LABORATORY SCIENCE

Contact inhibition of migrating lens epithelial
cells at the capsular bend created by a sharp-edged
intraocular lens after cataract surgery
Okihiro Nishi, MD, Naoki Yamamoto, PhD, Kayo Nishi, MD, Yutaro Nishi, MD

PURPOSE: To investigate whether the lens epithelial cells (LECs) at the capsular bend created bya sharp-edged intraocular lens (IOL) are in the G0 phase of the cell cycle.
SETTING: Nishi Eye Hospital, Osaka, Japan.
METHOD: A CeeOn Edge silicone IOL (AMO) with sharp edges was implanted in 1 eye and a PhacoFlex II silicone IOL (AMO) with rounded edges in the contralateral eye after standard cataract surgery in 6 rabbits. Immunohistochemical staining for the Ki-67 antibody was performed 1 day, 3, 4,
and 7 weeks after surgery.
RESULTS: In eyes with the sharp-edged IOL, LECs with thin, elongated nuclei accumulated at, but
did not extend beyond, the capsular bend and stained negative for the Ki-67 antibody, indicating thatthey were in the G0 phase of the cell cycle. In contrast, in the eye with the round-edged IOL, continuous migration of a predominantly monolayer of LECs over the IOL and onto the posterior capsule occurred. These cells were Ki-67 positive, indicating that they were proliferating.
CONCLUSIONS: Lens epithelial cells at the capsular bend of sharp-edged IOLs were in the G0 phaseof the cell cycle, indicating that they were contact inhibited. These findings support the theory the
sharp posterior optic edge of the IOL inhibits LEC migration, reducing formation of posterior capsule opacification. Whether these LECs can reactivate when the capsular bend is eliminated by later
formation of a Soemmerring’s ring requires further studies.
J Cataract Refract Surg 2007; 33:1065–1070 Q 2007 ASCRS and ESCRS

Experimental1–4 and clinical studies5–13 show that thecapsular bend formed by the sharp posterior optic
edge of an intraocular lens (IOL) inhibits lens epithelial
cell (LEC) migration onto the posterior capsule, reducing posterior capsule opacification (PCO). We postulated that contact inhibition of migrating LECs is
induced at the capsular bend.1–3 Our theory is based

Accepted for publication February 23, 2007.
From the Nishi Eye Hospital (O. Nishi, K. Nishi), Osaka, and the Fujita Health University Joint Research Laboratory (Yamamoto),
Toyoake, Japan; Universitäts-Augenklinik (Y. Nishi), Heidelberg,
Germany.
No author has a financial or proprietary interest in any material or
method mentioned.
Corresponding author: Okihiro Nishi, MD, Nishi Eye Hospital, 4-1426 Nakamichi, Higashinari-ku, Osaka 537-0025, Japan. E-mail:okihiro@nishi-ganka.or.jp.
Q 2007 ASCRS and ESCRS
Published by Elsevier Inc.

on the observation that cells in the rectangular wellbottom of a cell culture dish tend to form layers
when becoming confluent but cannot climb the vertical wall of the culture dish. The cell cycle consists of
the G1, S, G2, M, and G0 phases. When cells are in
the G0 phase, they are in a state of rest; that is, they
are not proliferating. Accordingly, we postulated
that the migrating LECs at the capsular bend should
also be in the G0 phase.
To test our hypothesis, we investigated whether
LECs at the capsular bend were influenced by contact
inhibition, and, if so, were in G0, the nonproliferatingphase.

