Vascular events associated with the appearance of the secondary center of ossification in the murine distal femoral epiphysis.

Floyd, Waldo E.; Zaleske, David J.; Schiller, A L; Trahan, Carol; Mankin, Henry J.

doi:10.2106/00004623-198769020-00004

Cited by 75 publications

(49 citation statements)

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“…During natural formation of the SOC, vascular invasion from the perichondrium is considered to take place by invagination and then canals in epiphyseal cartilage, leading to further mineralization of the chondroepiphysis. [38][39][40][41][42] However, angiogenesis should have been arrested after 12 h in either the presently loaded explants or control explants in organ culture medium, followed by 3 days of additional culture in a rotary bioreactor. It is unlikely that angiogenesis, at least in the sense of in vivo angiogenesis, has played any significant role in the formation of the SOC in the present ex vivo organ culture system.…”

Section: Discussionmentioning

confidence: 99%

Modulation of endochondral development of the distal femoral condyle by mechanical loading

Sundaramurthy

Mao

2005

Journal Orthopaedic Research

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Although previous theoretical modeling studies have predicted that various mechanical stresses accelerate or inhibit the ossification process of the neonatal chondroepiphysis, there is a paucity of experimental data to verify these models. The present study was designed to provide experimental evidence on whether the ossification of the chondroepiphysis is modulated by mechanical loading on the distal femoral condyle explant of the neonatal (5-day-old) rabbit in organ culture. Upon aseptic dissection, the right condyle explant was immersed in and fixated to an organ culture system, and received cyclic forces at 200 mN and 1 Hz for 12 h (N ¼ 8) directly on its slightly convex articular surface, whereas the contralateral, left condyle explant was immersed separately in organ culture (N ¼ 8). Subsequently, both loaded and control explants were placed in a bioreactor rotating at 20 rpm for 72 h. In each mechanically loaded specimen, a structure reminiscent of the secondary ossification center (SOC) appeared with an average area of 1.17 AE 0.13 mm 2 , or 15.2 AE 8.2% of the total epiphysis area. In contrast, no SOC was detected in any of the unloaded contralateral control specimens. The SOC in mechanically loaded specimens was stained intensively with fast green, whereas either the rest of the loaded epiphysis or the entire control epiphysis was stained intensely to safranin-O but lacked fast green staining. Immunolocalization revealed that the SOC of the mechanically loaded specimens expressed Runx 2 and osteopontin, both of which were absent in the unloaded control specimens. Type X collagen was expressed surrounding hypertrophic chondrocytes adjacent to the SOC, but was absent in the control specimen. Type II collagen and decorin were absent in the SOC of the loaded specimen, but were expressed throughout the rest of the loaded epiphysis and the unloaded control epiphysis. The intensity of type II collagen and decorin expression was significantly stronger among hypertrophic chondrocytes surrounding the SOC than the control. The numbers of hypertrophic chondrocytes surrounding the SOC and superior to metaphyseal bone were significantly higher in the loaded specimens than the unloaded controls. Taken together, mechanical stresses accelerate the formation of the secondary ossification center, and therefore modulate endochondral ossification. ß

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Section: Discussionmentioning

confidence: 99%

Modulation of endochondral development of the distal femoral condyle by mechanical loading

Sundaramurthy

Mao

2005

Journal Orthopaedic Research

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“…The ossification centers development inside the cartilage model of long bones has been extensively investigated in animal experimental models [12][13][14][15][16][17] …”

Section: Prenatal and Early Childhood Bone Growthmentioning

confidence: 99%

A Review of the Actual Knowledge of the Processes Governing Growth and Development of Long Bones

Pazzaglia

Beluffi²,

Benetti

et al. 2011

Fetal and Pediatric Pathology

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“…As development progresses, nutrition and oxygenation of the epiphysis by diffusion from surrounding vessels becomes insufficient, and vascular canals containing blood vessels and mesenchymal cells invade the cartilage (13)(14)(15). Both the initial vascular invasion and the subsequent development of the secondary ossification center were impaired in VEGF 188/188 mice.…”

Section: Figurementioning

confidence: 99%

“…The oxygen and nutrient supply of developing avascular cartilage is thought to depend largely on the elaborate epiphyseal vascular network overlying the cartilaginous surface (11,12). Invasion of these vessels into the epiphyseal cartilage represents a critical early step in the development of the secondary ossification center (13)(14)(15). The membrane-type 1 MMP (MT1-MMP) is the only known molecular signal implicated in this process (16,17).…”

Section: Introductionmentioning

confidence: 99%

Soluble VEGF isoforms are essential for establishingepiphyseal vascularization and regulating chondrocyte development and survival

Maes¹,

Stockmans²,

Moermans³

et al. 2004

J. Clin. Invest.

120

133

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VEGF is crucial for metaphyseal bone vascularization. In contrast, the angiogenic factors required for vascularization of epiphyseal cartilage are unknown, although this represents a developmentally and clinically important aspect of bone growth. The VEGF gene is alternatively transcribed into VEGF 120 , VEGF 164 , and VEGF 188 isoforms that differ in matrix association and receptor binding. Their role in bone development was studied in mice expressing single isoforms. Here we report that expression of only VEGF 164 or only VEGF 188 (in VEGF 188/188 mice) was sufficient for metaphyseal development. VEGF 188/188 mice, however, showed dwarfism, disrupted development of growth plates and secondary ossification centers, and knee joint dysplasia. This phenotype was at least partly due to impaired vascularization surrounding the epiphysis, resulting in ectopically increased hypoxia and massive chondrocyte apoptosis in the interior of the epiphyseal cartilage. In addition to the vascular defect, we provide in vitro evidence that the VEGF 188 isoform alone is also insufficient to regulate chondrocyte proliferation and survival responses to hypoxia. Consistent herewith, chondrocytes in or close to the hypoxic zone in VEGF 188/188 mice showed increased proliferation and decreased differentiation. These findings indicate that the insoluble VEGF 188 isoform is insufficient for establishing epiphyseal vascularization and regulating cartilage development during endochondral bone formation.

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Vascular events associated with the appearance of the secondary center of ossification in the murine distal femoral epiphysis.

Cited by 75 publications

References 0 publications

Modulation of endochondral development of the distal femoral condyle by mechanical loading

Modulation of endochondral development of the distal femoral condyle by mechanical loading

A Review of the Actual Knowledge of the Processes Governing Growth and Development of Long Bones

Soluble VEGF isoforms are essential for establishingepiphyseal vascularization and regulating chondrocyte development and survival

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