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Abstract
Keratoconus is defined as a disorder characterised by progressive corneal steepening, most typically inferior to the center of the cornea, with eventual corneal thinning, induced myopia, and both regular and irregular astigmatism (Sugar, 1999).
The prevalence of keratoconus in the general population appears to be relatively high and is reported to be between 50 - 230 per 100, 000 (Wang et al, 2000).
The disease has no racial predilection and it is usually bilateral. The reports and studies showed variable sex distribution of the disease.
Onset of keratoconus occurs during the teenage years. The prognosis is unpredictable and progression is variable (Leibowitz and Morello, 1998).
Most cases of keratoconus are sporadic. Hereditary transmission of keratoconus also had been reported. Dominant, recessive, and irregular transmissions all appeared to be implicated (Leibowitz and Morello, 1998).
The proposed etiology of keratoconus includes biochemical and physical corneal tissue changes, but no one theory fully explains the clinical findings and associated ocular and non-ocular disorders (Feder, 1999).
Various biochemical abnormalities have been repoted in keratoconic corneas including decrease in hydroxylation of lysine and glycolysation of hydroxylysine, decreased total collagen and relative increase in structural glycoprotein (Fukichi et al, 1994).
Numbers of entities, both ocular (e.g., retinitis pigmentosa, floppy eyelid syndrome, fuch’s corneal dystrophy, cotact lens syndromes, keratectasia after LASIK) and systematic (e.g.,atopic disease, down syndrome, turner syndrem, systematic collagen diseas) are associated with keratoconus. (Feder, 1999).
Although all layers of the cornea ultimately may show microscopic alterations, the earliest changes occur in the superficial layers of the cornea. The basal layer of epithelium involved in early stage and later the basal cells disappear, leaving only one or two layers of flattened superficial epithelial cells lying on an altered basement membrane. In advanced stage the Bowman’s layer is gradually destroyed, the stroma show abnormal thinning and anterior protrusion of the central portion of the cornea and the descemet’s membrane may be folded until becomes ruptured. Also the endothelial cells flattened and their nuclei lay father apart (Leibowitz and Morello, 1998).