Intravenous bisphosphonate therapy for osteoporosis: Where do we stand?

Bone, Henry G.; Schurr, W.

doi:10.1007/s11914-004-0011-5

Cited by 8 publications

(5 citation statements)

References 60 publications

(56 reference statements)

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“…The reduction in activation frequency of bone remodeling units along bone surfaces and the coupling between bone resorption and formation result in a decrease in bone formation following treatment (1). Further more, it has been argued that such profound inhibition of bone turnover could be contributing to rare, but significant, clinical complications such as osteonecrosis of the jaw (ONJ) and atypical subtrochanteric femoral fractures (2)(3)(4)(5). The profound decrease in bone remodeling associated with these drugs has also been sug gested to decrease the responsiveness of the skeleton to parathy roid hormone (PTH), the only anabolic drug currently available in the clinic (6).…”

Section: Introductionmentioning

confidence: 99%

Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation

Lotinun¹,

Kiviranta²,

Matsubara³

et al. 2013

J. Clin. Invest.

216

253

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Cathepsin K (CTSK) is secreted by osteoclasts to degrade collagen and other matrix proteins during bone resorption. Global deletion of Ctsk in mice decreases bone resorption, leading to osteopetrosis, but also increases the bone formation rate (BFR). To understand how Ctsk deletion increases the BFR, we generated osteoclast-and osteoblast-targeted Ctsk knockout mice using floxed Ctsk alleles. Targeted ablation of Ctsk in hematopoietic cells, or specifically in osteoclasts and cells of the monocyte-osteoclast lineage, resulted in increased bone volume and BFR as well as osteoclast and osteoblast numbers. In contrast, targeted deletion of Ctsk in osteoblasts had no effect on bone resorption or BFR, demonstrating that the increased BFR is osteoclast dependent. Deletion of Ctsk in osteoclasts increased their sphingosine kinase 1 (Sphk1) expression. Conditioned media from Ctsk-deficient osteoclasts, which contained elevated levels of sphingosine-1-phosphate (S1P), increased alkaline phosphatase and mineralized nodules in osteoblast cultures. An S1P 1,3 receptor antagonist inhibited these responses. Osteoblasts derived from mice with Ctsk-deficient osteoclasts had an increased RANKL/OPG ratio, providing a positive feedback loop that increased the number of osteoclasts. Our data provide genetic evidence that deletion of CTSK in osteoclasts enhances bone formation in vivo by increasing the generation of osteoclast-derived S1P.

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Section: Introductionmentioning

confidence: 99%

Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation

Lotinun¹,

Kiviranta²,

Matsubara³

et al. 2013

J. Clin. Invest.

216

253

View full text Add to dashboard Cite

show abstract

“…Thus, osteopenia is considered a major public health problem with high financial costs (Bravo et al, 1997), significant effects on quality of life (Dargent-Molina, 1998), and high mortality rates (Shin et al, 2010). Substantial efforts have been made to prevent or reduce bone loss, including the administration of calcitonin, calcium, and estrogen replacement (North American Menopause Society, 2002), as well as the use of anti-resorptive therapy, such as bisphosphonates (Bone & Schurr, 2004). However, the long-term administration of these drugs may result in gastrointestinal side effects, including gastric ulcers and reflux esophagitis (Abrahamsen, 2010).…”

mentioning

confidence: 99%

The osteogenic effects of swimming, jumping, and vibration on the protection of bone quality from disuse bone loss

Falcai

Zamarioli

Okubo

et al. 2014

Scandinavian Med Sci Sports

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We assessed and compared the effects of swimming, jumping, and vibration therapies on the prevention of bone loss because of unloading. Eighty Wistar rats were randomly divided into eight groups: S, permanent hind limb-suspended rats; CON, control rats; S + Swim, unloading interrupted by swimming exercise; S + C(Swim), suspension interrupted by regular weight-bearing with the same duration as in the S + Swim protocol; S + Jump, unloading interrupted by jumping exercise; S + C(Jump), suspension interrupted for regular weight-bearing as in the S + Jump group; S + Vibr, unloading interrupted by vibration; and S + C(Vibr), suspension with interruptions for regular weight-bearing with the same protocol as that used for the S + Vibr rats. At the end of the experiment, the bone mineral density, bone strength, histomorphometric parameters, and serum levels of the bone markers were analyzed. The hind limb-suspended rats exhibited bone quality loss. In contrast, the trained rats showed a significant increase in bone mass, bone strength, bone formation, and serum levels of bone markers compared with the respective controls. Although we did not find a significant difference among the three physical exercises, the osteogenic effect of vibration was slightly lower than that of swimming and jumping. Thus, all physical exercises were efficient in preventing bone loss because of unloading and preserving bone quality.

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“…Available anti‐resorptive drugs are efficient in inhibiting bone resorption but also have a profound inhibitory effect on bone formation [Nyman et al, ]. The decreased bone formation is thought to contribute to significant clinical complications (osteonecrosis of jaw and atypical sub‐trochanteric fractures) [Bone and Schurr, ; Khan et al, ; Koh et al, ; Carvalho et al, ]. Current drugs also reduce the responsiveness of the skeleton to parathyroid hormone, the only anabolic drug currently available in the clinic [Black et al, ].…”

Section: The Dogmamentioning

confidence: 99%

The Multifaceted Osteoclast; Far and Beyond Bone Resorption

Drissi

Sanjay

2016

J of Cellular Biochemistry

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The accepted function of the bone resorbing cell, osteoclast, has been linked to bone remodeling and pathological osteolysis. Emerging evidence points to novel functions of osteoclasts in controlling bone formation and angiogenesis. Thus, while the concept of a "clastokine" with the potential to regulate osteogenesis during remodeling did not come as a surprise, new evidence provided unique insight into the mechanisms underlying osteoclastic control of bone formation. The question still remains as to whether osteoclast precursors or a unique trap positive mononuclear cell, can govern any aspect of bone formation. The novel paradigm eloquently proposed by leaders in the field brings together the concept of clastokines and osteoclast precursor-mediated bone formation, potentially though enhanced angiogenesis. These fascinating advances in osteoclast biology have motivated this short review, in which we discuss these new roles of osteoclasts. J. Cell. Biochem. 117: 1753-1756, 2016. © 2016 Wiley Periodicals, Inc.

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Intravenous bisphosphonate therapy for osteoporosis: Where do we stand?

Cited by 8 publications

References 60 publications

Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation

Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation

The osteogenic effects of swimming, jumping, and vibration on the protection of bone quality from disuse bone loss

The Multifaceted Osteoclast; Far and Beyond Bone Resorption

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