Actinic Keratosis: Causes, Symptoms & Treatment Options

What Is Actinic Keratosis?

Actinic keratosis (AK) is a rough, scaly patch on the skin caused by years of sun exposure. Also called solar keratosis, it is considered a precancerous condition because a small percentage of lesions may develop into squamous cell carcinoma, a type of skin cancer, if left untreated.

Actinic keratoses develop when the DNA in skin cells becomes damaged by ultraviolet (UV) radiation from the sun or tanning beds. This damage accumulates over time, which is why AKs are most common in people over 40 and those with significant sun exposure history. The condition affects an estimated 58 million Americans, making it one of the most common reasons for dermatology visits.

The term "actinic" comes from the Greek word for ray (aktis), referring to the sun's rays, while "keratosis" means a thickening of the skin's outer layer (keratin). These lesions represent the earliest stage on the continuum from sun-damaged skin to invasive squamous cell carcinoma. Dermatologists often describe the surrounding sun-damaged skin as "field cancerization," indicating widespread cellular damage even in areas without visible lesions.

Understanding that actinic keratosis is a sign of significant sun damage is important for both treatment and prevention. When one AK develops, it often indicates that the entire area of sun-exposed skin has underlying damage, and more lesions may appear over time. This is why dermatologists recommend not only treating existing lesions but also implementing comprehensive sun protection strategies to prevent new ones from forming.

How Common Is Actinic Keratosis?

Actinic keratosis is extremely common, particularly in populations with fair skin living in sunny climates. Studies show that 11-25% of adults in North America and Europe have at least one AK. In Australia, where UV radiation is intense, prevalence reaches 40-60% in adults over 40. The condition is more common in men than women, likely due to historical differences in outdoor occupations and sun protection behaviors.

Age is a significant risk factor, with prevalence increasing dramatically after 40. By age 60, approximately 60% of people with fair skin have one or more actinic keratoses. The cumulative nature of sun damage means that even people who now practice good sun protection may develop AKs from exposure earlier in life.

Who Gets Actinic Keratosis?

People with fair skin (Fitzpatrick skin types I and II), light-colored eyes, and blond or red hair are at highest risk. However, anyone with significant cumulative sun exposure can develop actinic keratosis. Other high-risk groups include outdoor workers, people living in sunny climates, those who use tanning beds, and individuals with weakened immune systems. Organ transplant recipients have a particularly elevated risk, approximately 250 times higher than the general population, due to immunosuppressive medications.

What Are the Symptoms of Actinic Keratosis?

Actinic keratosis typically appears as rough, dry, scaly patches on sun-exposed skin. These lesions range from a few millimeters to over a centimeter in size, and may be skin-colored, red, pink, or brown. The texture is often described as sandpaper-like, and lesions may be easier to feel than see.

The appearance of actinic keratoses can vary considerably, which sometimes makes them difficult to identify. The most characteristic feature is the rough, scaly texture that persists over time. Unlike a temporary skin irritation that heals within days, AKs remain and may gradually become more prominent. Some lesions develop a thick, crusty surface, while others remain flat with fine scaling.

Color variation in actinic keratoses depends on the individual's skin tone and the lesion's characteristics. On fair skin, AKs often appear pink or red with white or yellowish scales. On medium skin tones, they may appear tan or brown. It's important to note that the redness associated with AKs is often not visible on darker skin tones, making tactile examination (feeling for rough patches) especially important for these individuals.

Some actinic keratoses cause symptoms beyond their appearance. Patients commonly report itching, burning, or tenderness at the site of lesions. These sensations may come and go, and some people describe a prickly feeling, as if small thorns are in the skin. While many AKs are asymptomatic, the presence of symptoms doesn't necessarily indicate a higher risk of progression to cancer.

