Arne Burkhardt’s research while affiliated with University of Tübingen and other places

In der 1.Auflage des Bandes 4 aus dem Jahr 1969 waren unter topographisch-anatomischen Gesichtspunkten vier Organregionen — Nase und Nasennebenhöhlen, Kehlkopf and Luftröhre, Schilddrüse, Mediastinum — abgehandelt worden, wobei der Schwerpunkt der Darstellung das Mediastinum betraf. Das damals von K. KÖHN gestaltete Kapitel umfaßte sowohl den Kehlkopf als auch die Luftröhre. Die vorliegende Fassung, die weitgehend der Pathologie des Kehlkopfes gewidmet ist und die der Luftröhre nur marginal streift, lehnt sich zwar zu einem geringeren Teil an die frühere Auflage an, besonders da, wo die entsprechenden Aussagen nach wie vor Gültigkeit haben, wie z. B. die Anatomie, die Mißbildungen oder die spezifischen Entzündungen. Insgesamt handelt es sich um eine völlig überarbeitete und aktualisierte Abhandlung des Stoffgebietes unter Berücksichtigung sowohl moderner Untersuchungsmethoden als auch der neuen revidierten WHO-Tumorklassifikation. Speziell bei den Larynxtumoren sind zahlreiche Befunde berücksichtigt und ergänzt, die in der von E. MEYER-BREITING und A. BURKHARDT verfaßten Monographie „Tumours of the Larynx. Histopathology and Clinical Inferences“ enthalten waren.

The spectrum of conventional and advanced morphological methods for the assessment of malignant potential of precancerous lesions of the laryngeal mucosa is discussed.

Cancer, if not in essence a genetic disease, is at least to a large extent determined in its behaviour by the interaction of a number of genetically coded products, which may enhance its growth (oncogenes) or suppress it (tumour suppressor genes or anti-oncogenes). However, the genetic changes of various cancers show considerable individual variations some of which maybe determined by geographic or aetiological factors. Overall, 50%–96% of oral carcinomas have abnormal karyotypes (Owen et al. 1992; Hittelman et al. 1993), and there is a high frequency of breakpoints and deletions (Owen et al. 1992; Patel et al. 1993; Partridge et al. 1994; Füzesi et al. 1994). All chromosomes may be involved, and it is noteworthy that those chromosomes encoding some of the well-known oncogenes (or tumour suppressor genes) are frequently altered, such as chromosome 1, 3, 7 (epidermal growth factor receptor, EGFR), 8 (myc), 9 (MTS), 11 (ras, bcll, intl), 13 (erb), 17 (neu, p53) and 18 (Patel et al. 1993; Voravud 1993; Tsuji et al. 1994). Details are outlined in the chapter by Scholes and Field in this volume.

Tissue markers of potential malignancy have been sought for many years. Cell surface markers, particularly blood group and histocompatibility antigens, have shown great promise and several squamous carcinoma antigens have been identified--but not fully studied in potentially malignant lesions. Growth factors and receptors also need further study. Cytoplasmic markers of potential malignancy have been examined and, of these, keratins, filaggrin, and some carcinoma antigens show most promise. Nuclear analyses have promise but are time-consuming and expensive. Image cytometric analyses appear to be sensitive and predictive: oncogene and tumour suppressor analyses remain to be fully evaluated. New investigative techniques at the cellular and molecular level show increasing promise at defining potentially malignant oral epithelial lesions but more prospective studies are required.

"Alveolitis", as opposed to "pneumonia" sensu strictiori, is a term used to denote diffuse inflammatory changes of the pulmonary parenchyma, excluding those that result from local bacterial, fungal or other extracellular microbial growth. The various types of alveolitis are classified according to their histological characteristics and range from "luminal phagocytic" or "mural lymphoplasmacellular" and "exudative" to "fibrosing" alveolitis. In this overview, various exogenous and endogenous causes of different types of alveolitis, and the cellular events in their pathogenesis are briefly discussed to illustrate the complex mechanisms involved. Particular emphasis is placed on the possible transition from diffuse exudative to fibrosing alveolitis. It appears that pulmonary fibrosis, which is usually patchy rather than truly diffuse, does not have a uniform pathogenesis. Besides the possibility of a certain degree of a diffuse fibrosis three major pathways are evident: (1) granulation tissue budding into alveolar lumina (luminal fibrosis) (2) exudate incorporation into alveolar walls (mural fibrosis) and--at least equally important--(3) so-called collapse (atelectatic) induration (obliterative-interseptal fibrosis), a process that has largely been neglected so far.

Von Albertini (1974) defined true neoplasms as ?irreversible autonomic overgrowths of the body?s tissue?. Autonomic growth excesses are, in part, also represented by those frequent hyperplasias which occur in the larynx, namely, tissue growth as a result of inflammation, polyps and cysts. These so-called pseudotumours must be separated from the irreversible neoplasms. To a large extent, this book follows, as regards content and classification, the International Classification of Tumours of the World Health Organization (WHO) (Shanmugaratnam and Sobin 1978). Pseudotumours (group VIII) and tumour-like malformations and dystopias (group V) will be described in Chap. 8.

Most malignant neoplasms of the larynx and the adjacent regions (hypopharynx and oropharynx with lingual epiglottic surface, valleculae, lower part of the retrolingual region) are squamous cell carcinomas (Table 5.1). In a survey of 1207 patients with malignant tumours of the larynx treated in the Frankfurt University Ear, Nose and Throat Clinic between 1962 and 1986, there were 998 squamous cell carcinomas; including the variants of the squamous cell carcinoma, i.e. the so-called carcinosarcoma, spindle cell carcinoma and verrucous carcinoma, results a good 97%, whereas all other types of malignant neoplasm were seen very rarely.

The incidence of malignant neoplasms of the larynx has risen in proportion to the increase in new cases of respiratory tract carcinomas in general (MC– MICHAEL 1978, STEINER 1984; review KLEINSASSER 1983); the overall mortality is 2.5 per 100000 person–years, and in the USA new laryngeal cancers form 1.5% of all new cases of cancer and laryngeal cancer mortality is 0.9% of total cancer mortality.