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Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis.
TLDR
The role and the molecular mechanism of action of regulatory molecules, such as cytokines and hormones, in osteoclast and osteoblast birth and apoptosis are reviewed to review the evidence for the contribution of changes in bone cell birth or death to the pathogenesis of the most common forms of osteoporosis. Expand
Matrix-embedded cells control osteoclast formation
TLDR
It is demonstrated that hypertrophic chondrocytes and osteocytes, both of which are embedded in matrix, are essential sources of the RANKL that controls mineralized cartilage resorption and bone remodeling, respectively. Expand
Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone.
TLDR
It is reported that daily PTH injections in mice with either normal bone mass or osteopenia due to defective osteoblastogenesis increased bone formation without affecting the generation of new osteoblasts, and the antiapoptotic effect of PTH was sufficient to account for the increase in bone mass. Expand
Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors Dissociation from Transcriptional Activity
TLDR
A novel paradigm of sex steroid action on osteoblasts, osteocytes, embryonic fibroblasts, and HeLa cells involving activation of a Src/Shc/ERK signaling pathway and attenuating apoptosis is demonstrated, providing proof of principle for the development of function-specific-as opposed to tissue-selective-and gender-neutral pharmacotherapeutics. Expand
Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
TLDR
Evidence is provided that glucocorticoid-induced bone disease arises from changes in the numbers of bone cells, whereas decreased production and apoptosis of osteoblasts would account for the decline in bone formation and trabecular width. Expand
Sex steroids and bone.
TLDR
Loss of nongenotropic anti-apoptotic effects on mature osteoblasts and osteocytes, in combination with an opposite effect on the lifespan of mature osteoclasts, may be responsible for the imbalance between formation and resorption and the progressive loss of bone mass and strength. Expand
Bone marrow, cytokines, and bone remodeling. Emerging insights into the pathophysiology of osteoporosis.
TLDR
Changes in the numbers of bone cells, rather than changes in the activity of individual cells, form the pathogenetic basis of osteoporosis is a major advance in understanding the mechanism of this disease. Expand
From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis.
TLDR
Emerging evidence provides a paradigm shift from the "estrogen-centric" account of the pathogenesis of involutional osteoporosis to one in which age-related mechanisms intrinsic to bone and oxidative stress are protagonists and age- related changes in other organs and tissues, such as ovaries, accentuate them. Expand
Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesis.
Both chronic excess of PTH, as in hyperparathyroidism, and intermittent elevation of PTH (by daily injections) increase the number of osteoblasts; albeit, the former is associated with boneExpand
The Pathophysiologic Roles of Interleukin-6 in Human Disease
TLDR
What makes interleukin-6 particularly interesting to physicians is its marked pleiotropy and its involvement not only in inflammation but in the regulation of endocrine and metabolic functions. Expand
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