الفهرس 
Anatomy of the vitreous
Microscopic morphologyOnly 14 pages are availabe for public view
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Abstract
The vitreous humour is a transparent colourless gel of a consistency firmer than egg white.
Posterior vitreous detachement has been regarded as an age-related degenerative process of the vitreous that results in the separation of the cortical vitreous gel from the retinal surface. Pharmacological vitreolysis is a promising new therapy to improve vitreoretinal surgery. There are many reasons for enzymatic-assisted vitreous surgery. The main goal is to manipulate the vitreous collagen, both centrally achieving liquefaction, as well as along the vitreoretinal surface to be able to achieve a cleavage plane cleaner than can be mechanically achieved. Enzymes used for pharmacological vitreolysis include: Hyaluronidase, Collagenase, Chondroitinase, Dispase, Nattokinase, Tissue plasminogen activator, Human plasmin and Microplasmin while non enzymatic agents include: Urea/Vitreosolve and Arginin-glycine-Aspartate peptides (RGD peptides).
Published researches showed the hyaluronidase enzyme with concentrations greater than 15 IU clinical and histological abnormalities were evident in most eyes.
Regarding collagenase enzyme, recent studies have showen that there are two machanismes by which collagenase act upon collagen: a triple helical peptidases activity and a collagenolytic activity. The former unravels the triple helix but does not cut the long strands into smaller pieces.Published researches showed the effect of chondroitinase as a human trials of diabetic retinopathy eyes and macular holes have never been released to allow complete analysis.
The dispase enzyme not optimal for application in the eye because it is obtained from bacillus polymyxa and contains endotoxin.
Regarding the PVD inducing mechanism, nattokinase have two major effects: one is the direct effect of liquefying the vitreous gel by its proteolytic activity and the other is the indirect effect of increasing the plasmin activity that induce the vitreoretinal dehiscence.
Tissue plasminogen activator inducing PVD is similar to plasmin enzyme by activating endogenous plasminogen which the converts to plasmin enzyme and works on the vitreoretinal juncture.
RGD peptide-assited vitrectomy facilitated PVD, suggesting that RGD peptide may prove to be effective adjuncts in producing posterior vitreous separation during vitreous surgery.
Human plasmin. The liquefaction of the vitreous gel by plasmin enzyme is based on its activity on collagenases especially type IV collagenase. Plasmin inducing a cleavage between the vitreous cortex and ILM without morphological changes to the retina leaving a smooth retinal surface.Plasmin induced vitreoretinal separation is limited to the posterior pole and to the equator.
At the vitreous base the cortical hyaloid remains firmly attached, indicating that plasmin does not cleave the vitreoretinal junction by secondary activation of collagenase.
Thus, one important disadvantage of plasmin injection without vitrectomy may be the risk of inducing retinal breaks at posterior margin of the vitreous base.
The human recombinant microplasmin which its molecular weight 29 KDa is much smaller than plasmin that enabling it to penetrate epiretinal tissue more effectively than plasmin.
Microplasmin can induce spontaneous PVD or reduce the amount of suction necessary to induce PVD with no apparent retinal toxicity with a 50% success rate.
As its role in diabetic retinopathy can induce a acomplete PVD with spontaneous resolution of macular edema and improvement of visual acuity.
Also ocriplasmin could potentially be applicable to a wide range of pediatric vitreoretinopathies.
The only available safety data supported the view that adverse ocular events were mild and limited largely to the first post injection week. A small percentage suffered from unexplained visual loss and most of these recovered within two weeks.