Abstract
Objectives:
Patellar dislocations are associated with patellofemoral cartilage degradation following injury and a high risk of patellofemoral post-traumatic osteoarthritis (PTOA). Obesity is also a primary risk factor for patellofemoral cartilage degradation and OA, but the influence of obesity on cartilage degradation follow patellar dislocations is unknown. The current study uses T1ρ-based relaxation time mapping of patellofemoral cartilage to evaluate the influence of body mass index (BMI) on cartilage properties in the acute phase following a patellar dislocation, and compares the results to healthy knees. The hypothesis of the study is increasing BMI is associated with cartilage matrix degeneration for injured and healthy knees.
Methods:
The IRB-approved study focused on a BMI range from underweight to obese (< 40 kg/m2). The population included 18 patients being treated conservatively for a unilateral, first-time patellar dislocation (20 ± 8 years, 9 females, BMI: 24 ± 5 kg/m2, 56 ± 39 days since dislocation), 12 patients being treated conservatively for multiple unilateral dislocations (19 ± 6 years, 9 females, 24 ± 5 kg/m2, 67 ± 35 days since most recent dislocation), and 16 healthy controls (21 ± 7 years, 7 females; 21 ± 7 kg/m2). MRI scans included a 3D water excitation double echo steady state (DESS) scan of the knee for segmentation of the cartilage surfaces (slice thickness of 0.7 mm) and a T1ρ relaxation time scan (fat saturated scan, slice thickness = 4 mm, spin lock times = 0, 10, 40, and 80 ms, spin-lock frequency = 500 Hz). Long T1ρ relaxation times indicate low proteoglycan concentration within cartilage. Automated algorithms based on machine learning were used to segment cartilage on the patella and within the trochlear groove. Additional automated algorithms mapped T1ρ relaxation times to the reconstructed cartilage surfaces (Fig. 1). Mean T1ρ relaxation times were quantified for patellar and trochlear groove cartilage for each knee. Linear regression were used to correlate T1ρ relaxation times with BMI for the single dislocation, multiple dislocations, and control groups. Statistical significance was set at p < 0.05.
Results:
Patellofemoral T1ρ relaxation times increased with BMI for healthy control subjects, but decreased with BMI following patellar dislocation. For control subjects, the increase in T1ρ relaxation times with BMI was significant for cartilage on the patella and within the trochlear groove (r2 > 0.4, p < 0.01). For patients being treated for a single dislocation and multiple dislocations, the decrease in T1ρ relaxation times with increasing BMI was significant for cartilage on the patella and within the trochlear groove (r2 > 0.25, p < 0.025 for single dislocations, r2 > 0.3, p < 0.05 for multiple dislocations).
Conclusions:
The expected increase in T1ρ relaxation times with BMI was observed for healthy control subjects, but not for patients being treated for patellar dislocations. Elevated T1ρ values indicate loss of proteoglycan content that reduces cartilage integrity and could be an initiation point for progression to OA. For cartilage throughout the patellofemoral joint, T1ρ relaxation times decreased as BMI increased following patellar dislocation. The relationships were similar following one dislocation and multiple dislocations. The regression lines for injured knees and controls crossed at a BMI of approximately 25 for patellar and trochlear groove cartilage, indicating T1ρ relaxation times are higher for injured knees than healthy controls only for patients with a BMI < 25 (underweight or healthy weight). Multiple previous studies have identified elevated patellofemoral cartilage relaxation times from quantitative MRI following single and multiple patellar dislocations, but no study has previously attributed the difference to patients with a low BMI. The mechanism by which a high BMI limits cartilage degradation following patellar dislocation is currently unknown. The opposing relationships between T1ρ relaxation times and BMI for injured knees and controls occur despite similar ranges for T1ρ times and BMI. The primary difference between injured knees and controls is the recent dislocation event, and the ensuing inflammatory response. The single and multiple dislocation groups have a recent dislocation and inflammation in common despite differences in time since the first dislocation. Impact injury to cartilage is primarily limited to the medial patella, so is unlikely to cause the difference in trends. Pathologic patellofemoral anatomy is a characteristic of knees with patellar instability that could also influence the relationship with BMI. Additional enrollment and characterization of anatomical factors and inflammatory conditions is needed to identify factors that interact with BMI. Follow up analyses are also needed to determine if these relationships weaken with time from injury.
