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. 2016 Dec 29;8(4):483–489. doi: 10.1111/os.12284

What Role Does Low Bone Mineral Density Play in the “Killer Turn” Effect after Transtibial Posterior Cruciate Ligament Reconstruction?

Yue Li 1, Xing‐zuo Chen 1, Jin Zhang 1, Guan‐yang Song 1, Xu Li 1, Hua Feng 1,✉
PMCID: PMC6584432  PMID: 28032708

Abstract

Objective

To explore the mechanism of the “killer turn”, which is reported to be a reason for postoperative residual laxity after transtibial posterior cruciate ligament (PCL) reconstruction, in a low bone mineral density (BMD) condition.

Methods

A total of 80 skeletally mature female New Zealand white rabbits were included for biomechanical evaluation after transtibial PCL reconstructions. The subjects were equally divided into low BMD (n = 40) and control groups (n = 40). Rabbits in the low BMD group were treated with surgery and drug injection to establish an osteoporotic model. Rabbits in the control group received sham surgeries and no injection. All assignments were conducted randomly according to random numbers generated by a computer. All grafts were then subjected to biomechanical testing with an MTS model‐858 Mini Bionix servohydraulic materials testing machine (MTS Systems, Minneapolis, Minnesota, USA). The experimental outcomes were the increment of total graft displacement, tunnel inlet enlargement, graft elongation, stiffness and failure load of the two groups, and the comparison between them.

Results

Among the 80 subjects, 1 subject of the low BMD group failed at the 30th cycle by proximal tibial fracture and 1 subject of the control group failed at the 20th cycle for the same reason. As a result, 39 subjects of the low BMD group and 39 subjects of the control group survived the cyclic loading test. Compared with the control group, the low BMD group demonstrated significantly larger total graft displacement (P = 0.006) and tunnel inlet enlargement (P = 0.041) than the control group. The number of subjects with less than 10% enlargement was significantly greater (57.1%) in the control group than in the low BMD group (P = 0.004). In the load‐to‐failure test, 26 (66.7%) subjects in the low BMD group failed by proximal tibial fracture (around the tunnel), 6 (15.4%) at the mounting site, 5 (12.8%) at the fixation site, and only 2 (5.1%) failed at the “killer turn.” In the control group, 20 (51.3%) failed at the “killer turn,” 9 (23.1%) at the proximal tibia (around the tunnel), 5 (12.8%) at the mounting site, and 5 (12.8%) at the fixation site. There were significantly fewer failures (10.0%) at the “killer turn” (P = 0.000) and 155.6% more for the para‐tunnel fracture (P = 0.000) in the low BMD group compared with the control group.

Conclusions

The low BMD group demonstrated an inferior biomechanical outcome to the control group with the transtibial technique. With low BMD, the “killer turn” effect compromises the posterior tibial cortex by enlarging the tunnel inlet.

Keywords: Bone mineral density, Killer turn, Posterior cruciate ligament, Reconstruction

Introduction

Posterior cruciate ligament (PCL) reconstruction is a common surgery in sports medicine. The transtibial technique is a popular technique of PCL reconstruction. Although the transtibial technique has the advantages of patient positioning and lower technical difficulty, the “killer turn” has frequently been documented as a primary drawback of this technique1, 2, 3. Given the anatomy of the tibial posterior cortex and the direction of tibial and femoral tunnels, there is a sharp angle of the graft at the inlet of the proximal tibial tunnel, which is referred as the “killer turn” after transtibial PCL reconstruction4.

The mechanism of the “killer turn” effect is conventionally believed to be a permanent elongation of the graft caused by thinning from repetitive abrasion between the bone and the graft1, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16. Because the ligament is less abrasion‐resistant compared to the posterior tibial cortex, it is usually the graft rather than the proximal posterior cortex that becomes attenuated and elongated. However, in the state of low bone mineral density (BMD), the posterior tibial cortex might be more vulnerable than in the normal state, leading to a compromise of the tibial tunnel inlet. Therefore, it can be assumed that, during the process of abrasion or micro‐motion between the bone and the graft, the tibial tunnel inlet might also be weakened and, thus, enlarged, especially in the case of low BMD.

