Definition
The term actinic keratosis describes a precancerous stage of skin cancer (precancerosis) that requires treatment and is triggered by chronic exposure to sunlight (UV light). It is the proliferation of atypical skin cells (keratinocytes) in the area between the dermis and the epidermis, which manifests itself as a cornification disorder. The keratosis can later develop into a squamous cell carcinoma.
Light-skinned, blue-eyed people (people with skin types I and II) with a permanently high sun exposure have a significantly increased risk of developing actinic keratosis. In contrast, dark pigmented people have hardly any risk of developing actinic keratosis. Men are more frequently affected by the disease than women.
Occupational groups such as seafarers, road, construction and agricultural workers are particularly susceptible because of the long exposure to the sun. According to an American study, the relative frequency of cases of illness (prevalence) among the over 20-year-olds is 11 % and 25 % among the over 30-year-olds. A British study found a 15% risk for those over 40.
Up to 10 million people are affected by actinic keratosis. In Australia, on the other hand, the prevalence of actinic keratosis in the over-40s is as high as 45%. In addition, the number of new cases (incidence) in Europe has risen significantly in recent decades due to the increasing frequency of travel to countries with higher UV radiation exposure and longer exposure to the sun for leisure activities, as well as higher environmental UV radiation.
As a result, the term senile keratosis is somewhat outdated, since nowadays many young people also fall ill, for example, who spend too much time in the sun or go to a solarium. People who are exposed to a permanent suppression of the immune system (immunosuppression), as is the case after an organ transplant, for example, also have a significantly increased risk of contracting the disease. But also diseases like albinism, Rothmund-Thomson syndrome, Cockayne syndrome.
Xeroderma pigmentosum and Bloom syndrome represent a genetic predisposition to the development of actinic keratoses. Permanent changes (mutations) caused by UVB rays develop after 10 to 20 years on chronically light-exposed skin cell clones of abnormal (atypical) cells that show irreversible damage to their DNA (genetic material). These mutated cells slowly penetrate the normal epidermis and lead to the loss of proper skin stratification and cornification disorders.
The actual repair system of the skin cannot prevent the formation of the pathologically altered skin cells under permanent sunlight or high UV radiation. Affected by these mutations are the so-called telomerase gene and the tumor suppressor gene TP53. These genes are proteins that control the cell cycle or trigger the death of atypical cells (apoptosis).
If their function is switched off by changes in the genetic material (mutations), the malignant cells can develop. Furthermore, the changes can also spread to the tissue under the epidermis, the dermis. If the basement membrane between the epidermis and the dermis is breached, this is known as an invasive tumour, an invasive squamous cell carcinoma, which develops in 5-10% of patients.
Thus, actinic keratosis represents an initial stage of cancer (carcinoma in situ). But not only the UVB rays of the sun with 280-320nm length can cause actinic keratosis. Forms of electromagnetic radiation such as UVA light, as used in the therapy of psoriasis, ionising radiation or infrared radiation can also trigger the disease.
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