Loss and gain of bone in spondyloarthritis:what drives these opposing clinical features?

Clunie, Gavin and Horwood, Nicole ORCID: https://orcid.org/0000-0002-6344-1677 (2021) Loss and gain of bone in spondyloarthritis:what drives these opposing clinical features? Therapeutic Advances in Musculoskeletal Disease, 12. pp. 1-17. ISSN 1759-720X

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The breadth of bone lesion types seen in spondyloarthritis is unprecedented in medicine and includes increased bone turnover, bone loss and fragility, osteitis, osteolysis and erosion, osteosclerosis, osteoproliferation of soft tissues adjacent to bone and spinal skeletal structure weakness. Remarkably, these effects can be present simultaneously in the same patient. The search for a potential unifying cause of effects on the skeleton necessarily focuses on inflammation arising from the dysregulation of immune response to microorganisms, particularly dysregulation of TH17 lymphocytes, and the dysbiosis of established gut and other microbiota. The compelling notion that a common antecedent pathological mechanism affects existing bone and tissues with bone-forming potential (entheses), simultaneously with variable effect in the former but bone-forming in the latter, drives basic research forward and focuses our awareness on the effects on these bone mechanisms of the increasing portfolio of targeted immunotherapies used in the clinic.

Item Type: Article
Uncontrolled Keywords: ankylosing spondylitis (as),axial spondyloarthritis (axspa),bone pathophysiology,enthesophyte,osteoimmunology,osteomicrobiology,osteoporosis,osteoproliferation,spondyloarthritis (spa),syndesmophyte,rheumatology,orthopedics and sports medicine ,/dk/atira/pure/subjectarea/asjc/2700/2745
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
UEA Research Groups: Faculty of Medicine and Health Sciences > Research Centres > Metabolic Health
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Depositing User: LivePure Connector
Date Deposited: 07 Nov 2020 01:09
Last Modified: 19 Oct 2023 02:49
URI: https://ueaeprints.uea.ac.uk/id/eprint/77578
DOI: 10.1177/1759720X20969260

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