According to Fanelli, 96.5% of posterior cruciate ligament injuries are PCL‐based multiligament injuries that usually result from high‐energy trauma, of which fractures and vascular injuries are the common concomitant injuries and demand a long immobilization and non‐weight bearing period17. Long‐term immobilization and non‐weight bearing are two vital risk factors of disuse osteoporosis. Because ligament injury treatment is only indicated after the management of fracture and vascular injuries, disuse osteoporosis has become inevitable when performing PCL reconstruction consequently18, 19. Chronic neglected PCL injury or multiligament injury that limit patients are other risk factors for low bone mineral density. It has been proven that low BMD is associated with tunnel inlet enlargement after anterior cruciate ligament (ACL) reconstruction. However, to our knowledge, there is a paucity of literature on the effect of the “killer turn” on the PCL tibial inlet in low BMD knees. Because the low BMD makes the bone less abrasion‐resistant, it can be presumed that the “killer turn” may also be attenuated by the graft, making the tunnel inlet enlargement a critical component of the total graft displacement.

The objective of this study was to compare the biomechanical properties of the grafts in a low BMD group with those of a control group. We hypothesized that: (i) the total graft displacement and tunnel inlet enlargement of the low BMD group would be greater than that of the control group; and (ii) the graft elongation would be smaller in the low BMD group.

Methods

Ethical Statement

This study was carried out in accordance to the guidelines of the Beijing Jishuitan Hospital. The protocol was approved by the Ethical Committee of Beijing Jishuitan Hospital. (Protocol Number: 20080812.)

Experimental Animals

Eighty skeletally mature female New Zealand white rabbits were included for PCL reconstruction. The mean age was 13.1 ± 1.2 months. The mean body weight was 4.1 ± 0.7 kg. All rabbits were housed separately on a 12/12 h light/dark cycle in a specific‐pathogen‐free (SPF) facility. All subjects had free access to sterile water and standard commercial rabbit feed during the acclimatization period of 1 week and the whole study period. Before the in vitro surgery and biomechanical testing, all rabbits were killed by intra‐cardiac administration of sodium pentobarbital (50 mg/kg) under general anesthesia.

Study Design

Among the 80 rabbits, 40 were allocated to the low BMD group and the other 40 subjects were assigned to the control group. Rabbits in the low BMD group were treated with surgery and drug injection to establish an osteoporotic model. Rabbits in the control group received sham surgeries and no injection. All assignments were conducted randomly according to random numbers generated by a computer. The flowchart of the study is shown in Fig. 1. A single animal was set as an experimental unit. All specimens underwent biomechanical testing. The experimental outcomes were the increment of total graft displacement, tunnel inlet enlargement, graft elongation, stiffness and failure load of the two groups and the comparison between them.

Figure 1.

Figure 1

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Flowchart of the study design.

Establishment of Osteoporotic Model

A verified low BMD rabbit model was then created according to the method of Castañeda et al. 20, 21: (i) bilateral ovariectomy on Day 1 in an operation room; (ii) daily i.m. injections of methylprednisolone hemisuccinate at a dose of 1 mg/kg/day from Day 1 to Day 28 at 16.00 hours; (iii) all rabbits were killed by intra‐cardiac administration of sodium pentobarbital (50 mg/kg) under general anesthesia on Day 43; (iv) at time of death, both tibias without fibula were dissected for further PCL reconstruction. The validity of this method was verified by a preliminary pathologic observation.

Surgical Technique

On the tibia specimens, the native PCL footprint was identified before the PCL fibers were removed, leaving the remnants of the fibrous attachments intact1, 22. The Achilles tendon autograft was then harvested. All reconstructions were performed using the transtibial technique. A tunnel was drilled with 3.5‐mm K‐wire from the anteromedial cortex of the tibia to the center of the native footprint at an angle of 60°. The Achilles tendon autograft was then fashioned to a diameter of approximately 3.0 mm and braided with 4‐0 Ethibond (Ethicon, Somerville, New Jersey, USA). The graft was then pulled through the tunnel and fixed with one Endobutton (Smith & Nephew Endoscopy, Andover, Massachusetts, USA) on the anteromedial cortex of the tibia. The other end of the graft was with the calcaneus on for the mounting on the device.

