Eyelid pathology 2

Eyelid pathology 2
Azza Mohamed Ahmed, MD

Viral infections of the
eyelid

1-Verruca vulgaris(wart)
 Caused by Human papilloma virus infects the eyelid skin.
 Clinically, it is usually an elevated papillary lesion.
 Mic: the lesions demonstrate hyperkeratosis and
acanthosis and exhibit a papillary growth pattern.
 Infected cells may demonstrate cytoplasmic clearing
(koilocytosis).
 A mixed inflammatory infiltrate is typically present in the
superficial dermis

 Caused by Poxvirus infection.
 Clinically, Dome-shaped, waxy epidermal nodules with
central umbilication form and, if present on the eyelid
margin, may cause a secondary follicular conjunctivitis.
 Mic: The lesions are distinctive, with a nodular proliferation
of infected epithelium producing a central focus of necrotic
cells (central crater) that are extruded to the skin surface.
2-Moluscum contagiosum

 As the replicating virus fills the cytoplasm, the nucleus
is displaced peripherally by large viral inclusions
(molluscum bodies) and finally disappears as the cells
are shed.
2-Moluscum contagiosum

Degenerative diseases of
the eyelid

1-Xanthelasma
 Common.
 Bilateral.
 Middle and elderly.
 Hyperlipidaemia found in 1/3
of patients.
 Mic : Fat is intracellular
with lipid laden
histiocytes (foam cells in
diffusely distributed, often
around blood vs in dermis
with no to minimal ass
inflammation.

 The term amyloid refers to a heterogeneous group of extracellular
proteins that exhibit birefringence and dichroism under
polarized light when stained with Congo red.
 Amyloid within the skin of the eyelid is highly indicative of a
systemic disease process, either primary or secondary,
whereas deposits elsewhere in the ocular adnexa but not in
the eyelid are more likely a localized disease process.
2-Amyloid

 Amyloid deposits in the skin are usually multiple, bilateral,
symmetric, waxy yellow white nodules.
 The deposition of amyloid within blood vessel walls in the skin
causes increased vascular fragility and often results in
intradermal hemorrhages, accounting for the purpura seen
clinically.
2-Amyloid

 Mic: amyloid appears as an amorphous, eosinophilic
extracellular deposit, usually within vessel walls but also in
soft tissue and around peripheral nerves and sweat glands.
Stains useful in demonstrating amyloid deposits include
Congo red, crystal violet, and thioflavinT.
 Electron microscopy reveals the deposits to be composed of
randomly oriented extracellular fibrils measuring7-10
nm in diameter.
2-Amyloid

Neoplasia of the eyelid
Epidermal
Benign
Precancerous
cancerous
Dermal Appendage Melanocytic
Seborrheic keratosis
Keratoacanthoma
Actinic keratosis
BCC
SCC

1-Epidermal Neoplasias
A. Seborrheic keratosis
 A common benign epithelial proliferation.
 Occurs in middle age.
 Clinically, it is a well-circumscribed, oval, dome-shaped
to verrucoid "stuck-on" papule, varying from pink to
brown in color.

A. Seborrheic keratosis

A- Seborrheic keratosis
 Mic: several architectural patterns are possible,
although all demonstrate hyperkeratosis, acanthosis,
and some degree of papillomatosis.
 The acanthosis is a result of the proliferation of
either polygonal or basaloid squamous cells without
dysplasia.

 A characteristic finding in most types of seborrheic
keratoses is the formation of pseudohorn cysts,
which are concentrically laminated collections of
surface keratin within the acanthotic epithelium.

 Irritated seborrheic keratosis, also termed inverted
follicular keratosis, shows nonkeratinizing squamous
epithelial whorling, or squamous "eddies;' instead of
pseudohorn cysts. Heavy melanin phagocytosis by
keratinocytes may impart a dark brown color to an
otherwise typical seborrheic keratosis, which may
then be confused clinically with melanoma.

