In more than 50% of cases, anterior cruciate ligament (ACL) lesions lead to post-traumatic osteoarthritis. Ligament reconstruction stabilizes the joint, but the tear seems to impair the poroelasticity of the cartilage: synovial membrane fluid inflammation is observed 3 weeks after tearing. There have been some descriptions of visible cartilage changes, but poroelasticity has never been analyzed at this early stage. The present animal study aimed to determine (1) whether cartilage showed early poroelastic deterioration after ACL tear; (2) whether an impairment correlated with macroscopic changes; and (3) whether cartilage poroelasticity deteriorated over time.

In the days following trauma, cartilage poroelasticity is greatly impaired, without macroscopically visible change.

ACL tear was surgically induced in 18 New-Zealand rabbits. Cartilage poroelasticity was assessed on indentation-relaxation test in 3 groups: “early”, at 2 weeks postoperatively (n=6), “mid-early” at 6 weeks (n=6) and in a non-operated control group (“non-op”). Macroscopic changes were scored in the same groups.

Poroelastic impairment was greatest at the early time-point (2 weeks). Permeability ranged from a mean 0.08±0.05×10⁻¹⁵ m⁴/Ns (range, 0.028–0.17) in the “non-op” group to 1.03±0.60×10⁻¹⁵ m⁴/Ns (range, 0.24–2.15) in the “early” group (p=0.007). Shear modulus ranged from 0.53±0.11MPa (range, 0.36–0.66) to 0.23±0.10MPa (range, 0.12–0.43), respectively (p=0.013). Macroscopic deterioration, on the other hand, differed significantly only between the “mid-early” and the “non-op” groups: p=0.011 for cartilage deterioration and p=0.008 for osteophyte formation. At the “mid-early” time point, poroelastic deterioration was less marked, with 0.33±0.33×10⁻¹⁵ m⁴/Ns permeability (range, 0.06–1.06) and shear modulus 0.30±0.10MPa (range, 0.13–0.41: respectively p=0.039 and p=0.023 compared to the “non-op” group.

The severe rapid deterioration in poroelasticity following ACL tear in an animal model, as notably seen in increased permeability, corresponds to changes in cartilage microstructure, with easier outflows of interstitial fluid. This mechanical degradation may underlie onset of microcracks within the cartilage, leading to physiological loading that the cartilage by its nature is unable to repair. Further investigations are needed to correlate these experimental data with clinical findings.

III; comparative study with control group.