Alterations in compositional and cellular properties of the subchondral bone are linked to cartilage degeneration in hip osteoarthritis

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@article{b5e3ab02332d4aaeaf7062c0d1b648d7,
title = "Alterations in compositional and cellular properties of the subchondral bone are linked to cartilage degeneration in hip osteoarthritis",
abstract = "OBJECTIVE: The subchondral bone is an emerging regulator of osteoarthritis (OA). However, knowledge of how specific subchondral alterations relate to cartilage degeneration remains incomplete.METHOD: Femoral heads were obtained from 44 patients with primary OA during total hip arthroplasty and from 30 non-OA controls during autopsy. A multiscale assessment of the central subchondral bone region comprising histomorphometry, quantitative backscattered electron imaging, nanoindentation, and osteocyte lacunocanalicular network characterization was employed.RESULTS: In hip OA, thickening of the subchondral bone coincided with a higher number of osteoblasts (controls: 3.7±4.5 mm-1, OA: 16.4±10.2 mm-1, age-adjusted mean difference 10.5 mm-1 [95% CI 4.7 to 16.4], p<0.001) but a similar number of osteoclasts compared to controls (p=0.150). Furthermore, higher matrix mineralization heterogeneity (CaWidth, controls: 2.8±0.2 wt%, OA: 3.1±0.3 wt%, age-adjusted mean difference 0.2 wt% [95% CI 0.1 to 0.4], p=0.011) and lower tissue hardness (controls: 0.69±0.06 GPa, OA: 0.67±0.06 GPa, age-adjusted mean difference -0.05 GPa [95% CI -0.09 to -0.01], p=0.032) were detected. While no evidence of altered osteocytic perilacunar/canalicular remodeling in terms of fewer osteocyte canaliculi was found in OA, specimens with advanced cartilage degeneration showed a higher number of osteocyte canaliculi and larger lacunocanalicular network area compared to those with low-grade cartilage degeneration. Multiple linear regression models indicated that several subchondral bone properties, especially osteoblast and osteocyte parameters, were closely related to cartilage degeneration (R2 adjusted=0.561, p<0.001).CONCLUSION: Subchondral bone properties in OA are affected at the compositional, mechanical, and cellular levels. Based on their strong interaction with cartilage degeneration, targeting osteoblasts/osteocytes may be a promising therapeutic OA approach.DATA AND MATERIALS AVAILABILITY: All data are available in the main text or the supplementary materials.",
author = "Julian Delsmann and Julian Eissele and Alexander Simon and Assil-Ramin Alimy and {von Kroge}, Simon and Herbert Mushumba and Klaus P{\"u}schel and Bj{\"o}rn Busse and Christian Ries and Michael Amling and Beil, {Frank Timo} and Tim Rolvien",
note = "Copyright {\textcopyright} 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.",
year = "2024",
month = may,
doi = "10.1016/j.joca.2024.01.007",
language = "English",
volume = "32",
pages = "535--547",
journal = "OSTEOARTHR CARTILAGE",
issn = "1063-4584",
publisher = "W.B. Saunders Ltd",
number = "5",

}

RIS

TY - JOUR

T1 - Alterations in compositional and cellular properties of the subchondral bone are linked to cartilage degeneration in hip osteoarthritis

AU - Delsmann, Julian

AU - Eissele, Julian

AU - Simon, Alexander

AU - Alimy, Assil-Ramin

AU - von Kroge, Simon

AU - Mushumba, Herbert

AU - Püschel, Klaus

AU - Busse, Björn

AU - Ries, Christian

AU - Amling, Michael

AU - Beil, Frank Timo

AU - Rolvien, Tim

N1 - Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.

