Keratoacanthomas (KC) are common skin lesions that frequently cause alarm due to their rapid development and distinctive appearance. They are characterized by an extremely fast growth phase that can occur over a matter of weeks, which is unusual for most skin growths. While KC lesions share many characteristics with skin cancers, they possess a unique life cycle. This article explores the nature of keratoacanthomas, detailing their physical traits, underlying causes, classification, and standard approaches to treatment.
Defining Keratoacanthomas
Keratoacanthomas typically present as dome-shaped nodules on the skin, often measuring between one and two centimeters in diameter. A defining feature is the presence of a central crater or core filled with keratin, which gives the lesion a volcano-like or crateriform appearance. These growths originate from the pilosebaceous unit (hair follicle) and are most commonly found on sun-exposed areas such as the face, head, neck, and the back of the hands.
The natural history of a KC follows three distinct phases. The first is the proliferative phase, marked by rapid expansion that can last for approximately six to eight weeks. This is followed by a maturation phase, where the lesion maintains its size and crateriform shape for several weeks to months.
The final stage is the involution or regressive phase, during which the lesion spontaneously begins to shrink and resolve. This regression process usually occurs over four to six months, often leaving behind a depressed, atrophic scar. However, because the lesion’s behavior can be potentially destructive, medical intervention is often sought long before this natural regression occurs.
Understanding the Causes and Risk Factors
The exact biological trigger for keratoacanthoma development is not fully understood, but the condition is strongly linked to several external and internal factors. The primary cause is chronic exposure to ultraviolet (UV) radiation from the sun, which leads to DNA damage in skin cells. KC lesions occur predominantly in fair-skinned individuals and older adults, reflecting the cumulative effect of sun damage over time.
Immune system suppression is another well-established risk factor, particularly in organ transplant recipients who take immunosuppressive medications. These patients have a significantly higher incidence of KC, which can also present more aggressively. Exposure to chemical carcinogens, such as industrial tar, pitch, and mineral oils, has been associated with an increased risk.
Genetic predisposition also plays a role, with some lesions linked to rare inherited conditions like Muir-Torre syndrome or Ferguson-Smith syndrome, which cause multiple KC lesions. Localized skin trauma, such as a previous injury or surgery, and infection with certain types of Human Papillomavirus (HPV) have also been implicated as potential triggering events.
Classification and Diagnosis
The classification of keratoacanthoma remains a long-standing debate among dermatologists and pathologists. Historically, it has been viewed as a benign, self-healing tumor, but its close resemblance to well-differentiated squamous cell carcinoma (SCC) complicates this classification. Many modern experts now classify KC as a low-grade variant of SCC, often referring to it as “squamous cell carcinoma, keratoacanthoma type” (SCC-KA type).
This reclassification reflects that it is nearly impossible to definitively distinguish KC from an aggressive SCC based on clinical appearance alone. A small percentage of lesions initially classified as KC may also progress or metastasize. Therefore, a definitive diagnosis requires a tissue biopsy to examine the cellular architecture.
An excisional biopsy, which removes the entire lesion, is generally preferred because a partial or shave biopsy may not provide enough tissue depth to differentiate KC from invasive SCC. Under the microscope, pathologists look for features that favor KC, such as a symmetrical, crateriform structure with an orderly growth pattern that typically does not invade past the sweat glands.
In contrast, a conventional SCC may exhibit more cellular disorganization and evidence of deeper invasion into the surrounding tissue. The decision to treat is often guided by the necessity of ruling out the more dangerous conventional SCC, rather than waiting for spontaneous regression.
Treatment Approaches and Expected Outcomes
Although keratoacanthomas can resolve on their own, treatment is typically recommended due to the potential for local destruction, scarring, and the risk of misdiagnosing a true SCC. The most common and preferred option is surgical excision, which involves removing the entire lesion with a small margin of healthy tissue. This method provides the tissue specimen necessary for a complete pathological analysis, confirming the diagnosis and ensuring the entire growth has been removed.
Mohs micrographic surgery is often utilized for larger lesions or those located in cosmetically sensitive areas, such as the face. This technique minimizes the removal of healthy tissue while ensuring clear margins. For patients who are not suitable candidates for surgery, alternative non-surgical options are available.
Non-Surgical Options
These include destructive methods like curettage and electrodesiccation (scraping and burning the tissue) or cryosurgery (freezing the lesion). Intralesional injections of medications, such as 5-fluorouracil or methotrexate, can also be used, particularly for multiple or very large lesions where surgery is impractical.
The prognosis for treated KC lesions is generally excellent, with a very low rate of recurrence after complete surgical removal. However, individuals with a history of KC have an increased likelihood of developing new lesions elsewhere, emphasizing the need for ongoing skin surveillance and consistent sun protection.