If you have spent years in the Australian sun, there is a very real chance you will develop actinic keratoses at some point in your life. I see them every single day in clinic. Sometimes they are obvious. Sometimes they are subtle. Often, there are far more damaged cells beneath the surface than what you can see in the mirror.

Actinic keratosis, also called solar keratosis, is not skin cancer. But it sits uncomfortably close to it. These are sun damaged cells with abnormal DNA that have the potential, over time, to progress to squamous cell carcinoma. That risk is why I take them seriously and why treatment choice matters.

This article is not a textbook summary. It is how I personally think about actinic keratosis and how I choose treatments for my own patients, based on experience, evidence, and long term skin outcomes.

First, a principle that guides everything I do

Sun damage is rarely isolated to a single spot. If you can see one actinic keratosis, there are almost always many more damaged cells nearby that have not yet declared themselves. This is why I strongly favour field treatments rather than spot treatments. Treat the whole area, not just the visible lesion, and let the treatment identify and target damaged cells for you. This philosophy influences my view on every treatment option below.

Liquid nitrogen freezing

Why I rarely use it

Liquid nitrogen cryotherapy is still widely used. It is fast and it is cheap. But I am not a fan, especially on the face. Freezing is indiscriminate. Good cells and damaged cells are destroyed equally. You are essentially burning tissue with cold, and precision is limited. There are three common problems I see. The freeze is not deep enough and abnormal cells survive. The freeze is too deep and causes permanent hypopigmentation. The surrounding healthy skin is unnecessarily damaged. That white scar you sometimes see after freezing is not rare in my world. It is permanent. For that reason alone, I avoid cryotherapy on cosmetically sensitive areas wherever possible. I still use liquid nitrogen in very limited circumstances, usually for isolated lesions in low risk areas. But it is not my go to treatment, and it never will be.

Surgical excision

Not appropriate for actinic keratosis

Excision has a role in skin cancer. It does not have a role in solar keratosis. Actinic keratosis is a field disease. Cutting out individual spots does nothing to address the surrounding sun damaged skin and exposes patients to unnecessary scarring. I do not excise actinic keratoses.

Photodynamic therapy

An excellent option if time allows

Photodynamic therapy, or PDT, is one of my favourite in clinic treatments. It works by applying a photosensitising agent to the skin, allowing it to preferentially absorb into damaged cells, and then activating it with a specific light source. The result is targeted destruction of abnormal cells while largely sparing healthy skin. The advantages are clear. Excellent cosmetic outcomes. True field treatment. Shorter visible downtime compared to some topical options. The trade off is cost and clinic time. PDT requires equipment, trained staff, and scheduled appointments. Time equals money, both for the clinic and the patient. For many patients, especially those who want effective treatment with controlled downtime, PDT is an outstanding option.

Efudix on its own

Effective but not for everyone

Efudix, which contains 5 fluorouracil, is a very effective topical treatment. It selectively targets rapidly dividing abnormal cells and causes a visible inflammatory reaction where sun damage exists. I use Efudix sparingly as a standalone treatment. It works, but patients need to be prepared. Treatment courses are longer, the reaction can be intense, and social downtime is real. Redness, crusting, and discomfort are part of the process. The major advantage is cost. Efudix is inexpensive and accessible. For patients with time on their hands and no upcoming social commitments, it can be a very good option.

Efudix combined with calcipotriol

My preferred topical treatment right now

This combination is currently my preferred topical approach for many patients. Efudix combined with calcipotriol enhances the immune response to sun damaged cells and allows for much shorter treatment courses. In many cases, around one week is sufficient, although shorter courses may also be appropriate depending on the individual. This combination is well researched and widely used internationally. At present, it is not formally recognised by Australian authorities for solar keratosis treatment. That will change. The data is there, and clinical practice has already moved ahead of regulation. The benefits are compelling. Short treatment duration. Strong efficacy. Field based treatment. Lower cost compared to in clinic procedures. When patients ask me what topical option I would choose for myself, this is usually the answer.

Oral nicotinamide

An important adjunct, not a replacement

In patients with significant sun damage or recurrent actinic keratoses, I often recommend high dose oral nicotinamide as an adjunct to procedural and topical treatments. Nicotinamide is a form of vitamin B3 that plays a key role in cellular energy metabolism and DNA repair. Ultraviolet radiation depletes energy within skin cells, impairing their ability to repair DNA damage. Nicotinamide helps restore this energy balance and supports normal DNA repair pathways. Well conducted clinical studies have shown that high dose oral nicotinamide can reduce the number of new actinic keratoses and lower rates of certain non melanoma skin cancers in high risk individuals when taken consistently. It is important to be clear about its role. Nicotinamide does not treat existing lesions on its own. It does not replace topical therapies, photodynamic therapy, or appropriate procedural treatment. Where it adds value is in reducing ongoing damage and recurrence, working quietly in the background while other treatments do the heavy lifting. For patients with chronic sun damage, I see nicotinamide as part of a long term skin health strategy rather than a short term fix.

A note on spot treating

Why I discourage it

I rarely encourage spot treatment for actinic keratosis. The strength of topical therapies is that you do not need to know where all the damage is. You treat the entire field, whether that is the face, scalp, or forearms, and allow the medication to identify abnormal cells. Damaged cells react. Healthy cells largely do not. This selective response is one of the most powerful advantages of field therapy and one that is often underappreciated.

Scarring risk

An important distinction

Scarring from topical treatments and PDT is rare. The treatment I associate most strongly with permanent scarring and pigment change is liquid nitrogen cryotherapy. This is another reason I avoid it, particularly on the face. When patients come to me concerned about cosmetic outcomes, this distinction matters.

Final thoughts

There is no single best treatment for actinic keratosis. The right option depends on the patient, the extent of sun damage, tolerance for downtime, cost considerations, and cosmetic priorities. What matters most is understanding that actinic keratosis is a marker of cumulative sun damage and future risk. Treating visible lesions is only part of the job. Addressing the field is where meaningful prevention happens. If you take one thing away from this article, let it be this. Think long term. Think whole skin, not single spots.

Medical disclaimer

This article provides general information only and does not constitute medical advice. It is not an exhaustive list of available treatments. Individual circumstances vary and treatment decisions should always be made in consultation with a qualified medical specialist who is familiar with your medical history and skin cancer risk.