Arcus Senilus

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Original article contributed by: Van Nguyen, Jessica E. Weinstein, MD
All contributors: Jessica E. Weinstein, MD
Assigned editor:
Review: Assigned status Update Pending by Jessica E. Weinstein, MD on April 13, 2017.

Arcus Senilus
Classification and external resources
OMIM 107800
DiseasesDB 17120

This article summarizes the clinical entity known as Arcus Senilis, a ring like opacity by the corneal limbus formed from lipid deposition. It can be associated with hyperlipidemia and several other risk factors, but overall has a good prognosis with little to no effect on visual acuity and ocular health.


Arcus senilis (AS), also known as gerontoxon, arcus lipoides, arcus cornae, or corneal arcus, is a deposition of lipid in the peripheal cornel stroma. It is the most common peripheral corneal opacity. Frequently it occurs with hyperlipidemia, especially in elderly individuals, and may be associated with dyslipidemia in younger patients (termed arcus juvenilis).[1]


This is not entirely known though it has been linked to hyperlipidemia and dyslipidemia.

Risk Factors

AS is associated with older age, male gender, smoking, systolic hypertension[2][3], African American heritage[4], and increased fasting serum triglyceride[5][6]. Due to its association with hyperlipidemia, AS is particularly common in people with familial hypercholesterolemia and xanthelasma[1][7][8][9].

Despite the risk factors of hyperlipidemia and dyslipidemia, there have been conflicting studies with regards to the association of AS with cardiovascular disease (CVD). In a population-based cross-sectional study in 2011 of 3397 ethnic Indians aged 40 to 80 in Singapore, presence of AS was associated with CVD (OR, 1.31; 95% CI, 1.02 to 1.7; P = .0038) independent of the risk factors in the paragraph above[3]. However, a prospective cohort study of 12,745 Danes followed up for a mean of 22 years found that AS had no clinical value as a predictor of CVD.[10] In a third study of white men (n = 3,930) and women non-hormone users (n = 2,139), ages 30-69, followed for an average of 8.4 years as part of the Lipid Research Clinics Mortality Follow-up Study, AS was associated with CHD (RR, 3.7; 95% CI, 0.9 to 14.7) and CVD mortality (RR, 4.0; 95% CI, 1.2 to 12.9) only in hyperlipidemic men ages 30-49 years[11].


AS is due to a deposition of lipid in the peripheral cornea and is generally considered a normal aging process and expected in the elderly patient. It is believed that increased permeability of limbal vessels with age allows for low-density lipoproteins to pass through the cornea, which may explain why it is found in > 70% of patients over the age of 60[4][5]. Tissue necrosis and atrophy are not present with this anomaly[12]. There is no increase in cellularity, fragmentation of the laminae, phagocytosis, unusual vascularity, nor any difference in lipogenesis on histological examination[4].

The lipid in AS is found to be concentrated mainly in two layers of the peripheral cornea: Descemet membrane and Bowman layer, with more deposition in the former[4][12]. Lipid deposition may not be confined to the cornea, and may be found in the ciliary body, ciliary processes, and iris as well[13].

Primary prevention

Primary prevention of AS would be directed towards management of hyperlipidemia and dyslipidemia, the main risk factor for development of AS.


Diagnosis of AS is clinically made. There are no lab tests or imaging to be performed to determine a diagnosis. However a lipid panel can help identify aforementioned risk factors.

Physical examination

Stromal lipid initially deposits in the superior and inferior perilimbal cornea, progressing circumferentially to form a mat-white or yellow-white band about 1 mm wide. The band is usually wider in the vertical than the horizontal meridian. The central border is diffuse and the peripheral edge is sharp and separated from the limbus by a clear interval that may undergo mild thinning[1].

Rarely, AS may contain scintillating crystals or “crystalloid” edges which are characteristic of many lipid keratopathies. Though, these opacities are not regularly fluorescent on exam[4].

Certain changes in the biomechanical properties of the cornea have been noted to be different when AS is present. One study found that corneal hysteresis and corneal resistance factor values of eyes with AS were lower when compared with age-matched controls, but there were no differences in other parameters, such as IOP, central corneal thickness, spherical equivalent value of the refractive error, axial length measurements, and mean keratometry[14].


Photo used under the creative commons license from this page:

Family members or friends may note a whitish or bluish looking ring-like opacity in the peripheral cornea by the limbus.


AS is usually an incidental finding on exam, as the ring itself is beyond the visual axis and therefore usually asymptomatic.