 Sudden onset of multiple seborrheic keratoses is
known as the Leser- Trelat sign and is associated with a
malignancy, usually a gastrointestinal adenocarcinoma;

B- Keratoacanthoma
 A rapidly growing epithelial proliferation with a potential for
spontaneous involution.
 There is strong evidence supporting the idea that
keratoacanthomas are a variant of a well-differentiated
squamous cell carcinoma.
 These studies are based on expression of proliferation
markers (cyclins and cyclin-dependent kinases) and
oncoproteins (mutated p53) that are expressed similarly by
both entities.

B- Keratoacanthoma
 Dome-shaped nodules with a keratin-filled central crater
may attain a considerable size, up to 2.5 cm in diameter,
within a matter of weeks to months .
 The natural history is typically spontaneous involution
over several months, resulting in a slightly depressed scar.

B- Keratoacanthoma
Mic:
 keratoacanthomas show a cup-shaped invagination of well-
differentiated squamous cells forming irregularly configured
nests and strands and inciting a chronic inflammatory host
response.
 The proliferating epithelial cells undermine the adjacent
normal epidermis.
 At the deep aspect of the proliferating nodules, mitotic activity
and nuclear atypia may occur, making the distinction between
keratoacanthoma and invasive squamous cell carcinoma
problematic.

B- Keratoacanthoma

C- Actinic keratosis
 Actinic keratoses are precancerous squamous lesions
that appear, clinically, as erythematous, scaly macules or
papules in middle age on sun-exposed skin, particularly on
the face and the dorsal surfaces of the hands.
 Actinic keratoses range from a few millimeters up to 1
cm in greatest dimension..

 Hyperkeratotic types may form a cutaneous horn, and
hyperpigmented types may clinically simulate lentigo maligna.
 Squamous cell carcinoma may develop from preexisting actinic
keratosis; thus, biopsy of suspicious lesions and long term
follow-up are necessary in patients with this condition.
However, when squamous cell carcinoma arises in actinic
keratosis, the risk of subsequent metastatic dissemination is
very low (0.5%-3.0%).

Mic:
 5 subtypes, ranging from hypertrophic to atrophic; all types demonstrate
changes in the epidermis with hyperkeratosis and parakeratosis.
 Cellular atypia such as nuclear hyperchromasia and enlargement, nuclear
membrane irregularities, and increased nuclear-to-cytoplasmic ratio is
present and ranges from mild (involving only the basal epithelial layers) to
frank carcinoma in situ, or full- thickness involvement of the epidermis.
 Dyskeratosis (premature individual cell keratinization) and mitotic figures
above the basal epithelial layer are often present.

C-Actinic keratosis

C-Actinic keratosis
 The underlying dermis shows solar elastosis (elastotic
degeneration of collagen) , which manifests as fragmentation,
clumping, and loss of eosinophilia of dermal collagen.
 A chronic inflammatory cell infiltrate is usually present in the
superficial dermis.
 The base of the lesion must be examined histologically to
determine whether invasive squamous cell carcinoma is
present; for this reason, shave biopsy not including the base of
the lesion is contraindicated.

 C-Actinic keratosis

D-Carcinoma
I- Basal cell carcinoma (BCC) is the most common malignant
neoplasm of the eyelids, accounting for > than 90% of all eyelid
malignancies.
 Exposure to sunlight is the main risk factor, although genetic
factors can play a role in familial syndromes.
 The lower eyelid is more commonly involved than the upper
eyelid, with the medial canthus being the second most
common site of involvement.

D-Carcinoma
I- Basal cell carcinoma (BCC)
 Tumors in the medial canthal area are more likely to be deeply
invasive and to involve the orbit.
 Clinically, BCC is a slowly enlarging, slightly elevated lesion with
ulceration and pearly, raised, rolled edges.

D-Carcinoma
 The morphea form, or sclerosing, variant of BCC is a flat or
slightly depressed pale yellow indurated plaque; this type is
often infiltrative, and its extent is difficult to determine
clinically.
 Other growth patterns include nodular (most common; and
multicentric.A small percentage of BCCs are pigmented.

