Trabecular Bone Turnover and Bone Marrow Cell Development in Tail-Suspended Mice

Sakata, Toshiie; Sakai, Akinori; Tsurukami, Hiroshi; Okimoto, Nobukazu; Okazaki, Yukio; Ikeda, Satoshi; Norimura, Toshiyuki; Nakamura, Toshio

doi:10.1359/jbmr.1999.14.9.1596

Cited by 102 publications

(119 citation statements)

References 41 publications

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“…Following hindlimb suspension, an accepted model of skeletal unloading, MSCs isolated from rats exhibited a significant decrease in proliferation potential 96 as well as an impaired differentiation capacity. 97,98 Similar observations have been made following the isolation of MSCs from mice, 99 and reloading partially rescues deficits in MSC proliferation and differentiation. 100 In humans, skeletal unloading is associated with an increase in bone marrow adipocity which may represent an alteration in MSC differentiation.…”

Section: Fluid Flow In Tissue Engineeringsupporting

confidence: 67%

From streaming‐potentials to shear stress: 25 years of bone cell mechanotransduction

Riddle

Donahue

2008

Journal Orthopaedic Research

129

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Mechanical loads are vital regulators of skeletal mass and architecture as evidenced by the increase in bone formation following the addition of exogenous loads and loss of bone mass following their removal. While our understanding of the molecular mechanisms by which bone cells perceive changes in their mechanical environment has increased rapidly in recent years, much remains to be learned. Here, we outline the effects of interstitial fluid flow, a potent biophysical signal induced by the deformation of skeletal tissue in response to applied loads, on bone cell behavior. We focus on the molecular mechanisms by which bone cells are hypothesized to perceive interstitial fluid flow, the cell signaling cascades activated by fluid flow, and the use of this signal in tissue engineering protocols. ß

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Section: Fluid Flow In Tissue Engineeringsupporting

confidence: 67%

From streaming‐potentials to shear stress: 25 years of bone cell mechanotransduction

Riddle

Donahue

2008

Journal Orthopaedic Research

129

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“…In the present study, WRS successfully reduced the BMD via a high bone turnover rate; WRS induced an increase in bone resorption and formation. There are several mouse models for the reduction of BMD, such as ovariectomy of female mice (25), administration of soluble receptor activator of nuclear factor κB ligand (RANKL) (26) and tail suspension (27). Ovariectomy leads to BMD loss for 8 weeks, but requires specific surgical skills, while the intraperitoneal injection of soluble RANKL reduces BMD for only 50 h; however, soluble RANKL is expensive and difficult to obtain.…”

Section: Discussionmentioning

confidence: 99%

Effect of vitamin K2 on the development of stress-induced osteopenia in a growing senescence-accelerated mouse prone 6 strain

Katsuyama

Fushimi

Yamane

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Vitamin K2 (VK2) has been used as a therapeutic agent for osteoporosis, since it has been suggested to be able to reduce the frequency of fractures by improving bone quality; however, bone turnover is strictly regulated by various cytokines and hormones. In the present study, the effect of menaquinone-4 (MK-4) on bone turnover was investigated using the senescence-accelerated mouse prone 6 (SAMP6) strain. Since water-immersion restraint stress (WRS) causes a significant decrease in bone mineral density (BMD), WRS was used as the bone resorption model in the SAMP6 strain. Six-week-old SAMP6 male mice were divided into the following three groups: Control, WRS and WRS + MK-4. WRS was performed for 6 h per day, 5 times a week, for 4 weeks. Following WRS, MK-4 (30 mg/kg) was injected subcutaneously 3 times a week for 4 weeks. No growth retardation was observed in the WRS groups as compared with the control group. In the WRS groups, the BMD was significantly lower than that in the control group. The levels of bone formation and resorption markers were increased in the WRS groups, indicating that WRS reduced the BMD by promoting high bone turnover. A bone histomorphometrical examination showed that the trabecular (Tb) bone mass in the secondary spongiosa at the distal femur was significantly reduced in the WRS mice, and this reduction was abrogated by MK-4 treatment. Specifically, the Tb bone reduction was caused by the activation of osteoclasts (Ocs), and Oc activity was suppressed by MK-4. The number of osteoblasts and the mineral apposition rate were significantly increased in the WRS and WRS + MK-4 mice, suggesting that WRS triggered a significantly higher mineral apposition rate. These results indicate that MK-4 can induce recovery from the bone mineral loss caused by WRS treatment. Further studies are required to clarify the association between bone quality and MK-4.

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“…Murine models have demonstrated unique potential for mechanistic exploration of muscle/ bone interactions in vivo [19], but bone loss in current murine models of disuse arises due to a combination of diminished osteoblast activity and enhanced osteoclastic resorption [34]. This response is distinct from that observed in humans and other mammals in which diminished muscle function precipitates reduced bone mass primarily via aggressive bone resorption with minimal contribution from altered osteoblast function [24].…”

Section: Introductionmentioning

confidence: 99%

Botox induced muscle paralysis rapidly degrades bone

Warner

Sanford

Becker

et al. 2006

Bone

180

193

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The means by which muscle function modulates bone homeostasis is poorly understood. To begin to address this issue, we have developed a novel murine model of unilateral transient hindlimb muscle paralysis using botulinum toxin A (Botox). Female C57BL/6 mice (16 weeks) received IM injections of either saline or Botox (n = 10 each) in both the quadriceps and calf muscles of the right hindleg. Gait dysfunction was assessed by multi-observer inventory, muscle alterations were determined by wet mass, and bone alterations were assessed by micro-CT imaging at the distal femur, proximal tibia, and tibia mid-diaphysis. Profound degradation of both muscle and bone was observed within 21 days despite significant restoration of weight bearing function by 14 days. The muscle mass of the injected quadriceps and calf muscles was diminished −47.3% and −59.7%, respectively, vs. saline mice (both P < 0.001). The ratio of bone volume to tissue volume (BV/TV) within the distal femoral epiphysis and proximal tibial metaphysis of Botox injected limbs was reduced −43.2% and −54.3%, respectively, while tibia cortical bone volume was reduced −14.6% (all P < 0.001). Comparison of the contralateral non-injected limbs indicated the presence of moderate systemic effects in the model that were most probably associated with diminished activity following muscle paralysis. Taken as a whole, the micro-CT data implied that trabecular and cortical bone loss was primarily achieved by bone resorption. These data confirm the decisive role of neuromuscular function in mediating bone homeostasis and establish a model with unique potential to explore the mechanisms underlying this relation. Given the rapidly expanding use of neuromuscular inhibitors for indications such as pain reduction, these data also raise the critical need to monitor bone loss in these patients.

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Trabecular Bone Turnover and Bone Marrow Cell Development in Tail-Suspended Mice

Cited by 102 publications

References 41 publications

From streaming‐potentials to shear stress: 25 years of bone cell mechanotransduction

From streaming‐potentials to shear stress: 25 years of bone cell mechanotransduction

Effect of vitamin K2 on the development of stress-induced osteopenia in a growing senescence-accelerated mouse prone 6 strain

Botox induced muscle paralysis rapidly degrades bone

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