Common Locations

Actinic keratoses develop almost exclusively on sun-exposed skin. The most common locations reflect areas that receive the most cumulative UV exposure over a lifetime:

• Face: Particularly the forehead, nose, cheeks, and around the eyes
• Ears: Especially the tops and rims of the ears
• Scalp: Common in people with thinning hair or baldness
• Neck: Both front and sides exposed during outdoor activities
• Forearms and hands: Backs of hands and outer forearms
• Lower legs: More common in women who wear skirts or shorts

Warning Signs of Progression

While most actinic keratoses remain stable or even resolve on their own, certain changes may indicate progression toward squamous cell carcinoma. Patients should monitor their lesions and report any concerning changes to their dermatologist. Warning signs that warrant prompt evaluation include rapid growth of a lesion, increasing thickness or elevation, bleeding without obvious trauma, persistent pain or tenderness, development of a hard base beneath the lesion, or a lesion that doesn't heal after treatment.

What Causes Actinic Keratosis?

Actinic keratosis is caused by cumulative ultraviolet (UV) radiation damage from sunlight or tanning beds. UV rays damage the DNA in skin cells called keratinocytes, leading to abnormal cell growth. This damage accumulates over years, which is why AKs are more common with age.

The development of actinic keratosis is a direct result of UV-induced DNA damage in the skin's keratinocytes, the cells that make up the outermost layer of skin (epidermis). When UV radiation penetrates the skin, it causes specific types of DNA mutations, particularly in the p53 tumor suppressor gene. Under normal circumstances, p53 acts as a "guardian of the genome," detecting DNA damage and either halting cell division to allow repair or triggering cell death if damage is too severe.

When p53 is mutated by UV exposure, this protective mechanism fails. Damaged keratinocytes survive and continue to divide, passing their genetic abnormalities to daughter cells. Over time, these abnormal cells accumulate and form the characteristic scaly patches of actinic keratosis. The process is cumulative, meaning that every episode of sun exposure adds to the total burden of DNA damage, even if no visible sunburn occurs.

Both UVA and UVB radiation contribute to actinic keratosis development. UVB rays (280-315 nm) are the primary cause of sunburn and direct DNA damage. UVA rays (315-400 nm) penetrate deeper into the skin and contribute to damage through the generation of reactive oxygen species. This is why broad-spectrum sun protection, which blocks both UVA and UVB, is essential for prevention.

Risk Factors for Actinic Keratosis

How Is Actinic Keratosis Diagnosed?

Actinic keratosis is usually diagnosed through visual examination by a dermatologist. The characteristic rough, scaly appearance on sun-exposed skin is often sufficient for diagnosis. In uncertain cases, dermoscopy (magnified skin examination) or skin biopsy may be performed to confirm the diagnosis and rule out skin cancer.

Clinical diagnosis of actinic keratosis relies on the experience and trained eye of the dermatologist. During examination, the physician looks for the characteristic features of AK: rough texture, scaly surface, and location on sun-exposed skin. The dermatologist will also feel the lesions, as the sandpaper-like texture is often more distinctive than visual appearance alone. A full-body skin examination is typically recommended, as patients with one AK often have multiple lesions.

Dermoscopy, a technique using a handheld device that magnifies and illuminates the skin, provides additional diagnostic information. Under dermoscopy, actinic keratoses show characteristic patterns including a "strawberry pattern" with red pseudo-network and white-yellow scales. This technique helps distinguish AKs from other skin conditions and can identify early signs of transformation to squamous cell carcinoma.

When the diagnosis is uncertain, or when there's concern about possible progression to skin cancer, a skin biopsy provides definitive answers. During a biopsy, a small sample of the lesion is removed under local anesthesia and examined under a microscope. The pathologist can confirm the diagnosis of actinic keratosis and determine if there's any evidence of invasive squamous cell carcinoma. Biopsy is particularly important for lesions that are thick, hard, bleeding, or not responding to standard treatment.

Differential Diagnosis

Several other skin conditions can resemble actinic keratosis and must be considered during diagnosis:

• Squamous cell carcinoma: AKs and early SCC can look similar; biopsy distinguishes them
• Seborrheic keratosis: Benign growths with a "stuck-on" appearance, usually darker
• Bowen's disease: SCC confined to the epidermis, requires biopsy to distinguish
• Psoriasis: Scaly patches that typically affect different body areas
• Eczema: Inflammatory condition with different distribution pattern

How Is Actinic Keratosis Treated?

