Posterior capsular opacification (PCO) is the most common complication of cataract surgery, occurring in up to 50% of cases,1 and a recent clinical survey suggested that the incidence is not declining in spite of improvements in surgical technique.2 At present PCO is treated by YAG capsulotomy, which carries a small risk of sight threatening complications such as cystoid macular oedema or retinal detachment and is expensive, costing the US Medicare programme $250 million in 1993.3 YAG laser capsulotomy is frequently not available in underdeveloped countries, adding considerably to the problems of treating third world blindness from cataract. The clinical and economic significance of PCO makes it an important public health problem, and in order to prevent it a clear understanding of the pathogenesis is needed.

Cataract surgery induces a wound healing response in the lens with cellular proliferation and laying down of extracellular matrix (ECM). PCO results from the proliferation of lens epithelial cells (LEC) remaining in the capsular bag after any type of extracapsular cataract extraction.1 Visual loss occurs as a result of centripetal migration of LECs associated with fibrosis and wrinkling of the posterior capsule. Histology has shown that there are two areas within the capsular bag where cellular activity leads to the formation of PCO4—the cuboidal anterior epithelial cells and the equatorial lens bow cells, which are both derived embryologically from ectoderm at 8 weeks' gestation. Clinically there are two morphological types of PCO—wrinkling and haze from fibrosis on the capsule and epithelial pearls from regeneration of lens fibres. McDonnell and co-authors,5 6 have shown that the anterior epithelial cells in both rabbits and humans initially undergo hyperplasia and, by 4 days after surgery, transform into spindle-shaped myofibroblast cells. This process starts at the cut edge of the anterior capsule …