Osteonecrosis of the femoral head of growing, spontaneously hypertensive rats

Hirano, Tôru; Iwasaki, Katsurô; Yamane, Yoshimichi

doi:10.3109/17453678809148778

Cited by 39 publications

(21 citation statements)

References 15 publications

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“…The histologic characteristics of osteonecrosis in our mouse model are consistent with those described in human patients and in other models of vascular disruption-induced ischemic osteonecrosis [4,5,49] which feature extensive cell death (osteoblasts, osteocytes, and marrow cells) and empty lacunae. In comparison to the rat model of osteonecrosis [14,29,38], our mouse model showed similar histologic changes and the temporal sequence of the repair process. Revascularization of the necrotic marrow space was followed by a gradual increase in the number of osteoclasts and osteoblasts on the bone surfaces from 2 to 6 weeks.…”

Section: Discussionmentioning

confidence: 83%

“…Revascularization of the necrotic marrow space was followed by a gradual increase in the number of osteoclasts and osteoblasts on the bone surfaces from 2 to 6 weeks. Furthermore, it appears to have a relatively fast healing process as seen in the rat model [14,29,38] compared with that of large animal models of osteonecrosis [25,26] and human disease [35]. The fast repair also may be related to relatively young mice (5 weeks old) used in this study.…”

Section: Discussionmentioning

confidence: 91%

“…The site of osteonecrosis in these models, however, is limited to the femoral head except in corticosteroid-induced models which tend to develop multifocal lesions. The experimental models also can be divided into large animal models such as canines [31,34,37], porcines [24,41], and sheep [44], and small animal models such as rabbits [5,[15][16][17][19][20][21] and rats [14,29,38]. These models can be further classified into immature and mature animal models that represent pediatric and adult osteonecrotic conditions [11].…”

Section: Introductionmentioning

confidence: 99%

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Development of a Mouse Model of Ischemic Osteonecrosis

Kamiya

Yamaguchi

Aruwajoye

et al. 2015

Clinical Orthopaedics &Amp; Related Research

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Background Availability of a reliable mouse model of ischemic osteonecrosis could accelerate the development of novel therapeutic strategies to stimulate bone healing after ischemic osteonecrosis; however, no mouse model of ischemic osteonecrosis is currently available. Questions/purposes To develop a surgical mouse model of ischemic osteonecrosis, we asked, (1) if the blood vessels that contribute to the blood supply of the distal femoral epiphysis are cauterized, can we generate an osteonecrosis mouse model; (2) what are the histologic changes observed in this mouse model, and (3) what are the morphologic changes in the model. Methods We performed microangiography to identify blood vessels supplying the distal femoral epiphysis in mice, and four vessels were cauterized using microsurgical techniques to induce ischemic osteonecrosis. Histologic assessment of cell death in the trabecular bone was performed using terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) and counting the empty lacunae in three serial sections. Quantitation of osteoclast and osteoblast numbers was performed using image analysis software. Morphologic assessments of the distal femoral epiphysis for deformity and for trabecular bone parameters were performed using micro-CT. Results We identified four blood vessels about the knee that had to be cauterized to induce total ischemic osteonecrosis of the distal femoral epiphysis. Qualitative assessment of histologic sections of the epiphysis showed a loss of nuclear staining of marrow cells, disorganized marrow structure, and necrotic blood vessels at 1 week. By 2 weeks, vascular tissue invasion of the necrotic marrow space was observed with a progressive increase in infiltration of the necrotic marrow space with the vascular tissue at 4 and 6 weeks. TUNEL staining showed extensive cell death in the marrow and trabecular bone 24 hours after the induction of ischemia. The mean percent of TUNELpositive osteocytes in the trabecular bone increased from 2% ± 1% in the control group to a peak of 98% ± 3% in the ischemic group 1 week after induction of ischemia (mean difference, 96%; 95% CI, 81%-111%; p \ 0.0001). The mean percent of empty lacunae increased from 1% ± 1% in the control group to a peak of 78% ± 15% in the ischemic group at 4 weeks (mean difference, 77%; 95% CI, 56%-97%; p \ 0.0001). Quantitative analysis showed that the mean number of osteoclasts per bone surface was -015-4172-6 Clinical Orthopaedics and Related Research ® A Publication of The Association of Bone and Joint Surgeons® decreased in the ischemic group at 1, 2, and 4 weeks (p \ 0.0001, \ 0.0001, and p = 0.02, respectively) compared with the control group. The mean number of osteoclasts increased to a level similar to that of the control group at 6 weeks (p = 0.23). The numbers of osteoblasts per bone surface were decreased in the ischemic group at 1, 2 and 4 weeks (p \ 0.0001 for each) compared with the numbers in the control group. The mean number of osteoblasts also increased to a level...

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Development of a Mouse Model of Ischemic Osteonecrosis

Kamiya

Yamaguchi

Aruwajoye

et al. 2015

Clinical Orthopaedics &Amp; Related Research

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“…Thin coronal sections of the proximal femurs were stained with hematoxylin-eosin and Mallory 's azan method. Histologic observation of the femoral heads disclosed various stages of osteonecrosis (Table 1; Hirano et al 1988a). Of51 femoral heads withosteonecrosis, 15 epiphyses showed fresh osteonecrosis, not yet invaded by reparative tissue (Figure 1).…”

Section: Methodsmentioning

confidence: 99%

Necrosis of the femoral head in growing rats: Occlusion of lateral epiphyseal vessels

Hirano

Iwasaki

Sagara

et al. 1989

Acta Orthopaedica Scandinavica

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“…This ION model is not considered to be a model of clinical osteonecrosis after traumatic hip dislocation. The established ION animal models such as rats and rabbits do not always lead to osteonecrosis (Hirano et al 1988;Yamamoto et al 1995;Norman et al 1998). We believe that ION animal models need to develop into osteonecrosis in the femoral head in order to investigate the effects of MPSS on bone regeneration.…”

Section: Model For Osteonecrosis Of the Femoral Headmentioning

confidence: 99%