Keratoacanthoma vs. squamous cell carcinoma in contrast with keratoacanthoma is squamous cell carcinoma

To the Editor Forslund et al. accept the premise that keratoacanthoma (KA) and cutaneous squamous cell carcinoma (SCC) are not within the same biological and diagnostic spectrum, in contrast with recent thinking by a number of authors, notably Ackerman, who regard solitary KA as a specific type of SCC. Forslund et al. state that ‘Keratoacanthomas are benign, clinically distinct skin tumors generally located at sun-exposed sites in elderly fair-skinned people. . .Histologically, keratoacanthomas are diagnosed by their architecture as well as their cytological features, and when also considering their characteristic clinical history most keratoacanthomas can be distinguished from SCCs.’ The authors do not state whether they believe KAs are examples of hyperplasia or neoplasia. This distinction, however, is important because hyperplasias are reversible conditions, whereas neoplasms, as a rule, do not resolve spontaneously. To approach this issue another way, if one were to develop the hypothesis that KA is hyperplasia, rather than neoplasia of keratocytes, the finding of human papillomavirus (HPV) is an intriguing premise on which to base that investigation, as any dermatologist or dermatopathologist knows from dealing with verrucae vulgares. In order to investigate that question scientifically, one would, however, need to identify a control group of uncontroversial squamous carcinomas as part of any such study, in addition to the experimental group, i.e. KAs. Further-more, it would also be extremely useful to find examples of ‘KAs’ that metastasized (i.e. unequivocal SCCs that are well differentiated) and to subject these lesions to a study of a possible association with HPV. In the study by Forslund et al., however, I do not see any evidence that they considered investigating controversial or uncontroversial cutaneous SCCs as a control group. Thus, how are the authors to know whether HPV might be detected in cutaneous SCCs? Furthermore, how would the authors respond to the advocates of KAs are squamous carcinomas? Those who include KAs as examples of SCCs would argue that some SCCs contain HPV, and, perhaps, that HPV is an inducer, not unlike HPV 16and 18-associated SCCs that have been documented well in the literature. They might also argue it that it is not causal at all – true, true but unrelated. In contrast, the argument from those who believe that KA is hyperplasia would probably favor the point of view that HPV causes KA, which regresses once the effects of HPV have played out. However, without using control groups of welldocumented examples that either camp would agree are KAs or SCCs, the presence of HPV in a KA has no scientific meaning whatsoever, at least regarding the question of KA vs. SCC in contrast with KA is SCC. Finally, the authors did not show examples photographically of what they were investigating, thus the reader cannot tell whether these are classical KAs or classical SCCs. I urge the authors to clarify their nosological position on KA and to show photographically what they mean by the use of that term. Yours sincerely