Posterior capsular opacification (PCO) is the most frequent complication of cataract surgery. Advances in surgical techniques, intraocular lens materials, and designs have reduced the PCO rate, but it is still a significant problem. The only effective treatment for PCO, Nd:YAG laser capsulotomy carries vision-related complications and risks and puts a significant financial burden on the health care system. This review contains current knowledge about the mechanisms of PCO development. Posterior capsular opacification is caused mainly by remnant lens epithelial cell proliferation and migration, epithelial-mesenchymal transition, collagen deposition, and lens fiber generation. All of these processes are influenced by cytokines, growth factors, and extracellular matrix proteins. We also describe advances and improvements in surgical techniques, intraocular lens materials, and the designs and use of therapeutic agents leading to safe, effective, and less expensive strategies to eradicate PCO.

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Posterior capsular opacification: a problem reduced but not yet eradicated.

The vertebrate lens has a distinct polarity and structure that are regulated by growth factors resident in the ocular media. Fibroblast growth factors, in concert with other growth factors, are key re

Transforming Growth Factor-β-Induced Epithelial-Mesenchymal Transition in the Lens: A Model for Cataract Formation

Posterior Capsule Opacification

Posterior capsule opacification: A cell biological perspective

Myofibroblast transdifferentiation: The dark force in ocular wound healing and fibrosis

Purpose. After intraocular lens (IOL) implant surger for cataracty , cell growth on the posteriorcapsule is responsible for renewed visual impairmen in approximatelt y 30% of patients. Theauthors have, therefore, develope a humad n lens capsule system to study this growth in vitro.Methods. Sham cataract surgery, including anterior capsulorhexis, nucleus hydroexpression,and aspiratio onf lens fibers, was performed on donor eyes I.n some cases, a polymethylmeth-acrylate IOL implant was place idn th capsulae r bag Th. e capsular bag was dissected free,pinned flat o an plastic culture dish, covered with Eagle's minimum essential medium supple-mented with 10% fetal calf seru anmd observed by phase-contrast and dark-field microscopyfor as long as 100 days. At the end-point, capsules were examined by fluorescence microscopyfor actin, vimentin. , and chromatin.Results. Withi 2n4 hours, there was evidenc oef cell growth in the equatorial region. Afte 2rto 3 days, cells were normally observed growin thg froe rhexims onto the posterior capsuleand acros ths e anterior surface o f the IOL i,f present. Growth proceeded rapidl so thayt theposterior capsule fo,r example, was totally covere byd a confluent monolaye of cellr s at 5.8± 0.6 days and 7.2 ± 0.7 days for capsules aged 60 years, respectively. Totalcover of the anterior IOL surface generally followe 4 to 5 dayds behind tha otf the capsule.Capsular wrinkles became increasingly apparent as time progressed, causin a markegd rise inlight scatter A. n increase in capsular tension also occurred and th, e actin filaments becamemore polarized nea thre wrinkles.Conclusions. The model presented her foer posterior capsule opacification shows o manf theychanges seen in vivo, including rapid lens cell growth, wrinkling, tensioning, and light scatterin the posterior capsule It wil. l b e possibl teo develop strategie fors inhibitin g cell growthwith this system. Invest Ophthalmol Vi 1996s Sci 37:906-914;. .An modern extracapsular cataract surgery, to restorethe best possible vision, a small artificial lens is im-planted into the remaining lens capsular bag fromwhich most of the fiber mass has been removed. Thisapproach is not without subsequent complications,however, and within 2 years as many as 35% of patientsexperience a significant loss of visual acuity.

A study of human lens cell growth in vitro : A model for posterior capsule opacification

Lens cytoplasmic calcium is controlled by calcium adenosine triphosphatases at the plasma and endoplasmic reticulum membranes. The former is inhibited by W7 and insensitive to thapsigargin whereas the latter is inhibited by thapsigargin, but insensitive to W7. The lens endoplasmic reticulum store is also controlled by an inositol (1,4,5) trisphosphate calcium-release mechanism. Na+/Ca2+ exchange plays a relatively minor role in calcium regulation, at least at resting calcium levels.

S. F. Webb

Papers

A study of human lens cell growth in vitro : A model for posterior capsule opacification

Calcium regulation in tissue-cultured human and bovine lens epithelial cells.

Calcium mobilisation modulates growth of lens cells.