Histopathological changes in the skin in various subtypes of actinic keratosis

BACKGROUND: Actinic keratosis is a precancerous skin condition caused by prolonged exposure to sunlight. Despite existing clinical and dermatoscopic diagnosis techniques, morphological examinations of skin biopsy samples remain the gold standard for preventing the progression of actinic keratosis to squamous cell carcinoma. Histopathological characteristics of various subtypes of actinic keratosis are essential for early diagnosis and assessing the risk of malignant transformation.

AIM: The work aimed to assess histopathological changes in the skin in various subtypes of actinic keratosis.

METHODS: The cross-sectional study included 90 patients (50 women and 40 men) with various clinical types of actinic keratosis aged 45–80 years. All patients had a diagnostic skin biopsy followed by a histological examination. The samples were classified into six subtypes: hypertrophic (n = 45), bowenoid (n = 20), atrophic (n = 15), lichenoid (n = 5), proliferative (n = 3), and acantholytic (n = 2). Morphological changes in the epidermis and dermis were assessed, including hyperkeratosis, acanthosis, dysplasia, atypical keratinocytes, pathologic mitoses, and inflammatory infiltrates.

RESULTS: The hypertrophic and bowenoid subtypes were the most common, whereas the acantholytic subtype was the least common. The hypertrophic subtype was characterized by hyperkeratosis and acanthosis, with dysplasia reported in some cases (KIN II–III). The bowenoid subtype was associated with significant cell polymorphism, numerous pathologic mitoses, and atypical keratinocytes in the basal and spinous layers. The atrophic subtype showed severe dysplasia and epidermal atrophy. The lichenoid subtype was characterized by local spongiosis and lichenoid infiltrate. The proliferative subtype demonstrated downward growth and dysplasia in the lower epidermis. The acantholytic subtype showed signs of suprabasal splitting and acantholysis. The dermis showed solar elastosis and basophilic degeneration of collagen, as well as perivascular and interstitial infiltration, primarily lymphocytic, in all cases.

CONCLUSION: The identified changes define several pathognomonic signs of actinic keratosis, including epidermal dysplasia, atypical keratinocytes, pathologic mitoses, and impaired stratification. Reactive changes (acanthosis, hypergranulosis, atrophy) should be considered non-specific. The histopathological classification of actinic keratosis is critical for assessing the risk of progression to squamous cell carcinoma and selecting treatment strategy.