Actinic keratosis: Understanding Your Pathology Report

by Jason Wasserman MD PhD FRCPC
April 24, 2026

Actinic keratosis (AK) is a pre-cancerous skin condition caused by long-term damage from ultraviolet (UV) radiation, most often from the sun. It is made up of abnormal skin cells called keratinocytes, which are the flat cells that form most of the epidermis (the outer layer of the skin). In actinic keratosis, the abnormal cells are confined to the lower part of the epidermis — they have not yet replaced the full thickness of the outer skin and have not invaded the deeper tissue below.

Actinic keratosis is considered pre-cancerous because, over time, a small percentage of these lesions progress to an early form of skin cancer called squamous cell carcinoma in situ (Bowen’s disease) and eventually to invasive squamous cell carcinoma. When actinic keratosis develops specifically on the lips, it is called actinic cheilitis. This article will help you understand the findings in your pathology report for actinic keratosis — what each term means and why it matters for your care.

What causes actinic keratosis?

The main cause of actinic keratosis is chronic exposure to ultraviolet (UV) radiation. Most of this damage comes from sunlight, but artificial UV sources, such as tanning beds, also cause similar injury. UV radiation damages DNA in keratinocytes, and over many years, these genetic changes accumulate, leading to abnormal growth.

Risk factors include:

• Older age — Most actinic keratoses develop after age 50 because UV damage accumulates over a lifetime.
• Fair skin — People with lighter skin, light-colored eyes, and red or blond hair are at higher risk because their skin contains less protective melanin.
• Outdoor lifestyle or work — People who spend long hours outdoors, such as farmers, sailors, and construction workers, are more likely to develop actinic keratoses.
• History of sunburns or tanning bed use — Repeated burns and artificial UV exposure increase the risk.
• Weakened immune system — People taking anti-rejection medications after an organ transplant, receiving other forms of immune suppression, or living with HIV are at much higher risk. Organ transplant recipients can develop hundreds of actinic keratoses, and their lesions are more likely to progress to invasive cancer.
• Male sex — Actinic keratoses are more common in men, particularly on the scalp in men who are bald or have thinning hair.

What are the symptoms of actinic keratosis?

Actinic keratosis usually appears as a rough, scaly patch of skin that feels like sandpaper. These patches are often easier to feel than to see, especially when they are small. Common features include:

• Rough, scaly patches — The surface may feel dry, crusty, or sandpapery and may flake off and reappear over time.
• Color variation — Patches can be red, pink, brown, or skin-colored.
• Mild discomfort — Some lesions itch, burn, or feel tender, particularly after sun exposure.
• Variable appearance — Lesions may be flat, raised, or form a thick crust.
• Multiple lesions — It is common to develop several actinic keratoses at the same time in areas of chronic sun damage.

Actinic keratoses most often develop on sun-exposed areas of the body, including the face, scalp (especially in men with thinning hair), lips, ears, hands, forearms, and lower legs. A lesion that bleeds, rapidly enlarges, becomes tender, or develops into a firm bump should be assessed promptly, as these features raise concern for progression to squamous cell carcinoma.

How is the diagnosis made?

Doctors often suspect actinic keratosis based on how a lesion looks and feels during a skin examination. Because actinic keratosis can resemble other skin conditions — including eczema, psoriasis, seborrheic keratosis, and early squamous cell carcinoma — a biopsy is performed whenever the diagnosis is uncertain or when a lesion has features suggesting possible progression to cancer. The biopsy is typically a shave biopsy, in which the surface of the lesion is shaved off, although a punch biopsy may be used for thicker or pigmented lesions. The sample is then examined under the microscope by a pathologist. Under the microscope, the pathologist looks for abnormal keratinocytes in the lower part of the epidermis, with cells of irregular size and shape replacing the normal, orderly arrangement of the bottom layers. The surface layer typically shows parakeratosis (cells that still contain their nuclei in the outermost layer, where they should normally be lost) alternating with areas of hyperkeratosis (thickened keratin). The dermis beneath the lesion usually shows solar elastosis — damaged elastic tissue that reflects long-term sun exposure — along with scattered inflammatory cells and small new blood vessels. Imaging is not required for actinic keratosis because it is confined to the outer layer of skin and cannot spread.

Variants of actinic keratosis

Actinic keratosis can look different under the microscope depending on the variant. Most behave similarly, but some carry a higher risk of progression to invasive squamous cell carcinoma.

• Classic actinic keratosis — The most common type, appearing as rough, scaly patches. The risk of progression from any single lesion is low but increases with the number of lesions and with time.
• Atrophic actinic keratosis — The epidermis is thinned and often lacks the usual surface keratin. Despite looking less impressive than classic AK, these lesions can still progress to invasive cancer.
• Hypertrophic actinic keratosis — Appears thick and crusted under the microscope, with prominent hyperkeratosis. This type may be harder to treat with topical therapy and carries a higher risk of progression, particularly if it persists or recurs.
• Pigmented actinic keratosis — Contains melanin pigment, making it appear brown clinically. It can resemble melanoma, lentigo, or seborrheic keratosis. The pigmentation itself does not increase cancer risk, but can delay recognition.
• Lichenoid actinic keratosis — Shows a dense band of inflammation beneath the epidermis that resembles another skin condition called lichen planus. The inflammation may represent the immune system’s response to the abnormal cells.
• Acantholytic actinic keratosis — The abnormal keratinocytes lose their connections to one another, creating small spaces or clefts within the epidermis.
• Bowenoid actinic keratosis — Shows more widespread atypia that approaches the features of squamous cell carcinoma in situ. Because the distinction between this variant and Bowen’s disease can be subtle, Bowenoid AK is often managed similarly to squamous cell carcinoma in situ.