PY - 2024/5

Y1 - 2024/5

N2 - OBJECTIVE: The subchondral bone is an emerging regulator of osteoarthritis (OA). However, knowledge of how specific subchondral alterations relate to cartilage degeneration remains incomplete.METHOD: Femoral heads were obtained from 44 patients with primary OA during total hip arthroplasty and from 30 non-OA controls during autopsy. A multiscale assessment of the central subchondral bone region comprising histomorphometry, quantitative backscattered electron imaging, nanoindentation, and osteocyte lacunocanalicular network characterization was employed.RESULTS: In hip OA, thickening of the subchondral bone coincided with a higher number of osteoblasts (controls: 3.7±4.5 mm-1, OA: 16.4±10.2 mm-1, age-adjusted mean difference 10.5 mm-1 [95% CI 4.7 to 16.4], p<0.001) but a similar number of osteoclasts compared to controls (p=0.150). Furthermore, higher matrix mineralization heterogeneity (CaWidth, controls: 2.8±0.2 wt%, OA: 3.1±0.3 wt%, age-adjusted mean difference 0.2 wt% [95% CI 0.1 to 0.4], p=0.011) and lower tissue hardness (controls: 0.69±0.06 GPa, OA: 0.67±0.06 GPa, age-adjusted mean difference -0.05 GPa [95% CI -0.09 to -0.01], p=0.032) were detected. While no evidence of altered osteocytic perilacunar/canalicular remodeling in terms of fewer osteocyte canaliculi was found in OA, specimens with advanced cartilage degeneration showed a higher number of osteocyte canaliculi and larger lacunocanalicular network area compared to those with low-grade cartilage degeneration. Multiple linear regression models indicated that several subchondral bone properties, especially osteoblast and osteocyte parameters, were closely related to cartilage degeneration (R2 adjusted=0.561, p<0.001).CONCLUSION: Subchondral bone properties in OA are affected at the compositional, mechanical, and cellular levels. Based on their strong interaction with cartilage degeneration, targeting osteoblasts/osteocytes may be a promising therapeutic OA approach.DATA AND MATERIALS AVAILABILITY: All data are available in the main text or the supplementary materials.

AB - OBJECTIVE: The subchondral bone is an emerging regulator of osteoarthritis (OA). However, knowledge of how specific subchondral alterations relate to cartilage degeneration remains incomplete.METHOD: Femoral heads were obtained from 44 patients with primary OA during total hip arthroplasty and from 30 non-OA controls during autopsy. A multiscale assessment of the central subchondral bone region comprising histomorphometry, quantitative backscattered electron imaging, nanoindentation, and osteocyte lacunocanalicular network characterization was employed.RESULTS: In hip OA, thickening of the subchondral bone coincided with a higher number of osteoblasts (controls: 3.7±4.5 mm-1, OA: 16.4±10.2 mm-1, age-adjusted mean difference 10.5 mm-1 [95% CI 4.7 to 16.4], p<0.001) but a similar number of osteoclasts compared to controls (p=0.150). Furthermore, higher matrix mineralization heterogeneity (CaWidth, controls: 2.8±0.2 wt%, OA: 3.1±0.3 wt%, age-adjusted mean difference 0.2 wt% [95% CI 0.1 to 0.4], p=0.011) and lower tissue hardness (controls: 0.69±0.06 GPa, OA: 0.67±0.06 GPa, age-adjusted mean difference -0.05 GPa [95% CI -0.09 to -0.01], p=0.032) were detected. While no evidence of altered osteocytic perilacunar/canalicular remodeling in terms of fewer osteocyte canaliculi was found in OA, specimens with advanced cartilage degeneration showed a higher number of osteocyte canaliculi and larger lacunocanalicular network area compared to those with low-grade cartilage degeneration. Multiple linear regression models indicated that several subchondral bone properties, especially osteoblast and osteocyte parameters, were closely related to cartilage degeneration (R2 adjusted=0.561, p<0.001).CONCLUSION: Subchondral bone properties in OA are affected at the compositional, mechanical, and cellular levels. Based on their strong interaction with cartilage degeneration, targeting osteoblasts/osteocytes may be a promising therapeutic OA approach.DATA AND MATERIALS AVAILABILITY: All data are available in the main text or the supplementary materials.

U2 - 10.1016/j.joca.2024.01.007

DO - 10.1016/j.joca.2024.01.007

M3 - SCORING: Journal article

C2 - 38403152

VL - 32

SP - 535

EP - 547

JO - OSTEOARTHR CARTILAGE

JF - OSTEOARTHR CARTILAGE

SN - 1063-4584

IS - 5

ER -