Morphology, Magic and the Clinical Legacy of A. Bernard Ackerman 

There are many authors of the Clinical Atlas, but I believe that all would agree that it was summoned into being by the daemon of A. Bernard Ackerman. Writing nearly a decade after his passing, the number of Dr. Ackerman’s students who remain as active practitioners of pathology, dermatology and dermatopathology is dwindling. The readership of, the website he founded and nurtured, is in vast part composed of physicians who did not know “Bernie” (as he insisted he be called), knew him in passing, were familiar with some of his work and teachings, or may not have known him at all. It is thus fitting that we begin this reworking of the Clinical Atlas with an introduction to how Bernie’s persona, cognitive style, mode of working and way of thinking shaped the Atlas and how our approach bears on this in the reimagining of it.

For those who know little of Bernie, he was certainly the most famous dermatopathologist of the last quarter of the twentieth century—and was also perhaps the most famous dermatologist and pathologist as well. There were many reasons for this. He accepted no received knowledge uncritically, measuring what he was taught against his own experience as well as the theories of others. Early on, this intellectual restlessness expressed itself in his medical education. In his three years of formal training in dermatology, he was a resident at Columbia, Penn and Harvard—the leading programs of the time. Bernie may have intuited the 80/20 rule long before its formalization—that 80% of what someone has to say can be garnered from the first 20% of what they say or write.

Bernie ascertained that dermatopathology was a field ripe for revision. One of his teachers at Columbia looked at slides of a basal cell carcinoma with him and remarked on “how much this aggregate of cells looked like a cloud and that one like a doggy”. Here then was discipline sorely in need of a comprehensive revitalization! His early ambitions to be a diplomat had been derailed by a domineering father who gave him a narrow choice—dentistry or medicine. Unlike now, dermatology was not a prestigious specialty, and Bernie’s choice of it was rebellious. But dermatopathology, this world within a world, was to be his oyster.

Both the pathology and dermatopathology of his time were based on experience, not method or criteria. This frustrated him. To answer this student, who wanted to know “why does this slide signify that the patient has melanoma?” with “in time, experience will tell you that it does”, was an insult to intellect and rational thought. Bernie began to amass criteria for diagnoses, and devised one of the first comprehensive algorithmic approaches to diagnosis in pathology or dermatology. From teaching himself, he branched out to teaching his method to others. He had little doubt that there was anyone in the world that had a functioning frontal cortex that he could not teach dermatopathology to. “I can teach a monkey to read slides” was his boast. Among the trainees at the multi-headed microscope that he taught at were not just residents and fellows, but high school and college students. None walked away untutored in how to recognize a seborrheic keratosis, basal cell carcinoma or nevus.

The method that animated Bernie’s work was pattern analysis. From clinical dermatology he had gleaned that one did not begin to observe a patient with one’s nose plastered against their skin but instead a few feet away at a sufficient distance to view the distribution of lesions. From there, one could move to evaluating the fundamental type of lesion, and lastly, details within it. For many pathologists of the time, cytologic observations were given precedence, and decisions about the benignancy or malignancy of a tissue specimen were made at high magnification. In his approach to diagnosis histopathologic, Bernie instead proposed to start by looking at the slide at the lowest power possible, and gleaning every detail that he could, before moving to high power. Most famously, for melanocytic neoplasms this meant looking first at size, symmetry, circumscription, and maturation with descent, and only later at cytologic features. The magic that Bernie wrought was to meld a connoisseur’s appreciation of clinical and histopathologic morphology with lively writing and artistic presentation—initially in the form of beautifully printed and meticulously illustrated monographs.

To say that Bernie was computer literate (a phrase showing its age in an era when infants navigate touch screens on tablets and computers before learning to walk) would be preposterous. He was a lover of books and published many of the most lucid and beautifully presented volumes in the modern era of medicine. While not his first love, he grasped early on how web-based publishing could enable dissemination of his ideas to worldwide in a way that print never could. A Clinical Atlas had among its aspirations to be comprehensible to those outside dermatology by dint of limiting the number of diseases it dealt with to the magic number of 101. It was first published as a paperback—hardly Bernie’s preferred form. His first and signature oeuvre, Histologic Diagnosis of Inflammatory Skin Diseases appeared in hardcover, looking to all the world like a product of the golden age of Unna, Kaposi and von Hebra. The democratic ideal of the Clinical Atlas was thus born from the mind of a man whose elitist instincts had driven most of his other projects. was a democratizing vehicle, but the contents were slated to be aspirational, and exceptional.

