Tendon properties in a mouse model of severe osteogenesis imperfecta
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Tendon properties in a mouse model of severe osteogenesis imperfecta. / Sinkam, Larissa; Boraschi-Diaz, Iris; Svensson, René B.; Kjaer, Michael; Komarova, Svetlana V.; Bergeron, Raynald; Rauch, Frank; Veilleux, Louis Nicolas.
In: Connective Tissue Research, Vol. 64, No. 3, 2023, p. 285-293.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Tendon properties in a mouse model of severe osteogenesis imperfecta
AU - Sinkam, Larissa
AU - Boraschi-Diaz, Iris
AU - Svensson, René B.
AU - Kjaer, Michael
AU - Komarova, Svetlana V.
AU - Bergeron, Raynald
AU - Rauch, Frank
AU - Veilleux, Louis Nicolas
N1 - Publisher Copyright: © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.
PY - 2023
Y1 - 2023
N2 - Purpose/Aim of the study: Osteogenesis imperfecta is a heritable bone disorder that is usually caused by mutations in collagen type I encoding genes. The impact of such mutations on tendons, a structure with high collagen type I content, remains largely unexplored. We hypothesized that tendon properties are abnormal in the context of a mutation affecting collagen type I. The main purpose of the study was to assess the anatomical, mechanical, and material tendon properties of Col1a1 Jrt/+ mice, a model of severe dominant OI. Materials and Methods: The Flexor Digitorum Longus (FDL) tendon of Col1a1 Jrt/+ mice and wild-type littermates (WT) was assessed with in vitro mechanical testing. Results: The results showed that width and thickness of FDL tendons were about 40% larger in WT (p < 0.01) than in Col1a1 Jrt/+ mice, whereas the cross-sectional area was 138% larger (p < 0.001). The stiffness, peak- and yield-force were between 160% and 194% higher in WT vs. Col1a1 Jrt/+ mice. The material properties did not show significant differences between mouse strains with differences <15% between WT and Col1a1 Jrt/+ (p > 0.05). Analysis of the Achilles tendon collagen showed no difference between mice strains for the content but collagen solubility in acetic acid was 66% higher in WT than in Col1a1 Jrt/+ (p < 0.001). Conclusions: This study shows that the FDL tendon of Col1a1 Jrt/+ mice has reduced mechanical properties but apparently normal material properties. It remains unclear whether the tendon phenotype of Col1a1 Jrt/+ mice is secondary to muscle weakness or a direct effect of the Col1a1 mutation or a combination of both.
AB - Purpose/Aim of the study: Osteogenesis imperfecta is a heritable bone disorder that is usually caused by mutations in collagen type I encoding genes. The impact of such mutations on tendons, a structure with high collagen type I content, remains largely unexplored. We hypothesized that tendon properties are abnormal in the context of a mutation affecting collagen type I. The main purpose of the study was to assess the anatomical, mechanical, and material tendon properties of Col1a1 Jrt/+ mice, a model of severe dominant OI. Materials and Methods: The Flexor Digitorum Longus (FDL) tendon of Col1a1 Jrt/+ mice and wild-type littermates (WT) was assessed with in vitro mechanical testing. Results: The results showed that width and thickness of FDL tendons were about 40% larger in WT (p < 0.01) than in Col1a1 Jrt/+ mice, whereas the cross-sectional area was 138% larger (p < 0.001). The stiffness, peak- and yield-force were between 160% and 194% higher in WT vs. Col1a1 Jrt/+ mice. The material properties did not show significant differences between mouse strains with differences <15% between WT and Col1a1 Jrt/+ (p > 0.05). Analysis of the Achilles tendon collagen showed no difference between mice strains for the content but collagen solubility in acetic acid was 66% higher in WT than in Col1a1 Jrt/+ (p < 0.001). Conclusions: This study shows that the FDL tendon of Col1a1 Jrt/+ mice has reduced mechanical properties but apparently normal material properties. It remains unclear whether the tendon phenotype of Col1a1 Jrt/+ mice is secondary to muscle weakness or a direct effect of the Col1a1 mutation or a combination of both.
KW - Col1a1
KW - Osteogenesis imperfecta
KW - Tendon properties
U2 - 10.1080/03008207.2022.2161376
DO - 10.1080/03008207.2022.2161376
M3 - Journal article
C2 - 36576243
AN - SCOPUS:85145383370
VL - 64
SP - 285
EP - 293
JO - Connective Tissue Research
JF - Connective Tissue Research
SN - 0300-8207
IS - 3
ER -
ID: 338361921