Are keloid and hypertrophic scar different forms of the same disorder? A fibroproliferative skin disorder hypothesis based on keloid findings

Abstract

Hypertrophic scars (HSs) and keloids are commonly seen as two different diseases by both clinicians and pathologists. However, as supported by histological evidence showing they share increased numbers of fibroblasts and accumulate collagen products, HS and keloid might be different forms of the same pathological entity, rather than separate conditions. To test this hypothesis, keloids from patients who underwent scar excisions (n = 20) in Nippon Medical School from 2005 to 2010 were examined histologically. The proportion and distribution of cellular and matrix collagen components were evaluated at the centre and periphery of each sample. In keloid samples, coexistence of hyalinised collagen, which is the most important pathognomonic characteristic of a keloid and dermal nodules that are considered to be characteristic of HS, was found. Moreover, hyalinised fibres appeared to initiate from the corner of the dermal nodules. Key features of inflammation such as microvessels, fibroblasts and inflammatory cells all decreased gradually from the periphery to the centre of keloids, indicative of reduced inflammation in the centre. Thus, we hypothesise that HS and keloid can be considered as successive stages of the same fibroproliferative skin disorder, with differing degrees of inflammation that might be affected by genetic predisposition.

Keywords: Fibroproliferation; Hypertrophic scar; Inflammation; Keloid; Scar pathology.

Figure 1

Haematoxylin–eosin stain for case 1. (A) Central area (40×). The expanded dermis was occupied by large and highly oeosinophilic hyalinised collagen bundles running parallel to the superficial epidermis. (B) Peripheral area (40×). The hyalinised keloidal collagens were mainly located in the upper reticular dermis, and were somewhat fragmented and shortened, and interrupted and surrounded by cellular components. The boundaries of the hyalinised keloidal collagens were clearer in the epidermal and central sides than in the dermal and peripheral sides. R side: central side; L side: peripheral side. (C) Coexistence of keloidal collagen and dermal nodules (40×) and its topical enlargement in panel (D) (100×). The dermal nodules, comprising focal fibroblast aggregates together with randomly oriented collagen fibres, had hyalinised collagens scattered on their tops. The character of the hyalinised collagen fibres changed with location. At the base the fibres were short, wavy, randomised in relation to the epidermis and non‐oeosinophilic, whereas at the top they were long, straight, parallel to the epidermis and strongly oeosinophilic.

Figure 2

Haematoxylin–eosin pictures for case 2. Hyalinised keloidal collagen fibres occupy the expanded reticular dermis in the central area, and the cellularity decreased from the central to the peripheral areas. (A) Panorama (40×). (B) Topical enlargement of central area (100×). (C) Topical enlargement of peripheral area (100×).

Figure 3

Dermal nodule (40×) in case 2. A typical dermal nodule in the dermis, together with a residual hair follicle and sebaceous gland. Hyalinised collagens first appear at the left corner of the nodule.

Figure 4

Combined haematoxylin–eosin pictures for case 3. Hyalinised keloidal collagens dominate the expanded reticular dermis in the central area, whereas large dermal nodules dominate the peripheral dermis. With increasing distance from the central area, the dermal nodules become larger, with fewer fibres. (A) Panorama (40×). (B) Topical enlargement of peripheral area (40×). (C) Topical enlargement of central area (100×).