A Multifaceted Holistic Review of the Literature on Scar Dermatoses.

Table  1 Numerous dermatoses reported in the literature find their origin in, or preferentially spare, injured skin [ 7 ]. The pathogenesis behind these observations has been studied and further classified into several well‐described phenomena, namely Köbner phenomenon, Wolf's isotopic response, and Renbök phenomenon. Pathophysiologic phenomena underlying dermatoses in scars. The Köbner phenomenon is a longstanding observation that was coined in 1877 by Heinrich Köbner, initially described in patients with psoriasis who witnessed new psoriatic lesions appearing on the uninvolved skin following trauma [ 8 ]. It is known to demonstrate an ‘all or none’ event; arising on all or none of the injured cutaneous sites [ 9 ]. This reproducible phenomenon affects a multitude of dermatoses, of which psoriasis, vitiligo and lichen planus represent the most well‐described entities demonstrating true köbnerization as per the Boyd and Nelder classification [ 10 ]. It can be triggered by numerous cutaneous insults including burns, excoriations, tattoos and friction. From the Greek ‘equal shape’, it is also referred to as the isomorphic response since the newly formed lesions are clinically and histologically similar to the patient's known underlying dermatosis [ 11 ]. To note, the phenomenon can happen prior to the appearance of cutaneous disease and will thus alert the dermatologist of the potential development of the dermatosis [ 12 ]. It is important to differentiate it from pathergy, classically reported in Behçet's disease and pyoderma gangrenosum, where a non‐specific pustular or papular rash develops secondary to trauma [ 13 ]. The pathophysiology of köbnerization remains unclear. The current adopted assumption is that it is immune‐mediated with the involvement of cytokines, T‐cell mediated responses, proliferation of keratinocytes along with angiogenesis but there are other postulated hypotheses with insufficient evidence to support one over another. Some experts believe that both the epidermis and the dermis have to be affected by the injury to induce köbnerization [ 11 ]. As previously mentioned, vitiligo, a known entity exhibiting köbnerization, can affect scars. In fact, Eun et al. [ 14 ] report a case of a middle‐aged man with a long‐standing history of vitiligo who develops a new lesion confined to a 25‐year‐old keloid scar. It is hypothesized that the stretching tension present in the keloid might have disturbed the adhesions between melanocytes and keratinocytes favouring the growth of a new vitiliginous lesion. In addition, patients with vitiligo can have köbnerization affecting striae distentiae [ 15 ], defined as dermal scarring related to stretching instigating a form of blunt trauma to the dermis [ 16 ]. Along with defective melanocyte adhesion, 3 other pathogenic pathways are believed to explain köbnerization in vitiligo, which are innate immunologic disorders, enhanced oxidative stress response, and growth factor deficiency explained in Figures  1 , 2 , 3 , 4 [ 29 ]. Striae distentiae and gravidarum are also reported as potential targets for both psoriasis and lichen planus [ 30 ]. A patient with palmoplantar psoriasis demonstrated periocular köbnerization on an external dacryocystorhinostomy scar [ 9 ]. A possible pathophysiologic mechanism was described by Ji et al. [ 31 ] and is summarised in Figure  5 . Another example of Köbner phenomenon is described by Musumeci et al. in a patient with known hidradenitis suppurativa with disease progressing to affect a recent surgical scar [ 39 ]. Furthermore, köbnerization is observed in a young woman known to have systemic lupus erythematosus presenting with an eruption of biopsy‐confirmed cutaneous lupus localising to a dermatome previously affected by herpes zoster [ 40 ]. Lastly, an exceptional case of acute febrile neutrophilic dermatosis or Sweet's syndrome is described as a Köbner response to a scar [ 41 ]. ‘The first mechanism of Köbner phenomenon in vitiligo’ In non‐lesioned skin of patients with vitiligo, NK cells and innate lymphocytes (ILC1) are increased in comparison to that of normal skin of people without vitiligo. Trauma induces these cells to release interferon‐gamma (IFN‐gamma), which in turn stimulates