D-Carcinoma
I- Basal cell carcinoma
Nodular type in XP

D-Carcinoma
Nodular type

D-Carcinoma
INFILTRATING

D-Carcinoma
 As the name implies, BCCs originate from the stratum basale,
or stratum germinativum, of the epidermis and the outer root
sheath of the hair follicle and occur only in hair-bearing tissue.
 Tumor cells are characterized by relatively bland,
monomorphous nuclei and a high nuclear-to-cytoplasmic ratio.
BCC forms cohesive islands with nuclear palisading of
the peripheral cell layer.

D-Carcinoma
Frequently, a clear space surrounds the islands of tumor
cells, presumably an artifact of tissue processing.
BCCs may exhibit a variety of histologic patterns,
including keratotic (hair follicle), squamous (metatypical),
sebaceous, adenoid, and eccrine (syringoid) differentiation.

D-Carcinoma

D-Carcinoma
I- Basal cell
carcinoma (BCC)
The morphea (sclerosing) variant shows thin cords and
strands of tumor cells set in a fibrotic stroma.

D-Carcinoma
 Complete excision is the treatment of choice, and surgical
margin control is required.
 Typically, margin control is achieved with frozen sections
or Mohs micrographic excision.
 Morbidity in BCCs is almost always the result of local
spread; metastasis is extremely unusual.

D-Carcinoma
2- Squamous cell carcinoma (SCC)
 Although squamous cell carcinoma may occur in the eyelids, it is at
least 10 - 40 times less common than BCC.
 Because most SCCs arise in solar damaged skin, the lower
eyelid is more frequently involved than the upper. However, the
proportion of SCCs occurring in the upper eyelid is larger
than the proportion of BCCs occurring in the upper eyelid.

D-Carcinoma
 The clinical appearance of SCC is diverse, ranging from
ulcers to plaques to fungating or nodular growths.
Accordingly, the clinical differential diagnosis is a long list,
and pathologic examination of excised tissue is necessary
for accurate diagnosis.

D-Carcinoma
I- Squamous cell carcinoma (SCC)
 Histologic examination shows atypical squamous cells forming
nests and strands, extending beyond the epidermal basement
membrane, infiltrating the dermis, and in citing a fibrotic tissue
reaction. Tumor cells may be well differentiated (forming keratin
and easily recognizable as squamous), moderately differentiated,
or poorly differentiated (requiring ancillary studies to confirm the
nature of the neoplasm).

D-Carcinoma
 The presence of intercellular bridges between tumor cells
should be sought when the diagnosis is in question.
 Perineural and lymphatic invasion may be present and
should be reported when identified microscopically. The
use of frozen section (conventional or Mohs
microsurgery) is indicated to treat this tumor adequately.

D-Carcinoma
 Regional lymph node metastasis is reported to occur in
up to 20% of patients with SCC of the eyelid.

Epidermal Dermal Appendage Melanocytic
Capillary
hemangioma

2-Dermal Neoplasias
Capillary hemangiomas are common in the eyelids of
children.
 They usually appear at or shortly after birth as a bright red
lesion, grow over weeks to months, and involute by
school age.
 Intervention is reserved for those lesions that affect
vision because of ptosis or astigmatism, promoting
amblyopia.

 Capillary hemangiomas
2-Dermal Neoplasias

 Capillary hemangiomas The histopathologic appearance
depends on the stage of evolution of the hemangioma.
 Early lesions may be very cellular, with solid nests of plump
endothelial cells and correspondingly little vascular luminal
formation.
 Established lesions typically show well developed, flattened,
endothelium -lined capillary channels in a lobular configuration.
 Involuting lesions demonstrate increased fibrosis and
hyalinization of capillary walls with luminal occlusion.
2-Dermal Neoplasias

Benign Malignant
•Syringoma
•Sebaceous
hyperplasia
•Sebaceous
adenoma
•Sebaceous
carcinoma

3- Appendage Neoplasms
A- Syringoma
 Syringoma is a common benign lesion of the lower eyelid
and typically manifests as multiple tiny papules.
 Syringomas result from a malformation of the eccrine sweat
gland ducts.
 Histologically, syringomas consist of multiple, comma-shaped
or round ductules lined with a double layer of epithelium
and containing a central lumen, often with secretory material.