Treatment options for actinic keratosis include cryotherapy (freezing) for individual lesions, topical medications like 5-fluorouracil and imiquimod for multiple lesions, and photodynamic therapy (PDT) for cosmetically sensitive areas. Treatment choice depends on the number and location of lesions, patient preferences, and potential side effects.

Treatment of actinic keratosis serves two primary purposes: eliminating existing precancerous lesions and preventing progression to squamous cell carcinoma. Because the 5-10% transformation rate is unpredictable, and we cannot determine which specific lesions will become cancerous, dermatologists generally recommend treating all diagnosed actinic keratoses rather than adopting a "watch and wait" approach.

Treatment selection is individualized based on several factors. For patients with only a few, isolated lesions, destructive therapies like cryotherapy or curettage are typically preferred due to their immediate effectiveness. For patients with numerous lesions or widespread sun damage (field cancerization), topical therapies or photodynamic therapy offer the advantage of treating larger areas simultaneously. The location of lesions also matters, as treatments with better cosmetic outcomes may be preferred for facial lesions.

Cryotherapy (Freezing)

Cryotherapy is the most commonly used treatment for individual actinic keratoses. Liquid nitrogen at -196 degrees Celsius (-321 degrees Fahrenheit) is applied to the lesion, typically using a spray device. The extreme cold destroys the abnormal cells by forming ice crystals within them, disrupting cell membranes and causing cell death.

The procedure takes only seconds per lesion. Patients typically feel a brief stinging or burning sensation during treatment. Within 24-48 hours, the treated area forms a blister or crust, which falls off over 1-3 weeks as new, healthy skin forms underneath. Treatment success rates range from 75-98% depending on the technique and lesion characteristics.

Side effects of cryotherapy include temporary redness, swelling, and blister formation. Some patients experience hypopigmentation (lightening of the skin) at the treatment site, which may be permanent. This cosmetic concern is more significant in patients with darker skin tones and should be discussed before treatment.

Topical Cream Treatments

Topical medications are particularly useful for patients with multiple actinic keratoses or extensive field cancerization. These treatments work by selectively destroying abnormal cells while sparing normal tissue, and they can treat subclinical lesions that aren't yet visible.

5-Fluorouracil (5-FU): This chemotherapy cream (brands include Efudex, Fluoroplex, Carac) works by interfering with DNA synthesis in rapidly dividing abnormal cells. Treatment typically involves applying the cream once or twice daily for 2-4 weeks. During treatment, the skin becomes red, irritated, and may develop crusting or erosions. This reaction is expected and indicates the medication is working. Healing occurs over 1-2 weeks after treatment ends, revealing healthier skin underneath.

Imiquimod: This immune-modulating cream (Aldara, Zyclara) stimulates the body's own immune system to recognize and destroy abnormal cells. Treatment schedules vary, but typically involve applying the cream 2-3 times per week for several weeks. Like 5-FU, imiquimod causes a local inflammatory reaction during treatment.

Diclofenac gel: This non-steroidal anti-inflammatory medication (Solaraze) is applied twice daily for 60-90 days. It causes less skin irritation than 5-FU or imiquimod but may be less effective. It's often chosen for patients who cannot tolerate the inflammation associated with other topical treatments.

Photodynamic Therapy (PDT)

Photodynamic therapy combines a light-sensitizing medication with specific wavelengths of light to destroy abnormal cells. A photosensitizing agent (aminolevulinic acid or methyl aminolevulinate) is applied to the affected area and allowed to absorb for 1-3 hours. During this time, the medication is preferentially taken up by rapidly dividing abnormal cells.

The area is then exposed to a specific wavelength of light, which activates the photosensitizing agent and generates reactive oxygen species that destroy the abnormal cells. The procedure takes about 15-20 minutes of light exposure. Patients typically experience burning or stinging during illumination, which can range from mild to significant. Pain management options, including cooling fans and local anesthesia, can help improve comfort.

PDT offers excellent cosmetic outcomes, making it particularly popular for treating facial actinic keratoses. The treatment causes temporary redness and swelling but typically heals without scarring. Some patients require multiple treatment sessions for complete clearance.