Testing Protocol

Device Parameters

According to the testing protocol of previous experiments, in both groups, after the tibial side of the graft was fixed, the other end of the graft was mounted onto an MTS model‐858 Mini Bionix servohydraulic materials testing machine (MTS Systems, Minneapolis, Minnesota, USA) for the cyclic loading test10, 12, 22, 23, 24, 25. Our device employed an MTS Model 858.11 load unit that is fatigue‐rated at 100 N, with a resolution of 0.001 N. This freestanding load unit can be operated at frequencies up to 30 Hz. The device can detect a displacement range of ±50 mm, with a resolution of 0.01 mm. The instrumental error was less than 0.5%. All specimens were subjected to 1500 cycles of loading at 3 Hz. The loading force was 50 N. Both tibias and calcaneus were secured with polymethyl methacrylate bone cement and then mounted on the device. The graft was secured at an angle of 45° to the tibial plateau on the sagittal plane (Fig. 2).

Figure 2.

Figure 2

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The establishment of the biomechanical device. (A) The front view of the device: both tibias and calcaneus were secured with polymethyl methacrylate bone cement and then mounted on the device. (B) The lateral view of the device: the graft was secured at an angle of 45° to the tibial plateau on the sagittal plane.

Testing Parameters

After the cyclic loading test, the elongation of the grafts (the length change of the mid‐third segment of the graft), the total displacement of the grafts (the difference of graft displacement between the 20th cycle and 1500th cycle at a loading of 30 N), the difference of graft stiffness [(the maximal axial force − minimal axial force)/(displacement at the maximal force − displacement at the minimal force)] at the 20th and the 1500th cycle, and the tunnel inlet enlargement were recorded and analyzed. The curve was continuously recorded from the 1st to the 10th cycle. Then it was recorded every 10 cycles from the 20th to the 100th cycle, and recorded every 100 cycles from the 200th to the 1500th cycle. The load‐to‐failure test was performed following the cyclic loading test, and the failure load was then recorded.

Tunnel Inlet Measurement

The tunnel inlet measurement was performed on the micro‐CT images (SKYSCAN 1172, BrukermicroCT, Belgium), and analyzed with CT vol (BrukermicroCT, Belgium): Realistic 3D visualization and CT analyzer software (BrukermicroCT, Belgium). The resolution was 2000 × 2000 pixels, with pixel size of 13.8 μm. The slice thickness was set as 5 μm. The long axis of the tunnel was measured on the 3D‐reconstruction model. First, the coordinate (expressed as pixels) of the two ends of the long axis was determined manually. Second, the distance between these two coordinates was calculated and expressed as pixels. Third, the pixel size in the present study was 13.8 μm, so the actual distance can be calculated. The tunnel inlet enlargement was expressed as the equation of difference of the pre‐testing and post‐testing long axis length divided by the pre‐testing long‐axis length. Validation of this method showed an inter‐group correlation coefficient of 0.935, and an intra‐group coefficient of 0.973.

Statistical Analysis

All data were expressed as average ± standard deviation. The variables included graft elongation, graft displacement, load to failure, stiffness, and the tunnel inlet enlargement. As confirmed by the Kolmogorov–Smirnov test, all variables were of normal distribution. The paired t‐test was used to analyze the tunnel inlet enlargement. Student's t‐test was used to determine the difference of the low BMD and control groups in terms of the graft elongation, graft displacement, load to failure, and stiffness. According to a power analysis, for a power of more than 0.80, the minimal sample size is 33. Therefore, in the present study, we included 40 rabbits in each group. The level of significance was P < 0.05.

Results

Inclusion Data

There were a total of 40 low BMD and 40 control subjects that underwent PCL reconstructions and biomechanical evaluations afterwards. Among them, 1 subject of the low BMD group failed at the 30th cycle by proximal tibial fracture and 1 subject of the control group failed at the 20th cycle for the same reason. As a result, 39 subjects of the low BMD group and 39 subjects of the control group survived the cyclic loading test.

