hyper oxygen-transmissible soft contact lens on bacterial binding and corneal epithelium

Are hypoxia or modulus causes of contact lens‐associated keratitis?

“…The Manchester Keratitis Study, [9][10][11] which was the first properly-controlled epidemiological study of keratitis with silicone hydrogel contact lenses, demonstrated a significantly reduced severity of keratitis in those wearing silicone hydrogel lenses versus those using hydrogel lenses for overnight wear. Although this finding is entirely consistent with the expectations of leading researchers in the contact lens field [3][4][5] and with the experimental works outlined above, [6][7][8] it conflicts with the findings of Stapleton and colleagues 1 and Dart and co-workers. 2 We believe that this discrepancy could be attributed partly to various confounding factors, the strongest candidate of which is lens modulus.…”

“…An irrigation chamber was used by Cavanagh and colleagues 7 to harvest human corneal epithelial cells from patients wearing conventional hydrogel and silicone hydrogel contact lenses. These cells were mixed with P. aeruginosa and the extent of bacterial binding to the epithelial cells was assessed.…”

Contact lens-related microbial keratitis: how have epidemiology and genetics helped us with pathogenesis and prophylaxis

“…42 The initiation of microbial keratitis probably requires a combination of unique bacterial virulence characteristics plus the physiological impact of contact lens wear on the cornea. Physiological changes as a result of contact lens wear, which are likely to affect resistance to infection, include inhibition of normal corneal epithelial cell shedding, 43 corneal epithelial thinning, 43 increased binding of bacteria to corneal epithelial cells 43 possibly through exposure of specific bacterial adhesins on basolateral cell membranes, 44 increased internalisation of bacteria through expression of membrane lipid rafts on corneal epithelial cells, 45 reduced tear exchange, 46 and disruption to the normal lid/cornea/tear resurfacing mechanism.…”

Corneal crystallins and the development of cellular transparency

“…1), the anterior corneal epithelium, the corneal stroma and the posterior corneal endothelium. While the thickness of the corneal epithelium is fairly constant, ranging from 45 to 50 μm in the human, mouse and rabbit [31][32][33], the corneal stromal thickness varies considerably depending on the species and can be quite thin in mice (70 to 90 μm depending on strain), thicker in rabbits and humans (325 μm to 500 μm, respectively) and very thick in pigs and cows (1 mm) [32][33][34][35]. The corneal stroma for the most part contains regularly arranged collagen fibers of uniform thickness and spacing that are organized into thicker collagen bundles or lamellae.…”