MATERIALS AND METHODS
Surgical Procedure
This experimental study used rabbits. All animal procedures were performed in compliance with the ARVO
Statement for the Use of Animals in Ophthalmic and Vision
Research.
0886-3350/07/$dsee front matterdoi:10.1016/j.jcrs.2007.02.022

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Six Dutch or albino rabbits weighing 1.5 to 2.0 kg had implantation of a PhacoFlex II SI-40NB silicone IOL (AMO)
with rounded edges in 1 eye and CeeOn Edge silicone IOL
with sharp edges (AMO) in the contralateral eye. All surgeries were performed with the animals under anesthesia. The
same surgeon (O.N.) performed standard phacoemulsification and aspiration and IOL implantation as previously
reported.1

Immunohistochemical Examinations
One day (1 rabbit), 3 weeks (2 rabbits), 4 weeks (2 rabbits),
and 7 weeks (1 rabbit) after surgery, immunohistochemical
examinations of each eye were performed using the following protocol: After the rabbit was killed by an intravenous injection of ketamine sulfate (0.3 mg/kg) and succinylcholine
chloride (0.15 mg/kg), the eyes were enucleated, and a small
incision was made at the limbus and equatorial sclera tofacilitate the uptake of the tissue-fixation solution. The specimen was immediately placed in a fixation solution (Yamamoto’s Rapid Fix Solution) for several days and thenembedded in paraffin. Briefly, this solution is neutrally buffered, with a low concentration of a protein cross-linker. The
specimen was sliced with a microtome and put on a slide
glass to permit Ki-67 and proliferating nuclear antigen(PCNA) staining.

Figure 1. Comparison between PCNA and Ki-67 staining. Lens epithelial cells beneath the anterior capsule at the preequatorial region 4
weeks after surgery in the eye that received a PhacoFlex II IOL withround edges. Left: The PCNA staining served as a control. Note thatthe lens fiber cells (elongated cells) are still positive, with decreasing
intensity of the brown nucleus staining in the consecutive row. Right:
Ki-67 staining. Note that the lens fiber cells are all Ki-67 negative.
This is because PCNA staining is still positive at the beginning of
the G0 phase.

Ki-67 Staining
Ki-67 is a nucleus protein that is detectable in all phases of
the cell cycle except the G0 phase.14,15 Paraffin sections (5 mm)
were incubated with anti–Ki-67 rabbit polyclonal antibody(1:50, Abcam Ltd.) for 30 minutes at 37 C. Bound antibody
was detected with the Histofine Simple Stain MAX-PO(R)reagent using diaminobenzidine tetrahydrochloride as thesubstrate, and the sections were counterstained with Mayer’s
hematoxylin.

Proliferating Nuclear Antigen Staining
This nucleus protein is detectable in all phases of the cell
cycle except the G0 phase. However, in the beginning phaseof G0, it is not negative and is still positive. This staining
usually serves as a control of Ki-67 staining. Paraffin sections(5 mm) were incubated with anti-PCNA mouse monoclonal
antibody (1:100, Ylem S.R.L.) for 30 minutes at 37 C. Bound
antibody was detected with the Histofine Simple Stain MAXPO(M) reagent using diaminobenzidine tetrahydrochloride
as the substrate, and the sections were counterstained with
Mayer’s hematoxylin.

RESULTS
Table 1 summarizes the histopathological findings.
Comparison Between Ki-67 and Proliferating
Nuclear Antigen Staining
In general, slightly more positive cells wereobserved with PCNA staining in all specimens, which
may verify that PCNA staining served as a control for
Ki-67 staining (Figure 1).

Capsules in Eyes with Sharp-Edged
Intraocular Lenses
One day after surgery in eyes with the sharp-edged
CeeOn IOL, the anterior subcapsular LEC layer contained many cells, the nuclei of which stained positive
for Ki-67. Migration of LECs from the preequatorial
germinative zone was not observed. No capsularbend formation was noted.
Three, 4, and 7 weeks after surgery, a sharp capsularbend was observed in all specimens (R2, R4, R5, andR6 in Table 1, Figure 1 (left)). Many anterior subcapsular LECs showed Ki-67 positive nuclei. Lens fiber cells
were seen on the posterior capsule, and their nuclei
were all Ki-67 negative.
Beneath the anterior capsule and lens fiber cells on
the posterior capsule was an accumulation of LECs,
some of which were Ki-67 positive. This accumulationof LECs tapered toward the capsular bend between theside edge of the IOL optic and posterior capsule, forming a narrow triangle. With the exception of 1 or 2 cells
that were not adjacent to the capsular bend but far
from it, all nuclei of these LECs were Ki-67 negative,
indicating that they were in the G0 phase of the cell
cycle (Figure 2, B).
At the sharp capsular bend, no LECs were found.
Behind the bend, a small amount of migrating LECs
were observed on the posterior capsule–forming
layers, (Figure 2, C) except in rabbit R5, in which no

