Journal of Experimental Medicine

1906

DOI: 10.1084/jem.8.3.365

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The Formation of True Bone With Cellular (Red) Marrow in a Sclerotic Aorta

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Cited by 58 publications

(26 citation statements)

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“…Common factors may underlie the pathogenesis of these two diseases. Some arterial calcium mineral deposits appear identical to fully formed lamellar bone, including trabeculae, lacunae, and islands of marrow (Bunting 1906;Haust and Geer 1970). Furthermore, calcified arteries have been shown to express several bone matrix proteins, including collagen type I, matrix GLA protein, osteocalcin, osteonectin, and bone morphogenic protein type 2 (Bostrom et al 1993(Bostrom et al , 1995Giachelli et al 1993;O'Brien et al 1995).…”

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osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification

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et al. 1998

Genes & Development

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Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG −/− mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.

“…Common factors may underlie the pathogenesis of these two diseases. Some arterial calcium mineral deposits appear identical to fully formed lamellar bone, including trabeculae, lacunae, and islands of marrow (Bunting 1906;Haust and Geer 1970). Furthermore, calcified arteries have been shown to express several bone matrix proteins, including collagen type I, matrix GLA protein, osteocalcin, osteonectin, and bone morphogenic protein type 2 (Bostrom et al 1993(Bostrom et al , 1995Giachelli et al 1993;O'Brien et al 1995).…”

mentioning

confidence: 99%

osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification

¹

,

et al. 1998

Genes & Development

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Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG −/− mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.

“…In vivo, tissues corresponding to these lineages form in the artery wall: bone, cartilage, fat, and even marrow. 33,34 The predominant form of metaplasia in human vasculature is bone, which is found in 5% to 15% of specimens. 35 Transitional stages between amorphous calcification and mature bone tissue are also seen, the latter apparently requiring microvascular invasion as in skeletal bone.…”

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confidence: 99%

Vascular Calcification

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2008

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M ost individuals aged Ͼ60 years have progressively enlarging deposits of calcium mineral in their major arteries. 1 This vascular calcification reduces aortic and arterial elastance, which impairs cardiovascular hemodynamics, resulting in substantial morbidity and mortality [2][3][4] in the form of hypertension, aortic stenosis, cardiac hypertrophy, myocardial and lower-limb ischemia, congestive heart failure, and compromised structural integrity. [5][6][7] The severity and extent of mineralization reflect atherosclerotic plaque burden 8 and strongly and independently predict cardiovascular morbidity and mortality. 9 Previously considered passive and degenerative, vascular calcification is now recognized as a pathobiological process sharing many features with embryonic bone formation. As evidence of this change in paradigm, research on vascular calcification has accelerated dramatically in the past decade. A search of PubMed (www.ncbi.nlm.nih.gov; US National Library of Medicine) under the key words vascular calcification returned Ϸ16 articles in 1982, 100 in 1994, and 250 in 2004. This year, 400 new publications are expected, for a total Ͼ3500.A breakthrough in this field was the recognition of its similarity to bone development and metabolism, in which endothelial, mesenchymal, and hematopoietic cells interact and respond to mechanical, inflammatory, metabolic, and morphogenetic signals governing skeletal mineralization; their counterparts in the artery wall govern arterial mineralization. With increasing age and dysmetabolic conditions in our population, the clinical burden of vascular calcification will continue to increase. Clinical Impact of Arterial CalcificationAortic calcification promotes congestive heart failure by eroding compliance and elastance. The hemodynamic demands of the cardiovascular system require that the aorta store energy in its elastance during systole and release it during diastole, which minimizes cardiac work and is the basis for balloon counterpulsation. This function, known as Windkessel physiology, is reflected in the high density of elastin in the arch, where mechanical energy is highest. Its loss is detectable as increased arterial pulse wave velocity in calcified arteries, resulting in thoracic summation of reflected and orthograde pressure waves, thereby increasing systolic and pulse pressures. It also increases cardiac work, promoting heart failure, left ventricular hypertrophy, and diastolic dysfunction, independently of atherosclerosis, aging, or diabetes. The link between aortic rigidity and heart failure is most evident in the hypertensive cardiomyopathy observed in patients with idiopathic infantile arterial calcification and in animal models with aortic banding.In the aortic valve, calcification produces life-threatening aortic stenosis. Although previously considered a passive, degenerative, untreatable disorder of "wear and tear" unrelated to atherosclerosis, recent findings now show that valvular calcification is regulated in a manner similar to that of atheroscler...

“…First described by pathologists centuries ago, the phenomenon has been termed metaplasia, and it appears in the form of ectopic cartilage, bone, fat, and marrow. [1][2][3][4][5][6] Its significance as evidence for mesenchymal stem cells (MSCs) in the artery wall has not been appreciated until recently.…”

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Mesenchymal Stem Cells and the Artery Wall

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2004

Circulation Research

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Abstract-The presence of ectopic tissue in the diseased artery wall is evidence for the presence of multipotential stem cells in the vasculature. Mesenchymal stem cells were first identified in the marrow stroma, and they differentiate along multiple lineages giving rise to cartilage, bone, fat, muscle, and vascular tissue in vitro and in vivo. Transplantation studies show that marrow-derived mesenchymal stem cells appear to enter the circulation and engraft other tissues, including the artery wall, at sites of injury. Recent evidence indicates that mesenchymal stem cells are also present in normal artery wall and microvessels and that they also may enter the circulation, contributing to the population of circulating progenitor cells and engrafting other tissues. Thus, the artery wall is not only a destination but also a source of progenitor cells that have regenerative potential. Although potential artifacts, such as fusion, need to be taken into consideration,

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