Squamous acanthoma of the oral mucosa Charles E. Tomich, D.D.S., M.S.D.,* and Will&n G. Shafer, D.D.S., M.S.,” Indianapolis, SCHOOL OF DENTISTRY,
INDIANA
UNIVRRSITY-PURDUE
Ind. UNIVERSITY
Eight cases of a heretofore unreported pathologic entity termed squamous aeanthoma are described. The lesion, which has no distinctive clinical appearance by which it can be identified, may occur virtually anywhere on the oral mucosa. It is seen predominantly in older men. The lesion is histologically distinct and consists of a welldelineated elevated and/or umbilicated epithelial proliferation with a markedly thickened layer of orthokeratin. It is postulated that the lesion is caused by trauma and develops its characteristic morphology by a series of epithelial alterations, beginning with pseudoepitheliomatous hyperplasia.
T
he oral epithelium generally does not manifest the wide variety of benign and malignant tumors or reactive lesions seen on the skin, presumably in part at least because of the absence of most of the various adnexal structures present in the skin. Conversely, there are seen occasional lesions of the oral epithelium which do not have an obvious dermal counterpart. The purpose of this report is to cite such an example that does not appear to have been previously described in the dental literature. The first instance of this lesion was seen in the tissue diagnosis service of Indiana University School of Dentistry, Department of Oral Pathology, in December, 1960. This was described as a sessile, well-circumscribed, mobile lesion measuring 10 by 15 mm. on the inner surface of the lower lip in a 6%year-old man with jagged anterior teeth that continued to irritate the lesion, which may have been preceded by a bite. This lesion was initially diagnosed histologically as pseudoepitheliomatous hyperplasia. Subsequently, seven additional lesions, all summarized in Table I, have been seen which have certain histologic features in common and which seem to represent a specific entity. We have been identifying this lesion as a %quamous acanthoma.” To the best of our knowledge, this lesion does not appear to have been described previously in the oral cavity. There are several lesions of the skin which bear a superficial resemblance to the oral squamous acanthoma, but there are some significant differences and the lesions in the two sites are probably *Associate Professor, Department of Oral Pathology. **Distinguished Professor and Chairman, Department
of Oral Pathology.
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756
Tomich and Shafer
Oral Surg. November, 1974
Pig. 1. Squamous acanthoma. A represents characteristic pseudo-epitheliomatous hyperplasia and B demonstrates elongation and confluence of rete ridges. C shows the %nmature” squamous acanthoma which precedes the fully established or “mature” form shown in D. (Hematoxylin and eosin stain. Magnification, x4.)
Volume Number
38 5
Squamous acanthoma of oral mucosa
757
Table I Irritant Location
Clinical
appearance
68
M
White
Lower lip, inner surface
Se&e, wellcircumscribed
+
72
F
White
Lateral
Elevated, white, verrucous area
+
55
M
White
Flat, white area, “sore spot”
29
M
White
Edentulous maxillary alveolar mucosa Palate
43
M
White
Palate
58
M
White
50
M
White
Anterior floor of mouth Mandibular retromolar pad
Raised, red, granular area White, verrucous lesion White, pedunculated pebbly, round Elevated, white area
53
M
White
tongue
Edentulous mandibular alveolar mueosa
Elevated,
white
area
N.S.
N.S.
Teeth (jagged) Denture with rough flange N.S.
N.S.
N.S.
2 months
N.S.
N.S.
Several years N.S.
N.S.
N.S.
N.S.
N.S.
“Quite some time” N.S.
