One of the most dramatic moments in my early career happened at a meeting of The Dermatology Section of The Royal Society of Medicine in 1978. A young girl was presented with very numerous moles quite a few of which were clinically atypical (increased size- generally 6mm or more in diameter, irregularly shaped with irregular borders ad variable pigment distribution). Wallace Clarke and co-workers had just described the “B-K mole syndrome” and Lynch and co-workers, “the familial atypical multiple mole melanoma syndrome”. As I remember it, the patient was the first case to be recognized with this condition in the UK. The excitement was palpable. For the dermatopathologists, at long last we had a fresh idea about what to do with those odd nevi that defied classification. In my Belfast days, our professor had called them “activated nevi”. We had nodded our heads wisely and said nothing more. Ah, the mystery of pathology! When they were described as occurring in patients with no evidence of a syndromic association and better still when they were identified as a single lesion, our life became so much easier or so it seemed at the time.

Nothing “good” lasts! There was quite a transatlantic divide. In the UK, many didn’t buy into the concept of the solitary dysplastic nevus, let alone its possible biological potential. In the States, the view was quite different. After all Boston was its birthplace and Wallace Clarke, its father! People didn’t seem to be able to agree on terminology, dysplastic, atypical and Clarke’s nevi all had their proponents. How to report them (if one believed in them) was another source of controversy. Should we grade them based on cytological atypia and if yes, how should we do it. Did grading mean anything? Was a high-grade lesion more likely to evolve into melanoma? Where was the proof? It became an almost personal matter- they didn’t exist, grading was worthless, they could be divided into low- and high-grade lesions (without giving very clear instructions on how to do this) or if one followed Ray Barnhill and his colleagues, they should be classified in 3 categories based on a comparison of the nevus nuclear size with that of a nucleus of a keratinocyte in the mid prickle cell layer. Mild, moderate, and severe atypia became solidly established in the lexicon of American dermatopathology. Equally problematical was what to do about them. Should they be re-excised if the initial biopsy showed lesion at a margin? How would one distinguish between a dysplastic nevus and in situ melanoma and did it really matter provided the lesion was fully excised?

When I crossed the great pond and found myself in Boston, it became very clear just how I was meant to deal with dysplastic nevi. Yes, they should be graded into three categories following the instructions that Ray and his colleagues recommended and yes, incompletely excised lesions must be re-excised. This was firmly entrenched in the minds of the dermatologist. I would receive phone calls from them asking what they should do and why hadn’t I included a recommendation in my report!

Nothing lasts forever, in the most recent WHO blue book, dysplastic nevi with mild cytological atypia became demoted and subsumed within the category of a banal nevus. What a strange world we live in.

Since the description of the dysplastic nevus, so many “new” entities have been described sometimes including the term atypical- atypical genital nevi, milk line nevi, atypical nevi of the ear and scalp, atypical common blue nevus, atypical cellular blue nevus and last but certainly not least, the atypical Spitz nevus- more about that later.

Melanocytic remains such a challenging topic and indeed it is the single most common source of litigation. I still have hopes that the scientists will one day put to rest all the controversy surrounding this common lesion. Hope springs eternal!

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