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Actinic Keratosis: Symptoms, Treatment, and Skin Cancer Risk. Learn what actinic keratosis looks like, how it differs from skin cancer, available treatments, when biopsy may be needed, and how to reduce future risk.
What Is Actinic Keratosis?
Actinic keratosis is a common precancerous skin condition that appears as rough, scaly, or gritty patches caused by years of sun damage. [1, 2]
Symptoms and Signs
Texture: Feels dry, rough, or gritty like sandpaper (often easier to feel than see).
Appearance: Small flat or raised spots that may be pink, red, tan, brown, or skin-colored.
Location: Most common on sun-exposed areas like the face, ears, lips, scalp, neck, forearms, and backs of hands.
Sensations: Can sometimes feel tender, itchy, prickly, or burning. [1, 2, 3, 4, 5]
Why UV exposure causes it
Ultraviolet (UV) exposure causes actinic keratosis by damaging the DNA in skin cells called keratinocytes, which leads to abnormal, uncontrolled cell growth. [1, 2]
How UV Damage Happens
DNA Mutation: UV rays from the sun or tanning beds penetrate the skin and alter cellular DNA. [1, 2]
Failed Repair: Normally, the body repairs this DNA damage or destroys the altered cells. Years of cumulative UV exposure overwhelm these repair systems. [1, 2]
Abnormal Growth: The damaged keratinocytes start multiplying in a disordered way. This creates the characteristic rough, scaly, or crusty patches known as actinic keratoses. [1, 2, 3]
Why Certain People Are at Higher Risk
Fair Skin: People with lighter skin have less melanin, a natural pigment that offers minor protection against UV rays.
Cumulative Time: Years spent outdoors or using artificial tanning equipment cause damage to add up over a lifetime.
Weakened Immunity: Individuals with compromised immune systems cannot fight off abnormal cell changes as effectively. [1, 2, 3, 4]
Typical Appearance
Actinic keratosis typically appears as a flat or slightly raised rough, scaly, or crusty patch of skin that often feels like dry skin or sandpaper. [1, 2, 3]
Mild itching, tenderness, or a burning/pricking feeling in the area.
Surrounding skin that shows general sun damage, such as wrinkles, blotchiness, or freckles.
Rare bleeding or persistent sores if a spot becomes irritated or changes. Detailed symptom overviews are available via the Cleveland Clinic and GoodRx. [1, 2, 3, 4]
Who is at increased risk
Anyone can develop actinic keratosis, but you are at increased risk if you have chronic or intense exposure to ultraviolet (UV) radiation from the sun or tanning beds. [1, 2]
Key Risk Factors
Light skin and hair: People with fair skin, blue or green eyes, and red or blond hair who burn or freckle easily face the highest risk.
Age over 40: Sun damage builds up over time, making these lesions much more common in older adults.
Outdoor lifestyle or work: Spending long hours outside or using indoor tanning beds increases your total UV exposure.
Geographic location: Living closer to the equator exposes you to stronger sunlight year-round.
Weakened immune system: People with suppressed immune systems from organ transplants, chemotherapy, or conditions like HIV have a higher chance of developing them.
Balding or thinning hair: Scalps and ears receive heavy sun exposure if unprotected by hair or hats. [1, 2, 3, 4]
Actinic keratosis is a precancerous skin lesion, while squamous cell carcinoma is an actual skin cancer that can develop from it if left untreated. [1, 2]
Key Differences
Classification:
Actinic Keratosis (AK): A pre-cancerous, non-cancerous patch caused by UV damage.
Squamous Cell Carcinoma (SCC): A true form of skin cancer where abnormal cells invade deeper skin layers. [1, 2, 3, 4, 5]
Texture & Feel:
AK: Feels dry, rough, or like sandpaper on a flat or slightly raised surface.
SCC: Feels thicker, firmer, or like a deeper lump under the skin. [1]
Symptoms:
AK: Usually flat or mildly raised, asymptomatic, or slightly itchy.
SCC: Often tender, painful, or prone to bleeding and forming open sores that do not heal. [1, 2, 3]
Speed of Change:
AK: Develops very slowly over years and remains stable.
SCC: Grows and changes visibly over weeks or months. [1]
Risk and Progression
About 5% to 10% of untreated actinic keratoses progress into squamous cell carcinoma over time. Because it is impossible to predict which specific AK spots will turn into cancer, dermatologists generally treat AK lesions as a precaution. [1, 2, 3]
You can learn more about skin care management through the American Academy of Dermatology.
