There were two principal findings of this study. First, the presence of MFLs on MRI was significantly lower in the ACL rupture group than in the control group. Second, the presence of MFLs decreased with increasing time from injury.
In this study, we evaluated the absence or presence of the MFLs in ACL ruptured and ACL intact patient knees. Compared with the control group, the ruptured ACL group had a significantly lower prevalence of MFLs. This ACL absence could be due to a congenital absence or a rupture. Two hypotheses can be proposed: MFLs rupture during ACL tearing or congenital pMFL-deficient knees have a higher risk of ACL rupture. Further studies are needed to evaluate these hypotheses.
The presence of the pMFL reportedly ranges between 66.4 and 100% in the literature (
7,
12,
17,
18). In our study, the presence of the pMFL was 78 and 49% in the intact and ruptured ACL groups, respectively. However, the presence of the aMFL has been lower (between 0 and 88.2%) than that of the pMFL in almost all previous studies (
9,
12,
17-
19). In our study, the presence of an isolated aMFL was 44 and 23% in the intact and ruptured ACL groups, respectively.
Anatomical studies have shown several variations in the proximal and distal adhesion sites of the MFLs (
17,
20). The aMFL may be thick or thin in two or three bands adjacent to the articular cartilage in the inferoanterior portion of the PCL, starting from the posterior part of the posterior meniscus and in the direction of the femur to the left. The pMFL is generally expressed from the posterior horn of the anterior horn and may be thick or thin in the posterosuperior part of the PCL or in the two bands within the posteromedial PCL band (
21). Bozkurt et al. observed that the MFL thickness ranged from 2.6 to 6.1 mm (average: 2.6 mm) (
22). In our study, the thickness and adhesion site variations in the MFL bonds were not evaluated. We accepted MFLs ≥ 3 mm as being present.
In the literature, the relationship between age and the presence of MFL is controversial. Rohrich et al. showed that there is no relationship between age and the presence of MFL (
23). On the other hand, there are studies showing a relationship between age and the presence of MFL (
17,
20). In our study, we found a negative correlation between age and the presence of MFL in both groups.
Forkel et al. found that MFL damage was observed in five of the 32 patients with lateral meniscus root ruptures who underwent arthroscopic evaluation for ruptured ACL (
6). Similarly, there was a relationship between posterior meniscus root tear and MFL absence in patients with ACL tear. Previously, when the meniscus was extruded, absence of the MFLs was more prevalent in patients with lateral meniscus root tear (
24-
26). In our study, we thought that instability causing degeneration of the MFLs would involve both weakening of the MFL structure and possible eventual MFL disappearance. The MFLs were less prevalent in the ACL ruptured group, which was consistent with other studies.
Several studies have shown a relationship between the lateral meniscus and MFLs, especially the discoid meniscus (
27,
28). Atypical thickness and atypical region pMFLs have been shown to cause discoid lateral meniscus rupture (
29,
30). However, findings in the literature have been inconsistent. A retrospective arthroscopic study by Lee et al. found no relationship between meniscus tear and the MFLs (
12). Similarly, Miller et al. found no significant relationship between meniscus tear and the MFLs by MRI (
11). Patients with meniscus rupture and meniscus root tears were not included in the present study because meniscus and ACL tears may have affected the results, and there were not enough patients to evaluate different meniscus tear types and ACL ruptures (
24-
26).
At present, there are no standardized guidelines for evaluation of MFLs by MRI. Proper evaluation of the MFLs on MRI should be performed for each plane and always include the sagittal plane (
23). Previous studies on the presence of the aMFL and pMFL in the coronal plane have shown that Cohen’s kappa coefficient was 0.62 for the aMFL and 0.72 for the pMFL. When evaluated in all available planes, Cohen’s kappa coefficient was found to be 0.84 for the aMFL and 0.96 for the pMFL (
23). In our study, MFLs were evaluated in each plane. We evaluated MFL by 1.5-T MRI because it has been shown to be sufficient in the literature (
31).
There were some study limitations that should be considered. The use of MRI to evaluate the MFLs was a potential major issue because there is no established arthroscopic or surgical correlation with MRI findings. MRI may give false-negative results if it misses the fine MFL bonds and may give false-positive results because of the oblique PCL fibers (
15,
32). We were careful to distinguish the oblique PCL and pMFL bundles. In our study, as anatomic markers, only BMI was evaluated. Such indicators as body fat, waist-hip ratio were not evaluated. Although we did not find any relation between the presence of MFL and BMI, other anatomic markers could be impacted by the presence of MFL. All patients were of a Caucasian population. MFLs vary according to race; different results may be obtained in different races (
17,
20). Other limitations were the small numbers of patients with intact and ruptured ACLs and that most of the subjects were male. However, no sex-related difference in the prevalence of MFLs in the normal population has been reported (
22,
33). Finally, we did not evaluate the cross-sectional areas, proximal/distal adhesion sides, and running angles in the MFLs in this study, which could have affected our results.
In conclusion, we observed the absence of MFLs (aMFL and pMFL) in a significant majority of patients with ruptured ACLs. Furthermore, we found a significant relationship between the time from injury to MRI and the absence of MFL in the ruptured ACL group. Future research is needed to evaluate correlations between arthroscopic or surgical findings and MRI features.