Subchondral damage after acute transarticular loading: An in vitro model of joint injury

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Abstract
Intact canine metacarpophalangeal and metatarsophalangeal joints were subjected to a variety of loads in vitro. Intraarticular fracture occurred in 19 joints loaded to an average force of 2.4 ± 0.4 kN with a corresponding loading rate of 88 ± 23 kN/s. The remaining 29 joints were without gross evidence of fracture with an average load and loading rate of 1.7 ± 0.9 kN and 64 ± 32 kN/s, respectively. In the fractured specimens, damage to the zone of calcified cartilage and subchondral bone was much more extensive than was initially evident by gross inspection when assessed by scanning electron microscopy. Cracks with associated step-off displacement at the zone of calcified cartilage were found distant to the gross fractures. These findings were confirmed histologically. In addition, cracks localized to the zone of calcified cartilage were commonly identified histologically in specimens loaded in the range of 1.9–2.8 kN, but were not grossly fractured. The contact area determined with pressure-sensitive film increased with increasing load up to the point of fracture. The average pressure generated at the articular cartilage surface at the time of fracture in this model is ≥40 MPa, and the fracture occurred at the contact site. Our findings suggest that failure in acute transarticular loading begins in the zone of calcified cartilage and subsequently involves the subchondral bone and overlying cartilage. This type of injury may contribute to the development of osteoarthritis after intraarticular fracture, or at high loads that do not result in gross fracture.