A wart is a common, non-cancerous skin growth resulting from an infection of the top layer of skin. This localized proliferation of tissue is caused by the Human Papillomavirus (HPV), a DNA virus with over 100 different types. To understand what a wart looks like beneath the surface, it is helpful to examine the structural changes the virus induces in the skin. The appearance of a wart in cross-section reveals a distorted architecture compared to normal, healthy tissue.
Understanding the Wart’s Overall Structure
A wart represents an overgrowth of the epidermis, the outermost layer of the skin. This growth is characterized microscopically by three major architectural hallmarks that distinguish it from a simple callus or a benign tumor.
The first is acanthosis, which describes the general thickening of the prickle cell layer of the epidermis. Hyperkeratosis is the excessive thickening of the stratum corneum, the skin’s outermost protective layer. This accumulation of dense, dead skin cells gives the wart its characteristic rough, often cauliflower-like surface texture.
The third feature is papillomatosis, which refers to the formation of numerous outward, finger-like projections of the dermal papillae. These projections cause the epidermis to grow in an uneven, undulating pattern, creating a deeply furrowed surface.
While many warts grow outward (exophytic), some, particularly those on the soles of the feet, are forced inward by pressure, resulting in an endophytic or “cup-shaped” growth. In these cases, the mass pushes down into the dermis, the layer beneath the epidermis.
Key Features Visible in the Cross Section
When a wart is viewed in a prepared cross-section, the internal structures provide clear evidence of the HPV infection. One of the most frequently observed features is the presence of vascular structures within the dermal papillae. These are small, tortuous blood vessels that have been drawn up closer to the surface due to the excessive epidermal proliferation.
These vessels are often described as thrombosed capillaries, meaning the small blood vessels have clotted. When a wart’s surface is shaved or worn away, these clotted capillaries appear as tiny, dark, punctate spots, often incorrectly called “wart seeds.” The dark color comes from the dried, trapped blood.
Microscopically, these capillaries are seen as small, dark, circular or oval profiles nestled within the upward-projecting dermal papillae. This density of vessels is a reliable way to differentiate a true wart from a simple callus, which lacks this specific vascular pattern.
The cross-section also highlights the extensive hyperkeratosis, showing a dense cap of keratin over the entire lesion. Scattered throughout this thick keratin layer are areas of parakeratosis, where the keratinocytes retain their nuclei instead of losing them during maturation.
The downward growth of the epidermis is also visible, with the rete ridges—the extensions of the epidermis into the dermis—elongated and often curving inward toward the center of the lesion. This inward-pointing feature helps contain the entire mass and is another microscopic identifier of the wart structure.
The Viral Mechanism of Wart Formation
The physical structure of the wart begins when the Human Papillomavirus gains entry into the basal layer of the epidermis, typically through a microscopic break in the skin barrier. The viral DNA begins to transcribe its genes, and the resulting viral proteins are the driving force behind the abnormal growth.
Two proteins, E6 and E7, are significant in driving the wart’s formation. These proteins interfere with the host cell’s normal regulatory mechanisms, specifically targeting tumor suppressor proteins like p53 and retinoblastoma protein (Rb). By inactivating these controls, the virus effectively removes the restraints on cell division.
This leads to the rapid and unregulated proliferation of the infected keratinocytes, resulting in the massive thickening of the epidermis. The virus commandeers the cell’s machinery to create more copies of itself as the infected cells mature and move toward the skin surface.
A defining cellular feature of HPV infection visible in the cross-section is the koilocyte, a pathognomonic marker for the virus. Koilocytes are mature squamous epithelial cells that exhibit an enlarged, irregular nucleus surrounded by a clear, hollow-looking area called a perinuclear halo or vacuole. The presence of these specific cells confirms the underlying viral etiology of the skin growth.