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. The recognition that many other skin diseases, such as vitiligo, lichen planus, Darier disease, and bullous dermatoses also arise at sites of cutaneous injury, led to the extension of the definition and to the attachment of the term isomorphic response.
    Types of Koebner response: Variations in the definition of KP led Boyd and Nelder to classify KP into four different groups.
    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 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 breakdown and not tissue proliferation.
    3. Occasional lesions: Where the phenomenon meets some criteria for the Koebner response, such as Darier disease, erythema multiforme, granuloma annulare, and Behμet disease.
    4. Questionable trauma-induced processes: Includes all disorders noted in case reports that have a questionable connection to trauma, such as pemphigus vulgaris, discoid lupus erythematosus, lupus erythematosus, and eruptive xanthoma.
    Studies have shown that a patient who reacts to a known Koebner inducing stimulus would react to all stimuli. A lack of a positive response, on the other hand, would predict failure of inducing KP by all other stimuli. This was termed the ball or none phenomenon.
    The pathogenesis of the Koebner response in psoriasis and other disease is not well understood. Much research has been geared toward explaining this unique phenomenon and assisting in understanding the mechanism of the underlying diseases. Two steps may be essential in KP. A first nonspecific inflammatory step contributes to the production of many substances, including cytokines, stress proteins, adhesion molecules, or autoantigens translocated from intracellular areas. In the second step there may be disease-specific reactions, including by T cells, B cells, autoantibodies, and immune deposits under the restriction of genetic backgrounds.

Koebner现象

    Koebner现象(KP又称同形反应)，于1876年由德国皮肤科医生Heinrich Koebner最先描述。这种现象为：银屑病患者受到外伤（如抓伤、纹身和马咬伤）后在损伤部位可出现银屑病样皮损。由于许多皮肤病如：如白癜风，扁平苔癣，毛囊角化病，大疱性皮肤病在受到外伤的部位亦可出现这种现象，因此KP的概念得到了进一步的扩展。
    由于KP概念的变化，Boyd和Nelder把KP分为4类：
    1、真性KP：KP在所有患者中出现，可被各种损伤（不包括皮肤感染和过敏因素）诱发。疾病包括银屑病、扁平苔藓、白癜风等。
    2. 假性KP：KP现象与感染因素定植在皮损周边组织或创伤部位有关。如：寻常疣、传染性软疣等。
    3、偶发皮损：偶然发生的现象符合同形反应标准。如毛囊角化病、多形性红斑、环状肉芽肿、白塞病等。
    4、可疑KP：在个别报道的病例中发现可疑的外伤诱导皮疹发生的现象。如：寻常型天疱疮、盘状红斑狼疮、发疹性黄瘤等。
    研究显示：同形反应也存在“全”或“无”现象，即一种刺激能诱发同形反应，则其他刺激也可诱发同形反应；若一种刺激不能诱发, 那么其他刺激亦不能。
    KP的发病机制目前不是很清楚，但是许多研究已经为这种独特的现象进行逐步的解读，以便更好的了解某些疾病的发病机制，在KP的发病机理中有两个环节可能是重要的。第一，非特异的炎症反应产生了某些炎症介质，包括：细胞因子、应激蛋白、粘附分子或来自细胞内部的自身抗原；第二，可能和疾病特异反应相关，包括T-细胞、B-细胞、自身抗体和遗产背景下的免疫沉积。