Using a special embedding method, autopsied eyes with proliferative diabetic retinopathy were studied. In areas with no posterior vitreous detachment, small proliferations may arise multifocally and grow within the vitreous cortex. The fibrous material of the vitreous cortex is densely interconnected with and obviously incorporated into the newly formed proliferated tissue, a process which causes coarse traction lines on the vitreous cortex lamellae. The clinical consequences of these findings are discussed.

Background: To evaluate the role of the vitreous in diabetic eyes, autopsy eyes from diabetic patients have been examined by means of light and electron microscopy. Methods: Twenty-five eyes were obtained from 19 patients. The duration of diabetes was from 8 to 26 years (average 17 years). All patients had type II diabetes. The glycerol-dehydrated globes were embedded in celloidin and hardened with chloroform. For light microscopy, areas of interest were cut from 200-μm-thick celloidin sections and embedded in paraffin, and 10-μm sections were cut. Such 200-μm and 10-μm sections were also used for scanning electron microscopy. For transmission electron microscopy, areas of interest were cut from thick celloidin sections and embedded in Epon for thin sectioning. Results: The vitreous in diabetic eyes exhibits delayed senile degeneration in case of early onset of diabetes. It shows intensified staining of the vitreous cortex. Posterior detachment is often incomplete without collapse. The vitreous collagen fibers are coarse and aggregated in the centrally located cortical region of the vitreous. Hyalocytes in diabetic eyes have a different shape than normally, and their number seems to be increased. All these structural changes were not demonstrated in nondiabetic eyes. Conclusion: The vitreous in diabetic patients is morphologically different from normal vitreous. Features of the diabetic vitreous are aggregated collagen fibers, increased density of the vitreous cortex and morphological changes of hyalocytes. It is discussed whether these findings arise from nonenzymatic glycosylation of collagen molecules resulting in diabetic vitreopathy.

Silicone oils (polymethylsiloxanes) with different viscosities (200, 1000 and 5000 cSt) and a fluorinated silicone oil (5000 cSt) were injected into the peritoneum of CBA mice. Three weeks after the injection, peritoneal exudates were obtained and investigated using light and electron microscopy. For each silicone-oil type, light-microscopic examination revealed the presence of abundant extracellular lipid-like droplets and a dense cellular infiltrate composed of macrophages, lymphocytes and multinucleated giant cells. Lipid-like inclusions were observed in macrophages and multinucleated giant cells. These intracellular inclusions were revealed to be membrane bound by transmission electron microscopy. We observed no differences with respect to the amount of phagocytotic activity for the different silicone-oil types tested. Purified silicone oils of lower viscosity (OP 200 and OP 1000) resulted in the mildest chronic inflammatory reaction. Our results suggest that emulsification, phagocytosis and granulomatous inflammation are associated with intraocular silicone-oil implantation. The question of which properties would make a silicone oil most suitable for clinical use requires further investigation.

No abstract

After vitrectomy and silicone oil instillation, several oil inclusions were found on histologic examination of recurrent epiretinal membranes 3-4 months after oil instillation. The authors discuss how far an early emulsification of silicone oil stimulates macrophages as well as other proliferating cells and thus leads to impregnation and reproliferation of epiretinal membranes. If highly refined oil is used, impregnation and its complications will perhaps become less significant.