Cartilage in the Anterior Lens Capsule of a Diabetic Patient

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 α smooth muscle actin (α-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 α-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.

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.

Light microscopy revealed a thickened anterior lens capsule and mature hyaline cartilage (Figure 2).

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 β, 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.

The authors would like to thank Sandra Mckay for her assistance.

Corresponding author and reprints: Noemi Lois, MD, PhD, Retina Service, Ophthalmology Department, Aberdeen Royal Infirmary, Foresterhill, Aberdeen AB25 2ZA, Scotland (e-mail: noemilois@aol.com).