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Does a sharp edge compress the posterior capsule in vivo?

2005; Lippincott Williams & Wilkins; Volume: 31; Issue: 2 Linguagem: Inglês

10.1016/j.jcrs.2004.12.012

1873-4502

Okihiro Nishi,

Glaucoma and retinal disorders

Nagamoto and Fujiwara1 conclude from their in vitro study that inhibition of cell migration at the optic edge of an intraocular lens (IOL) may be regulated by the degree of contact pressure between the optic edge and posterior capsule. A sharp capsule bend does not in itself inhibit cell migration. I have comments and questions for the authors. First, this conclusion is based on an in vitro study, which differs from in vivo conditions. Zonular tension, aqueous humor, and vitreous were not present in this model. Furthermore, the authors' conclusion is based on the assumption that contact pressure will arise at the optic edge clinically in vivo. Contradictory to their conclusion, there are some facts as well as in vivo experimental and clinical findings opposing the thesis that contact pressure arises at the optic edge. Some in vivo findings also indicate that a sharp capsule bend in itself inhibits cell migration. The volume and surface area of a human lens capsule (10 mm diameter, 4.0 mm thickness) have been mathematically calculated to be approximately 166 mm3 and 182 mm2, respectively, and those of an IOL, 12.5 mm3 and 60 mm2, respectively. Thus, an IOL has ratios of 1 to 10 and 1 to 3 in volume and area, respectively, to a lens capsule, indicating a capsule surplus. This suggests the capsule lies softly and gently on the IOL, deferring and complying to its form without compression, at least initially and unless the lens capsule contracts in a specific manner, as discussed below. Even several months after surgery, one can observe clinically in many eyes a slack posterior capsule apart from the IOL or posterior capsular folds by slitlamp. This indicates there is capsule surplus and, therefore, there is no tension in the capsule and there should be no tension at the IOL optic edge. Figure 1, A and B, show an extreme fold formation in the posterior capsule (arrows), indicating the capsule surplus. Myofibroblast-like cells in these folds could raise the tension. However, no cells are seen in these complex folds. If there were tension, the capsule at the optic edge would be pulled toward the fold. The capsule, however, lies closely and tightly on the side of the optic edge. These folds are simply the expression of capsule surplus. The capsule folds swallow the capsule surplus, so that the posterior capsule forms a bend, deferring to the sharp optic edge. In contrast, in Figure 1, C, there are no complex folds, so the posterior capsule is undulated due to its surplus and lies loosely on the IOL. As a result, the bend is not sharp and some lens epithelial cells (LECs) are seen. One can clearly recognize in this figure how excessively large the undulated posterior capsule is compared to the IOL.Figure 1.: A and B: Rabbit lens capsules containing an AcrySof IOL 3 weeks after surgery. The extensive folds in the posterior capsule indicate a large surplus of capsule (arrow) and contain no LECs in the folds. The posterior capsule lies tightly at the side of the optic edge, indicating the lack of pulling tension by the capsule folds. There is no adhesion between the anterior and posterior capsules (PC = posterior capsule). C: Rabbit lens capsule 3 weeks after surgery. There are no complex capsule folds in either eye, as shown in B and C. The undulated posterior capsule showing a surplus indicates that there may be no compression pressure at the optic edge.In capsule contraction syndrome, the posterior capsule conforms to the original form and is separated from the sharp optic edge. It becomes slack after neodymium:YAG (Nd:YAG) laser capsulotomy (Figure 2, A), indicating the posterior capsule simply lies on the optic without tension.Figure 2.: A: Scheimpflug photography of a case of capsule contraction syndrome shows the view before (left) and after (right) Nd:YAG laser capsulotomy. The posterior capsule is apart from the IOL edge and slack after the capsulotomy, indicating there is no compression pressure at the optic edge (courtesy of Satoshi Suzuki, MD, Showa Medical College, Tokyo). B: Rabbit lens capsule containing a capsule bending ring (CBR) 4 weeks after surgery. The LECs proliferated on the CBR, yet they never migrated onto the posterior capsule. Lens epithelial cells are found in a rectangular angle among the CBR and anterior and posterior capsules, indicating