Battle of words: Response to 'dysplastic' debate

October 1, 2007


I am delighted to respond to Michael Coverman, M.D.'s, letter and hope that I can shed some light on the topic. Let me start by asking "Why do we get moles, anyway?" In insects, melanin is the primary immune response mechanism. Humans have a more sophisticated defense system with antibodies and the like, but we retain our primordial immunological forms as well.

Melanocytes are not simply pigment-producing cells, but they manufacture substances with a range of biological functions, including structural strengthening by cross-linking proteins, antimicrobial defense, photon shielding and chemoprotection.

God gave us melanocytes and moles to provide several physiologically significant functions, including provision of communicatory links with several different systems, e.g., the skin, central nervous system and the immune/inflammatory response.

Thus, moles aren't necessarily all bad, as insinuated in your note. In an analogous situation, white blood cells can cause leukemia, but not every white blood cell is bad.

I concede that the terms "atypical" and "dysplastic" are confusing, especially when they are used to describe a type of harmless mole that typically has no atypia and no dysplasia. The NIH has recommended eliminating this terminology since 1992.

I am not the only one who considers dysplastic nevi to be one form of benign acquired melanocytic nevi; the NIH does, also. The loose use of the term "dysplastic" in our present histologic melanocyte terminology is, at best, misleading. The term "dysplastic nevus"' has probably been retained, not for historical reasons, but rather to facilitate reimbursement from third parties.

Our terminology must be in line with other pathological fields in which this term confers abnormal growth or development, as well as implying that the lesion is a direct precursor of malignancy. On point, some authors have stated that all nevi should be considered precursors of melanoma. If a progressive transformation exists from normal melanocyte to melanoma, where along this biologic continuum do we inform the public that a particular mole type should always be excised prophylactically?

I should add that nuclear atypia is not a separate criterion for dysplastic nevi but rather can be seen with any melanocytic nevi. As I have stated before in the literature (N Eng J Med. 2004;350:12; SKINmed. 2003;3:12-13), dysplastic nevi should be considered benign and treated accordingly, with repeated excisions reserved only for those showing clinically significant cytological atypia (just like with any other type of nevus). In short, a coherent, sensible classification of melanocytic nevi should be established.

In regards to Dr. Coverman's query of my integrity, I am a clinical professor at University of Toledo College of Medicine as well as clinical assistant professor at Ohio University of Osteopathic Medicine. Additionally, I have a master's in Public Health. I also try to practice in an "honorable and ethical fashion." Let me pray that all the readers of Dermatology Times do the same.

The terms "dysplastic" and "atypical" continue to confuse patients, internists, primary care physicians and dermatologists in terms of definition and significance. There continue to be many additional surgical excisions and repeat excisions that have been performed needlessly because of an improper understanding of dysplastic nevi.

I have pleaded in my article in the Journal of Cutaneous Pathology (2005;32:642-643) for a panel of dermatopathologists to expound the truth about this confusing terminology. So far, all they have provided us with is a survey relating to the confusion related to this entity (J Cutan Pathol. 2004;31:523-527).

In this latter publication, I compared this confusing terminology with dysplastic nevi to mondegreens, which are misinterpretations or mishearings of popular phrases and/or song lyrics. For example: