This longitudinal study examined changes in patellar cartilage morphologic features (i.e., cartilage volume and cartilage defects) in ACLR knees with or without combined meniscal pathology from 2.5 to 4.5 years post-surgery, as well as a control group assessed over 2 years. ACLR groups demonstrated an increase in patella cartilage volume whilst control participants exhibited no change over the study period. Moreover, the isolated ACLR group showed a higher level of patella cartilage volume increase than the combined ACLR and control groups. Patellar cartilage defect scores significantly regressed in the isolated ACLR group. Finally, baseline patellar cartilage defect scores were positively associated with the increase in patellar cartilage volume over 2 years in ACLR participants.
Consistent with H1, both isolated and combined ACLR knees showed significant increases in patellar cartilage volume at follow-up compared to baseline, while the patellar cartilage volume of the control group exhibited no significant change. Increase in patellar cartilage volume in ACLR knees is consistent with results of several recent longitudinal studies that have also reported increased knee cartilage volume or thickness within 1–5 years post-ACLR [15–17, 23] - albeit in the TF joint compartments. These findings may be indicative of early OA development that where cartilage increases have been reported prior to cartilage loss and may be due to tissue hypertrophy, repair and swelling [15]. In contrast to the current study, Culvenor et al. [14] reported decreased PF cartilage thickness at 5-years following ACLR- a finding which, given the follow-up period, may be reflective of a more advanced stage of cartilage degeneration than the current study. In the early stages of cartilage degeneration, cartilage increase is suggestive of accelerated metabolism and increased water - an adaptive response to repair cartilage damage and withstanding mechanical load [27, 28]. Whilst identifying the biomechanical mechanisms contributing to patella cartilage increase are beyond the scope of this study, PFJ ‘underloading’ during running in a comparable cohort of ACLR patients has been reported [29]. Decreased PFJ loading has been associated with early degenerative changes in ACL-transected animals [30, 31]. In humans, a relationship between TF joint underloading and the development of early-onset TF osteoarthritis has been identified [32]. Clearly, the definitive biomechanical conditions that contribute to the pathogenesis of PFJ OA post-ACLR need to be the focus of future studies.
In contrast to H2, ACLR isolated knees exhibited a greater increase in annual percentage change in patella cartilage volume than the combined ACLR and control knees. Meniscectomy and meniscal injuries have been associated with a higher prevalence of TF and PF joint OA following ACLR [7, 33, 34]. For this reason, we hypothesised (H2) that combined ACLR knees would demonstrate more pronounced cartilage volume change compared to isolated ACLR and control knees. However, our results indicate the opposite, and no differences were found between combined ACLR and control knees. This unexpected finding may be related to the fact that degenerative changes occur across cartilage sub-regions at different rates. In this respect, Eckstein et al.[15] whilst adopting a different technique for quantifying cartilage morphology, reported concurrent TF cartilage thickening and thinning in different sub-regions within the same cartilage compartment in post-ACLR participants. It has been widely accepted that an increase in cartilage volume precedes cartilage thinning during the process of cartilage degeneration [28]. Overall cartilage morphology is a direct result of the balance between cartilage hypertrophy and loss. The isolated ACLR group experienced greater patellar cartilage volume increase suggesting that, on balance, increasing cartilage volume was the predominant change across the plate sub-regions. In contrast, combined ACLR knees may have been undergoing a higher level of cartilage thinning in some sub-regions due to more rapid degeneration compared with isolated ACLR knees. This argument is also supported in the TF joint, as our previous research has demonstrated the same between-group difference in the lateral tibia [23].
Contrary to H1, the majority of participants in each of the three groups had stable cartilage defects meaning defect grades were unchanged between baseline and follow up assessment time points. The stability of the cartilage defects in both ACLR groups suggests that the cartilage defects persist from 2.5–4.5 years post-ACLR. This notion is supported by Potter et al. (2012) who found cartilage defects in all 40 patients at the time of ACL injury, and minimal subsequent change in cartilage defect size until ~ 7 years post injury, at which point there was a marked increase in defect [20]. It is likely that the increase at this latter time represents acceleration of the degenerative processes, and is consistent with the higher rates of OA development observed around this time period (i.e., over 10 years) post-injury[2, 4].
Notably and contrary to H1, patellar cartilage defect scores significantly regressed in the isolated ACLR group and 25% of knees exhibited improvements in PF cartilage defects from baseline to follow-up. These improvements seem to be independent of concurrent meniscal injury, as 24% of the combined ACLR knees also showed cartilage defect improvement. This finding is different from previous studies showing one-way progression of patellar cartilage defects from 2–11 years following ACLR [20, 35]. In support however, another study [36] demonstrated that in a relatively young (i.e., mean age of 45 years) cohort of 325 participants, largely without radiographic OA, 13% of participants showed improvement in patellar cartilage defects over two-year period [36]. Improvement in cartilage defects, due to cartilage synthesis or swelling, reflects an attempt to repair cartilage damage and withstand mechanical load [28]. The natural history of cartilage defects was also age-related. In older groups, improvement of cartilage defects appears to be less common. Specifically, in a study of 395 participants with mean age 62.7 years, 26% cartilage defects progressed at the patella over 3 years, with the majority of defects remaining stable, and defect improvement rarely occurring (~ 1% of participants) [37]. In another study of 86 healthy participants with a mean age of 57 years, approximately 36% had worsening in patellar cartilage defects, while approximately 18% improved over 2 years [38]. Moreover, a recent study reported that 17% of ACLR participants had cartilage defects or osteophytes in the PF joint and, as such, were categorised as exhibiting MRI-defined PF joint OA [6]. Although defining early OA is of great value [39], results of the current study suggest that the definition of early OA should be carefully selected. Specifically, using the presence of mild cartilage defects as a diagnostic criterion for early OA may be inappropriate in either research or clinical setting, considering the regression of cartilage defects in a substantial portion of ACLR patients.
Contrary to H2, there were no differences in changes in cartilage defects between the three groups. This lack of difference between groups may be attributable to the small change in cartilage defects over the 2-years, and/or the relatively small sample size with a lack of power to detect statistical differences.
In support of H3, higher baseline cartilage defect scores at the patella of ACLR participants were associated with greater patellar cartilage volume increases over the subsequent two years. The positive relationship indicates that mildly disturbed cartilage homeostasis (i.e., ICRS 1–2 cartilage defects) was associated with cartilage adaptation, which may be indicative of early cartilage degeneration. This positive association between cartilage defects and increases in cartilage volume are consistent with our previous finding in the lateral tibia [22]. It is important to note that ACLR participants in this study were different from those included in previous studies which reported that more severe cartilage defects (i.e., ICRS 3–4) were associated with an increased likelihood of developing radiographic OA [33] and worse patient-report outcomes [40–43].
This study has several strengths. First, this is the first study to compare the change in patellar cartilage morphology between ACLR participants with and without concomitant meniscal pathology. Second, in contrast to most other longitudinal studies, we included an age-matched control group for comparative purposes. By contrast, our study also has several limitations. Firstly, 49% of the participants were lost to follow-up. Importantly, no difference in participant characteristics were identified between those participants who remained in the study and those lost to follow-up. Also, the sample size was relatively small for the combined ACLR group and the control group, which could reduce the statistical power of the study [22].