Tendon properties in a mouse model of severe osteogenesis imperfecta

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 mice, a model of severe dominant OI.

The Flexor Digitorum Longus (FDL) tendon of Col1a1 mice and wild-type littermates (WT) was assessed with in vitro mechanical testing.

The results showed that width and thickness of FDL tendons were about 40% larger in WT (p < 0.01) than in Col1a1 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 mice. The material properties did not show significant differences between mouse strains with differences <15% between WT and Col1a1 (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 (p < 0.001).

This study shows that the FDL tendon of Col1a1 mice has reduced mechanical properties but apparently normal material properties. It remains unclear whether the tendon phenotype of Col1a1 mice is secondary to muscle weakness or a direct effect of the Col1a1 mutation or a combination of both.