Eyelid Lesions and Tissues of Origin

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The plethora of lesions that can occur on the eyelids is rather daunting, not to say confusing, to the average clinician. Many names are similar and while they may be meaningful to the pathologist based on details of microscopic findings, they often add little to the clinical recognition or management of these diseases. Placing such lesions into a more or less organized system based on anatomical tissues of origin may be a useful exercise.

All lesions that involve the eyelids or any other region of the body can be thought of as deriving from two basic sources. Those that arrive in the lids from other more remote sources are exogenous lesions. These include metastatic tumors from sites such as the breast or lung. Also included here are infiltrations in the dermis and epidermis of cellular or other materials that secondarily involve eyelid structures. Included here are diseases such as amyloidosis, sarcoidosis, infectious inflammations such as herpes and cellulitis, xanthelamas, acute atopic dermatitis, erythema multiforme, granuloma annulare, and lymphoid and myeloid infiltrates. All exogenous lesions disturb the normal eyelid architechture to some extent, and may be generalized or confined to specific eyelid tissue types.

The majority of lesions seen on the eyelids are derived from normal lid tissues and structures. The epidermis is the source for a large number of lesions that characteristically disturb the fine wrinkles and pores normally seen on the skin surface (Fig. 1). These include most of the common cutaneous malignancies seen on the lids. The basal cell carcinoma arises from basal cells in the deep epidermis. Squamous carcinomas are derived from stratified squamous cells of the epidermis. Malignant melanomas arise from melanocytes that normally reside in the basal epidermis, but some probably arise from dermal nevoid cells.

Of the benign lesions derived from the epidermis many can look rather similar clinically. Some may remain epidermal in location, but many extend into the underlying dermis. Epidermal lesions include the papilloma, actinic keratosis, seborrheic keratosis, inverted follicular keratosis, ichthyosis, keratoacanthoma, lentigo, milia, molluscum contagiosum, and acquired melanosis. When epidermal cells become buried beneath the surface, keratin can accumulate to form an epidermoid cyst.

The dermis is composed largely of collagen with a small amount of elastin. Few lesions arise directly from these materials, but the dermis is frequently involved with infiltrative and other processes (Fig. 2). In angioedema the dermis is edematous with an inflammatory cell infiltrate. White blood cell infiltration also predominates in blepharitis, cellulitis, insect bites, and in cicatricial phemphigoid. Leukemic infiltrates also accumulate within the dermal stroma.

Although melanocytes usually migrate to the epidermis during embryogenesis, they can arrest in the dermis where they form pigmented lesions. These include the junctional and compound nevus located at the epidermal/dermal junction and dermis, respectively, congenital blue nevus and cellular blue nevus within the dermis, and oculodermal melanocytosis. Lymphangiomas arise from lymphatic endothelium within the dermis. A number of lesions occur in the dermis but are of uncertain cellular etiology. The cylindroma may have eccrine relationships but also involves the dermal collagen to a large extent. Dermatofibromas demonstrate some relationship to fibroblasts but their specific etiology remains uncertain. The origin of Merkel cell tumors remains controversial, but they appear to have neuroendocrine relationships. Myxomas have an association with dermal fibroblasts which secrete the surrounding matrix, however their cellular etiology remains unclear. Microcystic adnexal carcinoma is derived from dermal ductal elements, but also includes epidermal relationships.

Microcystic Adnexal Carcinoma

Figure 1 A lesion of the epithelium with loss of epithelial surface characteristics of fine wrinkles and cellular structure.

Herpes Structure Lesion

Figure 2 Dermal lesions displace the epithelium upward usually without obliterating fine surface features.

Figure 1 A lesion of the epithelium with loss of epithelial surface characteristics of fine wrinkles and cellular structure.

Figure 2 Dermal lesions displace the epithelium upward usually without obliterating fine surface features.

