In this study, higher HPIE and greater SAPIE in the PCL-ruptured group were found compared to the PCL-intact group and it may be risk factors for the PCL rupture in knee flexion injury. In addition, patients with PCL injury had significantly greater SLPIE than PCL-intact patients.
The PCL originates from the anterolateral aspect of the medial femoral condyle and inserts onto the posterior aspect of the tibial plateau. It is the most important ligament in maintaining the posterior stability of the knee joint [15, 16]. It can be separated into the anterolateral and the posteromedial bundles [17, 18], of which the anterolateral bundle (65% of the body of the PCL) is about twice as large as the posteromedial bundle in cross-sectional area [15, 18, 19]. The anterolateral bundle is taut during knee flexion and lax in extension; conversely, the posteromedial bundle is taut during extension and lax in flexion [15, 18]. MRI of the knee in flexion shows the PCL gradually approaching the posterior intercondylar eminence [9, 10]. Therefore, we chose PCL-ruptured cases when its mechanism is knee flexion for this study. According to the biomechanical mechanism of the PCL, the anterolateral portion is commonly injured in knee flexion. In addition, the spectrum of PCL injuries includes intra-substance injury, complete substance tears and avulsion of the PCL insertion sites on the femur and tibia [11, 19]. In our study, substance tears were incorporated because of the injury mechanism.
Previous studies have focused on the bony morphology of the knee as a risk factor in ACL-ruptured patients [14, 20,21,22]. However, to our knowledge, few studies have focused on the anatomical risk factors for PCL rupture [7, 8]. A recent study found that patients with PCL rupture had higher tibial eminences than PCL-intact patients on anterior–posterior X-ray . However, that study just used a statistical shape model in X-ray and did not specifically measure the height of the tibial intercondylar eminence. In addition, it only described this phenomenon of higher tibial eminences resulting in PCL injuries without exploring the possible mechanism. In our study, we defined the HPIE, SLPIE and SAPIE and measured the specific data on MRI in PACS system (Fig. 2). The measurement method refers to other previously-published studies on the relationship between tibial slopes and ACL injuries on MRI .
In extension of the knee, the PCL is curved concave-forwards away from the posterior intercondylar eminence. It is straight, fully out-to length with the knee at 90° flexion and close to the posterior intercondylar eminence (Fig. 1). In full flexion, it curves convex-forwards over the roof of the intercondylar notch [9, 10]. It has been reported that in situ force in the PCL increases with knee flexion ranging from 35.6 ± 13 N at 0° flexion to 112.3 ± 28.5 N at 90° flexion, in response to 95% of posterior translational forces at 90° [6, 10, 23]. In addition, studies have found that the maximal length of the PCL in the living knee is at 90–100° of knee flexion and the PCL is closest to the posterior intercondylar eminence apex at this time [9,10,11]. At this time, a sudden posteriorly-directed force applied to the proximal tibia may cause collisions between the bony structures and stretched ligaments. In this study, we found that the mean HPIE, SLPIE and SAPIE of patients with PCL rupture were significantly greater than PCL-intact patients. HPIE and SAPIE were independently associated with PCL rupture using multivariable logistic analyses regression model which means that PCL is closer to the posterior intercondylar eminence apex in PCL-ruptured patients. In this study, as well as matching age, gender, height, weight, and side of injury, we specifically chose patients with knee trauma as the control group to make the groups more comparable than using healthy controls without a traumatic event. Research into anatomical risk factor for PCL rupture is rare. In a previous study, Kuijk  found that a more sharply angled intercondylar notch is related to a PCL rupture. In this study, we found that patients with PCL rupture may have a higher posterior intercondylar eminence compared to PCL-intact patients. It may be helpful for protecting the graft when polishing the high HPIE during posterior cruciate ligament reconstruction. Also, we think the anatomical risk factor may help to identify individual patients who are at great risk of PCL rupture.
We acknowledge some limitations to our study. In this study, the PCL injured group were only those that had PCL reconstruction performed so that the results may not be generalizable to the non-operatively managed PCL injured patients. Another limitation is that the theory of collision between the PCL and posterior intercondylar eminence during knee flexion was inferred from clinical data. There are no biomechanical studies on cadavers to directly explain the phenomenon. Third, we have chosen patients with ACL injuries but PCL-intact as the control group in this study, which may cause some misleading that lower HPIE, SLPIE and SAPIE were risk factors for ACL injuries. In terms of anatomical positional relationship, the posterior intercondylar eminence and ACL will not collide theoretically. However, it still needs biomechanical studies of cadavers to confirm this. In addition, patients in control group may not experience a similar mechanism of injury. And, we selected patients with sports injuries during the same period as controls to minimize errors. Fourth, there were no radiographs of uninjured knees in our study. The uninjured knees of patients in our study have no symptoms and they refused MRIs of uninjured knees. Thus, the parameters could not be measured to examine whether there are significant differences between the involved knees and uninjured knees.