Purpose: To assess long-term morphological and biometric corneal changes produced by overnight orthokeratology and to examine their recovery after cessation of contact lens wear. Methods: Prospective, single-center, longitudinal trial. Fifteen right eyes with low to moderate myopia underwent overnight orthokeratology for 1 year. The central cornea was examined using a confocal microscope and changes determined in visual acuity, refractive error and corneal topography. Cell counts were performed using both the confocal microscope’s software and the image analysis software of the USA Health Institute. All measurements were made during orthokeratology treatment and 1 month after discontinuing treatment. Results: No significant changes in endothelial cell density were observed over time but polymegethism increased significantly and baseline values were not recovered (p < 0.01). Stromal cell density remained unchanged though numbers of activated keratocytes increased during the study and returned to baseline when lens wear ceased. Basal epithelium cell densities significantly fell (p < 0.01) and epithelial wing and superficial cells showed enhanced visibility (p < 0.05). Superficial cells increased in height and width; this width increase being significant after 1 year of orthokeratology (p < 0.01). All epithelial cell changes returned to baseline. Corneal thickness, Bowman layer thickness, subbasal plexus thickness and epithelial thickness were reduced in the central cornea but the stroma was thickened. Of these changes, the decrease in epithelium thickness reached statistical significance (p < 0.01) and baseline values were not recovered. Conclusion: Overnight orthokeratology induces structural and optical changes particularly in the central corneal epithelium during myopia treatment. If confirmed, the irreversible changes detected indicate a need for further investigation.

To examine the morphological and biometric corneal changes produced over periods of 15 days and 1 month after overnight orthokeratology (OK). Prospective, single-center, longitudinal trial. Twenty-seven right eyes of 27 subjects (group 1) with low to moderate myopia wore OK lenses for 1 month. Ten right eyes of 10 subjects (group 2) with emmetropia to low myopia who did not wear any type of contact lens served as controls. Corneal morphometric measurements were obtained in vivo using a confocal microscope to examine the central and midperipheral cornea. Thickness measurements in the peripheral cornea were obtained by optical coherence tomography. Changes in visual acuity, refractive error, and corneal topography were also analyzed. No significant changes in either endothelial cell or stromal cell density were observed after 1 month of OK. Basal epithelial cells were, however, significantly reduced (P < 0.01), and epithelial wing and superficial cells showed enhanced visibility (P < 0.05). Superficial cells increased in height and width, the width increase after 1 month being significant (P < 0.01). Epithelial thickness was significantly reduced in the central cornea and 2 mm around the center. Corneal pachymetry increased significantly in the band from 5 to 10 mm from the corneal apex (P < 0.01). OK lenses for myopia induce significant structural and optical changes particularly in the central epithelium after 15 days or 1 month of wear. The central corneal epithelium responds to OK wear by undergoing significant epithelial cell shape and size alterations with no effects, however, on the cells of the corneal endothelium or the corneal stroma. Peripheral corneal thickness increased with respect to baseline values. These findings suggest that the corneal epithelium is the principal structure affected by the mechanical forces exerted by the OK lenses.

Arthritis is a chronic inflammatory illness that induces cachexia, which has a direct impact on morbidity and mortality. Fenofibrate, a selective PPARα activator prescribed to treat human dyslipidemia, has been reported to decrease inflammation in rheumatoid arthritis patients. The aim of this study was to elucidate whether fenofibrate is able to ameliorate skeletal muscle wasting in adjuvant-induced arthritis, an experimental model of rheumatoid arthritis. On day 4 after adjuvant injection, control and arthritic rats were treated with 300 mg/kg fenofibrate until day 15, when all rats were euthanized. Fenofibrate decreased external signs of arthritis and liver TNFα and blocked arthritis-induced decreased in PPARα expression in the gastrocnemius muscle. Arthritis decreased gastrocnemius weight, which results from a decrease in cross-section area and myofiber size, whereas fenofibrate administration to arthritic rats attenuated the decrease in both gastrocnemius weight and fast myofiber size. Fenofibrate treatment prevented arthritis-induced increase in atrogin-1 and MuRF1 expression in the gastrocnemius. Neither arthritis nor fenofibrate administration modify Akt-FoxO3 signaling. Myostatin expression was not modified by arthritis, but fenofibrate decreased myostatin expression in the gastrocnemius of arthritic rats. Arthritis increased muscle expression of MyoD, PCNA, and myogenin in the rats treated with vehicle but not in those treated with fenofibrate. The results indicate that, in experimental arthritis, fenofibrate decreases skeletal muscle atrophy through inhibition of the ubiquitin-proteasome system and myostatin.