Bowen’s disease (BD) represents a very early form of skin cancer, specifically classified as Squamous Cell Carcinoma in situ. This diagnosis means that the abnormal, pre-cancerous cells are confined solely to the outermost layer of the skin, the epidermis, and have not yet invaded the deeper skin layers. The development of this condition is not typically attributed to a single cause but is considered a complex outcome of multiple factors that collectively lead to damage in the DNA of skin cells. This cellular damage disrupts the normal growth and division cycle of the keratinocytes, which are the main cell type in the epidermis, ultimately driving the formation of the characteristic scaly or crusted patches. The reasons behind this transformation are explored through environmental exposure, specific viral infections, and a person’s underlying biological ability to fight off disease.
Environmental Triggers
The most common causal factor for Bowen’s disease globally is chronic, cumulative exposure to ultraviolet (UV) radiation from sunlight. Over decades, the skin absorbs high-energy photons from both UVA and UVB light, which leads to direct damage of the cellular DNA within the keratinocytes. This damage often results in specific mutations, particularly in tumor suppressor genes, preventing the cells from undergoing programmed cell death or repair.
The effect of UV radiation is cumulative, meaning the total lifetime sun exposure determines the risk. BD most frequently manifests on chronically sun-exposed areas of the body, such as the head, neck, lower legs, and arms. The condition is often seen in older individuals because cellular repair mechanisms become less efficient over time, allowing the total sun dose to reach a threshold that overwhelms the skin’s defenses.
A distinct chemical trigger for Bowen’s disease is exposure to inorganic arsenic compounds. Historically, this exposure resulted from certain medications, such as Fowler’s solution, or through contaminated drinking water. Today, occupational exposure in industries like smelting or pesticide manufacturing is the primary source. Arsenic acts as a co-carcinogen, disrupting DNA repair processes and interfering with cell signaling pathways that control growth.
A unique characteristic of arsenic-induced BD is that it can appear on non-sun-exposed areas of the body, such as the palms, soles, or trunk. This presentation differs significantly from the pattern seen with UV-related cases, emphasizing that arsenic represents a systemic, chemical-driven pathway to the disease. The resulting lesions are often multiple and widespread. The latency period between arsenic exposure and the onset of BD can be very long, often exceeding 20 or 30 years.
Viral Agents
Certain infectious agents, specifically high-risk types of the Human Papillomavirus (HPV), are strongly implicated as a separate cause of Bowen’s disease. This mechanism of disease development is independent of the environmental damage caused by UV radiation or arsenic exposure. HPV is a small DNA virus that infects epithelial cells, and specific strains contain proteins that can interfere with normal cell cycle regulation.
The HPV types most commonly associated with BD are the high-risk strains, such as HPV-16, HPV-18, and HPV-33. These viruses are well-known for their oncogenic potential. The viral proteins E6 and E7 produced by these high-risk types are particularly effective at inactivating the host cell’s tumor suppressor proteins, leading to uncontrolled proliferation of the infected keratinocytes.
When BD is caused by HPV, it typically affects the anogenital region, including the perianal area, vulva, and penis. On the glans penis, this manifestation is sometimes referred to by the specific term Erythroplasia of Queyrat. The presence of these high-risk HPV types in the lesions supports a direct viral etiology.
Underlying Biological Susceptibility
A person’s internal biological state determines their susceptibility to developing Bowen’s disease when exposed to environmental or viral triggers. The most significant host factor that increases risk is a compromised or suppressed immune system. The immune system is normally tasked with identifying and destroying cells that have undergone cancerous transformation or those infected by viruses like HPV.
Individuals who are immunosuppressed, such as organ transplant recipients taking anti-rejection medications or people with advanced HIV infection, have a markedly increased risk of developing BD. The inability of the weakened immune surveillance system to effectively recognize and eliminate damaged or pre-cancerous keratinocytes allows these abnormal cells to survive and proliferate. This failure explains why immunosuppressed patients often develop multiple and more aggressive lesions following exposure to the common triggers.
Beyond immune status, the natural process of aging contributes to an increased susceptibility to all forms of skin cancer, including BD. As people age, the efficiency of their cellular machinery responsible for repairing DNA damage naturally declines. This reduced capacity for repair means that the mutations caused by UV radiation or other carcinogens are more likely to persist and accumulate over time. Genetic predisposition also plays a role, as certain inherited variations in DNA repair genes can make some individuals less able to handle the burden of cumulative cellular damage.