Keloids are the result of aberrant tissue scarring typically occurring in injured skin, and are caused by the overgrowth of granulation tissue or collagen type III during the healing process. There is a genetic component, thus a predisposition can be genetically transmitted. Keloids are difficult to treat because of their postexcisional recurrence, and they have an impact on patient quality of life due to psychological distress caused by cosmetic concerns and functional disability. Treatment ranges from classic corticosteroid therapy to multimodal approaches such as injections, cryotherapy, laser, radiation, radiofrequency ablation and extracorporeal shockwave therapy. Recent discoveries into the pathogenesis of keloid have enabled clinicians to expand the therapeutic options for treatment. The aim of this paper was to review the literature, clarify the general concept of keloid development, and assess emerging treatment options such as stem cell therapy, mitomycin C, bleomycin, interferon, botulinum toxin type A, calcium channel blockers, angiotensin-converting enzyme inhibitors and fat grafting, and the evolutionary advancement towards epigenetic modifications and gene therapy.

<b><i>Background:</i></b> In the world scientific tradition, skin color is the primary physical characteristic used to divide humans into groups. Human skin has a wide range of tones and colors, which can be seen in a wide range of demographic populations. Many factors influence the color of people’s skin, but the pigment melanin is by far the most important. Melanin is produced by cells called melanocytes in the skin and is the primary determinant of skin color in people with darker skin. Indeed, &#x3e;150 genes have now been identified as having a direct or indirect effect on skin color. Vitamin D has recently been discovered to regulate cellular proliferation and differentiation in a variety of tissues, including the skin. The mechanisms through which the active vitamin D metabolite 1,25 dihydroxyvitamin D3 (or calcitriol) affects keratinocyte development are numerous and overlap with the mechanisms by which calcium influences keratinocyte differentiation. Ultraviolet (UV) is the most major modifiable risk factor for skin cancer and many other environmental-influenced skin disorders when it is abundant in the environment. Although the UV component of sunlight is known to cause skin damage, few researches have looked at the impact of non-UV solar radiation on skin physiology in terms of inflammation, and there is less information on the role of visible light in pigmentation. <b><i>Summary:</i></b> The quantity and quality of melanin are regulating by the expression of genes. The enzyme tyrosinase is primarily responsible for the genetic mechanism that controls human skin color. Genetics determines constitutive skin color, which is reinforced by facultative melanogenesis and tanning reactions. High quantities of melanin and melanogenic substances are typically accepted in darker skin to protect against UV radiation-induced molecular damage. Previous research has proposed that skin color variation is caused by a dynamic genetic mechanism, contributing to our understanding of how population demographic history and natural selection shape human genetic and phenotypic diversity. However, the most significant ethnic skin color difference is determined by melanin content. This current review aimed to assess the influence of skin color variations in skin structure and functions as well as difference in dermatological disease patterns. Also, this article reviewed several cases of skin color adaptation in different populations. <b><i>Key Messages:</i></b> Skin color impacts the composition and activity. Therefore, the contrast of dermatological ailments between distinct race-related categories is remarkable. Skin color adaptation is a challenging procedure. Refinement of skin color is an age-old craving of humans with ever-evolving drifts.

Botulinum toxin (BoNT) is a neurotoxin produced by the Clostridium botulinum bacterium with a well-known efficacy and safety profile in the focal idiopathic hyperhidrosis treatment. BoNT comprises seven different neurotoxins; however, only toxins A and B are clinically employed. BoNT is lately practiced in off-label therapies for a variety of skin diseases. Scar prevention, hyperhidrosis, rhytides, eccrine nevus, alopecia, psoriasis, Darier disease, bullous skin disease, pompholyx and Raynaud’s phenomenon are some of the novel indications for BoNT in cosmetic and notably non-cosmetic aspects of dermatology. To employ BoNT correctly in clinical practice, we must have a thorough understanding of the functional anatomy of the mimetic muscles. An intensive literature search was conducted to update all dermatology-oriented experiments and clinical trials on the described element of BoNT for this general overview of BoNT use in dermatology. This review aims to analyse the role of BoNT in dermatology and cosmetology.

Basal cell carcinoma (BCC) is the most common, accounting for 80-90% of skin cancers. It arises from the basal layer of the epidermis and its appendages. A complex interplay of environmental, phenotypic and genetic variables leads to the development of BCC. Literature has documented several clinical subtypes of BCC, the most common of which are nodular, superficial and morpheaform. Expeditious diagnosis and analysis are essential for improving the outcome of BCC. Preventive measures, particularly when implemented in childhood and adolescence, may play a critical role. Due to its low metastatic potential, treatment for BCC mostly focuses on local management. The standard treatment of basal cell carcinoma involved complete removal of the lesion by excision or Mohs surgery. In special circumstances, basal cell carcinoma can be treated with cryosurgery, electrodesiccation and curettage, topical medications and photodynamic therapy. This review aimed to evaluate the contemporary diagnosis and management of basal cell carcinoma.

Lentigo maligna (LM), also known as Hutchinson’s melanotic freckle, is a form of in situ melanoma characterized by the proliferation of atypical melanocytes along the basal epidermis in sun-damaged skin. If left untreated, LM will progress to lentigo maligna melanoma (LMM), a form of invasive melanoma with the same prognosis as other forms of invasive melanoma. LM is more common in the elderly, with a peak occurrence between the ages of 65 and 80 years. LM, however, is rarely present on the trunk and extremities. The diagnosis of LM, confirmed by histopathological and biopsy examination, is based on clinical and dermoscopic features. It typically begins as a tan-brown macule or patch, but it can progress to a variegated pigmentation with dark black color or even amelanotic characteristics. The risk factors involved in the LM development include a history of sunburns, lighter skin types, advanced age, history of nonmelanoma skin cancers, and tendency to form solar lentigines. This article explains the clinical presentation of LM, also reviews the available information on the diagnosis and management of LM, and discusses the potential of such information in facilitating the future prospective.