Hideki Kuwahara

Histochemistry of tartrate-resistant acid phosphatase and carbonic anhydrase isoenzyme II in osteoclast-like giant cells in bone tumours

Using routinely processed, paraffin-embedded tissue specimens, osteoclast-like giant cells in giant cell tumour of bone (GCT), chondroblastoma, osteoblastoma and osteoblastic osteosarcoma were examined histochemically for osteoclast-specific enzymes tartrateresistant acid phosphatase (TRAP) and carbonic anhydrase isoenzyme II (CA-II). Osteoclast-like giant cells and some mononuclear cells possessed TRAP activity. These were further classified with respect to CA-II immunoreactivity, i.e. cells with CA-II were seen in GCT and chondroblastoma, while those in osteoblastoma and osteoblastic osteosarcoma were negative for CA-II. All the cellular components in malignant fibrous histiocytoma and various extraosseous inflammatory lesions including malignant giant cells and macrophage polykaryons were negative for both TRAP and CA-II. These results indicate that osteoclast-like giant cells in GCT, chondroblastoma, osteoblastoma and osteoblastic osteosarcoma are all osteoclasts and generated by fusion of mononuclear cells with the same histochemical characteristics as osteoclast-like giant cells. The difference in CA-II immunoreactivity suggests the functional or maturational difference between osteoclast-like giant cells in GCT and chondroblastoma and those in osteoblastoma and osteosarcoma.

Experimental pulmonary fibrosis induced by trisodium citrate and acid-citrate-dextrose

A single intrapulmonary injection of 3.8% trisodium citrate and acid-citrate-dextrose (ACD) into rabbits results in extensive degeneration and necrosis of alveolar pneumocytes, including the type II pneumocyte, and of bronchiolar or bronchial epithelial cells. Subsequently, the alveoli and alveolar ducts collapse, and the septa and ductal walls adhere to each other, accompanied by the proliferation of interstitial fibroblasts. These fibroblasts produce fibrous connective tissue which is followed by pulmonary fibrosis in 1 week. Epithelial regeneration, especially that resulting from the proliferation of immature type II pneumocytes, occurs around the periphery of the fibrous lesions. The synthesis and release of large amounts of surfactant materials by the proliferated type II pneumocytes may induce the surfactant materials to reopen the air spaces of the collapsed and adhesive alveoli. By 4 weeks those fibrous areas in the pathological lungs become smaller and/or appear normal. These results suggest that this is a useful experimental animal model for pulmonary fibrosis, and that epithelial cells, especially type II pneumocytes, are associated with both the induction of and the recovery from the disorder; in the early stage, interference by reepithelization resulting from type II pneumocyte proliferation may elicit the proliferation of fibroblasts, and in later stages, reepithelization and surfactant synthesis by newly proliferated type II pneumocytes may permit the reopening of collapsed and adhesive air spaces.

Histochemical Demonstration of Carbonic Anhydrase Activity in the Odontogenic Cells of the Rat Incisor

Aldehyde-fixed, EDTA-demineralized frozen sections of the rat maxillary incisor were histochemically stained for carbonic anhydrase activity, by use of Hanssons method. Intense staining was observed in the odontoblasts, all types of epithelial cells of enamel organ in the maturation zone, cementoblasts, and the cells of the lingual dental sac. Less intense but consistent staining was observed in all types of epithelial cells of odontogenic origin directly facing the pulp and pulp cells adjacent to the odontoblast cell layer in the apical part of the pulp, and was considered due to the carbonic anhydrase-catalyzed reaction. Staining of these cells was completely inhibited by heat pretreatment (120°C, 30 min), 10-6 mol/L acetazolamide in the incubation medium, incubation by continuous immersion under the liquid surface, and omission of the substrate, NaHCO3. The dentin also exhibited heavy staining which was inhibited by the heat pre-treatment. However, this dentinal staining resisted the inhibition by 10-3 mol/L acetazolamide and was not inhibited by incubation by continuous immersion or incubation without the substrate NaHCO3. The dentinal staining was thus judged to have been due to non-enzymatic cobalt precipitation.

Autopsy case of hepatocellular carcinoma associated with lupoid hepatitis and complicated by malignant lymphoma

SummaryAn 81-year-old woman in whom liver dysfunction had been pointed out 3 years previously was diagnosed as having liver cirrhosis due to lupoid hepatitis. Considering the poor prognosis of cirrhosis and her age, immunosuppressive therapy was not adopted. Nine months later, a small liver tumor was found by ultrasonography and was diagnosed as hepatocellular carcinoma (HCC). The tumor was treated with trans-catheter arterial embolization, but grew continuously. She also developed gingival lymphoma that was successfully treated. Three years after initial diagnosis of lupoid hepatitis, she died of hepatic failure. An autopsy was performed and confirmed the clinical diagnosis, liver cirrhosis with HCC. HCC is regarded as a rare complication of lupoid hepatitis, but cases of HCC complicating lupoid hepatitis may increase with progress in treatment methods and elongation of survival. The present case suggests that any malignancy can be developed in long-term surviving patients with lupoid hepatitis.

Experimental emphysematous bullae

The effects of methylchoranthrene and carrageenan on the lungs of rabbits were studied. Four out of five animal which were injected via the bronchus with a suspension of 100 mg 20-methylchoranthrene in 8 ml solution of 0.75% lambda carrageenan in saline developed emphysematous bullae in the treated lobes of the lungs two months later. Animals treated with carrageenan solution (group 1), a suspension of methylchoranthrene in 10% tween 60 solution (group 2), and saline (group 3), failed to demonstrate cystic lesions in the lungs, except for one animal in group 1. These results suggest that this is a good experimental animal model for emphysematous bullae.

Healing Effects of Iodine and Thyroid Hormone on Experimental Rickets

The Steenbock 2965 diet has been regarded as a standard rachitogenic diet, but in 1961 Shimazaki and Yagi pointed out that this diet is also deficient in iodine, and the rachitic findings produced on this diet could be ameliorated with potassium iodide (KI). Further, in 1984 Shimazaki et al. (1) found that triiodothyronine (T3) is more effective in this respect than iodine and even vitamin D (v.D). In this study, to determine the physiological basis of this beneficial effect, the actions of T3 on mineral metabolism have been investigated and compared with those of v.D.