Cyclic Loading Test

Compared with the control group, the low BMD group demonstrated 86.5% larger total graft displacement (40.34% ± 23.75% vs 21.63% ± 24.62%, P = 0.006) and tunnel inlet enlargement (32.57% ± 37.73% vs 15.21% ± 20.82%, P = 0.041) than the control group (Fig. 3). In the low BMD group, there were 20 subjects (51.3%) with more than 30% enlargement, 5 subjects (12.8%) with 10%–30% enlargement, and 14 subjects (35.9%) with less than 10% enlargement. In the control group, there were 7 subjects (17.9%) with more than 30% enlargement, 10 subjects (25.6%) with 10%–30% enlargement, and 22 subjects (56.4%) with less than 10% enlargement (Fig. 4). The number of subjects with less than 10% enlargement was significantly more (57.1%) in the control than low BMD group (P = 0.004). No significant differences were detected in graft elongation, stiffness, and failure load. The baseline data and biomechanical results are illustrated in Table 1.

Figure 3.

Figure 3

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The measurement of tunnel inlet enlargement of pre‐cyclic and post‐cyclic loading test in 3D reconstruction model. (A) It showed a diameter of 3.56 mm before cyclic loading test, and (B) a diameter of 3.89 mm after the test, indicating an enlargement of 9.3%.

Figure 4.

Figure 4

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Comparison of tunnel inlet enlargement between the low bone mineral density (BMD) and control groups. In the low BMD group, there were 20 subjects (51.3%) with more than 30% enlargement, 5 subjects (12.8%) with 10%–30% enlargement, and 14 subjects (35.9%) with less than 10% enlargement. In the control group, there were 7 subjects (17.9%) with more than 30% enlargement, 10 subjects (25.6%) with 10%–30% enlargement, and 22 subjects (56.4%) with less than 10% enlargement. The number of subjects with less than 10% enlargement was significantly more in the control than low BMD group (P = 0.004).

Table 1.

Comparison of biomechanical properties between control and osteoporotic group with Transtibial technique (mean ± SD)

Control group Osteoporotic group
Indexes Difference Percentage (%) Difference Percentage (%) P value
Graft displacement (mm) 1.91 ± 0.74 21.63 ± 24.62 1.04 ± 0.85 40.34 ± 23.75 0.006
Graft elongation (mm) 0.21 ± 0.44 3.59 ± 6.77 0.37 ± 0.31 3.68 ± 6.94 0.601
Tunnel inlet enlargement (mm) 0.49 ± 0.66 15.21 ± 20.82 1.11 ± 1.28 32.57 ± 37.73 0.041
Stiffness (N/mm) 6.82 ± 6.58 21.10 ± 19.77 6.44 ± 9.18 20.75 ± 19.08 0.710
Failure load (N) 94.60 ± 22.70 86.11 ± 26.72 0.211
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Load‐to‐failure Test

At the load‐to‐failure test, 26 (66.7%) subjects in the low BMD group failed by proximal tibial fracture (around the tunnel), 6 (15.4%) at the mounting site, 5 (12.8%) at the fixation site, and only 2 (5.1%) failed at the “killer turn.” In the control group, 20 (51.3%) failed at the “killer turn,” 9 (23.1%) at the proximal tibia (around the tunnel), 5 (12.8%) at the mounting site, and 5 (12.8%) at the fixation site (Fig. 5). There were significantly fewer failures (10.0%) at the “killer turn” (P = 0.000) and 155.6% more for the para‐tunnel fracture (P = 0.000) in the low BMD group compared with the control group.

Figure 5.

Figure 5

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The comparison of failure site distribution between the low bone mineral density (BMD) and control groups. In the low BMD group, 26 (66.7%) subjects failed by proximal tibial fracture (around the tunnel), 6 (15.4%) at the mounting site, 5 (12.8%) at the fixation site, and only 2 (5.1%) failed at the “killer turn.” In the control group, 20 (51.3%) failed at the “killer turn,” 9 (23.1%) at the proximal tibia (around the tunnel), 5 (12.8%) at the mounting site, and 5 (12.8%) at the fixation site. There were significantly fewer failures at the “killer turn” (P = 0.000) and more for the para‐tunnel fracture (P = 0.000) in the low BMD group than the control group.

