Postinflammatory hypopigmentation is a common cause of acquired hypopigmentary disorders. It can be a result of cutaneous inflammation, injury or dermatological treatment. There are also many specific conditions that present with hypopigmentation other than postinflammatory hypopigmentation. Most cases of postinflammatory hypopigmentation improve spontaneously within weeks or months if the primary cause is ceased; however, it can be permanent if there is complete destruction of melanocytes. This article reviews the aetiology, pathogenesis, clinical features, differential diagnosis and therapeutic options for postinflammatory hypopigmentation.

Background: Melasma is a complex and multipathophysiological condition that is challenging to treat. The roles of each element in the dermis were highlighted in this recent year due to targeting it with emerging therapies. Although some studies have demonstrated abnormal findings in the dermis of melasma lesions, there are no integrated data regarding these findings. Purpose: This article aims to discuss each finding in the dermis of melasma lesions and to provide some ideas about treatment options. Methods: An Internet search was completed using the MEDLINE, Embase, Scopus, and Google Scholar databases for relevant literature through June 2021 and reference lists of respective articles. Only the articles published in English language were included. Results: Several studies have focused on the dermal changes in melasma. Common findings included basement membrane disruption, pendulous melanocytes, marked solar elastosis, increased melanophages, increased mast cells, and neovascularization. In addition, each of them had the specified mechanism that may relate with the others. Conclusion: Several changes in the dermis of melasma lesion may be connected with pathological changes in the epidermis. This may serve as a potential target treatment for melasma, which requires a multimodal approach.