PART 4 CORNEA AND OCULAR SURFACE DISEASES
SECTION 4 Conjunctival Diseases
Pterygium and Conjunctival
Degenerations
Roni M. Shtein, Alan Sugar
Definition:Secondary deterioration or deposition in the conjunctiva,
distinct from the dystrophies.
Key features
■ Common
■ Bilateral usually
■ Typically does not affect vision
Associated features
■ Increased prevalence with age
■ Often associated with chronic light exposure
■ May follow past inflammation
■ Not inherited
INTRODUCTION
Degenerations of the conjunctiva are common conditions that, in most
cases, have relatively little effect on ocular function and vision. They
increase in prevalence with age as a result of past inflammation, long-
term toxic effects of environmental exposure, or aging itself. Conjunc-
tival degenerations may be associated with chronic irritation, dryness,
or previous history of trauma. Progression to involve the cornea may
occur, as in pterygium.
PINGUECULA
Pingueculae are elevated, white to yellow in color, horizontally oriented
areas of bulbar conjunctival thickening that adjoin the limbus in the
palpebral fissure area (Fig. 4-9-1). They are less transparent than nor-
mal conjunctiva, often have a fatty appearance, are usually bilateral,
and are located nasally much more often than temporally. When a
pinguecula crosses the limbus onto the cornea, it is called a pterygium.
Current information, however, suggests that pinguecula do not progress
to pterygium and that the two are distinct disorders. Pingueculae are
associated with a 2- to 3-fold increased incidence of age-related macular
degeneration, possibly through a common light exposure effect.1
The causes of pingueculae are not known with certainty. Good evi-
dence exists, however, of an association with increasing age and ultra-
violet light exposure. Pingueculae are seen in most eyes by 70 years of
age and in almost all by 80 years of age.2 Chronic sunlight exposure has
been found to be a factor by association with outdoor work and equato-
rial residence. In some studies, the strength of this association is less
than that for pterygium.3, It is thought that the predominantly nasal
location is related to reflection of light from the nose onto the nasal
conjunctiva. The effect of ultraviolet light may be mediated by muta-
tions in the p53 gene.4
4.9
Fig. 4-9-1 Nasal pinguecula. Elevated conjunctival lesion encroaches on nasal
limbus.
Pingueculae are rarely associated with symptoms other than a mini-
mal cosmetic defect. They may become red with surface keratinization.
When inflamed, the diagnosis of pingueculitis may be given.
Distinguishing pingueculae from other lesions is usually not a prob-
lem because of the typical appearance. Conjunctival intraepithelial
neoplasia may be difficult to differentiate from keratinized pinguecula.
Gaucher’s disease type I is said to be associated with tan pingueculae,
but this is not a specific finding.5
Histopathologically, pingueculae are characterized by elastotic
degeneration of the collagen with hyalinization of the conjunctival
stroma, collection of basophilic elastotic fibers, and granular deposits,
and noninvolvement of the cornea.6
Pingueculitis responds to a brief course of topical corticosteroids or
nonsteroidal anti-inflammatory agents.7 Chronically inflamed or cos-
metically unsatisfactory pingueculae rarely warrant simple excision.
PTERYGIUM
Pterygium is a growth of fibrovascular tissue on the cornea and con-
junctiva. It occurs in the palpebral fissure, much more often nasally
than temporally, although either or both (“double” pterygium) occur
(Fig. 4-9-2). Elevated whitish opacities (“islets of Vogt”) and an iron
deposition line (“Stocker”) may delineate the head of the pterygium on
the cornea. Like pinguecula, it is a degenerative lesion, although it may
appear similar to pseudopterygium, which is a conjunctival adhesion to
the cornea secondary to previous trauma or inflammation, such as
peripheral corneal ulceration. A pseudopterygium often has an atypical
position and is not adherent at all points, so a probe can be passed
beneath it peripherally.
Like pinguecula, pterygium is associated with ultraviolet light expo-
sure.3 It occurs at highest prevalence and most severely in tropical areas
near the equator and to a lesser and milder degree in cooler climates.8,9 203
Outdoor work and both blue and ultraviolet light have been implicated
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CORNEA AND OCULAR SURFACE DISEASES
A under the medial rectus muscle insertion.
Fig. 4-9-2 Double pterygium. (A) Note both nasal and temporal pterygia in a
57-year-old farmer. (B) It is the invasion of the cornea that distinguishes a pterygium
from a pinguecula.
in its causation. The use of hats and sunglasses is protective.8,9 In the
past, the pathogenesis of pterygium was thought to be related to distur-
bance of the tear film spread central to a pinguecula. More recent theo-
ries include the possibility of damage to limbal stem cells by ultraviolet
light and by activation of matrix metalloproteinases.10,11 The histopa-
thology of pterygium is similar to that of pinguecula except that Bow-
man’s membrane is destroyed within the corneal component and
vascularization is seen.12 Recent evaluation using spectral domain opti-
cal coherence tomography revealed pterygium as an elevated, wedge-
shaped mass of tissue separating the corneal epithelium from Bowman’s
membrane, which appears abnormally wavy and interrupted and often
destroyed, with satellite masses of subepithelial pterygium tissue
beyond the clinically seen margins.13
Pterygia warrant treatment when they cause discomfort (not respon-
sive to conservative therapy), encroach upon the visual axis, induce
significant astigmatism, or become cosmetically bothersome. Aggres-
sive or recurrent pterygia may cause restrictive strabismus and distor-
tion of the eyelids. A variety of surgical techniques have been developed.
