The prevalence of diabetes mellitus worldwide has shown a pronounced increase in recent years. According to reports from the International Diabetes Federation, in 2015, more than 400 million people were living with diabetes. The Centers for Disease Control and Prevention (CDC) also reports that approximately 90-95% of all diagnosed cases of diabetes in adults are type 2. The prevalence of diabetes for all age groups worldwide was estimated at 2.8% during 2000 and is expected to increase to 4.4% in 2030. Diabetes is now considered the leading cause of newly diagnosed blindness in adults, and WHO predicts that mortality rates due to diabetes will double by 2030. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay The significance of vascular variations from normal and neuronal abnormalities in the pathogenesis of diabetic retinopathy has recently been indicated. Several studies have demonstrated that neuronal degeneration in diabetic retinopathy is due to caspase- and mitochondria-dependent cell death pathways, and that some neurotrophic components may hinder neuronal cell switching initiated by diabetic stress. Diabetes mellitus most commonly causes ocular complications in the retina, in the form of diabetic retinopathy, retinal vein and arterial occlusions, but can also cause others such as anterior ischemic optic neuropathy and cataracts. However, not much attention has been paid to its effects on the cornea, as it is a less frequent complication. However, it is one of the effects that needs to be studied due to its marked effect on vision and its difficulty in management. Neuronal irregularities are known to specifically affect vision in patients with diabetic retinopathy, however they may also be the cause of corneal changes in diabetic keratopathy. Several processes explain its effect; Diabetic neurotrophic keratopathy is part of systemic diabetic polyneuropathy. Another is during the management of proliferative diabetic retinopathy, whether surgical or medical, which disruptions may occur. This is due to endothelial decompensation and bullous keratopathy as a result of damage to diabetic endothelial cells. Complications of diabetes are related to the degree of control and duration of the disease. Anterior segment findings in eyes with diabetic keratopathy are more difficult to identify than those of the posterior segment. Although corneas may appear disease-free in diabetic patients, extreme biochemical and ultrastructural irregularities may be present that alter their role. Early diabetic anterior segment changes include conjunctival microaneurysms, uveal ectropion, and endothelial changes; which include folds of Descemet's film and pigment deposits in the endothelium. In 1970, Schwartz and Hynduik noted decreased corneal sensitivity in diabetic patients with sterile neurotrophic corneal ulcers. Current use of vitrectomy to treat diabetic retinopathy has found that these patients have problems with epithelial cell healing and stromal edema. Patients with diabetic keratopathy exhibit alterations in epithelial basement membrane (BM), epithelial wound healing, epithelial-stromal interactions, endothelial function, and corneal nerve functions. Corneal disorders associated with diabetic keratopathy are characterized histologically by subepithelial deposits and altered morphological aspects of the corneal epithelium and endothelium. The single-layer hexagonal corneal endothelium unfolds.