The dermis also contains epithelial appendages which are the source for many eyelid lesions. The pilosebaceous unit consists of the hair follicle and associated holocrine sebaceous gland and apocrine sweat gland of Moll. All of these structures can be the site of origin for eyelid lesions. The diverse cellular components of this apparatus can give rise to many different lesions that can look similar clinically. Lesions are grouped into four major categories depending upon differentiation towards sebaceous, hair follicle, apocrine, or eccrine tissues. Within these groups lesions are further subdivided into hyperplasias, hamartomas, adenomas, and carcinomas.

The hair follicle is a tubule with root cells at the base around the papilla and bulb (Fig. 3). Higher up follicular epithelium lines the follicle, and finally cortical cells lay down the outer keratin layers to the hair. Tumors arising from proliferations of cortical cells are termed piloma-trixomas. Solid proliferations of follicular cells manifest as trichofolliculomas, whereas an obstruction of the follicle results in a cystic lesion called a trichilemmal cyst. Solid tumors arising from the basal epithelial bulb are tichoepitheiomas.

Large sebaceous glands empty into the hair follicle. Proliferations of the secretory epithelium produce solid dermal tumors called sebaceous adenomas (Fig. 4). Occasionally the excretory

Sebaceous Adenoma

Figure 3 Hair follicle lesions.

Hair Follicle Nevus

Figure 4 The hair follicle and associated dermal lesions.

Figure 3 Hair follicle lesions.

Figure 4 The hair follicle and associated dermal lesions.

Gland Moll

Figure 5 Apocrine glands of Moll.

Apocrine Gland Carcinoma

Figure 6 The eccrine sweat gland can be the origin of several dermal lesions.

Figure 5 Apocrine glands of Moll.

Figure 6 The eccrine sweat gland can be the origin of several dermal lesions.

duct becomes blocked with accumulation of sebum, producing a sebaceous cyst (steatocystoma). More commonly, however, the block is higher up in the follicle and although the cyst is still contains some sebum the epithelial lining adds keratin and leads to the diagnosis of trichilemmal (= tricholemmal) or pilar cyst. Apocrine sweat glands of Moll normally produce a somewhat viscous secretion that empties into the hair follicle (Fig. 5). Solid tumors arising from the secretory epithelium give rise to apocrine adenomas. If the duct becomes obstructed, a cyst results that can have a layered precipitate of cellular debris. These are apocrine hidrocystomas.

Eccrine sweat glands empty directly to the skin surface (Fig. 6). Like the apocrine sweat glands, these can form solid and cystic lesions. Benign tumors arising from the ductal epithelium are called syringomas, whereas those from the tubular secretory epithelium are nodular hidradenomas. An obstruction of the secretory duct will result in an eccrine hidrocystoma filled with a clear fluid. Clinically, the eccrine and apocrine cysts may not always be distinguishable.

Vascular elements are present in the dermis and can give rise to a number of important eyelid lesions (Fig. 7). These include hemangiomas and angiosarcomas derived from endothe-lial cells, and hemangiopericytomas arising from the endothelial pericyte. Arteriovenous hemangiomas or malformations are abnormal vascular channels. Nerves are another component of the dermis and are the tissues of origin for neural tumors such as neurofibromas.

Lymphatic Endothelial Cells Dermis

Figure 7 Blood vessels and nerves in the dermis and subcutaneous tissues serve as the sites of origin for several vascular and neural lesions.

In addition to cutaneous layers and their included adnexal appendages eyelid lesions can arise from other eyelid structures. Most important in this group are the tarsal plate meibomian glands. These are modified holocrine sebaceous glands arranged as tubules, with about 25 to 30 in the upper eyelid and 20 in the lower lid. They are not associated with the eyelashes or a pilosebaceous unit, although they can occasionally revert to such a structure where they can be related to the development of abnormal hairs called distichiasis. An obstruction of the meibomian duct can result in an infected cyst called a chalazion. In contrast, a similar infection involving small isolated sebaceous glands (glands of Zeis) or those associated with the skin pilosebaceous units results in a more acute and superficial process called a hordeolum. Any of these sebaceous glands can also give rise to a malignant tumor, the sebaceous cell carcinoma.

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  • luigia
    Are all apocrine glands associated with hair follicle?
    8 years ago

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