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Here is an impressive tour de force which could also be called “40 years’ experience in microscopy of tissues from rheumatic disease patients”. The author, born in 1929, has probably seen more joint specimens under his microscope than anyone else and he is still head of a WHO centre of joint pathology in Mainz, Germany. This work is essentially based on his personal observations of histology and electron microscopy on biopsy, surgical, and perhaps postmortem material sent for diagnosis to his institution. It contains 31 chapters dealing with individual conditions and ends with a chapter called “Possibilities and limitations of synovial biopsy”, which summarises Fassbender’s legacy on three pages. Although the synovium is a loose tissue without definite structural components, it is possible to discern features distinguishing psoriatic arthritis and spondyloarthropathies from rheumatoid arthritis in its various stages and even to distinguish between osteoarthritis and “coxarthrosis”. But it may take a lifetime to convince oneself, and even longer to convince the world, that this is indeed possible.
One hundred of the 500 pages are devoted to rheumatoid arthritis, and it is in this disease that the author has made his most significant contributions. He points out that cartilage destruction seems to be initiated by a transient tumour-like aggressive tissue, consisting of undifferentiated mesenchymal cells, which precedes pannus. Another observation of interest is the relative absence of osteoclasts. His hypothesis is that synovial fibroblasts are the dominating bone destructive cells. The hypothesis has gained support from experimental work in Dr Steffen Gay’s laboratory in Zurich,1 but it would be wrong to say that it has gained general acceptance. One explanation for Fassbender’s relatively late recognition may be that most of his earlier work was published in German. The oldest English publication I could trace was from 1983.2.
Fassbender is well aware of modern classics in the rheumatological literature and cites, for example, Dr Bywaters’ paper on Jaccoud’s deformity in the chapter on rheumatic fever. I believe, however, that most of us, including Eric Bywaters, now consider Jaccoud’s deformity to be a manifestation of SLE. In synovial tissue obtained after joint replacement he finds giant cells as well as cement particles. Fibrin “exudation” (why not deposition?) is characteristic of rheumatoid joints and much less present in, for example, osteoarthritis or psoriatic arthritis. Some Germanisms can be found in the text. Interleukin 1α and tumour necrosis factor α are proinflammatory and not pure inflammatory cytokines. Skeletal muscle changes are described in polymyalgia rheumatica, but unfortunately also in fibromyalgia, although the latter has been retracted and re-interpreted as normal. Of osteoarthritis we learn that “It is only with onset of secondary synovitis that osteoarthritis becomes apparent”. It is stated (with no reference) that 70% of cases of gout start in the first metatarsophalangeal joint. These criticisms point to the sometimes superficial style of the book. It does not cover the current front line literature on pathophysiology, but then this may not have been its main mission. But I would have liked to read Fassbender’s comments on recent development in semiquantitative assessment of synovitis.3,4
This is a historical document and the enthusiastic foreword by J Claude Bennett phrases it well: “Although the illustrations and photomicrographs presented tell a convincing story, the real jewel of this volume is the skilful way in which the author has managed to integrate the pathogenic process in time, space, and molecular context”. In my view, the illustrations take the lead over the molecular interpretations and another dimension of authenticity would have been added had clinical data been provided about the donors of the specimens. This work will assume a place of honour on my bookshelf.