Early patellofemoral cartilage and bone pathology in a rat model of noninvasive anterior cruciate ligament rupture

• Published in: Connective tissue research Vol. 64; no. 2; p. 175
• Main Authors: Fleischer, Mackenzie M, Hartner, Samantha E, Newton, Michael D, Baker, Kevin C, Maerz, Tristan
• Format: Journal Article
• Language: English
• Published: England 04-03-2023
• Subjects: Animals; Anterior Cruciate Ligament - pathology; Anterior Cruciate Ligament Injuries - complications; Anterior Cruciate Ligament Injuries - pathology; Cartilage, Articular - diagnostic imaging; Cartilage, Articular - pathology; Female; Osteoarthritis - pathology; Rats; Rats, Inbred Lew; X-Ray Microtomography - adverse effects; Post-traumatic osteoarthritis; patellofemoral; bone; ACL rupture; cartilage
• ISSN: 1607-8438
• DOI: 10.1080/03008207.2022.2136571

Anterior cruciate ligament rupture (ACLR) is a risk factor for the development of post-traumatic osteoarthritis (PTOA). While PTOA in the tibiofemoral joint compartment is well-characterized, very little is known about pathology in the patellofemoral compartment after ACL injury. Here, we evaluated the extent to which ACLR induces early patellofemoral joint damage in a rat model.
Adult female Lewis rats were randomized to noninvasive ACLR or Sham. Two weeks post-injury, contrast-enhanced micro-computed tomography (µCT) of femoral and patellar cartilage was performed using 20% v/v ioxaglate. Morphometric parameters of femoral trochlear and patellar cartilage, subchondral bone, and trabecular bone were derived from µCT. Sagittal Safranin-O/Fast-Green-stained histologic sections were graded using the OARSI score in a blinded fashion.
Cartilage and bone remodelling consistent with an early PTOA phenotype were observed in both femoral trochleas and patellae. ACLR caused osteophyte formation of the patella and pathology in the superficial zone of articular cartilage, including surface fibrillation, fissures, increased cellularity, and abnormal chondrocyte clustering. There were significant increases in thickness of patellar and trochlear cartilage. Loss of subchondral bone thickness, bone volume fraction, and tissue mineral density, as well as changes to patellar and trochlear trabecular microarchitecture, were indicative of catabolic bone remodelling. Several injury-induced changes, including increased cartilage thickness and trabecular spacing and decreased trabecular number were more severe in the patella compared to the trochlea.
The patellofemoral joint develops mild but evident pathology in the early period following ACL rupture, extending the utility of this model to the study of patellofemoral PTOA.