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Superficial Morphea: Common morphea is basically an interface disease with the interface being between the reticular dermis and the subcutaneous
fat. In the latter location in a lesion of morphea, fibroblasts are increased in number per unit area; they also tend to be hypertrophied (individually enlarged with enlarged nuclei). In early lesions, interstitial
edema, and perivenular and interstitial infiltrates of lymphocytes, histiocytes, and plasma cells are features. The sclerosis usually begins at the interface between the reticular dermis and the fat. It progresses
upward to more superficial levels in the reticular dermis; it also expands into the domain of the fat. The extensions into the fat initially are thin plaques of delicate fibrous tissue that are based upon the lower
margin of the reticular dermis. Lipocytes become entrapped in this delicate fibrous matrix. The entrapped lipocytes provide a marker for a loss of the domain of the adipose tissue to the expanding reticular dermis.
In this interface reaction, involving both the reticular dermis and the adipose tissue, the contour of the interface eventually is altered. The interface loses its undulating quality; the protrusions of fat about
sweat glands are obliterated. In older lesions, the newly formed fibrous tissues in the domain of the adipose tissue is converted to dense fibrous tissue in which collagen bundles are coarse and are compactly
aggregated. In addition, the collagen bundles of the altered interface tend to be parallel rather than interlaced (an alteration that qualifies as “streaking” of collagen bundles). The collagen bundles, in this type
of interface reaction, may be more brightly acidophilic; they may show some degree of PAS positivity. The sclerosing process, that extends into the domain of the adipose tissue, qualifies as substitutive fibrosis.
With advancing age of the process, the sclerosis extends to more superficial layers of the reticular dermis; eventually, it tends to be pan-dermal in the reticular dermis.
For some examples of morphea, the initial manifestations are represented at both the superficial interface between the papillary dermis and the reticular dermis, and the interface between the reticular dermis and the
fat. The effects at the superficial interface are similar to those described above for the interface between the reticular dermis and the fat. The sclerosing process extends
into the papillary dermis to the dermal-epidermal interface; it extends in sclerosing patterns down into the reticular dermis. Eventually, the superficial process tends to merge with the component that is spreading upward from the interface between the reticular dermis and the fat. Interface changes (i.e., at the dermal-epidermal interface), with liquefaction degeneration of the basal layer of the epidermis, may be a feature.
Superficial morphea takes on significance when the process is isolated without an obvious deep component. For lesions of the latter type, or for superficial biopsy specimens that do not include the deeper portion of
the reticular dermis, superficial morphea presents a pattern (S15C7P1-1 & 2) that may be difficult to distinguish from the patterns of a lesion of LS&A.
The basic features of a classic lesion of LS&A are represented in S15C7P1-3-6. The edematous and
delicate hyaline matrix - in which unit fibrils rather than coarse bundles of fibrils are the rule - of a lesion of LS&A generally is not a prominent feature of the widened papillary dermis in a lesion of
superficial morphea - in which the fibrous tissue is densely fibrous and rarely is edematous.
Keratoacanthoma: Keratoacanthoma, beginning with its initial definition and continuing to the present, is a conceptual problem. The problems seem to
relate to an inability to observe the distinctions between neoplasia and immunostimulation. Some lesions, that are accepted as keratoacanthomas, are apparently non-neoplastic; this seems to be true of
the “keratoacanthomas” encountered in the setting of renal failure and renal dialysis. In these lesions, invasive growth and hypertrophy of keratinocytes are features, but cytologic atypia generally is not a
feature. Lesions in this clinical setting tend to spontaneously regress; they respect the restrictions imposed on the process in the original definitions. With this concession, some keratoacanthomas seem to be
examples of pure immunostimulation.
Lesions, in the most common category of keratoacanthoma (i.e., actinic keratoacanthoma), often do show cytologic atypia. Characteristically, not all of the invasive nests show a
comparable degree of atypia, but all of the invasive nests, in an active lesion, show the cytologic alterations associated with immunostimulation; they are individually hypertrophied and pale (glycogen-rich). In
addition, their cytologic features identify the cells as members of the superficial unit - by inference, cells of the superficial unit are committed to terminal differentiation. As an explanation for the irregular
representation of atypia in the advancing margin of a keratoacanthoma, some of the invasive nests may be neoplastic and some may be simply cells that have responded to a component of immunostimulation. In this
approach, a dual population is represented. The nests showing minimal or no atypia may be of follicular origin, while the nests showing atypia may be of epidermal origin - just as the common actinic keratosis shows
two defined populations, a neoplastic clone of epidermal origin and a benign clone representing the contribution of follicular components. In actinic keratoacanthoma both clones show the distinctive cytologic
features of immunostimulated cells; the cells of an actinic keratoacanthoma, whether atypical, or not, have abundant, pale cytoplasm
and show the cytologic features of keratinocytes of superficial unit of the epidermis; conceptually, by inference from cytologic features, both populations are committed to terminal differentiation and have made a phenotypic transformation to become like cells of the superficial unit of the epidermis - the greatest portion of the cellular population of an actinic keratoacanthoma is phenotypically dedicated to cell death.
