An experimental model for inducing chronic Achilles paratenonitis with tendinosis in the rabbit is presented. Thirteen rabbits were exercised in a kicking machine producing passive flexions and extensions of the ankle joint. Active contractions of the triceps surae muscles were induced by electric stimulation via surface electrodes. The animals were exercised for 5 to 6 weeks, with a rate of 150 flexions and extensions per minute for 2 h, three times a week. Light microscopic examination showed degenerative changes of the tendon, and increased number of capillaries, infiltrates of inflammatory cells, edema, and fibrosis in the paratenon. We conclude that chronic Achilles paratenonitis with tendinosis can be experimentally induced in a standardized manner in rabbits.

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Chronic recurrent multifocal osteomyelitis (CRMO) is characterised by an insidious onset of fever, local swelling and pain in affected bones, and radiological abnormalities suggestive of osteomyelitis. The histopathological features in 14 patients are described. Morphologically CRMO begins as an acute inflammatory process with a predominance of polymorphonuclear leucocytes, which occasionally form an abscess and osteoclastic bone resorption. At a later stage the predominant features are lymphocytes in the inflammatory infiltrates and occasional granulomatous foci and sigans of bone formation. The clinical course may be prolonged for many years.

Mice, 7-8-mo old, of the C57BL/Ks,l-db strain and homozygotic for the mutant gene db, exhibited marked hyperglycemia and moderately elevated serum insulin levels. Light and electron microscopy provided evidence of a slightly decreased proportion of ~ cells in the pancreatic islets, irregular islet architecture with intraislet ducts, and degenerative as well as hypertrophic changes in the individual cells. As a rule, islets microdissected from these mice did not release insulin in response to glucose, theophylline, iodoacetamide, or chloromercuribenzene-p-sulphonic acid. The absence of secretory responses was not simply due to lack of insulin. Although the islet content of insulin was decreased in C57BL/KsJ-db/db mice, the remaining amount was severalfold larger than that released from stimulated islets of normal controls. Another mutation, db 2J, an allele of db with identical phenotypic expressions in the C57BL/KsJ strain, was studied on the genetic background C57BI/6J. In contrast to the severely diabetic C57BL/KsJdb/db animals, the C57BL/6J-db2J/db ~J mice were characterized by highly elevated serum insulin levels and only moderate hyperglycemia. Their endocrine pancreas was enlarged and showed an increased proportion of ~ cells. Like the islets of normal mice, those of C57BL/6J-db~a/dbZJ mice responded to glucose and chloromercuribenzene-p-sulphonic acid, the glucose-induced responses being potentiated by theophylline or iodoacetamide. C57BL/KsJ-db/db mice should provide a valuable model for studying defects in insulin secretion in relation to diabetes mellitus. Mice of the C57BL/6J strain offer a control material that may help to elucidate the dependence of the insulin secretory defect on the background genome.

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