Daylight PDT

Daylight photodynamic therapy is an alternative to conventional PDT that uses natural sunlight instead of artificial light sources. After applying the photosensitizing cream, patients spend approximately 2 hours outdoors in daylight (avoiding direct intense sun). This approach causes less pain than conventional PDT while maintaining similar effectiveness. It's particularly useful for patients with multiple lesions over large areas.

How Can You Prevent Actinic Keratosis?

Prevention of actinic keratosis centers on protecting skin from ultraviolet radiation. Use broad-spectrum sunscreen (SPF 30+) daily, wear protective clothing and wide-brimmed hats, seek shade during peak sun hours (10 AM - 4 PM), and avoid tanning beds entirely. Early detection through regular skin examinations is also crucial.

Because actinic keratosis results from cumulative sun damage, prevention requires a lifelong commitment to sun protection. It's never too late to start protecting your skin, as limiting future UV exposure can help prevent new lesions even in skin that's already damaged. Studies show that regular sunscreen use not only prevents new actinic keratoses but can actually reduce the number of existing lesions over time.

Sunscreen is the cornerstone of AK prevention, but its effectiveness depends on proper use. Choose a broad-spectrum product with SPF 30 or higher that protects against both UVA and UVB rays. Apply generously (about one ounce for full-body coverage) at least 15 minutes before sun exposure. Reapply every 2 hours, or immediately after swimming or sweating. Don't forget commonly missed areas like ears, scalp (if thinning), tops of feet, and backs of hands.

Physical barriers provide the most reliable sun protection. Seek shade, especially during peak UV hours between 10 AM and 4 PM. Wear protective clothing, including long sleeves and pants when practical. A wide-brimmed hat (at least 3 inches) protects the face, ears, and neck. Ultraviolet protection factor (UPF) clothing is designed specifically to block UV rays and is particularly useful for outdoor activities.

UV-blocking sunglasses protect the delicate skin around the eyes and reduce the risk of both skin cancer and cataracts. Look for glasses labeled as blocking 99-100% of UVA and UVB rays. Wraparound styles provide the best protection.

Regular Skin Examinations

Early detection is a key component of actinic keratosis management. Perform monthly self-examinations of your skin, paying particular attention to sun-exposed areas. Use mirrors to check hard-to-see areas like your scalp, back, and behind your ears. Note any new rough or scaly patches and monitor existing lesions for changes.

Annual professional skin examinations by a dermatologist are recommended for people at increased risk, including those with fair skin, history of significant sun exposure, previous actinic keratoses, or family history of skin cancer. Your dermatologist can identify lesions you might miss and monitor suspicious areas over time.

What Is the Outlook for Actinic Keratosis?

The prognosis for actinic keratosis is generally excellent with treatment. Most AKs are successfully treated with standard therapies. However, patients often develop new lesions over time due to underlying sun damage, requiring ongoing monitoring and retreatment. The risk of progression to squamous cell carcinoma is 5-10% for untreated lesions.

Treatment for actinic keratosis is highly effective, with clearance rates of 75-95% depending on the method used. However, it's important to understand that treating existing lesions doesn't eliminate the underlying sun damage in surrounding skin. Patients with actinic keratoses often develop new lesions over time, which is why ongoing sun protection and regular skin examinations are essential components of long-term management.

The risk of an individual actinic keratosis progressing to squamous cell carcinoma is estimated at 5-10% over 10 years. While this may seem like a low percentage, patients with multiple AKs have a cumulative risk that can be substantial. A patient with 10 lesions has a significantly higher overall risk than someone with just one. This cumulative risk is why dermatologists recommend treating all diagnosed AKs rather than just watching them.

When actinic keratosis does progress to squamous cell carcinoma, it's typically the less aggressive, well-differentiated type with a good prognosis when treated early. This is another reason why regular monitoring and prompt treatment of changing lesions is important. The transition from AK to SCC is often gradual, and catching it early improves outcomes significantly.

Long-term Management

Actinic keratosis is best viewed as a chronic condition requiring ongoing management rather than a one-time problem to be fixed. Key elements of long-term care include continued sun protection to prevent new lesions, regular self-examination of skin, annual or more frequent dermatologist visits depending on risk level, prompt treatment of new lesions, and consideration of field therapy for patients with recurrent multiple lesions.