that the sharp discontinuous capsule bend induced contact inhibition as in vitro on a well bottom (reprinted with permission 2,3).These facts and findings indicate that contact pressure may not be clinically present at the optic edge in many eyes in which a capsule bend is present. Theoretically, contact pressure can only arise when the posterior capsule is pulled by extensive fibrosis along the optic edge toward the anterior capsule. I think such instances can occur, particularly with silicone IOLs, but not always. Furthermore, the condition would occur several months after surgery, if at all. Capsule tension created by the haptic would disturb bending of the capsule or compression pressure because it would work against pulling up the posterior capsule along the optic edge.These considerations inevitably lead to the idea that there must be an optimal size relationship and condition between capsule and IOL to bend the capsule optimally, preventing posterior capsule opacification. When a capsule is too large in relation to the IOL, it cannot form a bend at the optic edge because of the capsule surplus. Excessive capsule tension due to a large haptic may impede capsule bending.Finally, Figure 2, B, clearly shows that LECs do not migrate onto the posterior capsule when they are found in the discontinuous sharp angle, which contradicts the experimental in vitro results by Nagamoto and Fujiwara, thus the effect of a discontinuous capsule bend, which we call "contact inhibition of the cell."2,3 Nagamoto and Fujiwara say we have not used this term properly. However, as Molecular Biology of the Cell4 clearly states, when normal cells divide on the dish until a confluent monolayer, they stop proliferating—a phenomenon known as density-dependent inhibition of cell division. This phenomenon was originally described in terms of "contact inhibition." The in vivo finding shown in Figure 2, B, is analogous to the in vitro contact inhibition described. Thus, I think we used the term accurately. When the marginal cells knock into the rectangular well wall, cells are forced to or must be bent at the corner to overcome it, where they would undergo further mitosis (Figure 3). Can a cell bend itself at a rectangular corner, as Figure 3 illustrates? I suppose a signal inhibiting the cell cycle would arise at the rectangle so that the cells do not proliferate further.Figure 3.: A: Illustration of a cell population at the rectangular well bottom. A marginal cell is undergoing mitosis. B: When cells further proliferate by mitosis, they must discontinuously bend at the corner. C: A side view illustrates a dividing cell bent at the rectangular well corner. Can a cell containing dividing DNA (double helix, not linear) bend itself?The above in vivo findings speak clearly against the conclusion of Nagamoto and Fujiwara. My questions are as follows: Did the authors measure the pressure? How did they confirm there was pressure at the optic edge? Is it not an assumption? How did they bend the posterior capsule that was placed on the plastic sheet corner? How did they confirm it was sharply bent? The IOL with a ridge appears to be much thicker than the others the authors used in the experiment. This could affect the results. What is the thickness of each IOL? In conclusion, the most important finding is that a capsule bend is always formed at the sharp optic edge. This has been observed clinically and experimentally in vivo. In vivo clinical and experimental findings indicate that the excessively large posterior capsule (compared to an IOL) lies gently on the IOL, deferring to and complying with its shape without tension and, therefore, without compression pressure at the optic edge. However, some cases in which the posterior continuous curvilinear capsulorhexis was enlarged after surgery have been observed (Rupert Menapace, MD, personal communication), indicating that capsule tension can exert compression pressure at the optic edge. Some in vivo findings clearly support that contact inhibition can result from the square angle (capsule bend). Whether LECs stop migrating due to contact inhibition at this capsule bend or due to the compression pressure has not been definitively clarified in clinical situations. Finally, in vivo or clinical findings should be held in higher esteem than in vitro findings, although the former often cannot clarify pathogenesis and the latter can produce results that often differ significantly from clinical situations. Therefore, the authors should be careful about drawing conclusions based on in vitro study. Okihiro Nishi MD Osaka, Japan