Posterior capsule opacification (PCO) is the most common complication of cataract surgery. It causes a gradual deterioration of visual acuity, which would otherwise improve after a successful procedure. Despite recent advances in ophthalmology, this complication has not been eradicated, and the incidence of PCO can be as high as 10%. This article reviews the literature concerning the pathomechanism of PCO and examines the biochemical pathways involved in its formation and methods to prevent this complication. We also review the reported tests performed in cell cultures under laboratory conditions and in experimental animal models and in ex vivo human lens capsules. Finally, we describe research involving human eyes in the clinical setting and pharmacological methods that may reduce the frequency of PCO. Due to the multifactorial etiology of PCO, in vitro studies make it possible to assess the factors contributing to its complications and search for new therapeutic targets. Not all pathways involved in cell proliferation, migration, and contraction of the lens capsule are reproducible in laboratory conditions; moreover, PCO in humans and laboratory animals may be additionally stimulated by various degrees of postoperative reactions depending on the course of surgery. Therefore, further studies are necessary.
Keywords: animal model of PCO; cell cultures; experimental studies; posterior capsule opacification; tissue cultures.