Nishi's1 comments on the article by Nagamoto and Fujiwara2 were based on theoretical and animal studies. We would like to describe our experience based on the analysis of several thousand pseudophakic eyes obtained post-mortem. The capsular bend is based on the fusion of the peripheral posterior capsule and the peripheral aspect of the anterior capsule, thus creating a “nick” or “bend” in the capsule at the site where it contacts the posterior peripheral aspect of the square optic. It is predicated on the fact that little or no interfering material (eg, cortex or cells, specifically “E” cells, the source of posterior capsule opacification [PCO] within Soemmering's ring) rests in the space between the 2 capsules. If residual lens substance is in the space between the 2 capsules as they attempt to fuse, the process will be blocked. By this definition, the capsular bend can form completely only if there is a complete or almost complete removal of lens substance, allowing the 2 capsules to come into approximation (Figure 1). In these cases, PCO prevention is probably based on the first line of defense, namely, the complete removal of lens substance, and formation of the capsular bend is a secondary occurrence instead of the primary mechanism in retarding PCO.Figure 1: Photomicrograph of a human eye obtained post-mortem with an Alcon AcrySof IOL implanted in the capsular bag. There was complete removal of equatorial lens epithelial cells (E cells, the precursors of PCO). There is adherence of the peripheral anterior and posterior capsules around the haptic (left), extending toward the optic. A well-formed capsular bend has been created (lower left). A “cleanup” bag such as this is a prerequisite for capsular bend formation. The square-edged optic fills the bag. The biomaterial dissolves during processing, creating the large empty space (hematoxylin and eosin, original magnification ×5).In our autopsy series of several thousand eyes, we have seen numerous cases in which excellent PCO prevention was based on the barrier effect of the square-edge mechanism in the complete absence of a capsular bend (Figure 2). This seems to indicate that the capsular bend does not function as a primary mechanism in many cases.Figure 2: Photomicrographs clearly demonstrate examples of the barrier effect achieved with the square truncated edge of the 3-piece Alcon AcrySof IOL optic in the absence of a capsular bend. Retained cortex/lens epithelial cells are present in the intercapsular space in all 3 preparations (A to C), thus preventing the necessary adhesions between peripheral anterior and posterior capsules seen in these 4 preparations. The capsular bend is not necessary for effective lens epithelial cell/cortex blockage. Note the interface between the relatively exuberant Soemmering's rings (pink–red material, left) and the IOL optic (clear space, right). These are separated by the lens optic's square edge. Note also the clear posterior capsule in lower right. A: Masson's trichrome stain (original magnification ×50). B: Periodic acid-Schiff stain (original magnification ×150). C: Hematoxylin and eosin stain (original magnification ×40). D: Masson's trichrome stain (original magnification ×40).Figure 2: (continued)Figure 2: (continued)Figure 2: (continued)It is important to remember that the enhanced barrier effect provided by this optic geometry probably functions as icing on the cake by providing an additional reserve factor (in addition to the basic cortical cleanup that has proved to be of utmost importance in helping to reduce the overall incidence of visually significant PCO) in cases in which complete cortical cleanup was not achieved. As mentioned, the mechanism of action of the square edge in these cases cannot be related to the creation of a capsular bend but to a mechanical barrier effect.