The goal of treatment is prevention of recurrence. The recurrence rates
after simple excision are very high: of recurrences, 50% reoccur within
4 months of excision and nearly all within 1 year.14 Beta-radiation
applied postoperatively to the pterygium base was popular for many
years, but is associated with late scleral necrosis.15 Currently, the most
widely used techniques are conjunctival autografting, amniotic mem-
brane transplantation, and mitomycin-C application – either pre-,
intra-, or postoperatively.15,16 Fibrin-based glues have been used to
minimize operating time and discomfort associated with sutures, and
to reduce the amount of suturing required.17
SENILE SCLERAL PLAQUES
Senile scleral plaques occur in the sclera of elderly patients and are
204 frequently misinterpreted as a melting process similar to that of corneal
degenerations or as conjunctival depositions. These lesions appear as
Fig. 4-9-3 Senile scleral plaque. Calcium deposition appears as a gray scleral plaque
Fig. 4-9-4 Primary localized conjunctival amyloid. There is irregularity of the
conjunctiva superonasally with fixed folds. Resolving subconjunctival hemorrhages
noted superiorly are associated with amyloid deposition in blood vessel walls.
yellow, gray, or black vertical bands just anterior to the insertion of the
medial and lateral rectus muscles (Fig. 4-9-3). They become more com-
mon after the age of 60 years and, like pinguecula and pterygium, may
be related to ultraviolet light exposure.18 Histologically, calcium depos-
its along with decreased cellularity and hyalinization are seen. These
lesions do not need therapy.
CONJUNCTIVAL AMYLOID
Deposition of amyloid in the conjunctiva has been reported in both
primary and secondary localized forms (Fig. 4-9-4) and secondary to
systemic processes.19 Chronic conjunctival inflammation may cause
secondary localized amyloidosis, a true degenerative change. In the
primary localized forms, light-chain immunoglobulins deposited by
monoclonal B cells and plasma cells have been demonstrated by
immunohistochemistry.
In lesions secondary to systemic disease, other forms of amyloid
protein may be seen.20 All patients should be evaluated for lymphopro-
liferative and systemic diseases. Amyloid involving the skin of the
eyelids has been suggested to be a sign of systemic involvement.21
Conjunctival amyloid may appear as a yellowish, well-demarcated,
irregularly elevated mass. It generally involves the fornices, with the
superior fornix and tarsal conjunctiva most commonly affected. In vivo
confocal microscopy of conjunctival amyloid shows hyporeflective
material in a lobular pattern in the substantia propria and around the
blood vessels in the conjunctiva without associated inflammation.22
Recurrent subconjunctival hemorrhages may be associated with amy-
loid deposition in blood vessel walls. Biopsy is required for definitive
diagnosis.20
 Lesions are generally treated symptomatically, though debulking
excision can be performed for chronic irritation. Although it may not
cause full regression of deposited amyloid, radiotherapy may be used to
prevent progression.23
CONJUNCTIVAL MELANOSIS
Conjunctival melanosis is a common finding with advancing age. The
appearance is that of a flat, pigmented area on the conjunctiva. Primary
acquired melanosis is a risk factor for development of conjunctival
melanoma and is discussed in detail in Chapter 4-8.
Secondary melanosis of the conjunctiva is generally benign and
tends to be more frequently bilateral. Secondary melanosis occurs fol-
lowing trauma, chronic inflammation of the conjunctiva, and in indi-
viduals with darker skin pigmentation.24 Secondary melanosis is
generally not associated with atypia and can be observed. If the lesions
are noted to be elevated or where uncertainty exists, biopsies should be
performed.
KEY REFERENCES
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conjunctival amyloidosis. Clin Exper Ophthalmol 2008;36:173–5.
Chen PP, Ariyasu RG, Kaza V, et al. A randomized trial comparing mitomycin C and
4.9
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151–60.
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Clinicopathologic features. Ophthalmology 1989;96:436–61.
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management, and outcome. Ophthalmology 2006;113:1657–64.
Lucas RM. An epidemiological perspective of ultraviolet exposure – public health concerns.
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Ma DH, See LC, Liau SB, et al. Amniotic membrane graft for primary pterygium: comparison
with conjunctival autograft and topical mitomycin C treatment. Br J Ophthalmol
2000;84:973–8.
Mackenzie FB, Hirst LW, Battistutta D, et al. Risk analysis in the development of pterygia.
Ophthalmology 1992;99:1056–61.
Scroggs MW, Klintworth GK. Senile scleral plaques: a histopathologic study using
energy-dispersive X-ray microanalysis. Hum Pathol 1991;22:557–62.
Soliman W, Mohamed TA. Spectral domain anterior segment optical coherence tomography
assessment of pterygium and pinguecula. Acta Ophthalmol 2012;90:461–5.
Taylor HR, West S, Munoz B, et al. The long-term effects of visible light on the eye.
Arch Ophthalmol 1992;110:99–104.
Uy HS, Reyes JMG, Flores JDG, et al. Comparison of fibrin glue and sutures for
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