Lentigo Senilis

Cawley, Edward P.

doi:10.1001/archderm.1950.01530180024005

Cited by 21 publications

(13 citation statements)

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“…In a systematic comparison of lesional and perilesional histopathologic changes, we confi rmed the typical features of SL already noted by others [1,4,5] . Our investigation confi rms the opinion of Montagna et al [6] that 'the complex and distinctive architecture of SL is probably the result of concurrent proliferation of melanocytes and keratinocytes', but is also associated with a weakening of the dermal-epidermal junction ultrastructure.…”

Section: Discussionsupporting

confidence: 86%

Skin Ultrastructure in Senile Lentigo

Noblesse¹,

Nizard²,

Cario‐André

et al. 2006

Skin Pharmacol Physiol

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Senile lentigo is a common component of photoaged skin. It is characterized by hyperpigmented macules which affect chronically irradiated skin mostly after the age of 50. This study was undertaken to assess the morphology of senile lentigo on the dorsum of the hands. A systematic comparison between lesional and perilesional skin using histology and transmission electron microscopy was done to determine whether melanocytes or keratinocytes are affected in the evolution of lesions and which tissue structure is modified. The histology study showed that lesional skin is characterized by a hyperpigmented basal layer and an elongation of the rete ridges, which seem to drive deeply into the dermis. The epidermis contained clusters of keratinocytes, which retained and accumulated the melanin pigment. Electron microscopy studies showed important modifications in the lesional skin ultrastructure in comparison with perilesional skin. In melanocytes from perilesional and lesional skin, we observed normal size melanosomes at all stages of maturation in the cytoplasm and in migration within dendrites. No pigment accumulation was observed. However, the morphology of melanocytes in lesional skin revealed an activated status with numerous mitochondria and a well-developed endoplasmic reticulum, which could reflect intense protein synthesis. In basal keratinocytes from lesional skin, we observed numerous melanosome complexes called polymelanosomes, which formed massive caps on the nuclei. Observations in colored semi-thin sections also revealed perturbed structures in the basal layer region, which could explain the skin perturbation. Indeed, we observed keratinocytes that presented important microinvaginations and pendulum melanocytes, which sank into the dermis, beneath the basal layer of keratinocytes. These cell modifications seemed to be due to a perturbation of the dermal-epidermal junction, which appeared disorganized and disrupted and could directly disturb the basal support of the cells.

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Section: Discussionsupporting

confidence: 86%

Skin Ultrastructure in Senile Lentigo

Noblesse¹,

Nizard²,

Cario‐André

et al. 2006

Skin Pharmacol Physiol

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“…Besides an increase of melanin in the basal and, to a lesser extent, suprabasal layers of this epithelium, which is the basis for the clinical occurrence of SL, elongated rete ridges have been described by most authors. [1][2][3][4]10 The morphology of our samples was mostly in accordance with these findings confirming the clinical diagnosis histologically. The overall degree of rete ridge elongation, as quantified by the BM/E ratio, showed considerable overlap between perilesional and lesional skin (Fig.…”

Section: Discussionsupporting

confidence: 84%

“…Bar ¼ 100 lm (a-d). lesions compared with unaffected skin, as has been described elsewhere 2,4 (Fig. 2a-d).…”

Section: Analysis Of Epidermal Pigmentationsupporting

confidence: 65%

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Alterations in the epidermal-dermal melanin axis and factor XIIIa melanophages in senile lentigo and ageing skin

Unver¹,

Freyschmidt‐Paul²,

Hörster³

et al. 2006

British Journal of Dermatology

101

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“…The senile lentigo, consists of a localized proliferation of melanocytes at the dermoepidermal junction (20). In general, however, the number of dopa-positive melanocytes in both exposed and unexposed skin decreases in old age, though their size increases.…”

Section: E P L D E R M L Smentioning

confidence: 99%

Physiological background to skin ageing

Ebling

1982

Intern J of Cosmetic Sci

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Synopsis Ageing and ultimate death, when survival offers no reproductive advantages to the species, are essential to the evolutionary process. Yet the prolongation of youth has always been a human dream. The prevention of ageing in visible areas of skin is desirable not for physiological but for social reasons; the skin proclaims our sexuality and asserts our social image. Has the aspiration any hope of success? Ageing of the skin involves changes in the dermis, epidermis, pigment cells, hair follicles, sebaceous and sweat glands, and sense organs. Some of these changes appear intrinsic to the organs concerned; some are dependent on hormonal and other systemic mechanisms; some involve environmental factors such as radiation. If changes of the first type appear to be inevitable, those of the second may be modifiable, and those of the third may, to some extent, be preventable.

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Lentigo Senilis

Cited by 21 publications

References 0 publications

Skin Ultrastructure in Senile Lentigo

Skin Ultrastructure in Senile Lentigo

Alterations in the epidermal-dermal melanin axis and factor XIIIa melanophages in senile lentigo and ageing skin

Physiological background to skin ageing

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