Pre-osteoblastic Proliferation Assessed with BrdU in Undecalcified, Epon-embedded Adult Rat Trabecular Bone

Barou, Odile; Laroche, Norbert; Palle, Sabine; Alexandre, Christian; Lafage‐Proust, Marie‐Hélène

doi:10.1177/002215549704500902

Cited by 17 publications

(7 citation statements)

References 29 publications

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“…The above observations focused on the reversal phase, but of note, the canopy extends over bone-forming osteoblasts, which is actually the cell layer commonly considered to consist of osteoprogenitors, and where cell proliferation was also mentioned in mouse68 and rat 3169. This proliferation was stimulated by intermittent PTH 31.…”

Section: Bone-remodeling Compartment Canopiesmentioning

confidence: 99%

The reversal phase of the bone-remodeling cycle: cellular prerequisites for coupling resorption and formation

2014

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The reversal phase couples bone resorption to bone formation by generating an osteogenic environment at remodeling sites. The coupling mechanism remains poorly understood, despite the identification of a number of ‘coupling' osteogenic molecules. A possible reason is the poor attention for the cells leading to osteogenesis during the reversal phase. This review aims at creating awareness of these cells and their activities in adult cancellous bone. It relates cell events (i) on the bone surface, (ii) in the mesenchymal envelope surrounding the bone marrow and appearing as a canopy above remodeling surfaces and (iii) in the bone marrow itself within a 50-μm distance of this canopy. When bone remodeling is initiated, osteoprogenitors at these three different levels are activated, likely as a result of a rearrangement of cell–cell and cell–matrix interactions. Notably, canopies are brought under the osteogenic influence of capillaries and osteoclasts, whereas bone surface cells become exposed to the eroded matrix and other osteoclast products. In several diverse pathophysiological situations, including osteoporosis, a decreased availability of osteoprogenitors from these local reservoirs coincides with decreased osteoblast recruitment and impaired initiation of bone formation, that is, uncoupling. Overall, this review stresses that coupling does not only depend on molecules able to activate osteogenesis, but that it also demands the presence of osteoprogenitors and ordered cell rearrangements at the remodeling site. It points to protection of local osteoprogenitors as a critical strategy to prevent bone loss.

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Section: Bone-remodeling Compartment Canopiesmentioning

confidence: 99%

The reversal phase of the bone-remodeling cycle: cellular prerequisites for coupling resorption and formation

2014

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“…This type of administration spans several days and allows obtaining consistent and reproducible intensity of BrdU staining (Baldauf and Reymann, 2005; Cao et al, 2007; Soames et al, 1994; Tatematsu et al, 1989). Additionally, a previous study performed in bone showed sustained administration of BrdU via osmotic minipump provided a more substantial signal/ noise ratio and reproducible immunostainning of BrdU in the periosteal cells as compared to single and multiple injections (Barou et al, 1997). Preliminary studies in our laboratory confirmed these results.…”

Section: Methodsmentioning

confidence: 98%

The effect of aging on the density of the sensory nerve fiber innervation of bone and acute skeletal pain

Jiménez-Andrade

Mantyh

Bloom

et al. 2012

Neurobiology of Aging

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As humans age there is a decline in most sensory systems including vision, hearing, taste, smell, and tactile acuity. In contrast, the frequency and severity of musculoskeletal pain generally increases with age. To determine whether the density of sensory nerve fibers that transduce skeletal pain changes with age, calcitonin gene related peptide (CGRP) and neurofilament 200 kDa (NF200) sensory nerve fibers that innervate the femur were examined in the femurs of young (4 month old), middle-aged (13 month) and old (36 month) male F344/BNF1 rats. Whereas the bone quality showed a significant age-related decline, the density of CGRP+ and NF200+ nerve fibers that innervate the bone remained remarkably unchanged as well as the severity of acute skeletal fracture pain. Thus, while bone mass, quality and strength undergo a significant decline with age, the density of sensory nerve fibers that transduce noxious stimuli remain largely intact. These data may in part explain why musculoskeletal pain increases with age.

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“…An effective dose of 7 mg of BrdU per animal was administered. (34) Femurs for BrdU immunostaining were processed, embedded in paraffin, and sectioned in the University of Texas Southwestern Medical Center Molecular Pathology Core facility. Tissue sections were probed subsequently with an anti-BrdU Immunohistochemistry Kit (Oncogene, San Diego, CA, USA) according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

GPR30 deficiency causes increased bone mass, mineralization, and growth plate proliferative activity in male mice

Ford

Hajibeigi

Long

et al. 2010

Journal of Bone and Mineral Research

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Estrogen regulation of the male skeleton was first clearly demonstrated in patients with aromatase deficiency or a mutation in the ERα gene. Estrogen action on the skeleton is thought to occur mainly through the action of the nuclear receptors ERα and ERβ. Recently, in vitro studies have shown that the G protein–coupled receptor GPR30 is a functional estrogen receptor (ER). GPR30-deficient mouse models have been generated to study the in vivo function of this protein; however, its in vivo role in the male skeleton remains underexplored. We have characterized size, body composition, and bone mass in adult male Gpr30 knockout (KO) mice and their wild-type (WT) littermates. Gpr30 KO mice weighed more and had greater nasal-anal length (p < .001). Both lean mass and percent body fat were increased in the KO mice. Femur length was greater in Gpr30 KO mice, as was whole-body, spine, and femoral areal bone mineral density (p < .01). Gpr30 KO mice showed increased trabecular bone volume (p < .01) and cortical thickness (p < .001). Mineralized surface was increased in Gpr30 KO mice (p < .05). Bromodeoxyuridine (BrdU) labeling showed greater proliferation in the growth plate of Gpr30 KO mice (p < .05). Under osteogenic culture conditions, Gpr30 KO femoral bone marrow cells produced fewer alkaline phosphatase–positive colonies in early differentiating osteoblast cultures but showed increased mineralized nodule deposition in mature osteoblast cultures. Serum insulin-like growth factor 1 (IGF-1) levels were not different. These data suggest that in male mice, GPR30 action contributes to regulation of bone mass, size, and microarchitecture by a mechanism that does not require changes in circulating IGF-1. © 2011 American Society for Bone and Mineral Research.

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Pre-osteoblastic Proliferation Assessed with BrdU in Undecalcified, Epon-embedded Adult Rat Trabecular Bone

Cited by 17 publications

References 29 publications

The reversal phase of the bone-remodeling cycle: cellular prerequisites for coupling resorption and formation

The reversal phase of the bone-remodeling cycle: cellular prerequisites for coupling resorption and formation

The effect of aging on the density of the sensory nerve fiber innervation of bone and acute skeletal pain

GPR30 deficiency causes increased bone mass, mineralization, and growth plate proliferative activity in male mice

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