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Figure 2. A: Lens epithelial cells at the capsular bend 7 weeks after
surgery in an eye that received a CeeOn Edge IOL. Before the capsular bend, there is an accumulation of migrating LECs that narrow approaching the bend. B: Magnification of the LECs before the sharpedge of the IOL. All cells were Ki-67 negative, indicating these
LECs were contact inhibited. At the bend, there were no LECs. C:
Magnification of the LECs on the posterior capsule after the sharpedge. In contrast, on the posterior capsule after the bend, there
were ample LECs that stained positive for Ki-67, indicating they
were proliferating. These LECs must have migrated before the formation of the capsular bend.

LEC migration onto the posterior capsule was observed. The posterior capsule there showed complicated folds. These LECs diminished slowly, forminga monolayer, and disappeared centrally. The cells
were extremely thin and elongated. Many of the
LECs behind the capsular bend showed Ki-67 positive
nuclei indicating that they were proliferating (Figure 2,
A to C).
In summary, the typical common finding at the capsular bend or sharp edge was an accumulation of LECs
whose nuclei were mostly thin, elongated, and Ki-67
negative, indicating the G0 phase. At the equatorial
capsule, lens fiber cells (Soemmerring’s ring) wereseen, often in abundance. The Ki-67 negative cells
that accumulated at the sharp edge appeared to halt
the migration of the lens fiber cells. Beyond the sharpedge site and toward the posterior capsule, some
LECs were seen whose nuclei were round and notthin or elongated; that is, they had a normal appearance and were Ki-67 positive indicating that they
were proliferating. These LECs diminished in number
approaching the central posterior capsule, at which
point they disappeared.

Capsules in Eyes with Round-Edged
Intraocular Lenses
No sharp capsular bend formation was seen in eyeswith the round-edged PhacoFlex II IOL. Beyond thegerminating LECs, occasional lens fiber cells wereseen. Between these fiber cells and the LECs beneaththe anterior capsule was an accumulation of LECs,
which tapered toward the posterior optic edge area.
These LEC layers became narrower but were not disrupted at the posterior optic edge. They were narrowat the posterior round optic edge but migrated continuously onto the posterior capsule, as opposed to theposterior capsule in eyes with the sharp-edged IOL,
in which no cells were found at the bend (R2, R3, R5,
and R6 in Table 1) (Figure 3). The nuclei of these
LECs were round and not thin or elongated andwere predominantly Ki-67 positive.
DISCUSSION
This study would have been more exact had the 2 IOLs
differed only in the construction of their optic edge. Although theoretically ideal, this is not possible given the

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LABORATORY SCIENCE: INHIBITION OF LECS BY SHARP-EDGED IOL

Table 1. Accumulation of the Ki-67 negative LECs at the capsular bend.
Right

Rabbit Postop Period IOL Edge
R1

1d

R2

3 wk

R3

3 wk

R4

4 wk

R5

4 wk

R6

7 wk

Sharp
Round
Sharp
Round
Sharp
Round
Sharp
Round
Sharp
Round
Sharp
Round

Accumulation of
Ki-67 Negative
LECs

Left

Ki-67 Positive
LECs on PC

Accumulation of
Ki-67 Negative
LECs

Ki-67 Positive
LECs on PC

Many LECs beneath the anterior capsule stained Ki-67 positive, but no LEC migration onto PC
NA
NA
NA

