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Cartilage in the Anterior Lens Capsule of a Diabetic Patient
Arch Ophthalmol. 2002;120:1394-1396.
Posterior capsular opacification (PCO) is the most common complication
of cataract surgery. It occurs in as many as 50% of patients within the first
2 to 3 years following the procedure.1
Lens capsule opacification appears to be caused by lens epithelial cells
(LEC) retained in the capsular bag after surgery. Remnant LEC may undergo
regression or, alternatively, proliferate, migrate, and transdifferentiate
to myofibroblasts in a process called epithelial-mesenchymal transition. Myofibroblasts
are spindle-shaped cells that express the smooth muscle actin ( -SMA)
and secrete large amounts of extracellular matrix, including collagen types
I, III, and IV. Epithelial-mesenchymal transition is usually associated with
fibrosis and wrinkling of the lens capsule.2 Unaltered
nontransformed LEC do not produce extracellular matrix and do not express -SMA.3-4
The clinical and histopathologic findings in a diabetic patient with
marked anterior and posterior capsule opacification are presented. Histopathologic
evaluation of a specimen obtained from the anterior lens capsule disclosed
the unusual finding of cartilaginous tissue.
Report of a Case
A 54-year-old white woman with a 10-year history of type 2 diabetes
mellitus was referred to the Medical Retina Service at Aberdeen Royal Infirmary
(Aberdeen, Scotland) in October 2000 for evaluation of bilateral diabetic
macular edema. Her ocular history was remarkable for bilateral cataract extractions
for congenital cataracts, which were performed in 1991 (right eye) and 1994
(left eye). A polymethyl methacrylate intraocular lens (IOL) had been implanted
following extracapsular cataract extraction by nuclear expression in the right
eye. A silicone IOL (SI30; Allergan Medical Optics, Irvine, Calif) had been
used following phacoemulsification in the left eye. No other congenital or
developmental eye abnormalities, such as persistent hyperplastic primary vitreous,
had been detected. Posterior capsule opacification occurred in both eyes 1
year after cataract surgery, requiring bilateral Nd:YAG laser posterior capsulotomies.
Twelve months after this procedure, PCO was again noted in both eyes, and
Nd:YAG posterior capsulotomies had to be repeated.
On examination, her best-corrected visual acuity was measured at 20/120
OU. Intraocular pressures were normal. Slitlamp examination disclosed bilateral
pseudophakia and severe bilateral anterior capsular thickening and phimosis
that was more pronounced in the left eye. A small posterior capsulotomy was
present in each eye. On fundus examination, bilateral clinically significant
macular edema was suspected, although the view of the retina was poor owing
to anterior and posterior capsular thickening and phimosis.
A Nd:YAG anterior capsulotomy was performed in the left eye in an attempt
to enlarge the anterior capsule opening prior to retinal photocoagulation
for clinically significant macular edema. However, the Nd:YAG laser failed
to achieve any rupture of the anterior capsule, and surgical discission was
required. Intraoperatively, the anterior capsule appeared white, had a rubbery
consistency, and was extremely thick and hard (Figure 1), making it very difficult to excise. A specimen of the
anterior capsule was sent for histopathologic evaluation.
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Figure 1. Slitlamp photograph of the left
eye, obtained following anterior lens capsule biopsy. Thickening and opacification
of the anterior lens capsule is observed.
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Light microscopy revealed a thickened anterior lens capsule and mature
hyaline cartilage (Figure 2).
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Figure 2. Photomicrograph of the specimen
obtained from the anterior lens capsule. Mature cartilage cells immersed in
a cartilaginous matrix are seen (hematoxylin-eosin, original magnification
x178).
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Comment
The patient described in this report had marked anterior and posterior
lens capsule opacification and severe capsular phimosis. Rapid proliferation
of LEC and capsule opacification following Nd:YAG laser capsulotomy in patients
with retinal pathology has been reported.5 Thus,
the diabetic maculopathy present in this case and the fact that Nd:YAG capsulotomies
had been performed twice might have been contributing factors to the pronounced
capsule opacification present. It has also been shown that, in organ cultures,
LEC proliferate more rapidly when a high concentration of protein is present
in the culture medium. This could explain the increased rate of PCO observed
in patients with diabetes,6 in whom an increased
protein content in the aqueous humor has been detected,7 and
it is likely that it could have contributed to the capsular thickening observed
in our case. Furthermore, patients with diabetes seem to be more prone to
developing fibrotic changes in the lens capsule, rather than Elschnig pearls.8
Fibrotic changes in the lens capsule occur in the process of epithelial-mesenchymal
transition, a well-known phenomenon observed in many ocular tissues and in
tissue cultures.9 Epithelial-mesenchymal
transition appears to be involved in the pathogenesis of anterior subcapsular
cataract and PCO. The process of epithelial-mesenchymal transition seems to
be driven by cytokines, of which transforming growth factor , which
is also present in the aqueous humor, is the most important.2 Studies
on human capsular bags have shown that different parts of the lens capsule
have different histopathologic characteristics,2 which
could be at least partially related to being exposed to different environments
(ie, the anterior capsule is probably more exposed to the aqueous humor and
its cytokines than the posterior capsule, which is relatively protected by
the IOL).
To our knowledge, the finding of cartilage in the anterior lens capsule
in humans has not been previously reported. It could be hypothesized that
residual LEC could have undergone metaplasia when stimulated by various intraocular
cytokines, becoming chondrocytes. In this regard, it is interesting to note
that cartilage matrix proteins, including proteoglycan core protein, link
protein, and cartilage-matrix protein (CMP) have been found in the embryonic
chick lens capsule.10 It is unknown whether
LEC can undergo transformation into cartilage cells under the influence of
an altered microenvironment. Since lens capsules from diabetic patients with
capsule thickening are rarely available for histopathologic evaluation, it
is also difficult to judge whether this was an exceptional case or whether
cartilage can be found in some patients with marked lens capsule opacification.
Further clinicopathologic studies may give more insight into this unusual
phenomenon.
AUTHOR INFORMATION
The authors would like to thank Sandra Mckay for her assistance.
Kathrin Greiner, MD;
James M. Mackenzie, MD;
Noemi Lois, MD, PhD
Aberdeen, Scotland
Corresponding author and reprints: Noemi Lois, MD, PhD, Retina Service,
Ophthalmology Department, Aberdeen Royal Infirmary, Foresterhill, Aberdeen
AB25 2ZA, Scotland (e-mail: noemilois{at}aol.com).
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