Histologic Analysis of Keloids and Hypertrophic Scars

Ogawa, Rei; Akaishi, Satoshi; Izumi, Mitsuru

doi:10.1097/sap.0b013e3181855172

Cited by 27 publications

(27 citation statements)

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“…Keloidal collagen has also been reported as exclusively occurring in keloids, 3,5,29 although Lee et al 29 found it was not always expressed in keloids, with complete absence thereof in 45% of keloids. In line with our study, keloidal collagen in clinically diagnosed hypertrophic scars has been reported, 6,30 thus further complicating its usefulness as a definitive keloid marker. Finally, dermal nodules have been described as unique to hypertrophic scars, 3 but our results are more in line with the majority of studies reporting nodules in both abnormal scar types.…”

Section: Discussionsupporting

confidence: 86%

“…Finally, dermal nodules have been described as unique to hypertrophic scars, 3 but our results are more in line with the majority of studies reporting nodules in both abnormal scar types. [4][5][6]29,31 All things considered, the differences were of a gradient rather than absolute nature, with hypertrophic scars showing more intense a-SMA immunoreactivity and keloids showing a higher and constitutive presence of keloidal collagen (Fig. 7).…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Histologically, the distinction is not quite so clear cut. The presence of a-smooth muscle actin (a-SMA) 3 and dermal nodules 3,4 vs. thick hyalinized collagen bundles, also known as 'keloidal collagen' 5,6 have been put forward as features unique to hypertrophic scars or keloids respectively, However, conflicting results have been reported with regards to these features, and consequently there are still no definitive markers for either abnormal scar type.…”

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confidence: 99%

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Hypertrophic and keloid scars fail to progress from the CD 34 ⁻ /α‐smooth muscle actin (α‐ SMA ) ⁺ immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

et al. 2019

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Summary Background Our understanding of the pathogenesis underlying keloid scar formation is still very limited, and the morphological distinction between hypertrophic and keloid scars remains difficult. Objectives To test whether hypertrophic and keloid scars may reflect an inability to progress from immaturity to the desired mature normotrophic scar phenotype. Methods Using whole‐biopsy imaging and an objectively quantifiable way to analyse immunoreactivity, we have compared the immunohistopathological profiles of young immature scars with mature normotrophic scars, hypertrophic scars, and keloids with their surrounding‐normal‐skin. Results Abnormal scars (hypertrophic scars and keloids) maintain the immature scar phenotype, characterized by a CD34− (tumour biomarker) and α‐smooth muscle actin (α‐SMA)+ (myofibroblast) dermal region. This is in contrast to normal skin, surrounding‐normal‐skin and mature normotrophic scars that were CD34+/ α‐SMA−. Immature, hypertrophic and keloid scars showed abnormal epidermal differentiation (involucrin), but only hypertrophic scars and keloids showed increased epidermal thickness. Immature scars did show increased epidermal and dermal proliferation (Ki67), which was absent from abnormal scars, where mesenchymal hypercellularity (vimentin) and senescence (p16) were predominant. Keloidal collagen and α‐SMA were previously considered to distinguish between hypertrophic scars and keloids. However, α‐SMA staining was present in both abnormal scar types, while keloidal collagen was present mostly in keloids. There were no obvious signs of heterogeneity within keloid scars, and the surrounding‐normal‐skin resembled normal skin. Conclusions Both abnormal scar types showed a unique CD34−/α‐SMA+/p16+ scar phenotype, but the differences between hypertrophic scars and keloids observed in this study were of a gradient rather than absolute nature. This suggests that scar progression to the mature normal scar phenotype is, for as yet unknown reasons, hindered in hypertrophic and keloid scars. What's already known about this topic? Hypertrophic and keloid scars both have sustained epidermal barrier dysfunction, suggesting the persistence of an immature scar phenotype. Morphological distinction between hypertrophic and keloid scars remains a topic of debate, although α‐smooth muscle actin (α‐SMA) and keloidal collagen have been considered distinguishing features of hypertrophic and keloid scars, respectively. It has been suggested that keloids are not simply homogeneous growths, as heterogeneity within keloid scars and possible involvement of the surrounding‐normal‐skin have been reported. What does this study add? An extensive whole‐biopsy imaging and quantifiable immunohistochemical assessment of immature, mature normal, hypertrophic and keloid scars, including normal skin surrounding keloids. Hypertrophic and keloid scars maintain dermal characteristics of immature scars, rather than transitioning into the normal mature phenotype. Differences between hypertrophic and keloid scars...