keratinocytes to secrete CXCL10. CXCL10 binds CXCR3B on melanocytes which leads to their apoptosis and antigen release. Autoantigens are hence presented to CD8 T cells which stimulates the immune response and triggers Köbnerization of vitiligo [ 17 , 18 , 19 , 20 , 21 ]. ‘The second mechanism of Köbner phenomenon in vitiligo’ Some external triggers like UV radiation and trauma lead to the overproduction of reactive oxygen species by melanocytes. This results in melanocyte death, releasing DAMPs, especially HMGB1. Dendritic cells are hence activated. Moreover, these DAMPs increase the secretion of CXCL16 and IL‐8 from keratinocytes, favouring the migration of CD8 T cells, augmenting the immune response [ 22 , 23 , 24 , 25 , 26 ]. ‘The third mechanism of Köbner phenomenon in vitiligo’ E‐cadherin is the primary adhesion molecule that ensures the stability of melanocytes in the epidermal basal layer. External trauma/stress decreases E‐cadherin level, which detaches the melanocytes and enhances the hypopigmentation, which is the hallmark of vitiligo [ 27 ]. ‘The fourth mechanism of Köbner phenomenon in vitiligo’ Trauma, UV light, and H 2 O 2 cause the downregulation of stem cell factor and basic fibroblast growth factor, which normally control melanin metabolism. Hence, their downregulation causes less melanin production and more melanocyte apoptosis [ 28 ]. ‘The role of mast cells in psoriatic Köbnerization’ It is believed that tryptase levels increase following skin trauma. Tryptase increases the proliferation of epithelial cells and fibroblasts in the dermis. In addition, it activates proteinase‐activated receptors (PAR‐2) on mast cells, stimulating their secretion of IL‐8. Both mechanisms lead to the formation of new psoriatic lesions. In addition, keratinocytes secrete IL‐33 that directly stimulates mast cells to secrete IL‐6. Keratinocytes also secrete TLR‐3 which, along with IL‐17 secreted by mast cells, activate a downstream signalling cascade that contributes to the emergence of further psoriatic lesions [ 32 , 33 , 34 , 35 , 36 , 37 , 38 ]. As opposed to the isomorphic response detailed above, the Wolf's isotopic response is defined as the appearance of a new dermatosis localising to the site of another unrelated and healed skin disorder [ 42 ]. In 1955, Wyburn‐Mason first reports a series of patients developing malignant tumours, including skin cancers, laryngeal and breast carcinomas, confined to dermatomes of healed herpes zoster [ 42 ]. The isotopic response is then truly defined in 1985 and is now known to encompass a multitude of inciting factors in addition to the most reported herpes zoster [ 43 ]. Furthermore, the localisation and the preferential sites of development of dermatoses is not fully understood. It is conjectured that, although the two dermatoses do not share similar morphology, the microscopic derangements inflicted by the primary disease is a fertile area for another skin disorder to thrive. In fact, viral, neural, immunologic and vascular factors are hypothesized to be involved in the pathophysiology of this particular response [ 44 ]. The altered neural signalling hypothesis, currently gaining popularity, postulates that neurohumoral factors aid in the development of a new dermatosis through aberrant immune system activation along with the release of neuropeptides [ 45 ]. However, none of the abovementioned hypotheses is decisively proven and thus the mechanism remains unclear. As stated previously, scars represent one of the triggering factors of Wolf's isotopic response. A recent review by Wang et al. described several entities arising in areas of healed herpes zoster including lichen planus, psoriasis, acne vulgaris, lichen sclerosis et atrophicus, vitiligo, prurigo, bullous pemphigoid and impetigo [ 46 ]. More recently, several case reports described the emergence of eosinophilic dermatitis in skin lesions previously infected with herpes zoster [ 47 ]. A possible explanation of Wolf's phenomenon following herpes zoster is that the virus causes damage of dermal nerve endings, which alters immunity. Eventually, this might lead to immune hyperreactivity, immunosuppression, or abnormal angiogenesis, each of which can result in different cutaneous pathologies shown in Figure  6 [ 48 ]. Furthermore, Prieto‐Torres