Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis.
By S. Manolagas. Endocrine reviews, 2000
2,580 citations recorded by the source corpus.
Subfields: Molecular Biology, Obstetrics and Gynecology, Oncology
View Paper: https://www.semanticscholar.org/paper/78ee77456c9eb3aed00217f52eb04c02b17985dc
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Citations in the corpus
- Matrix-embedded cells control osteoclast formation (2011, background): “Excessive bone resorption causes the most common bone disorders, including osteoporosis, Paget's disease and osteolysis from cance”
- Sex steroids and bone. (2002, background): “Similar results were obtained subsequently by others in rats as well as in humans, in the bone marrow and in the peripheral blood (Manolagas, 2000a; Scheidt-Nave et al., 2001).”
- Stable Isotopes of Carbon and Nitrogen as Tracers for Paleo-Diet Reconstruction (2012, background): “The average residence time of C and N atoms in bone collagen is about 10 y but can be longer than 20 y in older individuals ( Manolagas 2000; Hedges et al. 2007).”
- Role of RANK ligand in mediating increased bone resorption in early postmenopausal women. (2003, background): “These cytokines increase bone resorption mainly by increasing the pool size of preosteoclasts in bone marrow (1, 3, 4); however, MCSF also enhances fusion of preosteoclasts to form osteoclasts (5) and, recently, direct effects of TNF-α on osteoclasts have been demonstrated (6, 7).”
- Molecular and cellular mechanisms of the anabolic effect of intermittent PTH. (2007, background): “The control of osteoblast number is determined by the balance between their production and their death [17].”
- Sex steroids and the construction and conservation of the adult skeleton. (2002, background): “As with E, T also increases the lifespan of both osteoblasts (32) and osteoclasts (44) by affecting apoptosis.”
- Buried alive: How osteoblasts become osteocytes (2006, background): “© 2005 Wiley-Liss, Inc. 1990); “osteoblasts are buried within the bone matrix” (Manolagas, 2000); and “osteoblasts merge progressively into the bone matrix” (Meunier, 1989).”
- Minireview: the OPG/RANKL/RANK system. (2001, background): “These include (among others) the identification of sex steroid receptors in bone cells (1, 2); the cloning and characterization of PTHrelated peptide (PTHrP) as the major factor responsible for the syndrome of humoral hypercalcemia of malignancy (3, 4) and as an important locally active cytokine in ”
- Natural Polymeric Scaffolds in Bone Regeneration (2020, background): “Size of the bone cells is also in the micro-domain, going from 1 to 2µm for bone lining cells to 50–100µm for mature osteoclasts (Manolagas, 2000).”
- From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “Almost 10 yr ago, I had reviewed in this journal the cellular and molecular mechanisms of osteoporosis and highlighted the overriding importance of osteoclast, osteoblast, and osteocyte numbers for bone homeostasis, as well as the paramount importance of the aberrations of the rate of birth and deat”
- RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β (2002, background): “jpg" NDATA ITEM> ]> Osteoclasts are cells of monocyte/macrophage origin that erode bone matrix: regulation of their differentiation is central to the understanding of the pathogenesis and treatment of bone diseases such as osteoporosis”
- The Amazing Osteocyte (2010, background): “It was proposed by Manolagas(9) that the matrix-producing osteoblast either can become an osteocyte, a lining cell, or can undergo programmed cell death.”