Tendon properties in a mouse model of severe osteogenesis imperfecta.

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.