et al. report a case of necrobiosis lipoidica arising in a surgical scar of a non‐diabetic 22‐year‐old patient as an example of Wolf's isotopic response, an infrequent observation [ 49 ]. In fact, the entity is more commonly described as an example of Köbner phenomenon in surgical scars of diabetic patients [ 50 ]. The propensity of granulomatous disease to affect scars is postulated to be related to a decrease in resistance of connective and vascular tissue [ 51 ]. Herpes simplex arising from a scrofuloderma scar is yet another example of Wolf's isotopic response manifesting in scars [ 52 ]. In addition, granulomatous diseases such as sarcoidosis, granuloma annulare [ 53 ], and granulomatous vasculitis can exhibit this phenomenon on injured skin [ 54 ]. Moreover, secondary syphilis confined to healed superficial scarring sites of previous varicella infection can manifest as isotopic response [ 55 ]. Last but not least, it is important to keep in mind that malignancy can present as such. To illustrate, a rare case of diffuse primary cutaneous large B‐cell lymphoma is observed to demonstrate a postherpetic isotopic response [ 56 ]. ‘Wolf's isotopic response in herpetic lesions’ Herpes virus destroys dermal nerve fibres, leading to an altered immunity. It can either be hyperreactive, favouring granulomatous dermatitis or lichenoid dermatitis, or hyporeactive, favouring infections and tumours. It has also been hypothesized that angiogenesis might result from nerve damage, giving rise to Kaposi sarcoma, a vascular tumour [ 42 ]. The Renbök phenomenon, described by Happle in 1991, is predominantly reported in patients with alopecia areata of the scalp that are concomitantly affected by psoriasis [ 57 ]. These patients witness reversal of alopecia areata with evidence of hair regrowth limited to areas where psoriasis plaques arise. More recently, Renbök phenomenon was described in a woman with significant alopecia areata but retained hair adjacent to a co‐existing nevus flammeus [ 58 ]. In opposition to Köbner isomorphic response where local inflammatory disruption attracts a pre‐existing skin disease, Renbök phenomenon entails the suppression of an inflammatory response by the appearance of another. The mechanism behind this observation is not fully understood. One of the proposed hypothesis attempting to explain the antagonism seen between different inflammatory conditions revolves around a T‐cell mediated switch in the local cytokine milieu [ 59 ]. In fact, it claims that each T‐cell population (Th1, Th2 and Th17) tends to accentuate its proper response and inhibit that of other subsets through the release of particular cytokines. That being said, at each point in time, one subset of inflammatory response will dominate allowing for a particular skin disease to take control of the area [ 60 ]. For instance, Th1 cells have the ability to suppress Th2 and Th17 mediated skin diseases at an overlapping site through the release of cytokines including interferon gamma. This mutually exclusive situation described might explain Renbök phenomenon that allowed Th17 mediated psoriasis [ 61 ] to suppress the presumed Th1 response of alopecia areata [ 62 ]. It is important to note that the reason behind an inflammatory response taking control over the other is uncertain; it remains unclear whether one subset is intrinsically dominant [ 60 ]. Table  2 As formerly stated, a plethora of pathologies can arise in scars. The mechanism behind the preferential localisation of diseases to these areas with a disrupted immune milieu is elucidated above. The following section tackles the entities known to affect healed wounds. Entities affecting scars: Summary of key categories. As portrayed above, lichen planus, vitiligo and psoriasis make up the three most frequently described dermatoses affecting scars and injured skin, a typical illustration of true köbnerization. In addition to these entities, a multitude of inflammatory disorders preferentially develop on sites of healed wounds. Sarcoidosis is an impeccable illustration, an inflammatory disease characterised by noncaseating granulomas affecting multiple organs with T cells and an inverted CD4 to CD8 ratio playing a central role in its pathogenesis [ 63 ]. Cutaneous involvement is reported in around