Clinical diagnosis

This is done at the slit lamp. A whitish yellow band is noted first in the superior and inferior perilimbal cornea, progressing circumferentially to form a mat-white or yellow-white band about 1 mm wide.

Diagnostic procedures

Gross examination or a slit lamp examination are all that is needed to diagnosis AS.

Laboratory test

Lab abnormalities associated with AS include elevated fasting serum triglyceride levels,5 total cholesterol,15 and low density lipoprotein[15][16].

Differential diagnosis

Pseudogerontoxon can develop in recurrent limbal disease. It is characterized by a paralimbal band of superficial scarring adjacent to a previously inflamed segment of the limbus resembling AS. An example of this is a mild superior pannus which may be seen in long-standing superior limbic keratoconjunctivitis[1].

The fine yellow-white refractile stromal opacities of Terrien marginal degeneration may resemble AS[1].

Ocular manifestations of osteogenesis imperfecta include blue sclera, megalocornea, and corneal arcus[1].


Patients can be followed at yearly intervals as would be expected for follow up in a patient with a normal eye exam. There is no specific management necessary.

General treatment

As AS is asymptomatic, no treatment is necessary.

Medical therapy


Medical follow up

Regular follow up exams as indicated for any patient being follow by an ophthalmology.


AS is usually asymptomatic, but a prominent AS is often associated with decreased clarity on surgical view, as are other stromal opacitie


Prognosis is generally good in terms of vision and ocular health.


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  2. 2. Hashemi, H., Khabazkhoob, M., Emamian, M. H., Shariati, M. & Fotouhi, A. A population-based study of corneal arcus and its risk factors in Iran. Ophthalmic Epidemiol. 21, 339–344 (2014).
  3. 3.0 3.1 Ang, M. et al. Corneal Arcus is a Sign of Cardiovascular Disease, Even in Low-Risk Persons. Am. J. Ophthalmol. 152, 864–871.e1 (2011).
  4. 4.0 4.1 4.2 4.3 4.4 Patterson, L. Arcus senilis. Am. J. Forensic Med. Pathol. 3, 115–118 (1982).
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  6. Finley, J. K., Berkowitz, D. & Croll, M. N. The physiological significance of gerontoxon. Arch. Ophthalmol. 66, 211–213 (1961).
  7. Forsius, H. Arcus senilis corneae; its clinical development and relationship to serum lipids, proteins and lipoproteins. Acta Ophthalmol. Suppl. 42, 1–78 (1954).
  8. Rodstein, M. & Zeman, F. D. ARCUS SENILIS AND ARTERIOSCLEROSIS IN THE AGED. Am. J. Med. Sci. 245, 104–111 (1963).
  9. Winder, A. F. Factors influencing the variable expression of xanthelasmata and corneal arcus in familial hypercholesterolaemia. Birth Defects Orig. Artic. Ser. 18, 449–462 (1982).
  10. Chambless, L. E. et al. The association of corneal arcus with coronary heart disease and cardiovascular disease mortality in the Lipid Research Clinics Mortality Follow-up Study. Am. J. Public Health 80, 1200–1204 (1990).
  11. Walton, K. W. & Dunkerley, D. J. Studies on the pathogenesis of corneal arcus formation II. Immunofluorescent studies on lipid deposition in the eye of the lipid-fed rabbit. J. Pathol. 114, 217–229 (1974).
  12. 12.0 12.1 Walton, K. W. & Dunkerley, D. J. Studies on the pathogenesis of corneal arcus formation II. Immunofluorescent studies on lipid deposition in the eye of the lipid-fed rabbit. J. Pathol. 114, 217–229 (1974).
  13. Walton, K. W. & Dunkerley, D. J. Studies on the pathogenesis of corneal arcus formation II. Immunofluorescent studies on lipid deposition in the eye of the lipid-fed rabbit. J. Pathol. 114, 217–229 (1974).
  14. Ayhan, Z., Ozturk, T., Kaya, M., Arikan, G. & Gunenc, U. Corneal Biomechanical Properties in Patients With Arcus Senilis. Cornea 35, 980–982 (2016).
  15. Wu, R., Wang, J. J., Tai, E. S. & Wong, T. Y. Cardiovascular risk factors, inflammation, and corneal arcus: the singapore malay eye study. Am. J. Ophthalmol. 150, 581–587.e1 (2010).
  16. Macchiaiolo, M. et al. Corneal arcus as first sign of familial hypercholesterolemia. J. Pediatr. 164, 670 (2014).