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Hypertrophic and keloid scars fail to progress from the CD 34 ⁻ /α‐smooth muscle actin (α‐ SMA ) ⁺ immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

et al. 2019

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“…Unfortunately, it is not always easy to make an accurate diagnosis of keloid scar based on its clinical appearance or even histopathologically especially due to its evolving nature [17,18]. This fact is highlighted in our case in which a histological misinterpretation of the biopsied specimen occurred.…”

Section: Discussionmentioning

confidence: 67%

Challenging Diagnosis of a Rare Case of Spontaneous Keloid Scar

Tiong

2014

J Med Cases

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Keloid scars are benign dermal collagenous lesions that arise in the reticular layer of the dermis as a result of a period of prolonged wound healing due to injurious cutaneous insult. It is diagnosed clinically by a history of injury preceding its appearance and its pathognomonic encroachment beyond the boundary of the original wound. There are multiple factors that predispose an individual to keloid scar formation but no single hypothesis sufficiently explained its complex pathogenesis. The spontaneity of keloid scar to arise de novo without prior cutaneous injury is very rare. Although the non-specific appearance of spontaneous keloid scar can resemble various malignant or benign tumors, it is of paramount importance to accurately diagnose it due to the difficulty and complexity of keloid scar treatment or the atrocious outcome of its mismanagement. Here, we presented a rare case of spontaneous keloid scar over an unusual site of occurrence, and its disfiguring consequences as a result of misdiagnosis and treatment. We also highlighted the diagnostic challenge facing many clinicians when spontaneous keloid scar occurred in an individual without significant predisposing factors. Therefore, extra vigilance should be exercised in our practice and the spontaneity origin of keloid scar should be borne in one's mind.

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“…Keloid research showed significant progress in the last few years [13][14][15][16] but there is still deficit in the literature regarding the mechanisms behind keloid development, recurrence and limited effective therapy. The available research data are mostly from in vitro studies and this often fails to represent in vivo pathophysiology.…”

Section: Introductionmentioning

confidence: 99%

Co-upregulation of Transforming Growth Factor Beta-1 and Nitric Oxide Synthase in Keloid by comparison to normal human skin-A possible role for TGFβ1 and NOS in pathogenesis of keloid

El-Aleem¹,

Abdelwahab²,

Osman³

2017

J Cytol Histol

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Keloid disease is a benign but progressive form of abnormal wound healing associated with skin fibrosis and can cause a major functional disability and morbidity. TGF beta (TGFβ) and Nitric Oxide (NO) are active biomarkers known to regulate phases of wound healing and have been implicated in pathogenesis of fibrotic disease. There are three isoforms of TGFβ (1, 2 and 3) TGFβ1 and 3 have a crucial role in fibrosis, with TGFβ1 profibrotic and TGFβ3 antifibrotic. NO is produced by Nitric Oxide Synthase (NOS) which exist in three isoforms, inducible NOS (iNOS), endothelial NOS (ecNOS) and neuronal NOS (nNOS). TGFβ isoforms and NO were found to be associated with fibrotic disorders affecting the skin. We hypothesis that the interaction between TGFβ and NO in keloid could promote the excessive collagen deposition associated with this disorder.Using immunohistochemistry, we investigated the profile of TGFβ isoforms (TGFβ1, 3) and NOS isoforms (iNOS and ecNOS) in keloid tissues and normal human skin. The cellular distribution of all the isoforms were studied and the protein levels were assessed by using H-Scoring and Image J Scoring systems.

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Histologic Analysis of Keloids and Hypertrophic Scars

Cited by 27 publications

References 3 publications

Hypertrophic and keloid scars fail to progress from the CD 34 ⁻ /α‐smooth muscle actin (α‐ SMA ) ⁺ immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

Hypertrophic and keloid scars fail to progress from the CD 34 ⁻ /α‐smooth muscle actin (α‐ SMA ) ⁺ immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

Challenging Diagnosis of a Rare Case of Spontaneous Keloid Scar

Co-upregulation of Transforming Growth Factor Beta-1 and Nitric Oxide Synthase in Keloid by comparison to normal human skin-A possible role for TGFβ1 and NOS in pathogenesis of keloid

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Histologic Analysis of Keloids and Hypertrophic Scars

Cited by 27 publications

References 3 publications

Hypertrophic and keloid scars fail to progress from the CD 34 − /α‐smooth muscle actin (α‐ SMA ) + immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

Hypertrophic and keloid scars fail to progress from the CD 34 − /α‐smooth muscle actin (α‐ SMA ) + immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

Challenging Diagnosis of a Rare Case of Spontaneous Keloid Scar

Co-upregulation of Transforming Growth Factor Beta-1 and Nitric Oxide Synthase in Keloid by comparison to normal human skin-A possible role for TGFβ1 and NOS in pathogenesis of keloid

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Hypertrophic and keloid scars fail to progress from the CD 34 ⁻ /α‐smooth muscle actin (α‐ SMA ) ⁺ immature scar phenotype and show gradient differences in α‐ SMA and p16 expression

Hypertrophic and keloid scars fail to progress from the CD 34 ⁻ /α‐smooth muscle actin (α‐ SMA ) ⁺ immature scar phenotype and show gradient differences in α‐ SMA and p16 expression