What Is a Solitary Keratoacanthoma? A Benign Follicular Neoplasm, Frequently Associated with Squamous Cell Carcinoma

Abstract

We present histopathological criteria for diagnosing keratoacanthoma (KA). In KA, four histological stages are recognized, which are the early/proliferative stage, well-developed stage, regressing stage and regressed stage. In diagnosing KA, we emphasize that KA consists of the proliferation of enlarged pale pink cells with ground glass-like cytoplasm without nuclear atypia, other than crateriform architecture. KA sometimes exhibits malignant transformation within the lesions. We describe the characteristics of benign and malignant epithelial crateriform tumors that should be differentiated from KA. We also present the data of histopathological diagnosis of lesions clinically diagnosed as KA, its natural course and related lesions after partial biopsy, and incidence of crateriform epithelial neoplasms. Based on these data, we recommend complete excision of the lesion when KA is clinically suspected, especially when the lesion is located on a sun-exposed area of an elderly patient. If complete excision is impossible, partial excision of a sufficient specimen with intact architecture is required. In such a case, however, careful investigation after biopsy will be needed, even if the histopathological diagnosis is KA, because there is some possibility that a conventional SCC lesion remains in the residual tissue.

Keywords: crater form of infundibular SCC; crateriform Bowen disease; crateriform SCC arising from actinic keratosis; crateriform neoplasms; crateriform seborrheic keratosis; crateriform verruca; keratoacanthoma; keratoacanthoma with malignant transformation; keratoacanthoma-like SCC; squamous cell carcinoma (SCC).

Figure 1

Histopathological findings of KA en plaque/nodule. Gross findings of the lesion reveal an exo-endophytic and non-crateriform architecture (a). The lesion consisted of proliferation of large pale eosinophilic cells with a few layers of basophilic cells at their periphery (b). Large pale eosinophilic cells show no nuclear atypia (b).

Figure 2

Histopathological findings of KA at the early/ proliferative stage. Gross findings of the lesion include crateriform architecture with a central keratinous plug (a). A lip-like structure is observed (b). Pale pink keratinocytes with a glassy appearance are observed. In the deeper areas, pale pink keratinocytes with a glassy appearance are noted (c). The deeper areas of the lesion are poorly demarcated from the surrounding stroma and exhibit slightly invasive growth (d).

Figure 3

Histopathological findings of KA at the well-developed stage. Gross findings of the lesion include crateriform and exo-endophytic architecture with a central keratinous plug (a). Overhanging epithelial lips with a normal overlying epidermis are observed (b). Characteristic proliferation of large pale pink cells with a glassy appearance showing compact keratinization is observed in most parts of the lesion (c). The deeper areas of the lesion are slightly poorly demarcated from the surrounding stroma and exhibit slightly invasive growth (d).

Figure 4

Histopathological findings of KA at the regressing stage. Gross findings of the lesion include crateriform architecture (a) and a lip-like structure (b). The lesion shows infundibular characteristics of laminated keratinization (b,d) and often loses the pale pink keratinocytes with a glassy appearance (c). Fibrosis in the dermal papillae and mixed cell inflammation are also observed (b).

Figure 5

Histopathological findings of KA at the regressed stage. A depressed epidermal lesion with overhanging and rising edges is observed (a), and the epidermis is flattened and atrophic with loss of rete ridges (b).

Figure 6

Histopathological findings of KA-like SCC. Gross findings of the lesion include crateriform architecture with a central keratinous plug (a). In part of the lesion, the histopathological features of KA are observed (b,c), whereas the SCC component is composed of tumor cells with keratinocytic differentiation and apparent nuclear atypia and shows invasive growth pattern (d).

Figure 7

Histopathological findings of mKA. Crateriform architecture is observed, and there is a clear distinction between KA and SCC (a). Both sides of the lesion show regressing KA (b), whereas the SCC component is in the center (c). The boundary between the two components is clear-cut (a).

Figure 8

Histopathological findings of CFV. A crateriform configuration with finger-like exophytic projections accompanied (a) by epithelial lip-like structures at the periphery (b) is exhibited. Arborization is observed and the base is well demarcated without endophytic growth (a). Focal hypergranulosis and koilocytes are visible between the papillary projections (c). The lesion consists of several lobular structures composed of the proliferation of keratinocytes of a similar size and regular arrangement (d).

Figure 9

Histopathological findings of CSK. The lesion is crateriform with finger-like exophytic projections (a), showing hyperkeratosis and acanthosis with proliferation of basaloid cells (b). Pseudohorn cysts (a) and squamous eddies (b) are evident.

Figure 10

Histopathological findings of crateriform Bowen disease. The lesion shows crateriform and exo-endophytic proliferation with a central keratotic plug and overhanging epithelial lip-like structures (a). Typical features of Bowen’s disease, which are full-thickness dysplasia with markedly atypical keratinocytes, are seen in the epidermis (b).

Figure 11

Histopathological findings of cSCC. A multilobular crateriform lesion (a) with epithelial lip-like structures (b) is observed. The full epidermal thickness of atypical keratinocytes with bowenoid features is evident at the base of the crater (c). There are no large, pale pink keratinizing cells with a glassy appearance featuring isthmic differentiation in the lobules (c). The histopathological features of solar keratosis are also observed in the periphery of the lesion (b).

Figure 12

Histopathological findings of crater form of infundibular SCC. The lesion has a crateriform KA-like configuration with a central low keratin-filled ulcer (a). The tumor shows neoplastic aggregates of SCC expanding from a follicular infundibulum (b) and neoplastic cells invade deeply into the dermis (a,c). The features of KA or features of bowenoid dysplasia (solar keratosis or Bowen’s disease) are absent in the interfollicular epidermis (a).