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Benign lichenoid keratosis, otherwise known as lichen planus-like keratosis, is a common, cutaneous entity that is often confused with cutaneous malignancy. Few studies have examined the multiple clinical and pathologic guises of this entity, particularly within the context of clinical pathologic correlation or magnitude of this study. We examined the epidemiologic, clinical, and pathologic attributes of 1040 consecutive cases of benign lichenoid keratosis referred for pathologic examination at a busy laboratory over an entire year. Clinical parameters assessed included the age, anatomic location, gender, and multiplicity of the lesions. Pathologic attributes were assessed yielding discernment of five different subtypes that included a classic type, bullous type, atypical type with cytologically atypical lymphocytes, an early or interface type, and a late regressed or atrophic type. The results yielded an average age at presentation of 59.5 years with an age range of 36 to 87 years. The gender frequency was 76% female, 24% male. The trunk was the most common location (76%), followed by the extremities (33%) and head and neck (7%); 8% of patients presented with two lesions and less than 1% with three lesions prompting consideration of lichen planus. The classic, atypical, and bullous forms of the disease clinically presented with erythematous papule/plaque(s). The early or interface type showed erythematous to hyperpigmented brown macules and the regressed or atrophic type presented as violaceous papules or irregularly distributed macular pigmentation; 81% of the lesions showed the classic histology consisting of epidermal acanthosis with a band-like lichenoid lymphocytic infiltrate. Variable numbers of plasma cells, eosinophils, and neutrophils were identified as well as epidermal parakeratosis distinguishing these lesions from typical lichen planus. The bullous variant showed intraepidermal or subepidermal bullous cavities with a dense associated lymphocytic infiltrate and increased numbers of necrotic basilar layer keratinocytes. The atypical variant showed features of the classic type with scattered enlarged CD-3, CD-30 (+) lymphocytes possessing hyperchromatic, irregular nuclei. The early interface type showed single lymphocytes aligned along the dermoepidermal junction without epidermal acanthosis and adjacent lentigo. The regressed or atrophic variant showed epidermal atrophy with papillary dermal scarring, patchy lymphocytic infiltrates and melanin incontinence. The clinicopathologic spectrum of benign lichenoid keratosis is broad and encompasses several unrelated entities. An awareness of its expanded presentation is essential to avoid misdiagnosis and may serve as an important forerunner of pathogenic discernment.

Trichilemmal keratosis (TK) is an uncommon epidermal tumor that exhibits a keratinizing surface with the formation of a cutaneous horn and that clinically resembles a hyperkeratotic actinic keratosis. Histologically, there is verrucous hyperplasia of the epidermis with orthokeratotic hyperkeratosis. TK is characterized by abrupt keratinization without formation of a granular cell layer, in the same manner as that in which the outer root sheath keratinizes (trichilemmal keratinization). The epidermis is acanthotic and contains pale-staining keratinocytes. Epithelial lobules and small trichilemmal cysts are connected to the thickened epidermis. We describe the clinical, histologic, and immunohistochemical findings of two cases of TK.

The distribution of A, B, and H blood group antigens was studied by means of peroxidase-antiperoxidase technique in normal skin and in lesions of carcinomas in situ (solar keratoses, Bowen's disease), squamous cell carcinoma, keratoacanthomas, and verrucae. In normal skin, the epidermis of persons of blood group O showed H antigens throughout the epidermis; of blood group A, H and A antigens; and of blood group B, H and B antigens. In lesions of solar keratoses, there were no antigens of blood groups in the irregular downward proliferations. In five of 11 cases of Bowen's disease, there were no antigens of blood groups in the epidermis. In eight out of 10 cases of squamous cell carcinoma, no antigens of blood groups were found in the islands of the neoplastic process, but in two cases they were present in a patchy distribution. In the benign lesions examined, the antigens of A, B, and H blood groups were always present, although in verrucae the staining was confined to the upper layers of the epidermis only.

Common benign skin abnormalities and related tumours were investigated for the presence of carcinoembryonic antigen (CEA) using immunohistological techniques in formalin-fixed tissue. CEA could be detected in all 10 squamous cell carcinomas examined, a finding which contrasted with those in earlier reports. CEA was not seen in normal skin but was present in the skins of 12-18-wk-old fetuses. Hence, CEA can be considered to be a true oncofetal antigen for ectodermal tissue. The antigen was not detected in seborrheic keratoses but was present in all 10 cases of keratoacanthoma. CEA was found in only one out of 10 basal cell carcinomas, the tumour being metatypical (basosquamous) in type. CEA was also observed in the minority of cases of solar keratosis and Bowen's disease. If the presence of CEA in proliferating epidermal tissue is associated with malignant transformation, both solar keratosis and Bowen's disease are indeed premalignant lesions whilst keratoacanthoma is the non-metastasizing variant of squamous cell carcinoma. Finally, the absence of CEA in basal cell carcinoma may help to explain its 'reluctance' to spread by metastasis.