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Tenascin expression in actinic keratosis.

BACKGROUND: Tenascin is an extracellular matrix protein frequently expressed around neoplastic and non-neoplastic lesions of the skin. Actinic keratoses (AKs) are intraepidermal neoplastic lesions of the sun-exposed skin. They are classified according to the extension of dysplasia in four stages; they also present different histological varieties. METHODS: We performed an immunohistochemical study using tenascin monoclonal antibody diluted 1 : 50 on 150 cases of AKs classified, respectively, in histotypes (38 hypertrophic, 18 atrophic, 21 bowenoid, 19 acantolytic, and 40 mixed) and in stages (27 stage I, 46 stage II, 42 stage III, and 35 stage IV; 14 in tumoral progression). RESULTS: Tenascin positivity was observed in all cases at the dermal level close to the epithelial lesion. The intensity of reaction increased from stage I to stage IV and, of course, also in tumoral progression. Its expression was not related to the histotypes. In very few cases, the atypical keratinocytes were positive. CONCLUSIONS: Tenascin expression in AKs is related to the stages of dysplasia. In fact, the immunostaining intensity corresponds to the degree of the dysplasia rather than the thickness of the involved epidermis. Tenascin plays a role in neoplastic progression working as an anti-adhesive factor.

Actins↗

A retrospective study of the effect of long-term topical application of retinaldehyde (0.05%) on the development of actinic keratosis.

BACKGROUND: The role of topical retinoids on photocarcinogenesis is still unclear. Retinaldehyde is a natural metabolite of vitamin A used as a cosmetic product. Its effect on actinic keratoses has not been studied to date. OBJECTIVE: To study the incidence of actinic keratoses during long-term application of retinaldehyde in order to evaluate a possible chemoprophylactic effect. METHODS: We conducted a retrospective study on 61 patients who had applied retinaldehyde on photoexposed body areas for a period ranging from 6 to 142 months. We counted the total number of actinic keratoses and cutaneous tumors that appeared over the time of exposure to retinaldehyde. RESULTS: The epidemiological characteristics of actinic keratoses were not modified by the application of retinaldehyde. Irregular application as compared to regular application of retinaldehyde was not associated with a change in the risk of actinic keratoses, suggesting that continuous use is not associated per se with a higher risk of actinic keratoses. CONCLUSION: With the statistical power limitation of this study, retinaldehyde applied alone does not appear to have prophylactic effects on the development of actinic keratoses. The design adopted is feasible to study the safety of cosmetic products applied for a long period of time.

Administration, Topical↗

Actinic keratosis: the key event in the evolution from photoaged skin to squamous cell carcinoma. Therapy based on pathogenetic and clinical aspects.

Skin aging is the result of intrinsic and extrinsic factors. Extrinsic aging, also called photoaging, is mainly caused by ultraviolet radiation from the sun and leads to a state which has been termed dermatoheliosis. The aim of this article is to provide an overview of photoaged skin addressing actinic keratoses (AKs) in particular. This review will describe the clinical features of photoaged skin and briefly summarize the underlying histological, photobiochemical and molecular mechanisms responsible for photoaging. The concept of the disease continuum from AK to squamous cell carcinoma will also be presented. A special focus will be on established and new therapeutic approaches to undo photoinduced skin damage.

Carcinoma, Squamous Cell↗