Actinic Keratosis Treatment
Cryotherapy
5-Fluorouracil
Imiquimod
Diclofenac
Tirbanibulin
Photodynamic Therapy
Evidence-Based Complementary and Non-Conventional Approaches
Evidence-based complementary and non-conventional approaches for actinic keratosis (AK) focus on botanical, natural, or alternative mechanisms, though many lack the robust clinical validation of standard therapies like 5-Fluorouracil or Photodynamic Therapy. [1, 2]
Notable Non-Conventional and Complementary Agents
Curaderm (BEC5): An eggplant extract containing solasodine glycosides that targets cancer cell lectins and induces apoptosis (programmed cell death). Small studies show promise for non-melanoma skin cancers, but it requires larger clinical trials. [1]
Ingenol Mebutate: Derived from the milkweed plant (Euphorbia peplus), this compound induces cellular death via the Hedgehog pathway. While initially FDA-approved as a topical gel for AK, its marketing authorization has faced restrictions or withdrawals in certain regions due to risk-benefit profiles and local skin reactions. [1, 2]
St. John’s Wort (Hypericum perforatum): Exhibits potential photodynamic properties by generating reactive oxygen species under light exposure, though research remains largely in vitro or experimental for skin malignancies. [1]
Green Tea Extract (EGCG): Studied for its antioxidant and anti-inflammatory properties that may help modulate sun-damaged skin pathways, though it is used primarily preventively rather than as a curative lesion clearance tool.
Dangerous Alternatives to Avoid
Black Salve: A corrosive escharotic paste (often containing bloodroot and zinc chloride) that causes non-specific tissue destruction. Medical experts strongly advise against its use because it leads to severe scarring, disfigurement, and incomplete cancer removal that allows hidden malignancy progression. [1]
Complementary and non-conventional approaches
PeopleBeatingCancer Evidence Rating.
Therapy
Evidence for AK
PBC Evidence Rating
UV protection
Strong
★★★★★
Cryotherapy
Strong
★★★★★
5-FU
Strong
★★★★★
Photodynamic therapy
Strong
★★★★☆
Nicotinamide
Moderate/high for prevention in high-risk patients
★★★★☆
Vitamin D
Preliminary/insufficient for routine AK treatment
I’m bald. I have spots on my head (AK?) I got sunburned as a kid. I had a bone marrow transplant and radiation therapy for a different cancer in 1995. I have six of the risk factors listed below.
When I found the study below, I learned how complicated AK or pre-skin cancer can be. At the same time, I was researching and writing a blog post abouthow important a dermoscope was when makingdiagnoses of any and all skin lesions.
The bottom line is that evidence-based, non-toxic, non-conventional therapies have been shown to reduce your risk of pre-skin cancer becoming melanoma.
To learn more about other evidence-based therapies that can help prevent the development of non-melanoma skin cancer or relapse, please watch the short video below:
I am both a cancer survivor and cancer coach. To learn more about evidence-based, non-toxic therapies to reduce your risk of skin cancer, scroll down the page, post a question or a comment, and I will reply to you ASAP.
“Little is known about the dermoscopic features of keratinocyte skin cancer…
We sought to determine the dermoscopic features of facial actinic keratosis (AK), intraepidermal carcinoma (IEC), moderately to poorly differentiated invasive squamous cell carcinoma (SCC), and well-differentiated SCC of the keratoacanthoma type…
A total of 243 (70 AK, 71 IEC, 78 SCC, and 24 keratoacanthomas) tumors of the face from 243 patients were analyzed. The majority of patients had a fair skin type, history of melanoma or nonmelanoma skin cancer, and multiple AK. A red pseudonetwork was significantly associated with AK, whereas dotted/glomerular vessels, diffuse yellow opaque scales, and microerosions were significantly more prevalent among IEC.
Hairpin vessels,
Linear-irregular vessels,
Targetoid hair follicles,
White structureless areas,
A central mass of keratin, and
Ulceration
were significantly associated with invasive SCC (P < .001 for all criteria). Similar patterns as in SCC were observed among keratoacanthomas.”
Background: The accuracy of clinical diagnosis of nonpigmented, facial actinic keratosis (AK) is often suboptimal, even for experienced clinicians.
Objectives: To investigate the dermoscopic features of nonpigmented AK located on the head/neck that may assist the clinical diagnosis.
Methods: Forty-one nonpigmented AKs on facial sites were examined by dermoscopy for any consistent underlying features. Lesions were gathered from skin cancer centres in Australia, Austria, Italy and the U.S.A. All cases were diagnosed histopathologically.
Results: Four essential dermoscopic features were observed in facial AK: (i) erythema, revealing a marked pink-to-red ‘pseudonetwork’ surrounding the hair follicles (95%); (ii) white-to-yellow surface scale (85%); (iii) fine, linear-wavy vessels surrounding the hair follicles (81%); and (vi) hair follicle openings filled with yellowish keratotic plugs (66%) and/or surrounded by a white halo (100%). These features combined, in 95% of cases, to produce a peculiar ‘strawberry’ appearance.
Conclusions: A dermoscopic model of ‘strawberry’ pattern is presented, which may prove helpful in the in vivo diagnosis of nonpigmented, facial AK. A limitation of this study is the lack of testing of the specificity of the described dermoscopic criteria in differentiating nonpigmented AKs from other nonpigmented skin lesions at this site.”