one‐fourth of patients, presenting as macules, papules, plaques, nodules, ulcers, lupus pernio, localised alopecia among others [ 64 ]. Scar sarcoidosis, characterised by erythematous swelling along with the appearance of papules and nodules within a scar, is an infrequent yet specific and well‐described skin manifestation of sarcoidosis and when reported is often associated with systemic involvement [ 65 ]. In fact, these patients are at a greater risk of developing pulmonary disease, bone cysts, parotid enlargement, uveitis and lymphadenopathy [ 66 ]. Thus, they should be screened for systemic involvement at the time of diagnosis and followed‐up on a regular basis. To note, scar sarcoidosis can be the first manifestation of systemic sarcoidosis, underlining the importance of investigating scar reactivation [ 67 ]. A recent case report described erythematous papules and nodules in scars acquired 9 years ago in a motor vehicle accident; skin biopsy then showed sarcoidosis [ 68 ]. Mimicking sarcoidosis, granuloma annulare represents another granulomatous disorder with known propensity to arise in scars [ 69 ]. For instance, postherpetic granuloma annulare, a classic example of Wolf's isotopic response, is frequently reported [ 70 ]. Also under the umbrella of granulomatous diseases, granulomatous vasculitis can arise in healed wounds such as scars of previous herpes zoster [ 71 ]. Another example described is the cutaneous involvement confined to a surgical scar by Churg‐Strauss syndrome [ 72 ]. Moreover, necrobiosis lipoidica and silicotic granulomas manifesting on phlebectomy scars represent another illustration of rare granulomatous eruptions on injured skin [ 73 ]. An exceptionally rare pathology known as pseudotuberculoma silicoticum, a delayed granulomatous foreign body reaction, is described arising in an old scar. As the name implies, materials containing silicone such as brick, glass and dirt are the culprit. This entity should be considered when dealing with an erythematous, raised, rubbery lesion growing in a scar [ 74 ]. Moving on to other inflammatory dermatoses, morphea or localised scleroderma, has the predilection to develop at sites of skin trauma [ 75 ]. For instance, Arif et al. report a case of morphea ‘en coup de sabre’ arising from a healed herpes zoster ophthalmicus [ 76 ]. Likewise, lichen sclerosis et atrophicus, a chronic inflammatory skin disorder, can arise in healed wounds. As an illustration, this condition is described arising in a urethrostomy scar [ 77 ] and within a skin graft scar [ 78 ]. In like manner, bullous pemphigoid can manifest on cicatrices [ 79 ]. It is reported as a blistering eruption confined to the surgical scar formed post calf vein harvesting as part of a bypass procedure [ 80 ]. Along the same lines, pyoderma gangrenosum, an inflammatory dermatosis that can occur as a result of trauma or in the context of a known systemic condition, is also identified in scars. In fact, it is described arising in a 7‐year‐old reduction mammoplasty scar with no near history of trauma [ 81 ]. Similarly, Jessner lymphocytic infiltrate, a rare disorder involving the benign buildup of lymphocytes, can present on healed skin namely a cutaneous leishmaniasis scar [ 82 ]. Also, giant cell lichenoid dermatitis is described at the site of herpes zoster scar in a patient who underwent bone marrow transplant [ 83 ]. Lastly, acne, a common skin disorder, can arise in scars. For example, a herpes zoster scar can trigger acne comedones [ 84 ] or an eruption of acne keloidalis nuchae reported in an HIV positive patient [ 85 ]. Tumours grow in scars the same way inflammatory pathologies do. As a matter of fact, scars represent hubs where chronic irritation, exposure to toxins, and poor vascularization in the setting of dysregulated immune control facilitate the emergence of neoplasms [ 86 ]. The term ‘scar tissue carcinoma’ encompasses numerous malignancies that affect scars, the most common being squamous cell carcinomas [ 87 ]. In fact, Marjolin's ulcer, most often a highly aggressive squamous cell carcinoma, is a well‐known cutaneous malignancy that has the propensity to grow in injured skin, most commonly burn scars, with an incidence of 0.1%–2.5% [ 87 ]. Although they are more often than not well‐differentiated