Actinic keratosis versus squamous cell carcinoma in situ

Actinic keratosis and squamous cell carcinoma in situ (Bowen’s disease) are part of the same continuum of sun-induced skin damage, but they differ in the extent of epidermal involvement by abnormal cells.

• Actinic keratosis — The abnormal keratinocytes are limited to the lower part of the epidermis. It is considered pre-cancerous.
• Squamous cell carcinoma in situ — The abnormal cells replace the full thickness of the epidermis. It is considered an early stage of skin cancer.
• Invasive squamous cell carcinoma — The abnormal cells break through the bottom of the epidermis and grow into the dermis below. It is considered a true skin cancer with the potential to spread.

Because these conditions can look similar both clinically and under the microscope, a biopsy is often needed to distinguish them.

Margins

If an actinic keratosis is completely removed rather than biopsied, the pathologist may examine the edges of the tissue — called the margins — to see whether any abnormal cells are present at the cut edge.

• Negative margin — No abnormal cells are seen at the cut edge.
• Positive margin — Abnormal cells are present at the cut edge. For actinic keratosis, a positive margin does not usually require re-excision because the remaining cells can be treated with topical therapy, cryotherapy, or other field treatments.

For most actinic keratoses, margin status is less important than it is for true skin cancers, because AK is pre-cancerous and because the surrounding sun-damaged skin often harbors additional abnormal cells that cannot be seen with the naked eye.

Risk of progression to skin cancer

Most actinic keratoses remain stable or even regress on their own over time. Only a small percentage progress to invasive squamous cell carcinoma. The risk from any single lesion is low — generally less than 1% per year — but the risk increases with certain features.

Factors that increase the risk of progression include:

• Number of lesions — People with many actinic keratoses have a higher overall risk because the chance that at least one will progress increases with the total number.
• Immunosuppression — Organ transplant recipients and others on long-term immunosuppressing medications have a much higher rate of progression, sometimes developing invasive skin cancer from an AK within a year or two.
• Persistence or recurrence — Lesions that do not respond to treatment or that keep coming back are more likely to harbor or develop into cancer.
• High-risk variants — Bowenoid and hypertrophic actinic keratoses have a higher risk of progression than classic AK.
• Rapid change — A lesion that suddenly grows, thickens, bleeds, becomes tender, or develops into a firm bump may already contain invasive squamous cell carcinoma.

Because actinic keratosis is a marker of chronic sun damage, having one or more AKs also indicates a higher overall risk of developing other skin cancers, including basal cell carcinoma and melanoma, at other sites on the body.

What happens after the diagnosis?

Treatment of actinic keratosis is typically managed by a family doctor or dermatologist. The goal is to destroy or remove the abnormal cells, treat the surrounding sun-damaged skin where additional AKs may be developing, and prevent new lesions from forming.

Lesion-directed treatments are used for isolated or easily identified lesions:

• Cryotherapy — The lesion is frozen with liquid nitrogen. This is the most common treatment for small numbers of AKs.
• Curettage and electrodesiccation — The lesion is scraped off, and the base is cauterized. This is often used for thicker or hypertrophic AKs.
• Surgical excision — Used mainly when there is concern that an AK may already harbor squamous cell carcinoma or for lesions that have not responded to other treatments.

Field treatments treat an entire area of sun-damaged skin, including both visible lesions and nearby cells that are abnormal but not yet visible:

• Topical 5-fluorouracil — A cream that destroys abnormal cells; usually applied for several weeks.
• Topical imiquimod — A cream that activates the immune system to attack the abnormal cells.
• Topical diclofenac — An anti-inflammatory gel used over several months.
• Photodynamic therapy (PDT) — A photosensitizing medication is applied to the skin and then activated with a specific wavelength of light, destroying the abnormal cells.
• Chemical peels or laser resurfacing — Occasionally used for extensive field damage.

After treatment, regular skin examinations are important to detect new or recurring actinic keratoses and early signs of skin cancer. The frequency depends on the number of AKs, the history of prior skin cancers, and overall risk — from once a year for most people to every few months for those at the highest risk, such as transplant recipients.

Ongoing sun protection is a key part of prevention. Broad-spectrum sunscreen, sun-protective clothing, a wide-brimmed hat, and avoiding tanning beds all reduce the risk of developing new actinic keratoses and other skin cancers.

Questions to ask your doctor

• What variant of actinic keratosis did my lesion show?
• Is there any concern that my lesion may already be squamous cell carcinoma in situ or invasive squamous cell carcinoma?
• Do I need treatment, or can this lesion just be monitored?
• Which treatment option is best for my lesion — cryotherapy, a topical cream, photodynamic therapy, or excision?
• Do I need a lesion-directed treatment, a field treatment, or both?
• How long will treatment take, and what side effects should I expect?
• What is my personal risk of progression to skin cancer?
• Am I at higher risk because of medications or a weakened immune system?
• How often should I have full skin examinations going forward?
• What warning signs should I watch for when checking my own skin?
• What sun-protection strategies do you recommend for me?
• Should I be screened for other sun-related skin cancers?