There are a great many different types of lesions that occur in the eyelids. Numerous, sometimes confusing names have been applied to different tumors that often offer little help for identification or management. Placing such lesions into a more or less organized system based on anatomical tissues of origin can help the clinician understand the etiology of these diseases.¹

Lesions arising in the eyelids can be thought of as originating from two sources. Those that grow in the eyelids but derive from remote sources in the body are exogenous lesions and include metastatic tumors from sites such as the breast, lung, or prostate. Infiltrative lesions also are exogenous to the eyelid and only secondarily involve eyelid structures. Included here are diseases such as amyloidosis, sarcoidosis, infectious inflammations such as herpes and cellulitis, xanthelasmas, acute atopic dermatitis, erythema multiforme, granuloma annulare, and lymphoid and myeloid infiltrates. All exogenous lesions disturb the normal eyelid architecture to varying degrees and may be generalized throughout the eyelid or be confined to specific locations of eyelid tissues.

The majority of lesions seen on the eyelids are endogenous, derived from normal eyelid tissues and structures. The epidermis is the source of a large number of lesions that characteristically disturb the fine wrinkles and pores that are normally seen on the skin surface (Figure 4.1). These include many common cutaneous malignancies. Basal cell carcinoma arises from the basal cells in the deep epidermis. Squamous cell carcinoma is derived from stratified squamous cells of the epidermis. Malignant melanoma develops from melanocytes that normally reside in the basal epidermis, but some may arise from dermal nevoid cells.

Of the benign lesions that arise from the epidermis, many clinically look similar. Some may remain within the epidermis, whereas others may extend deeply into the underlying dermis. Epidermal lesions include papilloma, actinic keratosis, seborrheic keratosis, inverted follicular keratosis, ichthyosis, keratoacanthoma, lentigo, molluscum contagiosum, and acquired melanosis.¹ 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 number of elastin fibers. Few lesions arise directly from these two materials, but the dermis is frequently involved with infiltrative and other processes (Figure 4.2). In angioedema, the dermis is edematous with an inflammatory cell infiltrate. White blood cell infiltration also predominates in blepharitis, cellulitis, and insect bite and sting reactions. 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 can form pigmented dermal lesions. These include the junctional and compound nevi located at the epidermal/dermal junction and dermis respectively, common blue nevus and cellular blue nevus within the dermis, and oculodermal melanocytosis. Lymphatic malformations arise from lymphatic endothelium within the dermis. Several lesions occur in the dermis but are of uncertain cellular etiology. Among these, the cylindroma may have eccrine relationships but also involves the dermal collagen to a large extent. Dermatofibroma demonstrates some relationship to fibroblasts, but its 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 that secrete the surrounding matrix, but their cellular etiology remains unclear. Microcystic adnexal carcinoma is derived from dermal ductal elements but also includes epidermal relationships.