The first edition of the Clinical Atlas incorporated the essence of Bernie’s ideas about how to teach clinical dermatology. At its heart was an appreciation of clinical morphology. An atlas is only as good as its pictures, and those chosen (from many times the number published) were iconic. Many came from the collections of former students; most notably those at the University of Graz, Austria, where a professional photographer impeccably lit patients to bet effect and employed a black velvet background. Such resources are regrettably shrinking in a world in which molecular biology is king and morphology is given lip service but not honored with resources. Oddly enough, while Bernie developed algorithms for both inflammatory and neoplastic dermatopathology, he never fully realized the project of a grand algorithm for clinical dermatology.

What the Atlas lacked in terms of a method, it made up for in succinctness and relevance. Its overarching purpose was to make an important disease come alive, so that the non-specialist or a trainee first approaching the subject could grasp the essence of a disease. To that end, references to technology that was unlikely to be found in the developing world were minimized, while the use of eyes connected to the cortex was maximized. For each disease, a definition, a description and depiction of its lesions, a statement about the clinical course (sometimes with and without treatment) and integration were delineated. For all his love of dermatopathology, detailed descriptions of histopathology did not find their way to the Atlas. Instead, a thumbnail of an iconic photomicrograph stood among the initial images in each chapter, and pathology was interwoven into integration. In this edition of the Clinical Atlas, we have somewhat maintained this forbearance but will make histopathology and microscopic images of all 101 diseases available via hypertext.

Many of Bernie’s concepts about the nature of skin disease have now been tested by scientific developments; some have been found flawed and will herein be revised, while others have proven sound. Others are yet debated. Foremost among Bernie’s hypotheses was the “big bang” theory of cancer. For him, a neoplasm (he eschewed the term “tumor”, as it originally implied the formation of a mass, while some neoplasms, e.g., melanoma in situ, Kaposi’s sarcoma, mycosis fungoides began with flat, nearly substanceless lesions) was either benign or malignant, and one could tell that he regarded the development of cancer from a benign neoplasm with suspicion. Borderline lesions did not exist in his mind—only borderline pathologists. Advances in molecular pathology have proven Bernie wrong about this in a large sense and right about it in a small but not insignificant one. For many neoplasms, we now know that there are initiating mutations and that the layering on of additional mutations can lead to genetic instability, and thence to cancer. This multistep theory of cancer progression is now dogma. Yet, for many neoplasms, the early steps are slow, and while there is no “big bang” at the beginning of tumorigenesis, there is one toward its end. For example, nevi are often initiated by mutations in the oncogene b-raf, grow for years, then undergo mutations in the hTERT promoter gene and only develop into full-blown melanoma when a tumor suppressor, CDKN2A, is lost. Along with that aberration, increased proliferation occurs, and nuclear atypia becomes marked. Other flawed concepts about melanoma include the hypothesis that melanoma is one disease (it is genetically diverse) and that the sun has little to do with its genesis (C to T mutations, a hallmark of actinic damage, are ubiquitous in melanomas in severely sun-damaged skin). Hence, we aim to revise the discussions of nevus vs. melanoma and other neoplasms to reflect this without dwelling on the exact molecular aberrations except when memorable, vital to clinical practice, or a tool to learning.

A few entities, such as pyogenic granuloma and dermatofibroma, were presented in the original Clinical Atlas as inflammatory, rather then neoplastic, skin diseases. For Bernie, the history of trauma (in both cases) often related by patients was given weight disproportionate, as was the mixture of cell types. The line between hyperplasia and neoplasia are now known to be far fuzzier that when Virchow formulated them.

The task of revising the text of the Atlas is easier with respect to inflammatory skin disease. While there has been an explosion of knowledge about the immune system, it has not lead to an overhaul of our concepts regarding these entities. There is no comprehensible classification based on “diseases of T regulatory cells” or “diseases of CD4+ lymphocytes.” However, a group of conditions clearly represents disorders of innate immunity, with over-activity of neutrophils. This is not just conceptually interesting, but provides a rationale for therapy. Still, to keep the Atlas intellectually sound (and in Bernie’s tradition), the diseases are listed alphabetically without an attempt to superimpose an artificial structure on them.

I hope that our revisions will prove useful as the Atlas enters a new century, and reaches practitioners in new and innovative ways.

Philip E. LeBoit, MD
Departments of Pathology and Dermatology
University of California, San Francisco