Renaut bodies in the sciatic nerve of beagle dogs.

182 control Beagle dogs from 23 historical studies (14 chronic, 9 subchronic) were reviewed histologically for the presence of Renaut bodies in the sciatic nerve. Renaut bodies were found in 36.1 percent of the subchronic-study dogs and in 46.4 percent of the chronic-study dogs. The Renaut bodies most often resided in the distal sections of the sciatic nerve, specifically in the tibial branch as it traversed the knee joint in situ. There was no sex predilection. Renaut bodies were located predominately in the endoneurium, in the center of the nerve sections. There was no associated axonal degeneration, reactive gliosis, or encapsulation. The Renaut bodies were characterized as large (20 to 500 microns diameter in cross section), well-demarcated elliptical structures with an onion-skin arrangement of loosely textured, filamentous strands intermixed with sparse numbers of dark spindle-shaped nuclei. Occasionally the core displayed a more dense, intensely eosinophilic arrangement of fibers. Histochemical results included: positive acidic alcian blue, Gomori's trichrome, and Verhoeff Van Gieson's; and negative Periodic-acid Schiff, Congo Red, and Luxol fast blue/cresyl violet. Immunohistochemical results included: positive vimentin and collagen (subtypes I, II, and VI); and negative NSE, S-100, GFAP, amyloid A component, desmin, alpha-sarcomeric actin, pancytokeratin, EMA, and von Willebrand factor. Transmission electron microscopy revealed loosely arrayed, circumferentially oriented collagen fibers intermixed with varying amounts of amorphous substance and finely fibrillar material. Most of the cells comprising the Renaut body were identified as fibroblasts. No nerve fibers entered or left the Renaut body, and nearby nerves appeared to be normal structurally. Based on this characterization of Renaut bodies and in conjunction with the past literature, Renaut bodies appear to have little or no pathological significance, but rather are suggestive of a physiological adaptation in response to mechanical stress imposed on nerves.

Tumors in long-term rat studies associated with microchip animal identification devices.

Tumors surrounding implanted microchip animal identification devices were noted in two separate chronic toxicity/oncogenicity studies using F344 rats. The tumors occurred at a low incidence rate (approximately 1 percent), but did result in the early sacrifice of most affected animals, due to tumor size and occasional metastases. No sex-related trends were noted. All tumors occurred during the second year of the studies, were located in the subcutaneous dorsal thoracic area (the site of microchip implantation) and contained embedded microchip devices. All were mesenchymal in origin and consisted of the following types, listed in order of frequency: malignant schwannoma, fibrosarcoma, anaplastic sarcoma, and histiocytic sarcoma. The following diagnostic techniques were employed: light microscopy, scanning electron microscopy, and immunohistochemistry. The mechanism of carcinogenicity appeared to be that of foreign-body induced tumorigenesis.

C-cell hyperplasia in secondary hyperparathyroidism.

Calcitonin is a hypocalcaemia producing hormone and is secreted by C-cells of the thyroid. The current study was undertaken on a hypothesis that C-cell hyperplasia may develop in the secondary hyperparathyroidism of chronic renal failure in response to sustained hypercalcaemia. With an immunoperoxidase staining method for calcitonin, C-cell hyperplasia was noted in four of six cases of autosomal dominant polycystic kidney disease and in three of six cases of acquired renal cystic disease, an overall incidence of 58% compared with an incidence of 36% (five of 14) in cases of primary hyperparathyroidism with parathyroid adenoma. Thus, both primary and secondary hyperparathyroidism may trigger C-cell hyperplasia in an attempt to produce a hypocalcaemic effect.