NA
NA
NA
CC

C

NA
C
None
CC

CC
CCC

C

CC
C
CCC

CCC

C
CC
NA
CC
C (isolated)
None
CCC
C
CCC

C Z few; CC Z moderate; CCC Z abundant; LECs Z lens epithelial cells; NA Z not applicable; PC Z posterior capsule; Right and Left Z both sides of thecapsular bag in a histological sectioncommercially available IOLs. Moreover, many experimental and clinical studies have shown that it is theedge design that is the crucial and decisive factor in
the inhibition of LEC migration, regardless of IOL
material or design. Therefore, we used 2 types of silicone IOLs, the edges of which were sharp or round,with the full awareness that there was some dissimilarity between the IOLs in the silicone’s chemistry constituents and their design. As discussed in the study
methodology, the specific histopathological findingsin this study were interpreted and correlated with theedge design of the IOL optic alone.
Ki-67 is a protein in the cell nucleus and can always
be observed in all phases of the cell cycle except the G0
phase. Therefore, a cell-staining pattern negative for
Ki-67 indicates the cell is in the G0 phase and is notproliferating.14,15
In this study, we investigated the expression of theunique protein Ki-67 in the nuclei of LECs at the capsular bend in the eyes with a sharp-optic-edge IOL
design. In these eyes, all LECs that accumulated in
multiple layers along the side edges of the IOLs before
the capsular bend were Ki-67 negative in their nuclei,
with the exception of a few cells in some eyes, indicating that most LECs were in the G0 phase. These findings stand in stark contrast to the Ki-67 positive
LECs abundantly observed beyond the capsularbend toward the posterior capsule.
We postulate that contact inhibition of the LECs is
induced by the posterior capsular bend. We haveshown in vitro and in vivo16,17 that contact inhibitionof LECs can be induced at the capsular bend. In a rectangular well bottom in cell culture, LECs never climb

up the well wall. The histopathological sections of animal eyes show that in eyes with a capsular bending
ring, LECs at the ring form layers but never migrate
centrally along the posterior capsule.17 Lens epithelial
cell migration has been occasionally observed clinically at the slitlamp in human eyes with a capsularbending ring. However, in these cases, the migration
was a result of the discontinuity of the capsularbend. This phenomenon can occur when the eyeletsof the capsular bending ring are widely separated, as

Figure 3. Lens epithelial cells at the capsular bend in an eye witha PhacoFlex II with rounded edges. The LECs showed continuous
migration over the bend and contained Ki-67 positive nuclei, indicating that the LECs were not contact inhibited.

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is the case with large-diameter capsular bags. However, LECs will be contact inhibited at a rectangularstructural impasse. The results in the present experimental study are further evidence at a molecularbiological level of our concept of contact inhibition.
Migrating LECs were contact inhibited at the capsularbend created by the sharp optic edge of an IOL.
This contact inhibition theory is not without controversy. Bhermi et al.18 cultured bovine LECs in a welllike poly(methyl methacrylate) pit. They reported
that LECs migrated along the side wall out of thewell, concluding that the rectangular circumstance
did not induce contact inhibition of the LECs. The
LECs in their study, however, might have been transformed after 6 or 7 cell culture passages. Furthermore,because the formed well was shallow, the possibility
that the cells migrated out of the well when the cell
layers reached the level of the well cannot be excluded,
although in their illustration the single layer of LECs
climbed out of the side wall of the well. It is generally
accepted that with the exception of cancer cells, normal
cells have, to date, not been observed to ascend thevertical well wall as contact inhibition of the cells
is induced when they become confluent in the floor of
the well.
Nagamoto and Fujiwara19 grew cultured LECs on
the surface of a bent collagen membrane. They concluded that contact inhibition was not induced by therectangular configuration because the cells extended
beyond the point of the bent line of the membrane. In
their study, however, neither the bending techniqueof the collagen nor a description of whether the line
was sharp or discontinuous could be established.
Knowing these factors is important because if thebent line is not discontinuous LECs can migrate consistently over the allegedly discontinuous bent line.
In our study, LECs that migrated beyond the posterior capsule bend contained many Ki-67 positive nuclei, indicating that LECs were proliferating. This is
in contrast to findings that LECs before the bend
were Ki-67 negative. Capsular bending is experimentally and clinically complete within 2 to 3 weeks.5,20,21
In vitro and clinically in vivo, LECs are known to migrate onto the posterior capsule within 1 week.5,22,23
All these findings strongly suggest that the LECs
found beyond the capsular bend on the posterior capsule migrated before the capsular bend was formed because once it forms, contact inhibition will be induced
and LECs cannot migrate and accumulate before thebend. Therefore, the LECs observed beyond the bend
are considered have migrated before the formation of
the capsular bend.
The above findings and considerations strongly suggest that PCO in the eyes that receive an IOL withsharp edges is caused by LECs that migrate before

