Systemic sclerosis skin is a 'primed' microenvironment for soft tissue calcification - a hypothesisCitation formats

Standard

Systemic sclerosis skin is a 'primed' microenvironment for soft tissue calcification - a hypothesis. / Burgess, Kyle A; Herrick, Ariane L; Watson, Rachel E B.

In: Rheumatology (Oxford, England), Vol. 60, No. 6, 15.02.2021, p. 2517-2527.

Research output: Contribution to journalArticlepeer-review

Harvard

APA

Vancouver

Author

Burgess, Kyle A ; Herrick, Ariane L ; Watson, Rachel E B. / Systemic sclerosis skin is a 'primed' microenvironment for soft tissue calcification - a hypothesis. In: Rheumatology (Oxford, England). 2021 ; Vol. 60, No. 6. pp. 2517-2527.

Bibtex

@article{c4b488b78060455f94a1de8ca0332ce4,
title = "Systemic sclerosis skin is a 'primed' microenvironment for soft tissue calcification - a hypothesis",
abstract = "Calcinosis cutis, defined as sub-epidermal deposition of calcium salts, is a major clinical problem in patients with systemic sclerosis (SSc), affecting 20-40% of patients. A number of recognised associates of calcinosis have been identified, including disease duration, digital ischaemia and acro-osteolysis. Yet to date, the pathogenesis of SSc-related calcinosis remains unknown and currently there is no effective disease-modifying pharmacotherapy. Following onset of SSc, there are marked changes in the extracellular matrix (ECM) of the skin, notably a breakdown in the microfibrillar network and accumulation of type I collagen. Our hypothesis is that these pathological changes reflect a changing cellular phenotype and result in a primed microenvironment for soft tissue calcification, with SSc fibroblasts adopting a pro-osteogenic profile and specific 'driving forces' promoting tissue mineralisation. Considering the role of the ECM in disease progression may help elucidate the mechanism(s) behind SSc-related calcinosis and inform the development of future therapeutic interventions.",
author = "Burgess, {Kyle A} and Herrick, {Ariane L} and Watson, {Rachel E B}",
note = "{\textcopyright} The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.",
year = "2021",
month = feb,
day = "15",
doi = "10.1093/rheumatology/keab156",
language = "English",
volume = "60",
pages = "2517--2527",
journal = "Rheumatology (Print)",
issn = "1462-0324",
publisher = "Oxford University Press",
number = "6",

}

RIS

TY - JOUR

T1 - Systemic sclerosis skin is a 'primed' microenvironment for soft tissue calcification - a hypothesis

AU - Burgess, Kyle A

AU - Herrick, Ariane L

AU - Watson, Rachel E B

N1 - © The Author(s) 2021. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

PY - 2021/2/15

Y1 - 2021/2/15

N2 - Calcinosis cutis, defined as sub-epidermal deposition of calcium salts, is a major clinical problem in patients with systemic sclerosis (SSc), affecting 20-40% of patients. A number of recognised associates of calcinosis have been identified, including disease duration, digital ischaemia and acro-osteolysis. Yet to date, the pathogenesis of SSc-related calcinosis remains unknown and currently there is no effective disease-modifying pharmacotherapy. Following onset of SSc, there are marked changes in the extracellular matrix (ECM) of the skin, notably a breakdown in the microfibrillar network and accumulation of type I collagen. Our hypothesis is that these pathological changes reflect a changing cellular phenotype and result in a primed microenvironment for soft tissue calcification, with SSc fibroblasts adopting a pro-osteogenic profile and specific 'driving forces' promoting tissue mineralisation. Considering the role of the ECM in disease progression may help elucidate the mechanism(s) behind SSc-related calcinosis and inform the development of future therapeutic interventions.

AB - Calcinosis cutis, defined as sub-epidermal deposition of calcium salts, is a major clinical problem in patients with systemic sclerosis (SSc), affecting 20-40% of patients. A number of recognised associates of calcinosis have been identified, including disease duration, digital ischaemia and acro-osteolysis. Yet to date, the pathogenesis of SSc-related calcinosis remains unknown and currently there is no effective disease-modifying pharmacotherapy. Following onset of SSc, there are marked changes in the extracellular matrix (ECM) of the skin, notably a breakdown in the microfibrillar network and accumulation of type I collagen. Our hypothesis is that these pathological changes reflect a changing cellular phenotype and result in a primed microenvironment for soft tissue calcification, with SSc fibroblasts adopting a pro-osteogenic profile and specific 'driving forces' promoting tissue mineralisation. Considering the role of the ECM in disease progression may help elucidate the mechanism(s) behind SSc-related calcinosis and inform the development of future therapeutic interventions.

U2 - 10.1093/rheumatology/keab156

DO - 10.1093/rheumatology/keab156

M3 - Article

C2 - 33585894

VL - 60

SP - 2517

EP - 2527

JO - Rheumatology (Print)

JF - Rheumatology (Print)

SN - 1462-0324

IS - 6

ER -