Keloid vs. Hypertrophic scar

Differential Diagnosis

Keloid Hypertrophic Scar 1. Lesion usually elevated markedly above the skin surface; little tendency to regression without therapy 1. Lesion elevated slightly above the skin surface; even without treatment, tends, in time, to become flush with the surface of the skin or depressed below it as an atrophic scar 2. No subepidermal clefts or vesicles 2. Subepidermal clefts or vesicles form occasionally 3. Markedly thickened bundles of collagen with few fibrillary ones in a lesion developed fully 3. Fibrillary bundles of collagen only; no markedly thickened ones 4. Collagen bundles brightly eosinophilic 4. Collagen bundles slightly eosinophilic or amphophilic 5. Collagen bundles in haphazard array 5. Collagen bundles generally oriented parallel to the surface of the skin 6. Plump oval fibrocytes alongside thickened collagen bundles also arrayed in haphazard pattern 6. Oval fibrocytes alongside fibrillary bundles of collagen arranged mostly parallel to the skin surface 7. Widely dilated blood vessels oriented randomly 7. Widely dilated blood vessels oriented somewhat perpendicular to the skin surface 8. Abundant mucin between bundles of collagen often, especially in an early lesion 8. Little mucin between bundles of collagen except in an early lesion when it may be copious 9. Infiltrates of lymphocytes around dilated blood vessels at the periphery of a lesion especially 9. Infiltrates of lymphocytes around dilated blood vessels throughout a lesion

Discussion

Keloids and hypertrophic scars have many findings histopathologic in common (e.g., fibroplasia, telangiectases, infiltrates of inflammatory cells, mucin) and, in some instances, attributes of what seem to be both keloid and hypertrophic scar may be found together in sections from the same biopsy specimen. Almost always such a lesion turns out to be a keloid early in the course of development, i.e., prior to the appearance of thick bundles of collagen. When distinct, brightly eosinophilic, thick bundles of collagen are arrayed haphazardly in a lesion made up entirely of fibroplasia, the diagnosis, by convention, is keloid. No such bundles of collagen are found in a hypertrophic scar.

Hypertrophic scars usually are linear lesions that follow trauma such as those of a surgical incision and an accidental laceration. The scars have no predilection for individuals with any particular intensity of pigmentation, unlike the situation for keloids whose proclivity is for dark-skinned individuals. As a rule, hypertrophic scars tend to flatten without treatment, a process that takes years, whereas keloids do not shrink appreciably on their own.

Both keloids and hypertrophic scars are types of fibrosing dermatitis, i.e., inflammatory processes that resolve with fibroplasia. The entire spectrum of inflammation from granulation tissue to sclerosis may be found in keloids and hypertrophic scars depending on when in their course a biopsy specimen is obtained.

In an early lesion of a keloid, only abundant fibrillary bundles of collagen are present in nodular aggregations that contain numerous plump fibrocytes in random array. No brightly eosinophilic thickened bundles of collagen are found in an early keloid. The clue most valuable to diagnosis of a keloid, even at this early stage, is the presence of fibrillary bundles of collagen like those of a scar but in a lesion whose configuration is distinctly nodular. In time, foci of brightly eosinophilic, markedly thickened collagen bundles arranged haphazardly appear in the mass of fibrillary bundles of collagen. Those thickened bundles of collagen, in that particular setting, are signs of a keloid. The diagnosis histopathologic of keloid has implications important for a patient, among those being prevention of future keloids and treatment of existing ones.

Thickened collagen bundles like those in a keloid also are seen, episodically, in otherwise typical lesions of dermatofibroma (a type of fibrosing inflammation with keloidal attributes), nodular fasciitis (a type of fibrosing inflammation with keloidal characteristics), and basal-cell carcinoma (a malignant neoplasms associated with keloidal features). The factors that induce fibrocytes to manufacture collagen with various appearances morphologic are not understood, e.g., thick collagen bundles in haphazard array, as in a keloid developed fully; fibrillary collagen bundles, as a keloid early in its course and in a scar; short, coarse collagen bundles in random array, as in a dermatofibroma; thickened collagen bundles arranged compactly and in parallel, as in morphea at its apogee; wiry bundles of collagen in random distribution associated with patchy lichenoid infiltrates of lymphocytes as in mycosis fungoides; bundles of collagen arranged in lamellae in the papillary dermis immediately beneath nests of melanocytes positioned at the base of rete ridges and parallel to undulations of rete ridges as in proliferations of melanocytes like simple lentigines, junctional nevi of Clark's type especially, and malignant melanoma in situ; sclerotic collagen in the upper part of the dermis, as in the lichen sclerosus et atrophicus; expression of morphea; "homogenized" in the form of sclerosis and concentric whorls of collagen bundles around infundibulofollicular structures, as in a fibrous papule of the face. Why fibrocytes produce bundles of collagen arranged in vertical streaks in a thickened papillary dermis is known well. Those coarse bundles that occur in lichen simplex chronicus, prurigo nodularis, and picker's nodule result from prolonged, persistent rubbing of the skin. The mechanisms whereby the distinctive changes come into being have yet to be unraveled.

Ref:

Differential Diagnosis In Dermatopathology I, Ii, Iii, Iv.chm