lesions, they tend to be aggressive with a poor prognosis and a high recurrence rate [ 88 ]. As an example, squamous cell carcinoma is described as arising in a sporotrichosis scar [ 89 ], sternotomy scar [ 90 ], lupus vulgaris scar treated with radiation [ 91 ], epidermolysis bullosa acquisita scar [ 92 ], leishmania scar [ 93 ], soft‐tissue trauma scar [ 94 ] among others. Also, Bowen's disease or squamous cell carcinoma in situ [ 95 ], verrucous carcinoma, a low‐grade locally aggressive histologic variant of squamous cell carcinoma [ 96 ], and keratoacanthoma, commonly classified as a variant of squamous cell carcinoma [ 97 ] can localise in scars. For instance, keratoacanthoma centrifugum marginatum is described in a long‐lasting scar [ 98 ]. Keratoacanthoma is also reported as a complication following skin cancer excisions and should be part of the differential diagnosis of a rapidly growing lesion arising from a surgical site [ 99 ]. Basal cell carcinomas represent the second most common tumour arising in burn scars [ 100 ], chickenpox scars [ 101 ], leishmania scars [ 102 , 103 ], and surgical scars [ 104 ]. As opposed to other neoplasms, they often develop at a later age and exhibit a shorter latency period between injury and tumour formation [ 100 ]. In addition, melanomas have the ability to grow in scars. In fact, malignant melanoma [ 105 , 106 , 107 , 108 ], spindle cell melanoma [ 109 ], and amelanotic desmoplastic melanoma [ 110 ] are described in burn and surgical scars. Other types of skin and adnexal tumours displaying this phenomenon include trichoepithelioma [ 111 ], pigmented basal cell epithelioma [ 112 ], eccrine poroma and porocarcinoma [ 113 ], and nodular hidradenoma [ 114 ]. Furthermore, mimicking Marjolin's ulcer, Kaposi's sarcoma is reported as an infrequent complication of a burn scar [ 115 ]. It is also described in a postherpetic site as a single lesion in an HIV positive patient, an illustration of an ‘immunocompromised district’ in an immunocompromised patient [ 116 ]. A variety of other sarcomas can grow in scar tissue, albeit rarely. For instance, extraosseous osteosarcoma [ 117 , 118 ], cutaneous angiosarcoma [ 119 , 120 ], myxofibrosarcoma [ 121 ], cutaneous carcinosarcoma [ 122 ], low grade myofibroblastic sarcoma [ 123 ], fibrosarcoma [ 124 ], dermatofibrosarcoma protuberans [ 125 , 126 ] atypical fibroxanthoma [ 127 , 128 ], malignant fibrous histiocytoma [ 129 ], malignant mesenchymoma [ 130 ], and cutaneous leiomyosarcoma [ 131 , 132 ] among others, are reported in the literature. In addition, lymphoproliferative disorders occasionally grow in scar tissue. As a matter of fact, primary cutaneous CD4+ small/medium‐sized pleomorphic T‐cell lymphoproliferative disorder [ 133 ], primary cutaneous anaplastic large cell lymphoma [ 134 ], lymphoplasmocytoid lymphoma [ 135 ], and cutaneous infiltrates of B‐cell chronic lymphocytic leukaemia [ 136 ] can arise in scars. To note, the latter can be the first manifestation of the disease. For example, a case of systemic B‐cell chronic lymphocytic leukaemia is reported where the first presentation of the disease is a cutaneous lymphoid infiltrate at a herpes simplex scar [ 137 ]. Likewise, nerve sheath tumours represent another entity found in scars. In fact, a malignant nerve sheath tumour is described in an infantile hemangioma scar [ 138 ] and a malignant schwannoma is reported in a burn scar [ 139 ]. Moreover, there are rare reports portraying infrequent entities exhibiting this phenomenon such as extramammary Paget's disease affecting the borders of a burn scar [ 140 ], multiple pyogenic granulomas appearing in a scald burn scar caused by boiling milk [ 141 ], giant cell tumours of soft tissue arising in surgical scars [ 142 ], primary lymphoepithelioma‐like carcinoma of the skin localising in a basal cell carcinoma excision scar [ 143 ], cutaneous perivascular myoma growing in an old scar [ 144 ], and clear cell carcinoma arising from a surgical cesarian section scar [ 145 ]. Last but not least, lesions appearing in scars can be metastatic in origin. To illustrate, Tummidi et al. describe a scar site metastasis of renal cell carcinoma arising in a radical nephrectomy scar [ 146 ]. That being said, clinicians should keep a high index of suspicion when examining