Experimental Steroid-Induced Osteonecrosis in Adult Rabbits With Hypersensitivity Vasculitis

Matsui, Minoru; Saito, Susumu; Ohzono, Kenji; Sugano, Nobuhiko; Saito, Masanobu; Takaoka, Kunio; Ono, Katsuhiko

doi:10.1097/00003086-199204000-00008

Cited by 63 publications

(39 citation statements)

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“…Recent animal models of ON were produced by serum sickness (28) and the Shwartzman reaction (26) in addition to corticosteroid treatment, but the O N model reported herein, which is simple and reproducible, may be useful not only in researching the effects of corticosteroids on the bone and bone marrow tissue, but also in clarifying the etiology and early pathogenesis of steroidinduced ON. Moreover, in order to design appropriate drug treatment for the prevention of ON after corticosteroid treatment in humans, further research into the pathogenesis of this model may thus result in many useful findings, while taking into account the several differences between ON in this model and ON in humans, such as the distribution and extent of ON.…”

Section: Discussionmentioning

confidence: 99%

Effects of pulse methylprednisolone on bone and marrow tissues. Corticosteroid‐induced osteonecrosis in rabbits

Yamamoto

Irisa

Sugioka

et al. 1997

Arthritis & Rheumatism

226

181

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Objective. To investigate the effects of pulse methylprednisolone acetate on bone and bone marrow tissues and to clarify the causal factors of corticosteroidinduced osteonecrosis (ON) by using an experimental animal model.Methods. Male adult Japanese white rabbits were injected once with 20 mg/kg of methylprednisolone into the right gluteus medius muscle. Seven rabbits were killed at 4 weeks, 4 at 6 weeks, 4 at 8 weeks, and 6 at 10 weeks. Both histopathologic and hematologic studies were performed every week.Results. By 4 weeks after the steroid injection, 43% of the rabbits studied had developed multifocal ON lesions in the femur and/or humerus. In 1 rabbit, a thrombus was detected in an arteriole adjacent to the necrotic area at 4 weeks. After 6 weeks, there was also progressive histologic evidence of revascularization, with granulation tissue, and osteoblastic repair, with appositional bone formation. Hyperlipemia, fatty liver, and intraosseous fat embolism were observed in conjunction with thrombocytopenia and hypofibrinogenemia.Conclusion. A single injection of high-dose corticosteroids was found to be capable of inducing thrombocytopenia, hypofibrinogenemia, and hyperlipemia with multifocal ON in several bones.

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Section: Discussionmentioning

confidence: 99%

Effects of pulse methylprednisolone on bone and marrow tissues. Corticosteroid‐induced osteonecrosis in rabbits

Yamamoto

Irisa

Sugioka

et al. 1997

Arthritis & Rheumatism

226

181

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“…Matsui et al [72] described a rabbit ON model induced by employing a combined protocol of hypersensitivity vasculitis caused by horse serum and administration of highdose corticosteroids. Fourteen of 20 specimens (70%) showed histological evidence of ON in the femoral metaphysic.…”

Section: On Induced By Steroid In Combination With Horse Serummentioning

confidence: 99%

Experimental animal models of osteonecrosis

et al. 2011

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Osteonecrosis (ON) or avascular necrosis (AVN) is a common bone metabolic disorder, mostly affecting femoral head. Although many biological, biophysical, and surgical methods have been tested to preserve the femoral head with ON, none has been proven fully satisfactory. It lacks consensus on an optimal approach for treatment. This is due, at least in part, to the lack of ability to systematically compare treatment efficacy using an ideal animal model that mimics full-range osteonecrosis of femoral head (ONFH) in humans with high incidence of joint collapse accompanied by reparative reaction adjacent to the necrotic bone in a reproducible and accessible way. A number of preclinical animal ON models have been established for testing potential efficacy of various modalities developed for prevention and treatment of ON before introduction into clinics for potential applications. This paper describes a number of different methods for creating animal experimental ON models. Advantages and disadvantages of such models are also discussed as reference for future research in battle against this important medical condition.

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“…The diagnosis of osteonecrosis was made in a blind way by two researchers. When the two examiners did not agree, they discussed the Wndings (still blind) to reach a consensus, based on the diVuse presence of the empty lacunae or the pyknotic nuclei of the osteocytes within the bone trabeculae, accompanied by the surrounding bone marrow cell necrosis [8]. The rabbits that had at least one osteonecrotic lesion in the area examined could be considered to have developed osteonecrosis.…”

Section: Evaluation Of Osteonecrosismentioning

confidence: 99%

Lipoic acid prevents steroid-induced osteonecrosis in rabbits

2011

Rheumatol Int

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The objective of this study was to investigate in vivo effects of lipoic acid (LA) in preventing steroid-induced osteonecrosis and the possible pathway in a rabbit model. Sixty rabbits were divided into 2 groups: rabbits were intraperitoneally injected with LA aqueous solution at 36 mg/kg of body weight per day for 4 weeks in Group A and rabbits were injected with physiologic saline (PS) as a control in Group B. At 2 weeks after starting treatment, they were intramuscularly injected once with 20 mg/kg of methylprednisolone acetate (MPSL). The femora were histopathologically examined for the presence of osteonecrosis. The plasma levels of total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), glutathione (GSH), endothelin (ET) and malondialdehyde (MDA) were assayed at 2 weeks after the injection of MPSL. The incidence of osteonecrosis was significantly higher in Group B (73.1%) than in Group A (20.8%). The GSH level was higher in Group A than in Group B after the LA injection. The plasma MDA and ET levels were lower in Group A than in Group B at 2 weeks after the MPSL administration. Lipoic acid can prevent the development of steroid-induced osteonecrosis in rabbits. Inhibited oxidative stress and amendment of vascular endothelial dysfunction is a possible mechanism for this effect.

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Experimental Steroid-Induced Osteonecrosis in Adult Rabbits With Hypersensitivity Vasculitis

Cited by 63 publications

References 0 publications

Effects of pulse methylprednisolone on bone and marrow tissues. Corticosteroid‐induced osteonecrosis in rabbits

Effects of pulse methylprednisolone on bone and marrow tissues. Corticosteroid‐induced osteonecrosis in rabbits

Experimental animal models of osteonecrosis

Lipoic acid prevents steroid-induced osteonecrosis in rabbits

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