Anterior cruciate ligament and meniscus tears are injuries that are known risk factors for post-traumatic OA in humans, presumably because of residual abnormal knee mechanics. This work sought to determine whether abnormal motion of the tibiofemoral joint surfaces was related to early cartilage damage in two ovine joint injury models: combined anterior cruciate and medial collateral ligament transection (ACL/MCLx), and lateral meniscectomy (Mx). Five descriptions of in vivo tibiofemoral inter-surface motion (i.e., "surface interactions") were selected based on their speculated relationship to mechanical mechanisms known to damage cartilage in vitr. The hypotheses were: H₁. increasingly abnormal surface interactions would correlate with cartilage damage, H₂. the number of significant correlations would be greatest in ACL/MCLx sheep, and H₃. locations of cartilage damage would qualitatively coincide with that of altered surface interactions. 21 sheep were allocated to four groups: 6 ACL/MCLx, 5 Mx, 4 sham-operated, and 6 non-operated controls. Baseline in vivo kinematics were measured prior to injury, and serially up to 20 weeks post-injury, and expressed as the diference from Intact. Cartilage damage was quantified and mapped at sacrifice. Repeated measures ANOVAs and Pearson correlation coeficients were used to determine whether surface interactions were significantly diferent from Intact and correlated with cartilage damage. Results partially supported the hypotheses. ACL/MCLx surface interactions were significantly abnormal, and 3/5 interactions correlated with the magnitude of cartilage damage but not its distribution. The number of significant correlations was greatest in ACL/MCLx sheep and had a cumulative efect on cartilage damage that was individual- and surface-specific, suggesting that diferent surace interactions may be more damaging in diferent individuals. Lateral compartment joint space was significantly reduced following meniscectomy, but only correlated with cartilage damage at discrete gait points for two surface interactions 20 weeks post-Mx, suggesting that surface interactions presently quantified did not reflect the primary mechanism responsible for damage in this model, likely contact stress. The presence of significant correlations between multiple surface interactions and cartilage damage in both injury models add strong support to the paradigm that altered mechanics play a pivotal role in the aetiology of early cartilage damage following these joint injuries.