scars as reactivation in the form of an ulceration or a nonhealing lesion can have a malignant potential and hence should be biopsied and followed‐up accordingly [ 88 ]. Clinicians should keep a high index of suspicion when evaluating chronic scars, and monitor for any red flags such as but not limited to a persistently non‐healing ulcer despite appropriate care, rapid increase in size or change in morphology, ulceration or spontaneous bleeding, development of induration or nodularity, or a new lesion arising within a chronic scar or burn site. When these signs are appreciated, a biopsy may be warranted to exclude malignant degeneration and receive prompt management. Numerous pathologies are reported in the literature to erupt from scar tissue in addition to inflammatory conditions and neoplastic growths. To start with, cutaneous endometriosis, an infrequent manifestation of the disease, is often confined to scar tissue with an incidence of 0.3% [ 147 ]. It is described in surgical scars of hysterectomies, caesarean sections [ 148 ], laparoscopies, episiotomies, umbilical trocar sites known as ‘Villar's nodule’ and surgical drain sites where a rare case of combined inguinal endosalpingiosis and endometriosis is reported [ 149 ]. This condition should be part of the differential diagnosis of a painful scar with skin changes in pre‐menopausal women and warrant further investigation as 14% of patients diagnosed with gynaecological scar endometriosis have concomitant pelvic endometriosis [ 150 ]. It is important to keep in mind that, although extremely rare with an incidence no more than 0.3%–1% [ 151 ], scar endometriosis lesions have the potential to undergo malignant transformation with a histopathology showing endometrioid or clear cell carcinoma [ 150 ]. In addition, disorders involving the deposition of mucopolysaccharides such as primary cutaneous dermal mucinosis arising in a postherpetic scar [ 152 ] and reticular erythematous mucinosis developing in a surgical scar [ 153 ] are reported. Likewise, cutaneous dirt‐adherent disease, an uncommon psychogenic pathology frequently described in young Chinese and Japanese women, can develop in scar tissue. As a matter of fact, a unique report illustrates the development of this dermatosis in a keloid scar [ 154 ]. Also, milia can arise in sites of previous pemphigus vulgaris, porphyria cutanea tarda, burn, herpes zoster among others [ 155 ]. Additionally, the recurrent melanocytic nevus is a well‐described phenomenon denoting the proliferation of melanocytes at the site of an incompletely excised melanocytic nevus [ 156 ]. It can prompt a misdiagnosis of melanoma due to the uneven pigmentation along with the asymmetric appearance of the lesion at the site of a shave excision scar. Other rare presentations reported to arise from scars include inflammatory linear verrucous epidermal nevus [ 157 ], acquired dermal melanocytosis [ 158 ], porokeratosis [ 159 ], and circumscribed palmar hypokeratosis [ 160 ]. In addition, although the hyperpigmentation seen in Addison's disease is usually generalised, it can be particularly flagrant on scars formed after the onset of the systemic disease [ 161 ]. Some medications also have the ability to perpetrate changes in scars. In fact, minocycline is a known trigger of hyperpigmentation in cicatrices [ 162 ]. It is also described in a case of minocycline‐induced fixed drug eruptions confined to scars [ 163 ]. An uncommon presentation of a drug‐induced photosensitivity reaction causing a change in appearance of an established scar is described [ 164 ]. Clindamycin‐induced maculopapular rash involving preferentially striae distensae [ 165 ] and Cefuroxime‐induced cutaneous leukocytoclastic vasculitis in a skin graft site [ 166 ] are also reported among other drug‐induced cutaneous reactions. Moreover, cutaneous horns can arise in scars; they should be accorded special attention since they are commonly associated with a malignant lesion at the base [ 167 ]. Furthermore, cutaneous cytomegalovirus infection can present as multiple ulcers in a herpes zoster scar in HIV positive patients [ 168 ]. Finally, pretibial myxedema can be the cause of scar infiltration, manifesting as non‐pitting and firm nodules and plaques in patients with hyperthyroidism [ 169 ].