2 weeks
1 year
unrelated. Such skin lesions include the basosquamous-cell epidermal tumor (basosquamous-cell acanthoma) and invasive acanthosis (invasive acanthoma) , the latter actually constituting a variety of clinical lesions related to pseudoepitheliomatous hyperplasia, described by Lund1 in the Armed Forces Institute of Pathology fascicle on Tumors of the Sikl CLINICAL FEATURES The eight cases of squamous acanthoma occurred predominantly in men, there being only one case in a woman, and usually in the sixth decade or beyond. The youngest patient was 29 years old; the oldest was 72. The sites of occurrence of the lesion were quite varied; there were two cases on the palate and one case each on the lower lip, lateral tongue, edentulous maxillary alveolar mucosa, edentulous mandibular alveolar mucosa, anterior floor of the mouth, and retromolar pad. The known duration of the lesions varied from 2, weeks to several years, although in the majority of cases the duration was not stated. The clinical appearance of the lesions was usually described as being a white area, either flat or elevated, sometimes granular, verrucous, and sessile or pedunculated. HISTOLOGIC
FEATURES
The squamous acanthoma appears to arrive at its fully mature state through a series of alterations in the epithelium, consisting of elongation, broadening, and confluence of the rete pegs, progressing to a compact, uniform mass of acanthotic epithelium, smoothly rounded on the inferior margin, with no evidence of remaining rete pegs (Fig. 1). Early in the process of the epithelial alteration, the proliferating rete pegs commonly exhibit varying degrees of
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Ton&h
Oral Surg. November, 1974
trod Shafer
"MATURE" HYPERPLASIA
-SQUAMOUS
ACANTHOMA-SQUAMOUS
ACANlHOMA
Fig. 8. Proposed pathogenesis of the squamous acanthoma.
pseudoepitheliomatous hyperplasia. The surface of the lesion in the early stages is covered by a thickened layer of either orthokeratin or parakeratin, while in the fully mature lesion there is usually a very marked hyperorthokeratosis. The outline of the surface may be smoothly elevated, elevated with a central umbilication, or flat with umbilication. Occasionally, the surface, particularly when it is covered by parakeratin, is shaggy in texture. The lesion is generally rather well circumscribed or demarcated from adjacent normal epithelium, sometimes very strikingly so (Fig. 1, C and D) . Epithelial dysplasia is absent, although an occasional epithelial pearl may be found. In most cases, a mild inflammatory infiltrate is present in the underlying connective tissue, but this is usually limited in degree. DISCUSSION The cause of the squamous acanthoma is not known for certain; however, trauma most likely plays an important etiologic role. Likewise, the pathogenesis of the lesion is unknown, but it is speculated that it develops in the following manner: We postulate that the squamous acanthoma begins its biologic life as pseudoepitheliomatous hyperplasia and “matures” into the discrete, welldelineated lesion that has been described (Fig. 2). Between these two stages, there is an “immature” stage which is characterized histologically by a confluence of the epithelial proliferations into broad rete ridges or acanthotic bands of epithelium. Pseudoepitheliomatous hyperplasia is a well-recognized epithelial response to a variety of noxious stimuli. This histologic phenomenon is reversible and therefore, if the irritant is removed, the epithelium will, in time, assume its characteristic morphology. On the other hand, if the irritant persists, the epithelium may ulcerate, become hyperplastic, or possibly even become neoplastic. It is tempting to speculate, therefore, that one of the latter alternatives ensues in certain situations and gives rise to the squamous acanthoma. The fate of the squamous acanthoma is, obviously, unknown. SUMMARY A heretofore unreported pathologic entity termed squamous acanthoma has been described. The lesion, which has no distinctive clinical appearance by which it can be identified, may occur virtually anywhere on the oral mucosa. It is seen predominantly in older men. The lesion is histologically distinct and consists of a well-delineated elevated and/or umbilicated epithelial proliferation
Volume Number
38 5
Squamous acanthoma of oral mucosa
759
with a markedly thickened layer of orthokeratin. It is postulated that the lesion is caused by trauma and develops its characteristic morphology by a series of epithelial alterations, beginning with pseudoepitheliomatous hyperplasia. REFERENCE
1. Lund, H. Z.: Tumors of the Skin, Atlas of Tumor Pathology, Section ington, D. C., 1957, Armed Forces Institute of Pathology, pp. 42, 64. Reprint
requests
to:
Dr. Charles E. Tomich Department of Oral Pathology Indiana University School of Dentistry 1121 West Michigan St. Indianapolis, Id. 46202
1, Fascicle
2, Wash-