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Cited by 432

The DOI matches its Crossref record; 82 of the 82 references it cites were found in a registry or an index.

Bone modeling and remodeling: potential as therapeutic targets for the treatment of osteoporosis

Open access
Langdahl, Bente, Ferrari, Serge, Dempster, David W.·2016·Therapeutic Advances in Musculoskeletal Disease

Abstract

The adult skeleton is renewed by remodeling throughout life. Bone remodeling is a process where osteoclasts and osteoblasts work sequentially in the same bone remodeling unit. After the attainment of peak bone mass, bone remodeling is balanced and bone mass is stable for one or two decades until age-related bone loss begins. Age-related bone loss is caused by increases in resorptive activity and reduced bone formation. The relative importance of cortical remodeling increases with age as cancellous bone is lost and remodeling activity in both compartments increases. Bone modeling describes the process whereby bones are shaped or reshaped by the independent action of osteoblast and osteoclasts. The activities of osteoblasts and osteoclasts are not necessarily coupled anatomically or temporally. Bone modeling defines skeletal development and growth but continues throughout life. Modeling-based bone formation contributes to the periosteal expansion, just as remodeling-based resorption is responsible for the medullary expansion seen at the long bones with aging. Existing and upcoming treatments affect remodeling as well as modeling. Teriparatide stimulates bone formation, 70% of which is remodeling based and 20–30% is modeling based. The vast majority of modeling represents overflow from remodeling units rather than de novo modeling. Denosumab inhibits bone remodeling but is permissive for modeling at cortex. Odanacatib inhibits bone resorption by inhibiting cathepsin K activity, whereas modeling-based bone formation is stimulated at periosteal surfaces. Inhibition of sclerostin stimulates bone formation and histomorphometric analysis demonstrated that bone formation is predominantly modeling based. The bone-mass response to some osteoporosis treatments in humans certainly suggests that nonremodeling mechanisms contribute to this response and bone modeling may be such a mechanism. To date, this has only been demonstrated for teriparatide, however, it is clear that rediscovering a phenomenon that was first observed more half a century ago will have an important impact on our understanding of how new antifracture treatments work.

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Metadata

Authors
Langdahl, B., Ferrari, S., & Dempster, D. W.
Venue
Therapeutic Advances in Musculoskeletal Disease
Published
2016-10-06
Volume
8
Issue
6
Pages
225-235
ISSN
  • 1759-720X (ISSN-L)
  • 1759-7218
OpenAlex
W2529535353
Cited by
432
References
82
FWCI
13.54
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Bone modeling and remodeling: potential as therapeutic targets for the treatment of osteoporosis. https://app.cochat.ai/papers/10.1177/1759720x16670154
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Langdahl, B., Ferrari, S., & Dempster, D. W. (2016). Bone modeling and remodeling: potential as therapeutic targets for the treatment of osteoporosis. Therapeutic Advances in Musculoskeletal Disease. https://doi.org/10.1177/1759720x16670154

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.