Characteristics and pathogenesis of Koebner phenomenon

Abstract

The Koebner phenomenon, also known as isomorphic reaction, refers to the development of secondary lesions with the same clinical manifestations and histopathological characteristics as the primary lesions in normal skin after trauma or other stimuli. The triggering factors of Koebner phenomenon include physical trauma, chemical stimulation, mechanical stress, iatrogenic stimulation and pathogenic infection. Vitiligo, psoriasis and lichen planus are considered true Koebner phenomenon. Recent studies have shown that immunological disorders, oxidative stress, defective melanocyte adhesion and growth factor deficiency are the main pathological mechanisms of vitiligo Koebner phenomenon. In psoriasis, triggers may drive skin inflammation to induce a psoriatic phenotype through multiple signalling pathways and thereby cause Koebner phenomenon in susceptible individuals. Significantly, keratinocytes mediate the occurrence of Koebner phenomenon in psoriasis through mechano‐induced signalling pathways after sensing mechanical signals and explains the high frequency of psoriasis lesions on the extensor side of the elbow and knee joints. On the contrary, TRPA1‐driven mechano‐transduction, autoimmunity and actinic damage are the underlying mechanisms of Koebner phenomenon in lichen planus. In this review, we have summarized the current understanding of the characteristics and pathogenesis of Koebner phenomenon.

Clinicopathologic Overlap of Vulvar Psoriasis and Candidiasis

“…23 The vulva is exposed to numerous koebnerizing events to include minor surgery, sexual friction, hair management, and contact dermatitis. 23,24 A subtype of koebnerization is the Wolf isotopic response, defined as the appearance of a new dermatosis in the same place as an unrelated lesion, initially described as infections or immune disorders within resolving herpes zoster. 25 The tricolor vulva of psoriasis superimposed on vitiligo may represent a Wolf response.…”

“…The Koebner phenomenon describes initiation or provocation of skin conditions in an injured area of previously healthy skin, first described in psoriasis but also documented in LS, LP, and vitiligo 23 . The vulva is exposed to numerous koebnerizing events to include minor surgery, sexual friction, hair management, and contact dermatitis 23,24 .…”

“…The Koebner phenomenon describes initiation or provocation of skin conditions in an injured area of previously healthy skin, first described in psoriasis but also documented in LS, LP, and vitiligo 23 . The vulva is exposed to numerous koebnerizing events to include minor surgery, sexual friction, hair management, and contact dermatitis 23,24 . A subtype of koebnerization is the Wolf isotopic response, defined as the appearance of a new dermatosis in the same place as an unrelated lesion, initially described as infections or immune disorders within resolving herpes zoster 25 .…”

Acquired diffuse palmoplantar erythema with keratoderma in Chinese patients with pustular psoriasis: A predictor for IL36 receptor antagonist c.115+6T>C mutation?

“…5,28 Trauma is also a known trigger of both palmoplantar psoriasis and ACH. 29,30 IL36 is involved in epidermal inflammation underlying Koebnerization, 31,32 and is up-regulated following mechanical stimulation in a variety of tissues. 33,34 In murine models, transgenic IL36α expression resulted in epidermal hyperplasia and hyperkeratosis, 35 which were further aggravated in Il36rn −/− mice, an established animal model of DITRA.…”

Downregulation of Semaphorin 4A in keratinocytes reflects the features of non-lesional psoriasis

“…While the infiltration of immune cells into skin plays a critical role in the development of psoriasis, as evidenced by interleukin (IL) -23/IL-17 axis (Fitch, Harper, Skorcheva, Kurtz, & Blauvelt, 2007; Hawkes, Yan, Chan, & Krueger, 2018; Kim & Krueger, 2017), recent studies have revealed that cells constructing skin structure, such as keratinocytes, fibroblasts, and endothelial cells, also play pivotal roles in the development (Heidenreich, Röcken, & Ghoreschi, 2009; Lowes, Russell, Martin, Towne, & Krueger, 2013; Zhang et al, 2023) and maintenance (Arasa et al, 2019; Francis et al, 2024; Li et al, 2023; Ma et al, 2023; Tan et al, 2015; Zhu et al, 2020) of psoriasis. Among these cells, keratinocytes function as a barrier and produce cytokines, chemokines, and antimicrobial peptides against foreign stimuli, resulting in the activation of immune cells (Ni & Lai, 2020; Zhou, Chen, Cui, Shi, & Guo, 2022).…”