Diabetic retinopathy pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rohan Bir Singh, M.B.B.S.[2] Priyamvada Singh, M.B.B.S. [3], Afsaneh Morteza, MD-MPH [4]
Overview
Diabetic retinopathy is the result of microvascular abnormalities of the retina.
Pathophysiology
The retina is a multicellular photon sensor, a unique component of the central nervous system, which is structured on the vessels.
Promoted by the observations that there is a selective loss of pericytes early in diabetic retinopathy, many researchers were attracted to these cells as the origin of the disease.[1]. Pericytes are enigmatic cells, which are regular components of all human tissues and organs. In contrast to arteries and arterioles where the coverage consists of the smooth muscle cells, the capillary system is individually covered by the pericytes. Pericytes are codependent on the endothelial cells. Normal pericytes have a contractile function that helps to regulate capillary blood flow. The loss of pericytes, due to diabetic inflammation, is followed by the loss of capillary endothelial cells. Apoptosis of the pericytes, leads to the disappearance of both types of cells. Since neurons in the retina have high metabolic requirements, the hypoxia that results from extensive retinal capillary cell death is a probable stimulus for the increased expression of molecules that enhance the breakdown of the blood–retinal barrier and lead to vascular proliferation or angiogenesis. [2] Angiogenesis is a complex process, characterized by a cascade of events:
1: Initial vasodilatation of existing vessels
2: Increased vascular permeability and degradation of the surrounding matrix,
3: Migration and tube forming of the activated and proliferating endothelial cells
4: Maturation and remodeling of these new vessels takes place to form a vascular network.
These new blood vessels are abnormal and fragile. They grow along the retina and along the surface of the vitreous. By themselves, these blood vessels do not cause symptoms or vision loss. However, they have thin, fragile walls, and they ultimately leak blood. Retinal damage can result from persistent vitreous haemorrhage. On the other hand, contraction of associated fibrous tissue formed by proliferative disease tissue can result in deformation of the retina and tractional retinal detachment. The detachment may tear the retina (rhegmatogenous) or may not (non-rhegmatogenous). The non-rhegmatogenous retinal detachment is worse and is characterized by the
1: Confined retina
2: A taut and shiny appearance
3: Concave retina toward the pupil
4: Disappearance of the sub retinal fluid shifting
The cascade of these events causes vision loss.[3]
Recent studies which are focused on the neural component of the retina, have shown that diabetic neuropathy of the neuroglial cells may play an important role in the pathophysiology of disease.[4]
Hyperglycemia-induced pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damages change the formation of the blood-retinal barrier and also make retinal blood vessel become more permeable.[5]
Nonproliferative Diabetic Retinopathy (NPDR)
Small blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar control. An overaccumulation of glucose and/or fructose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any changes in their vision.
Macular Edema
Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.
Proliferative Diabetic Retinopathy
As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage. The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause Neovascular Glaucoma. Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages. Even so, the advanced proliferative diabetic retinopathy (PDR) can remain asymptomatic for a very long time, and so should be monitored closely with regular checkups.
References
- ↑ Understanding diabetic retinopathy by Pardianto G et al., in Mimbar Ilmiah Oftalmologi Indonesia.2005;2: 65-6.
- ↑ Frank RN (2004). "Diabetic retinopathy". N Engl J Med. 350 (1): 48–58. doi:10.1056/NEJMra021678. PMID 14702427.
- ↑ Witmer AN, Vrensen GF, Van Noorden CJ, Schlingemann RO (2003). "Vascular endothelial growth factors and angiogenesis in eye disease". Prog Retin Eye Res. 22 (1): 1–29. PMID 12597922.
- ↑ Berner AK, Brouwers O, Pringle R, Klaassen I, Colhoun L, McVicar C; et al. (2012). "Protection against methylglyoxal-derived AGEs by regulation of glyoxalase 1 prevents retinal neuroglial and vasodegenerative pathology". Diabetologia. 55 (3): 845–54. doi:10.1007/s00125-011-2393-0. PMID 22143324.
- ↑ Understanding diabetic retinopathy by Pardianto G et al., in Mimbar Ilmiah Oftalmologi Indonesia.2005;2: 65-6.