Acanthosis is defined as a thickened epidermis. Acanthosis may be “regular” with rete ridges of similar length (resembling psoriasis) or “irregular” with rete ridges with marked difference in length and width such as what is seen in pseudoepitheliomatous hyperplasia (Fig. 2.2). The clinical correlation of acanthosis is the sense of thickening of the skin upon palpation. Acanthosis is frequently associated with changes in the stratum corneum such as parakeratosis or orthokeratotic hyperkeratosis. Acanthosis is evidence of chronicity and does not occur in the acute setting. Thus, one may think of plaque-stage psoriasis that has been present for a while when there is regular acanthosis. This finding would not be expected in a relatively acute lesion of psoriasis. In addition, psoriasis of the genital site can exhibit spongiosis and only focal mounds of parakeratosis containing neutrophils. Similarly, chronic spongiotic (eczematous) processes will demonstrate regular acanthosis, though acute spongiotic processes will not show this change. Lichen simplex chronicus may show either regular or irregular acanthosis, and this always occurs with hypergranulosis and orthokeratotic hyperkeratosis as well as vertical papillary dermal fibrosis. In acanthosis nigricans, there is frequently regular acanthosis. Regular (psoriasiform) acanthosis is a common feature of syphilis, and in these cases plasma cells are almost always seen in the inflammatory infiltrate. Many other infectious diseases including viral, bacterial, and fungal infections demonstrate irregular acanthosis, and most commonly, there is a brisk inflammatory infiltrate in these cases.

See regular acanthosis above.

Parakeratosis is the preservation of nuclei into the stratum corneum (Fig. 2.2). The clinical correlate of parakeratosis is the presence of a superficial scale. Lesions that demonstrate parakeratosis are invariably described as scaly processes. This finding occurs in two basic types of conditions. It may be seen with abnormal maturation of keratinocytes such as what may be seen in squamous cell carcinoma, vulvar intraepidermal neoplasia (VIN), or bowenoid papulosis. It may also be seen in hyperproliferative states such as psoriasis and spongiotic dermatitis and with infectious processes. The observation of cytological atypia would point the diagnostician in the direction of a condition with abnormal maturation, while the presence of spongiosis and/or neutrophils might be helpful in pointing one toward a diagnosis of a spongiotic process or toward psoriasis.

Hyperkeratosis is defined as the excess stratum corneum for the site. Orthokeratosis describes the case when the excess keratin is devoid of nuclei (unlike parakeratosis). The excess keratin may demonstrate a basket-weaved pattern or may be compact (Fig. 2.2). The clinical correlate is that of a scale that may demonstrate a brownish color when the orthokeratosis is marked in extent. Orthokeratotic hyperkeratosis is most commonly encountered in lichen simplex chronicus and is often a clue to chronic irritation or rubbing. This is especially true when the basket-weaved pattern is lost and there is compaction of the stratum corneum. Despite the atrophic epidermis that characterizes well-developed lesions of lichen sclerosus, the stratum corneum tends to be hyperkeratotic and orthokeratotic in this condition. The difference in the thickness of the epidermis (acanthotic vs. atrophic) can be a useful additional clue to distinguish lichen simplex chronicus from lichen sclerosus, although one can see superimposed changes of lichen simplex chronicus in long-standing lichen sclerosus due to rubbing.

Hypergranulosis is defined as a relative increase in the thickness of the granular layer (Fig. 2.2). This is site specific and one would expect to see a much thicker granular layer on acral skin than is normal on vulvar skin. Hypergranulosis often correlates with a whitish color clinically. Depending upon the extent of the hyperkeratosis, the white coloring may be focal and “lacy” (lichen planus) or diffusely white (some cases of lichen simple chronicus). When the observer notes hypergranulosis, several diagnostic entities become likely. Lichen simplex chronicus demonstrates this finding in concert with psoriasiform epidermal hyperplasia, compact orthokeratotic hyperkeratosis, and dermal fibrosis. In lichen planus, one sees hypergranulosis accentuated in eccrine acrosyringium along with a lichenoid inflammatory infiltrate. A verruca vulgaris may demonstrate hypergranulosis and frequently papillomatosis. If cytological atypia is noted, bowenoid papulosis should be considered as a diagnostic possibility.

Hypogranulosis is defined as a relative thinning of the granular layer (Fig. 2.2). In some cases, it may be completely absent. Hypogranulosis frequently occurs in concert with parakeratosis. There is no reproducible clinical correlation to the observation of hypogranulosis. The most common situations where the observation of hypogranulosis is encountered in vulvar biopsies include psoriasis, relatively acute spongiotic dermatitis, and bowenoid papulosis. The presence of neutrophils may point toward the diagnosis of psoriasis, while the presence of spongiosis (see below) might lead to a diagnosis of some type of spongiotic (eczematous) process. Cytological atypia in the presence of hypogranulosis might favor a diagnosis of bowenoid papulosis.

Dyskeratosis refers to the abnormal keratinization of individual cells within the lower portions or midportions of the epidermis (Fig. 2.3). This change may occur in situations with abnormal keratin production or in situations with exocytosis of lymphocytes into the epidermis. There is no clinical correlate to this finding except when it is extensive and may give rise to small vesicles. Dyskeratosis is a prominent finding in Darier’s disease and in warty dyskeratoma. In both cases, there is also a prominent hyperkeratosis. Warty dyskeratoma will demonstrate a cup-shaped architecture that is not seen in Darier’s disease. Dyskeratosis may be seen in inflammatory entities such as lichen planus in concert with hypergranulosis, orthokeratotic hyperkeratosis, and a band-like inflammatory infiltrate. Similarly, dyskeratotic cells may be seen in erythema multiforme and in graft-versus-host disease, though the inflammatory infiltrate is not usually as pronounced as that seen in lichen planus. Cases of bowenoid papulosis may similarly demonstrate dyskeratosis and cytological atypia that is more diffuse than what is encountered with chemotherapeutic changes.