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Disorders of Pigmentation
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Michael Joseph Lavery, Charles Cathcart, Hasan Aksoy
Melanin synthesis is controlled by the melanocyte-stimulating hormone (MSH), which is derived from propiomelanocortin (POMC). POMC is also the precursor for adrenocorticotropic hormone (ACTH), which is raised in Addison’s disease. This accounts for the cutaneous hyperpigmentation seen in this condition. Once synthesized, melanin is then packaged into melanosomes and transported to neighboring keratinocytes.
Comparative Anatomy, Physiology, and Biochemistry of Mammalian Skin
Published in David W. Hobson, Dermal and Ocular Toxicology, 2020
Little is known about melanosome transfer from the melanocyte to neighboring keratinocytes. The melanosomes migrate to the dendritic processes of the melanocyte, which then become pinched off and transferred to the keratinocyte. The area of contact between the keratinocyte and dendritic processes of the melanocyte undulates in vitro. This undulation of the membrane has been attributed to intracellular microfilaments.101 Studies in vitro have demonstrated pigment transfer. When the fungal metabolite cytochalasin B is added to the culture medium, melanocytes shrink, undulations of the keratinocyte membrane cease, and microfilaments disappear. However, the attachment site between melanocytes and keratinocytes remains intact, while desmosomal attachments between keratinocytes split apart. This indicates that the melanocyte-keratinocyte attachment is stable and can withstand the tension, which the keratinocyte-keratinocyte desmosome attachment cannot. Other organelles are not affected by cytochalasin B treatment. The effects of cytochalasin B on microfilaments are reversible 1 h after removal of the drug.90
Exploring the Plant Kingdom for Sources of Skincare Cosmeceuticals
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Mayuri Napagoda, Sanjeeva Witharana
Skin color is primarily determined by the amount of melanin present in the skin. Melanin is a pigment produced by melanocytes through a process known as melanogenesis, from which the amino acid L-tyrosine gets converted by the enzyme tyrosinase into dopaquinone (Cooksey et al. 1997). Although melanogenesis and skin pigmentation are considered as natural photoprotective approaches in response to UV-induced skin photocarcinogenesis, the increased melanin synthesis and accumulation of these pigments give rise to many aesthetic and dermatological problems, such as melasma, periorbital hyperpigmentation, freckles, or lentigines (Smit et al. 2009, Zolghadri et al. 2019). Pigmentation is either dependent on the number, size, composition, and distribution of melanocytes, or activity of melanogenic enzymes. Furthermore, cutaneous pigmentation is resulted from melanin synthesis by melanocytes and transfer of melanosome to keratinocytes (Lin et al. 2008).
Periocular invasive melanoma manifestation in a patient using bimatoprost: case report and literature review
Published in Orbit, 2023
Adam P. Deveau, Flávia Nagel da Silva, Thai Yen Ly, Ahsen Hussain
PGF2a analogs appear to only affect aspects of melanogenesis but not melanocyte proliferation. In one study, a skin biopsy of a patient from bimatoprost-induced hyperpigmentation was analyzed by electron microscopy.42 This demonstrated a variable abundance of mature melanosomes in melanocytes and basal keratinocytes suggesting an increase in melanogenesis, yet there was no indication of an increased melanocyte cell number. Another study showed that in vitro treatment of melanocytes with latanoprost did not elicit a proliferative effect on the cells.29 Lastly, latanoprost has not been shown to increase the mitotic index of human cutaneous melanoma cells.43 Taken together, PGF2a analogs appear to increase melanogenesis through an increased expression of tyrosinase and possibly post-inflammatory processes; however, this does not help to determine why the frequency of patients with hyperpigmentation is so variable.
Development of piperine nanoemulsions: an alternative topical application for hypopigmentation
Published in Drug Development and Industrial Pharmacy, 2022
Burcu Ozkan, Ebru Altuntas, Rabia Cakir Koc, Yasemin Budama-Kilinc
Melanin biosynthesis is a complex mechanism that occurs within melanocytes, very specialized pigment cells within membrane-bound organelles called melanosomes [1]. Melanogenesis has different stages, and when this process is disrupted, different types of pigmentation disorders can be seen, classified as hypo- or hyperpigmentation [2,3]. Melanocytes are largely destroyed in hypopigmentation disorders such as vitiligo due to the loss of functional epidermal melanocytes. Therefore, depigmented lesions occur on the skin [4]. Vitiligo is a common disease affecting 0.5–2% of the general population. This bothersome disease begins on average at the age of 20 but is most common between the ages of 10 and 30 [5]. This apparent disorder can lead to many psychological, social and physiological problems in individuals [6].
Postinflammatory hypopigmentation: a comprehensive review of treatments
Published in Journal of Dermatological Treatment, 2022
Pamela N. Madu, Nicole Syder, Nada Elbuluk
Postinflammatory hypopigmentation occurs secondary to an intrinsic or external insult to the skin. A thorough clinical history is essential to diagnosing this condition and identifying the underlying cause. The pathogenesis of PIH has not been fully elucidated. Proposed mechanisms include decreased melanin production, blocked transfer of melanosomes to keratinocytes, and melanocyte loss (14). Histopathological studies suggest that suppression of melanogenesis serves a primary role in postinflammatory hypopigmentation as opposed to melanocyte loss (1,14). In a theory known as ‘individual chromatic tendency’, Ruiz et al. proposed a genetic predisposition toward hyperpigmentation or hypopigmentation through the inheritance of ‘strong’ and ‘weak’ melanocytes, respectively (15). They purport that ‘weak’ melanocytes are easily damaged in response to inflammation leading to hypopigmentation, and ‘strong’ melanocytes are more likely to respond with hyperpigmentation (15). Since the emergence of this theory, there have been no countering theories or additional studies to evaluate this hypothesis further.