Introduction

ACL tears are a common knee injury and are associated with an elevated risk of developing OA. Bone plays an important role in OA development, and bone mass has been shown in animal models and human studies to decrease immediately following injury before partially recovering. ACL transection models have confirmed this bone loss is driven by trabecular structure degradation, however, this has not been confirmed in humans due to limited in vivo image resolution. The recent development of high-resolution peripheral quantitative computed tomography (HR-pQCT) provides an unprecedented opportunity to longitudinal assess bone microarchitecture in the knee, and magnetic resonance imaging (MRI) complements this technology so that both hard and soft tissues can be simultaneously tracked. This allows, for example, the monitoring of bone marrow lesions, which commonly occur in post-traumatic knee injury, and we are particularly interested in early joint changes that may lead to long-term development of knee osteoarthritis.

The objective of this study was to establish bone microarchitectural changes in the human knee within the first year following a unilateral acute ACL tear, using HR-pQCT and MRI.

Content

METHODS: Participants with unilateral ACL tears (n=15, 22-44 years of age, 10 female and 5 male) were followed with HR-pQCT with up to four time points (baseline, +2 months, +4 months, +8months). The baseline measurement occurred within 6 weeks of injury. Both the ACL deficient and uninjured contralateral knees were imaged at 61μm isotropic voxel size (XtremeCTII, Scanco Medical). Bone microarchitecture was assessed up to 7.5 mm below the weight bearing surfaces of the medial and lateral tibia and femur. The subchondral bone plate (density, thickness), and trabecular bone (density, thickness, number, separation) were quantified. Longitudinal bone changes within each knee were assessed using quadratic temporal mixed effects models, which were compared to linear and intercept-only mixed effects models using chi-squared tests (level of significance: p<0.05). 95% confidence intervals for each model parameter were assessed using bootstrapping (200 samples with replacement). MRI captured regions of bone marrow lesions, and by multimodal image registration between HR-pQCT and MRI it was possible to establish the changes to bone microarchitecture that occur specifically in the BML region.

RESULTS: Bone loss occurred throughout the injured knee (-4.6% to -15.8%; Fig 1). Bone loss occurred in a non-linear manner, with loss occurring within the first 7 to 8 months post-injury before indicating the start of a recovery phase. The loss was driven by trabecular structure degradation as reflected by an increase in trabecular separation (6.4% to 10.6%) and decrease in number (-3.1% to -7.8%) of trabecular elements. The subchondral bone plate of the lateral femur significantly decreased in thickness (-9.0%). Regions of BMLs had accelerated microarchitectural adaptations compared to the rest of the knee. The contralateral knee was mostly unaffected.

CONCLUSION: Bone loss in the injured knee during the first year following ACL tears is driven by loss of trabecular elements. This likely cannot be reversed as for any future ‘recovery’ of bone mass there is no known mechanism to re-establish the original bone structure. Thus, permanent structural changes may persist, which indicates there may be a short window for intervention to reduce the risk of long-term OA development.

Acknowledgments

This study was funded by The Arthritis Society, SOG-15-226.