A- Syringoma

B-Sebaceous hyperplasia
 Sebaceous hyperplasia is an uncommon benign lesion of
the eyelid and face.
 Clinically, it appears as a small, yellow papule.
 Histologically, it is typically a single enlarged sebaceous
gland with numerous glandular lobules attached to a
single central duct.

B-Sebaceous hyperplasia

C-Sebaceous adenoma
 Sebaceous adenoma is a rare benign lesion of the eyelid
that typically manifests as a yellow, circumscribed
nodule.
 Histologically, it is composed of multiple sebaceous
lobules that are irregularly shaped and incompletely
differentiated.
 Muir-Torre syndrome should be considered when
sebaceous adenoma is diagnosed.

C-Sebaceous adenoma

D-Sebaceous carcinoma
 A sebaceous carcinoma most commonly involves the upper
eyelid of elderly persons.
 It may originate in the meibomian glands of the tarsus, the
glands of Zeis in the skin of the eyelid, or the sebaceous glands
of the caruncle.
 Clinical diagnosis is often missed or delayed because of this
lesion's propensity to mimic a chalazion or chronic
blepharoconjunctivitis

 Histologically, well-differentiated sebaceous carcinomas are
readily identified by the microvesicular foamy nature of the
tumor cell cytoplasm.
 Moderately differentiated tumors may exhibit some degree of
sebaceous differentiation.
 Poorly differentiated tumors, however, may be difficult to
distinguish from the other, more common epithelial
malignancies. The demonstration of lipid within the cytoplasm
of tumor cells by special stains, such as oil red 0 or Sudan
black, is diagnostic, but it must be performed on tissue prior
to processing and paraffin embedding.

Sebaceous carcinoma, histology. A, Tumor cells often have
hyperchromatic, atypical nuclei. The cytoplasm frequently has a
foamy or vacuolated appearance. Note mitotic figure (arrow)

 When sebaceous carcinoma is suspected clinically, the
pathologist should be alerted so that frozen section slides
can be generated for lipid stains.
 Another feature, characteristic of but not pathognomonic
for sebaceous cell carcinoma, is the dissemination of
individual tumor cells and clusters of tumor cells within
the epidermis or conjunctival epithelium, known as
pagetoid spread
 Another pattern in the conjunctiva is that of complete
replacement of conjunctival epithelium by tumor cells, or
sebaceous carcinoma in situ.

. B, Pagetoid invasion
of epidermis by
individual tumor cells
and small clusters
of tumor cells (arrows).
C, Sebaceous
carcinoma in situ with
complete replacement
of normal conjunctival
epithelium by tumor
cells (between arrows).

Benign Malignant
•Nevus Malignant
melanoma

A- Eye lid Skin nevi
 It is benign neoplastic proliferations of melanocytic cells
(hamartomatous lesions).
 At birth or acquired.
 Giant congenital melanocytic nevi.
 Congenital nevi of the eyelid may develop in utero before
the separation of the upper and lower eyelids and result
in a "kissing" nevus.
4- Melanocytic Neoplasms

A-Eye lid Skin naevus

 Histologically, most nevi are composed of nevus cells.
 Specialized melanocytes that have a round rather than
dendritic shape and tend to cluster together in nests.
 The cytoplasm of the nevus cell contains a variable
amount of melanin pigment.
 Other characteristics of these cells include growth within
and around adnexal structures, vessel walls, and the
perineurium; and extension into the deep reticular dermis
or subcutaneous tissue.
 Junctional, compound and epithelial types.

B- Malignant melanoma of eyelid
 There are 3main histologic subtypes of eyelid skin
melanoma:
• Superficial spreading.
• Lentigo maligna.
• Nodular.

 Pagetoid intraepidermal spread of atypical melanocytic nests.
 Band-like lymphocytic host response along the base of the
mass is more common in melanoma than in benign
proliferations.
 Prognosis is correlated with depth of invasion
 Metastases, when they occur, typically involve regional lymph
nodes first.
A-Eye lid Skin MM

Eyelid pathology 2

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