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Review Article
Mechanisms of Disease
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Volume 332:305-311 February 2, 1995 Number 5
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Bone Marrow, Cytokines, and Bone Remodeling — Emerging Insights into the Pathophysiology of Osteoporosis
Stavros C. Manolagas, M.D., Ph.D., and Robert L. Jilka, Ph.D.

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Bone is remodeled continuously during adulthood through the resorption of old bone by osteoclasts and the subsequent formation of new bone by osteoblasts. These two closely coupled events are responsible for renewing the skeleton while maintaining its anatomical and structural integrity. Under normal conditions, bone remodeling proceeds in cycles in which osteoclasts adhere to bone and subsequently remove it by acidification and proteolytic digestion. Shortly after the osteoclasts have left the resorption site, osteoblasts invade the area and begin the process of forming new bone by secreting osteoid (a matrix of collagen and other proteins), which is eventually mineralized. After . . . [Full Text of this Article]

Role of Bone Marrow in Bone-Cell Development

Origin of Osteoblasts

Origin of Osteoclasts

Pathophysiology of Osteoporosis

Bone Remodeling and Osteoporosis

Role of Interleukin-6 in Osteopenia Associated with Loss of Gonadal Function

Loss of Estrogens and Formation of Osteoblast Precursors in Marrow

Senescence and Osteoblast Development in Marrow

Summary


Source Information

From the Division of Endocrinology and Metabolism, Department of Internal Medicine, Center for Osteoporosis and Metabolic Bone Diseases, University of Arkansas for Medical Sciences, and the McClellan Veterans Affairs Medical Center — both in Little Rock.

Address reprint requests to Dr. Manolagas at the University of Arkansas for Medical Sciences, 4301 W. Markham, Mail Slot 587, Little Rock, AR 72205.

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