Senile Scleral Plaque
Senile scleral plaques are well circumscribed, slate-grey, oblong areas of the sclera found posterior to the limbus and anterior to the insertions of the horizontal rectus muscles. The characteristic grey color of the plaque is due to hyaline degeneration of the sclera, which allows the underlying uvea to become visible. While the plaques are usually asymptomatic and clinically insignificant, expulsion of calcified plaques can occur on rare occasions, resulting in senile scleromalacia. Because one-third of cases of calcified senile scleral plaques only involve a single plaque and 11% of calcified lesions are associated with a beam-hardening artifact on CT scan, calcified scleral plaques can be confused for foreign bodies when analyzing the CT image. However, the clinical appearance and asymptomatic nature of a calcified plaque should make it distinguishable from a foreign body.
Senile scleral plaques are most frequently seen in elderly persons above 70 years of age, and incidence increases with age. Calcification of senile scleral plaques has been observed in less than half of studied cases. The overall prevalence of calcified senile scleral plaques is between 3% and 6.2%, while a prevalence of 22.6% has been recorded for patients above 70 years old. A higher prevalence in women has also been noted.
On light microscopy, H&E stain reveals increased hematoxylin density and decreased scleral cellularity in the region of the plaque. The episclera covering the lesion contains fibers with a distinctive corkscrew appearance, and the scleral thickness of the plaque is the same as that of normal sclera. Dystrophic calcification of senile scleral plaques often occurs in the center of the translucent lesions, and calcified plaques usually cover the pars plana of the ciliary body. Calcifications are most often found in large lesions, suggesting that plaque calcification is secondary to a loss of scleral cellularity. Furthermore, plaques with different calcific compositions have been reported, including calcium phosphate, calcium carbonate, and calcium sulfate. A positive reaction between calcified tissue and Koassach, alizarin red, and von Kossa stains indicates calcium phosphate or calcium carbonate deposition.
The pathogenesis of senile scleral plaques remains unclear. However, various causes have been proposed. One suggested mechanism includes anterior scleral ischemia secondary to atherosclerosis. The location of the plaques immediately anterior to the horizontal rectus muscles may also be explained by repetitive mechanical stress and strain on the sclera by these muscles. A third proposed mechanism involves ultraviolet damage from the sun: exposure to solar radiation causes accumulation of actinic damage, leading to structural degeneration and eventual plaque formation. This hypothesis is supported by the fact that senile scleral plaques are found within a palpebral fissure distribution, which receives maximal exposure to solar irradiation. Finally, several factors may act in concert, such as mechanical stress combined with solar damage, to form these plaques.
Scleral plaques are diagnosed clinically, either through pen-light or slit lamp examination of the eye. They are generally in the shape of a vertical, angular ellipse, averaging 2 mm in width and 5-6 mm in height. In addition, calcified senile scleral plaques can be seen on CT scan. While there are many causes of periocular calcifications, including trauma, infection, tumors, and inflammation, senile scleral plaques can be distinguished based on their characteristic location posterior to the limbus and anterior to the rectus muscle insertions. Other calcifications, such as optic nerve head drusen, choroidal osteomas, and trochlear calcification can also be observed on CT scan and distinguished from senile scleral plaques based on their location.
In extremely rare cases, a defect in the sclera can form from sequestration and expulsion of a calcified senile scleral plaque. This phenomenon is known as senile scleromalacia and its appearance must be distinguished from scleromalacia perforans. Senile scleromalacia typically presents in advanced age. It is solely located anterior to the horizontal rectus muscles, appearing as a vertical, irregular, and oval shaped scleral defect covered by a thin layer of conjunctiva. It may have a glassy, yellow-grey hardened plaque residue at the base of the defect, just superficial to the uvea. There are usually both ipsilateral and contralateral senile scleral plaques. Rheumatoid scleral nodules or rheumatic disease are absent in this condition. Histologically, the residual scleral floor is flat, thin, intact, and covered by a continuous layer of healthy epithelium. There are smooth sharp margins, no necrosis, and minimal inflammation. Finally, the floor of the lesion and surrounding sclera show normal fibrillar architecture and birefringence with loss of cellularity.
However, unlike senile scleromalacia, scleromalacia perforans often presents in patients with less advanced age, can involve any part of the anterior sclera, will result in a bare uvea at the base of the hole, is not associated with senile scleral plaques, develops from a necrotizing scleritis, and is histologically characterized by necrosis of the affected sclera such that the lesion has poorly defined borders. The necrotic granulomatous inflammation of scleromalacia perforans often spreads into the uvea and scleral tissue surrounding the lesion. Despite the differences between senile scleromalacia and scleromalacia perforans, the early clinical manifestations of these conditions may be quite similar. Both are initially painless and exhibit minimal inflammation, and it is possible that numerous cases of senile scleromalacia have been misdiagnosed as scleromalacia perforans.
Because scleral plaques are usually an incidental finding and asymptomatic, they are not treated. However, cases of senile scleromalacia in which a scleral defect poses a high risk of spontaneous perforation can be treated surgically with scleral graft placement over the defect. Finally, plaque calcification may complicate surgical treatment of other ocular diseases by increasing the affected sclera’s resistance to incision.
- Alorainy. (2000). Senile scleral plaques: CT. Neuroradiology, 42, 145-148
- Manschot, W. A. (1978). Senile scleral plaques and senile scleromalacia. British Journal of Ophthalmology, 62, 376-380
- Gossner J & Larsen J. (2009). Calcified senile scleral plaques. Journal of Neuroradiology, 36, 119-20.
- Scroggs, M. W. & Klintworth, G. K. (1991). Senile scleral plaques: a histopathologic study using energy-dispersive x-ray microanalysis. Human Pathology, 22, 557-562.
- Carroll, C. P., Peyman, G. A., Raichand, M. (1980). Surgical management of senile scleromalacia. Ophthalmic Surgery, 11(10), 719-721.
- Klien-Moncreiff, B. (1932). Isolated foci of calcification in the sclera: anatomic and clinical aspects. Archives of Ophthalmology, 7(5), 757-762.