Effects of vascular occlusion on the femoral head in growing rabbits

Calvert, P; Kernohan, J.; Sayers, D.C.J.; Catterall, A.

doi:10.3109/17453678408992952

Cited by 18 publications

(7 citation statements)

References 18 publications

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“…By 6 weeks, necrotic marrow space was completely replaced by fibrovascular tissue and in some areas by hematopoietic marrow. 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.…”

Section: Discussionsupporting

confidence: 71%

“…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: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Development of a Mouse Model of Ischemic Osteonecrosis

Kamiya

Yamaguchi

Aruwajoye

et al. 2015

Clinical Orthopaedics &Amp; Related Research

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“…Breech delivery occurred in only 6.5%. The incidence of late DDH in all of Norway was 2.4 [347]: 1.7 in Oslo and 0.76 in southern Finland [348]. In Glasgow it was 0.84 before and 0.57 after institution of a selective ultrasound screening program [349].…”

Section: Resultsmentioning

confidence: 99%

The Epidemiology and Demographics of Hip Dysplasia

2011

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The etiology of developmental dysplasia of the hip (DDH) is unknown. There are many insights, however, from epidemiologic/demographic information. A systematic medical literature review regarding DDH was performed. There is a predominance of left-sided (64.0%) and unilateral disease (63.4%). The incidence per 1000 live births ranges from 0.06 in Africans in Africa to 76.1 in Native Americans. There is significant variability in incidence within each racial group by geographic location. The incidence of clinical neonatal hip instability at birth ranges from 0.4 in Africans to 61.7 in Polish Caucasians. Predictors of DDH are breech presentation, positive family history, and gender (female). Children born premature, with low birth weights, or to multifetal pregnancies are somewhat protected from DDH. Certain HLA A, B, and D types demonstrate an increase in DDH. Chromosome 17q21 is strongly associated with DDH. Ligamentous laxity and abnormalities in collagen metabolism, estrogen metabolism, and pregnancy-associated pelvic instability are well-described associations with DDH. Many studies demonstrate an increase of DDH in the winter, both in the northern and southern hemispheres. Swaddling is strongly associated with DDH. Amniocentesis, premature labor, and massive radiation exposure may increase the risk of DDH. Associated conditions are congenital muscular torticollis and congenital foot deformities. The opposite hip is frequently abnormal when using rigorous radiographic assessments. The role of acetabular dysplasia and adult hip osteoarthritis is complex. Archeological studies demonstrate that the epidemiology of DDH may be changing.

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“…As cartilage nutrition is derived from synovial fluid, it is unlikely that alterations in femoral head blood supply will influence chondrocyte metabolism, given the relatively brief period of vascular compromise before the rats were killed. Experimental studies involving temporary vascular occlusion of rabbit femoral heads show that osteonecrosis is best seen histologically after 2 weeks 18 . In these hips, no structural abnormality of the articular cartilage was seen.…”

Section: Discussionmentioning

confidence: 90%