Actinic Keratosis
Actinic keratosis (AK), also referred to as solar keratosis or senile keratosis, is a common premalignant skin lesion that arises due to chronic ultraviolet (UV) radiation exposure, primarily in fair-skinned individuals. It is characterized by thickened, scaly, rough patches that form on sun-exposed areas of the skin, particularly the face, ears, scalp, neck, forearms, and the backs of the hands. These lesions represent early squamous cell carcinoma in situ, confined to the epidermis, with potential to evolve into invasive squamous cell carcinoma (SCC) over time. AKs are one of the most common reasons for dermatologic consultations in older adults and are considered part of a spectrum of UV-induced epidermal neoplasia. Although many AKs remain stable or regress, their cumulative presence is a marker of field cancerization and increased skin cancer risk.
Symptoms
Most actinic keratoses are asymptomatic and discovered incidentally on skin examination. When symptomatic, patients may report mild pain, burning, itching, or a sensation of roughness. Clinically, lesions appear as small (usually <1 cm), rough, scaly, or crusted papules or plaques that are often easier felt than seen. They may be skin-colored, red, brown, or yellowish and can have an adherent, dry scale. AKs typically arise on chronically sun-exposed areas such as the forehead, scalp (especially in bald men), ears, dorsal hands, forearms, and lower legs. Lesions may be solitary or, more commonly, multiple and occur in clusters over sun-damaged skin. Variants include hypertrophic, atrophic, pigmented, lichenoid, and actinic cheilitis, the latter involving the lower lip and carrying a higher risk of malignant transformation.
Risk Factors
The primary risk factor for actinic keratosis is long-term exposure to ultraviolet radiation, particularly in people with fair skin types (Fitzpatrick I–III), light-colored hair and eyes, and a tendency to sunburn easily. Additional risk factors include increasing age, male sex, outdoor occupations or hobbies, use of tanning beds, and geographic location with high UV indices. Immunosuppression—such as from organ transplantation, HIV infection, or chemotherapy—substantially increases both the incidence and malignant transformation rate of AKs. Genetic conditions impairing DNA repair, such as xeroderma pigmentosum, also predispose individuals to early and aggressive actinic damage. Individuals with a history of frequent sunburns or prior nonmelanoma skin cancers are at elevated risk for developing multiple actinic keratoses.
Diagnosis
Diagnosis of actinic keratosis is primarily clinical and based on characteristic appearance and distribution of lesions in individuals with significant sun exposure. Dermatologists often use tactile examination to detect the roughness typical of AKs. Dermoscopy may aid in differentiating AKs from other pigmented lesions or early malignancies, revealing features such as a strawberry pattern, rosettes, or white-to-yellow scale. In cases where the diagnosis is uncertain or there are features concerning for invasive squamous cell carcinoma—such as induration, ulceration, rapid growth, or bleeding—a biopsy is warranted. Histopathological analysis confirms the presence of atypical keratinocytes confined to the epidermis, distinguishing AK from in situ or invasive carcinoma. Given the concept of field cancerization, dermatologic surveillance should assess for subclinical lesions and nearby actinic damage.
Treatment
Treatment of AKs is essential due to the potential for progression to invasive SCC and is chosen based on the number, thickness, location, and patient-specific factors. Lesion-directed therapies include cryotherapy with liquid nitrogen, which is the most widely used method and induces necrosis via rapid freezing and thawing. Cryotherapy is effective for isolated lesions but may cause hypopigmentation or blistering. Curettage and electrodesiccation, as well as surgical excision, are reserved for thicker or suspicious lesions. Field-directed therapies, used when multiple lesions are present or to treat subclinical disease, include topical agents such as 5-fluorouracil, imiquimod, diclofenac gel, and tirbanibulin. These agents exert their effects through mechanisms including antimetabolite activity, immune stimulation, cyclooxygenase inhibition, and inhibition of tubulin polymerization, respectively. Photodynamic therapy (PDT) using topical aminolevulinic acid or methyl aminolevulinate followed by light activation is another highly effective field therapy with good cosmetic outcomes, although it may cause transient pain and erythema. Other modalities include laser resurfacing and chemical peels, though these are less commonly employed. Adherence to therapy and proper education on inflammatory reactions during treatment are critical for success.
Outlook
The overall prognosis for individuals with actinic keratosis is favorable with appropriate treatment and sun protection. While many lesions remain stable or spontaneously regress, some progress to squamous cell carcinoma over months to years. The estimated annual risk of malignant transformation per lesion is less than 1%, but this risk increases with lesion thickness, patient immunosuppression, and the presence of numerous lesions. Importantly, the majority of cutaneous squamous cell carcinomas are believed to originate from AKs, particularly those with hypertrophic or ulcerated features. Early detection and treatment, as well as regular dermatologic follow-up, significantly reduce the likelihood of progression and morbidity.
Complications
The main complication of untreated or inadequately treated actinic keratosis is progression to invasive squamous cell carcinoma, which can metastasize and become life-threatening, especially in immunocompromised individuals. Other complications include local discomfort, cosmetic disfigurement, and treatment-related side effects such as scarring, pigment changes, and photosensitivity. Multiple lesions or field cancerization may require repeated treatments over time, impacting quality of life.
Prevention
The most effective preventive strategy against actinic keratosis is consistent and lifelong photoprotection. This includes applying broad-spectrum sunscreen daily, wearing protective clothing, avoiding tanning beds, and limiting sun exposure during peak UV hours. Behavioral interventions such as public education on UV risks, especially targeting adolescents and outdoor workers, can reduce long-term incidence. For high-risk populations, such as transplant recipients, chemopreventive measures including retinoids or topical agents like 5-fluorouracil may be considered to reduce the burden of new lesions. Regular dermatologic evaluations allow for early identification and treatment of AKs and related skin cancers.
Support
Patients should be advised to practice rigorous sun protection, including the daily use of broad-spectrum sunscreens with SPF 30 or higher, wearing sun-protective clothing and hats, and avoiding peak sunlight hours. Self-examination of the skin is important for early detection of new or changing lesions. Patients with multiple or recurring AKs may benefit from long-term dermatologic care, support groups, and educational resources on skin cancer prevention. Counseling on adherence to topical therapies, managing side effects, and regular follow-up is essential for optimal outcomes.
Sources
The information presented above is supported by reputable medical sources and research publications. These references provide additional clinical insights and evidence-based findings for healthcare professionals and individuals seeking comprehensive understanding of this medical condition.