For the population showing cytologic atypia, the atypia should not be accepted as a quality defining the process as a fully evolved carcinoma, even though the process is clearly
invasive. Keratoacanthomas, in their period of rapid growh, initially invade dermal connective tissue without inducing tumor stoma; they break into the reticular dermis. In the process, connective tissue fibers of
the reticular dermis become entrapped in the interstitium of the invading epithelium. This period, lasting several weeks, is one of rapid growth; patterns of regression are not prominent and inflammation usually is
mild. Tumor stroma is not a feature; this initial phase might be characterized as an immunostimulatory phase with refractory stroma.
In the common actinic keratoacanthoma, the next phase is characterized by the emergence of an inflamed tumor stroma and by the appearance of patterns of focal regression. This is a
phase of stromal reactivity. In duration, this phase evolves over a period of a few months. Eventually, most lesions tend to stabilize with downward growth limited at about the level of sweat glands. Some examples,
after being arrested at the level of the sweat glands, continue to enlarge centrifugally. Such a lesion in late stages tends to show regression along the base, but usually shows focal or eccentric active growth
laterally (in patterns of both stromal refractoriness and stromal reactivity). Interestingly, the common actinic keratoacanthoma rarely extends beyond the confines of the interface between the reticular dermis and
the fat. Those that do are aggressive variants.
In the final phase, regression is the dominant feature. Microcysts, containing keratinized debris and surrounded by histiocytes and giant cells, provide a marker for sites in
which invasive nests have been destroyed by interaction with host immune response and tumor stroma. Such a lesion tends to present in the pattern of a shallow, irregular crater that is lined by a rather uniform
layer of squamous epithelium (that has reverted to a more normal pattern of differentiation with a loss of cytoplasmic pallor). Even in lesions showing patterns of advanced regression, there may be small foci
showing continued active growth in the patterns of stromal refractoriness (S15C7P2-1-5).
Currently, “solitary” keratoacanthoma is equated with a diagnosis of squamous cell carcinoma; the diagnosis is often qualified (i.e., keratoacanthoma-like carcinoma) to indicate this
compromise. A recommendation to completely excise such a lesion is included in the comments. In this approach, what is the rationale for perpetuating the concept of keratoacanthoma? The answer probably is to be
found in the ploys that are designed to discourage medico-legal claims.
Keratoacanthoma is a squamous cell tumor, expressive of the influence of immunostimulation on the growth of epithelium. The immunostimulation may be operative in a site that is not
neoplastic; in this setting, atypia is not likely to be a feature. It may be operative in the site of squamous cell neoplasia, such as actinic keratosis. In the latter setting, the growth and behavior of a
keratosis, or a incipient squamous cell carcinoma will be altered by immunostimulation. The basic nature and outcome cannot be discerned by the examination of a lesion in the refractory, or reactive stromal phases.
On this basis, keratoacanthoma is keratinocytic tumor of uncertain malignant potential; the lesion should be additionally qualified as to degree of atypia and as to extent of atypia along the advancing margin of the
tumor. The treatment generally is surgical excision. A alternate form of treatment, by choice, or necessity, should be approached with caution and should include consultation with the respective pathologist. On
small, inadquate biopsy specimens, the distinction between keratoacanthoma and carcinoma may be impossible; this is an additional indication for the surgical treatment of lesions in this borderline category.
It should be noted that there are squamous cell carcinomas which show cytologic and structural features of keratoacanthoma, but apparently do not enter a phase in which a reactive
stroma is a significant feature; in the absence of a reactive stroma, these carcinomas do not regress to a significant degree. These lesions commonly show nerve sheath invasion and invasion of the subcutis. They are
aggressive squamous cell carcinomas in the pattern of an immunostimulated lesion; they invade the dermis in the absence of a tumor stroma and, in the act, entrap connective tissue fibers. These lesions often
do not show significant atypia, or nuclear pleomorphism. They commonly invade subcutaneous tissue and, in the act, come to qualify as aggressive variants.
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