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the capsular bend is formed and from the site where
the capsular bend fails to form. Therefore, PCO depends on the extent to which LECs migrate onto theposterior capsule before capsular bend formationand on the mitotic capacity of the cells, which is a function of the patient’s age. Clinically, localized and limited PCO in the periphery of IOL optics can often be
observed during the second or third postoperative
years in older cataract patients. This PCO may becaused by LECs that migrated before the capsularbend was formed. Because their mitotic function was
limited as a result of the age of the patient, they could
not reach the visual axis and remained as a local accumulation of cells peripherally.
Therefore, it is the early postoperative period, thefirst or second postoperative week, that is the crucial
period for the prevention of PCO. Bhermi et al.18 andNagamoto and Fujiwara19 deny the possibility of‘‘contact inhibition’’ and emphasize the importanceof ‘‘compression.’’ However, it not likely that an IOL
causes compression to the posterior capsule within
this time period as the human crystalline lens ismore than 10 times (mathematically calculated)
greater than the IOL in volume. Compression might
happen in the presence of strong capsular fibrosis in
the few months after surgery.
It was further observed that lens fiber cells (Soemmerring’s ring) accumulated within the equatorial
capsular bag and their growth appeared to havebeen stopped or hindered by the Ki-67 negative
LECs that accumulated at the sharp optic edge. It is
possible that because the LECs were contact inhibited,the subsequent LECs derived from the germinativezone were polarized and were transformed into lens
fiber cells de novo, forming the so-called Soemmerring’s ring cataract.
Another important question is whether Ki-67 negative LECs at the capsular bend will be reactivated in
the future. In other words, will they again enter thecell cycle, undergoing mitosis, when the increasing
Soemmerring’s cataract abolishes the capsular bend?
Clinical slitlamp observations indicate that LECs at
the posterior optic edge do not migrate beyond thecapsular bend despite elimination of the capsularbend by the bulky Soemmerring’s ring, suggestingthat Ki-67 negative LECs may stay permanently in
the G0 phase. However, years later, we have encountered the loss of the capsular bend as a consequenceof Soemmerring’s ring and PCO. Whether this PCO
is the result of the reactivation of the LECs found in
the G0 phase or, as described, of the proliferation of
the LECs that migrated before the capsular bend
formed should be clarified in a future study.
It may appear inconsistent with findings that
PCO-free capsules have been observed clinically on

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occasion, even in eyes with a round-edged IOL. As
shown in our previous studies,24,25 sharp, blunt, or
round edges are a relative notion and do not produce
an all-or-nothing effect. Rather, they create a transitionzone that may not necessarily be continuous. This may
be an explanation for this clinical observation.
In conclusion, we found that the LECs at the capsular bend created by the sharp optic edge of an IOL
were Ki-67 negative; that is, they were in the G0 phaseof the cell cycle. Thus, the posterior capsular bend
formed induced contact inhibition of LECs in eyesthat received an IOL with sharp edges, substantiating
our theory of the effect of a sharp optic edge on PCO
formation. Because LECs will not migrate once a capsular bend forms, PCO in eyes with a sharp-edged IOL
is caused by the proliferation of the small amount of
LECs that migrated onto the posterior capsule before
the posterior capsular bend formed or they migrated
through the site where the bending failed to form.
Whether the LECs will be reactivated into the cell cyclefrom the G0 phase when the capsular bend is abolishedneeds clarification in future studies. This concept of
PCO pathogenesis contributes to the development of
new strategies for the prevention of PCO.
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J CATARACT REFRACT SURG - VOL 33, JUNE 2007

First author:
Okihiro Nishi, MD
Nishi Eye Hospital, Osaka, Japan