The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Vascular pathology and osteoarthritis
Abstract
There is mounting evidence that vascular pathology plays a role in the initiation and/or progression of the major disease of joints: osteoarthritis (OA). Potential mechanisms are: episodically reduced blood flow through the small vessels in the subchondral bone at the ends of long bones, and related to this, reduced interstitial fluid flow in subchondral bone. Blood flow may be reduced by venous occlusion and stasis or by the development of microemboli in the subchondral vessels. There are several likely effects of subchondral ischaemia: the first of these is compromised nutrient and gas exchange into the articular cartilage, a potential initiator of degradative changes in the cartilage. The second is apoptosis of osteocytes in regions of the subchondral bone, which would initiate osteoclastic resorption of that bone and at least temporarily reduce the bony support for the overlying cartilage. It may be important to recognize these potential aetiological factors in order to develop more effective treatments to inhibit the progression of OA.
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Cites
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“Thirdly, recent work points to a broader role for osteocytes in systemic mineral metabolism [ 25 ].”
BackgroundOsteocyte control of bone formation via sclerostin, a novel BMP antagonist
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Cited by
Is osteoarthritis a metabolic disease?
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Bone–cartilage crosstalk: a conversation for understanding osteoarthritis
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Self-citationType 2 diabetes mellitus and osteoarthritis
Veronese, N., Cooper, C., Reginster, J.-Y., Hochberg, M., Branco, J., Bruyère, O., Chapurlat, R., Al-Daghri, N., Dennison, E., Herrero-Beaumont, G., et al. (2019) · Seminars in Arthritis and Rheumatism · doi:10.1016/j.semarthrit.2019.01.005 · Cited by 258
Metabolic stress-induced joint inflammation and osteoarthritis
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Metadata
- Authors
- Findlay, D. M.
- Venue
- Rheumatology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-08-05
- Volume
- 46
- Issue
- 12
- Pages
- 1763-1768
- ISSN
- 1462-0324 (ISSN-L)
- 1462-0332
- OpenAlex
- W2135213015
- Cited by
- 305
- References
- 65
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.
