Histopathological Differential Diagnosis of Keloid and Hypertrophic Scar

Abstract

Distinguishing hypertrophic scar (HS) from keloid histopathologically is sometimes difficult because thickened hyalinized collagen (keloidal collagen), the hallmark of keloid, is not always detectable and alpha-smooth muscle actin (alpha-SMA), a differentiating marker of HS, is variably expressed in both forms of scar. The aim of this study was to investigate additional distinguishing features to facilitate differentiation between keloid and HS. We compared various histologic features and the expression of alpha-SMA in 40 specimens of keloid and 10 specimens of HS. The features more commonly seen in keloids were: (a) no flattening of the overlying epidermis, (b) no scarring of the papillary dermis, (c) presence of keloidal collagen, (d) absence of prominent vertically oriented blood vessels, (e) presence of prominent disarray of fibrous fascicles/nodules, (f) presence of a tongue-like advancing edge underneath normal-appearing epidermis and papillary dermis, (g) horizontal cellular fibrous band in the upper reticular dermis, and (h) prominent fascia-like fibrous band. The last three features were found in keloid specimens only, including the ones lacking detectable keloidal collagen. Our study confirmed the diagnostic value of keloidal collagen, but it was only found in 55% of keloid specimens. Alpha-SMA expression was found in both HS (70%) and keloid (45%), thus it would not be a differentiating marker. In scars with no detectable keloidal collagen, the presence of the following feature(s) favors the diagnosis of keloid: non-flattened epidermis, non-fibrotic papillary dermis, a tongue-like advancing edge, horizontal cellular fibrous band in the upper reticular dermis, and prominent fascia-like band.

Scar Management in the Pediatric and Adolescent Populations

“…8 In addition to differences in clinical appearance, keloids often differ histopathologically from hypertrophic scars in a variety of ways, with the most distinguishing feature being the presence of thickened hyalinized collagen (keloidal collagen). 9 Keloid formation has also been associated with a family history of keloids, hyperimmunoglobulin E syndrome, blood type A, and hormone peaks during puberty and pregnancy. [10][11][12][13] …”

Angiotensin-II Mediates Nonmuscle Myosin II Activation and Expression and Contributes to Human Keloid Disease Progression

“…The sine qua non of keloids is the growth of the lesion beyond original wound margins (2)(3)(4). Keloids consist of a quiescent central area surrounded by an active leading edge that is frequently erythematous and pruritic (1).…”

“…Keloids consist of a quiescent central area surrounded by an active leading edge that is frequently erythematous and pruritic (1). Histologically, keloids are seen to invade adjacent reticular dermis beneath normal-appearing papillary dermis and epidermis (2). Previous research has demonstrated that keloid fibroblasts proliferate and migrate more rapidly than control dermal fibroblasts (5)(6)(7)(8)(9).…”

Effect of eccentric exercise on the healing process of injured patellar tendon in rats

“…A hallmark of myofi broblasts is the expression of α-SMA. 18,19 Therefore, α-SMA may be a marker for fi brosis and scar formation. We analyzed α-SMA expression by immunohistochemistry at day 14 after injury and found that deposition of α-SMA in the eccentric exercise group was more subdued than that in the concentric exercise group.…”