Koebner Phenomenon

Issues of Concern

Underlying Pathophysiology

The underlying pathophysiology of this phenomenon remains unclear.[1][2] The current thought is that it is immune-mediated, involving cytokines and autoantigens, or disease-specific reactions, such as T-cell mediated reactions, keratinocyte proliferation, and angiogenesis in psoriasis.[2] Other theories suggest that it is a vascular process, as it appears the microvasculature in psoriatic patients exhibiting Koebnerization responds differently to trauma. Some believe that the papillary dermis must be involved to induce a Koebner response, suggesting injury to epidermal cells and dermal inflammation are required—other possible underlying mechanisms include enzymatic, neural, genetic, infectious, and hormonal. However, there is currently insufficient evidence to support any particular theory over another.[4]

Classification and Subtypes of the Koebner Phenomenon

Boyd and Nelder classified clinical entities with reported Koebnerization into 4 categories: true Koebnerization, pseudo-Koebnerization, occasional traumatic localization of lesions, and poor or questionable trauma-induced processes.[4] (table 1) 

The first group [category I], called true koebnerization, includes psoriasis, lichen planus, and vitiligo. In these 3 conditions, the Koebner phenomenon is reproducible in all patients by various insults. Boyd and Nelder argued that the term Koebner phenomenon should typically be reserved for this disease group.

The second group [category II], referred to as pseudo-koebnerization, includes diseases such as molluscum contagiosum and verruca vulgaris. The Koebner phenomenon is produced by the seeding of infectious agents along with sites subjected to trauma, usually from scratching.

The third group [category IIII],  occasional lesions, includes Darier disease and erythema multiforme, which meet some criteria for the Koebner phenomenon but not all. Finally, the fourth group [category IV], questionable trauma-induced process, includes all disorders with a dubious association with trauma, such as pemphigus vulgaris and lupus erythematosus.

Since this publication in 1990, other conditions have demonstrated the Koebner phenomenon, such as leukocytoclastic vasculitis, mycosis fungoides, and eruptive xanthomas, among others mentioned in this topic.[7][8][9]

Type and Severity of Trauma Inducing Koebner Phenomenon

Different types of cutaneous injury may trigger this phenomenon, including excoriations, tattoos, friction, trauma, surgical instrumentation, burns, and ultraviolet or irradiation (see Table. Cutaneous Injuries Associated With Koebnerization).[1][2] The Koebner phenomenon exhibits an “all or nothing” pattern of reactivity, where a patient who reacts to 1 traumatic stimulus is likely to react to all stimuli, and a patient who does not react to a traumatic stimulus is likely to be non-reactive to all other stimuli as well.[10][11] The severity of the response varies, as well. Severity can be classified into 4 grades: none, abortive (lesions vanish spontaneously after approximately 2 weeks), minimal (focal lesions around the area of trauma), and maximal (wide-spread lesions).[2]

Time from skin insult to the appearance of new skin lesions varies. In psoriasis, new lesions typically arise within 10 to 20 days after a skin injury; however, this ranges from 3 days to 20 years.[2] The latent period between traumatic insult to the uninvolved skin and Boyd and Nelder considered the appearance of new lesions to be 10 to 14 days on average. However, Koebner has suggested the variability of the duration ranges from just 3 days to up to several years.[4][12] This wide range suggests varying sensitivity for developing the Koebner phenomenon, which may be a unique characteristic of the patient's skin or the underlying disease process. Moreover, diseases such as vitiligo and psoriasis typically have a waxing-waning course and may develop over different intervals after several simultaneous insults in the same patient.[1]

Clinical Significance

The Koebner phenomenon is typically associated with preexisting skin disease. Clinical entities commonly displaying the Koebner phenomenon include psoriasis, vitiligo, and lichen planus.[1] The incidence of Koebnerization ranges broadly within these entities; estimates of the prevalence of the Koebner phenomenon are approximately 11 to 75% in psoriasis and 21 to 62% in vitiligo.[4][13]

Koebnerization may significantly impact patients with psoriasis, as any insult to their skin, including tattoos and injections, can cause their disease to flare.[1] One study found that many patients surveyed had developed psoriasis within a few weeks following the tattooing process.[14] A minority had psoriasis limited to the tattoo site, but a larger subset of patients exhibited generalized psoriasis after tattooing.[14] Because the Koebner phenomenon is not a unique disease process but rather activation of underlying cutaneous disease, managing lesions arising from Koebnerization depends on managing the primary disease. Relative to vitiligo, studies have found that the affected body surface area is significantly higher when Koebnerization is present.[15] The presence of Koebnerization in vitiligo also appears to correlate with higher disease activity within the past 12 months. Lower response to treatment also appears to occur in vitiligo patients who exhibited Koebnerization. This study concluded that Koebnerization might function as a clinical indicator of disease activity in vitiligo and serve as a predictor of treatment response.[15]

Nursing, Allied Health, and Interprofessional Team Interventions

Dermatologists often test for the Koebner phenomenon as part of a complete physical exam. However, by the time a patient reaches a dermatologist, it is almost certain that they received a referral from other providers because they have an underlying cutaneous disease. As a result, awareness of the Koebner phenomenon by other health professionals is likely to help patients faster diagnose and refer. Primary care providers and emergency medicine physicians may often be the first health care professionals to encounter a patient with cutaneous disease. It may be helpful for these specialties to incorporate testing for Koebnerization (with a scratch test) into their physical exam to aid in building their differential diagnosis. Additionally, nurses may be the first to notice when minimal trauma induces a cutaneous response in a patient (ie, a patient develops psoriasiform plaques along venipuncture sites or tape lines). Nurses may thus help the interprofessional team by reporting such findings.