Elsevier

Clinics in Dermatology

Volume 29, Issue 2, March–April 2011, Pages 231-236
Clinics in Dermatology

The Koebner phenomenon

https://doi.org/10.1016/j.clindermatol.2010.09.014Get rights and content

Abstract

The Koebner phenomenon is one of the most well-known entities in dermatology. It was first described by Heinrich Koebner in 1876 as the formation of psoriatic lesions in uninvolved skin of psoriatic patients after cutaneous trauma. This isomorphic phenomenon is now known to involve numerous diseases, among them vitiligo, lichen planus, and Darier disease. The pathogenesis of the Koebner phenomenon is still obscure but may involve cytokines, stress proteins, adhesion molecules, and autoantigens. This contribution reviews the clinical manifestations of Koebner phenomenon, its provocative factors, suggested pathogenesis mechanisms, and the various skin conditions that exhibit this unique response.

Introduction

The Koebner phenomenon (KP) was first described in 1876 by Heinrich Koebner, a German dermatologist who was the founder of the dermatology department at the University of Breslau. He reported the formation of psoriasiform lesions in uninvolved skin of psoriatic patients after cutaneous trauma, such as excoriations, tattoos, and horse bites.1

The recognition that many other skin diseases, such as vitiligo, lichen planus, Darier disease, and bullous dermatoses also arise at sites of cutaneous injury,2, 3, 4, 5 led to the extension of the definition and to the attachment of the term isomorphic (from Greek, “equal shape”) response. Today, the definition of KP has been extended even further to describe patients who did not have preexisting dermatosis before trauma or in whom the response did not reoccur on additional trauma.

Section snippets

Types of Koebner response

Variations in the definition of KP led Boyd and Nelder to classify KP into four different groups6:

  • 1.

    True koebnerization: Where the phenomenon is reproducible in all manner of patients, by a variety of insults, and not due to disbursement of external infective or allergic elements such as psoriasis, lichen planus (Figure 1), and vitiligo.

  • 2.

    Pseudo-koebnerization: Where the phenomenon is produced by seeding of an infectious agent to surrounding tissue (eg, verrucae, molluscum contagiosum) or by skin

Associated conditions

Table 1 lists the skin conditions exhibiting the Koebner response.7 KP has been studied most extensively in psoriasis, but the pathogenesis of this phenomenon is still obscure. KP occurs in approximately 25% of psoriatic patients after various traumatic insults, but these might be unrecognized or forgotten.6 Various environmental stress factors on the skin have provoked KP, including trauma, such as burns, friction, insect bites, and surgical incision, as well as allergic and irritant

Possible drug induction

Certain pharmacologic agents, such as lithium, β-adrenergic blockers, nonsteroidal antiinflammatory drugs, and local application of crude coal tar and anthralin, may exacerbate psoriasis and induce koebnerization by chemical interaction with genetically susceptible epidermal cells. Potential mechanisms include alteration of polymorphonuclear leucocyte chemotaxis, diminished or enhanced synthesis of arachidonic acid metabolites, changes in the cyclic nucleotide system, and modified lymphokine

Miscellaneous types

Topical application of white soft paraffin was reported to have an inhibitory action,38 probably due to the antimitotic effect that bland ointments have been shown to possess. In contrast, other topical application did not prove useful in preventing or inhibiting KP.9 These include transient applications of heat or cold, topical, or intradermal methotrexate, lidocaine, antimycin A, and colchicine.

Reverse koebnerization is defined as clearing of a psoriatic plaque after injury. One of the early

Conclusions

The Koebner response has been described in numerous diseases since its early recognition at the end of the 18th century. This response is important dermatologists and also for surgeons, who should be aware of this entity and its consequences. The pathogenesis of this unique phenomenon is not well understood and requires further investigation. Understanding the mechanism of KP may contribute to unveiling the pathogenesis of psoriasis and other underlining diseases.

Acknowledgment

Mrs Yael Sagi assisted in the preparation of the manuscript.

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