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The study is a narrative review on the literature present regarding scar dermatoses. MedLine (via OVID), PubMed, Embase, Google Scholar, and Cochrane databases were systematically searched by two authors (FFH and DMK) using search terms: Scar Dermatoses, Cicatrix, Cicatrix/complications*, Cicatrix/pathology*, and Scars. Papers were flagged for inclusion by both authors independently and compared with each other. The literature was primarily comprised of case reports and case series, which may limit the strength of the conclusions of this paper.

The authors have nothing to report.

Locus minoris resistentiae, ‘place of lesser resistance’ in Latin, is an ancient concept that has provided the basis for the understanding of several pathologies in medicine [ 1 ]. It upholds the notion that any region of the human body that becomes compromised, from a congenital or acquired insult, becomes inherently weaker than the surrounding healthy tissue. Hence, this focus becomes somewhat defenceless and turns into a nidus for pathogens, malignancy, inflammatory processes among other pathologies to flourish. For instance, a well‐described illustration of this phenomenon is seen in damaged heart valves which serve as prey for bacterial proliferation. Along the same train of thought, the immunocompromised cutaneous district is a novel extrapolation of the aforementioned [ 2 ]. It highlights the disruption of the immune milieu in injured skin allowing for the preferential and opportunistic localisation of diseases to this area [ 3 ]. The skin can be weakened by several entities encompassing, but not limited to, infections, vaccinations, tattoos, burns, radiation therapies and trauma. Scars fall under the umbrella of compromised skin and thus represent another vulnerable cutaneous district and potential site for diseases to develop. Scars are formed as part of the process of tissue repair following an injury to the skin. The scarring process is hypothesized to be evolutionarily selected for as it provides an advantage due to its ability to allow for a fast wound recovery protecting the exposed injured area from more damage or infection [ 4 ]. The rapid activation of an effective inflammatory response takes place, typically described in three intersecting stages [ 5 ]. It starts the first three days post‐injury with the inflammatory phase in which a homeostatic fibrin and platelet plug is initially formed. Then, neutrophils followed by macrophages are recruited to the site of injury allowing for phagocytosis to take place. Macrophages release inflammatory mediators including chemokines and cytokines which allow for the recruitment of fibroblasts. Transforming growth factor‐beta and platelet‐derived growth factor are among the most recognised cytokines released. The proliferative stage of wound healing thus begins at day 4 with the formation of granulation tissue involving macrophages, fibroblasts and endothelial cells. Activated fibroblasts deposit type III collagen and angiogenesis takes place. Lastly, the remodelling stage starts at around day 21 with the replacement of type III collagen with type I collagen. Myofibroblasts' contractile properties allow for the scar to occupy a smaller surface [ 6 ]. The whole process described starting from the initial insult to the inflammatory cascade that follows compromise the integrity of the skin and thus contributes to scars being regions of potentially disturbed local environment. This hypothesis attempts to explain the notion behind a scar being a weaker focus—a ‘locus minoris resistentiae’–compared to the adjacent healthy tissue. This review will focus on the different entities that have a propensity to affect cicatrices. Although not frequently encountered in daily practice, many of the described pathologies arising in sites of injury are malignant. It is thus of utmost importance for dermatologists to get familiar with the different pathologies reported. This will allow for early diagnosis and hence timely treatment.

The authors declare no conflicts of interest.