Discussion

The principal purpose of the current study was to discover the mechanism of graft residual laxity at the “killer turn” under low BMD conditions. The most important findings of this study were twofold: (i) in the low BMD group, a greater total graft displacement was detected, which confirmed our first hypothesis; and (ii) the graft elongation was similar between the low BMD and the control group, which contradicted our second hypothesis.

Effect of “Killer Turn”

The mechanism of the “killer turn” has been illustrated by several biomechanical studies10, 24, 25, 26. The excessive load at the acute bend, and repetitive friction because of non‐isometric graft placement are possible explanations of the “killer turn” effect. Bergfeld et al. (2005) discovered that the grafts in transtibial groups had significant thinning and fraying at the site of the “killer turn23”. Another biomechanical testing by McAllister et al. (2002) detected that 2 of 12 grafts (16.7%) ruptured at the “killer turn” after 50 cycles of loading25. In a cadaveric study by Markolf et al., 10 grafts (32%) failed at the “killer turn” before 2000 cycles of testing at 200 N loading were completed4. For the surviving 21 grafts, the mean reduction of thickness was 40.6% (at the “killer turn”) in the grafts using the transtibial technique. The graft displacement was significantly increased by 18.2%, which returned the knee to the condition of having no posterior cruciate ligament4. Consistent with previous studies, in the control group, our study demonstrated a total graft displacement of 21.63%, and graft elongation of 3.59%. In the present load‐to‐failure test, with normal BMD, the “killer turn” became the site of rupture of the most grafts (51.3%) in the control group. In addition to the above findings, the present study also focused on the tunnel inlet enlargement of the control group (15.21% ± 20.82%), which has seldom been discussed in the literature. In the low BMD group, we detected a similar graft displacement pattern in which both graft elongation (3.68% ± 6.94%) and tunnel inlet enlargement (32.57% ± 37.73%) contributed to the total graft displacement (40.34% ± 23.75%). However, the tunnel inlet enlargement was significantly larger, with significantly fewer failures at the “killer turn” in the low BMD group.

Mechanism of Tunnel Inlet Enlargement

It has been well acknowledged that tunnel inlet enlargement is a frequent phenomenon after ACL reconstruction27. According to the published literature, the amount of tibial tunnel volume enlargement ranged from 18.2 to 73.9%3, 27. Two broad categories of risk factors have been proposed: mechanical and biological factors. Mechanical factors include micro‐motion within the tunnel, improper graft placement, and accelerated rehabilitation28. Low BMD was a critical biological risk factor. In a biomechanical research study on an ACL sheep model, the prevalence of tunnel inlet enlargement was 77.3%, and the overall enlargement was approximately 80% at the 24th postoperative week29. In addition, a positive correlation between tunnel inlet enlargement and BMD was also found. However, very few studies have focused on tunnel inlet enlargement after PCL reconstruction and even fewer on the influence of BMD27. Using arthroscopic transtibial PCL reconstruction with allograft and mixed grafts, Kwon et al. report an incidence of tibial tunnel inlet enlargement of 5.4% (3 of 56 patients)27. The definition of enlargement in Kwon's study was a volume increase greater than 44%, which is a relatively high standard, so the incidence was as low as only 5.4%27. At 1‐year follow‐up, the mean increase of the tibial tunnel volume was 9.9% in the allograft group and 11.2% in the mixed graft group. However, in the present study, it was the diameter of the tunnel inlet instead of the volume that was measured. The tunnel inlet of both the low BMD group and the control group was enlarged; however, the enlargement was greater in the control group than in the low BMD group (15.21 vs 32.57%).

In the present study, the tunnel inlet of both the low BMD group and the control group was enlarged, and there were more failures at the “killer turn” in the control group. Therefore, we hypothesized that, in addition to the conventional mechanism of the “killer turn” on the graft, the repetitive abrasion also had negative effects on the posterior tibial cortex. It seemed that the grafts in both groups were not only compromised by the “killer turn” effect on the graft (elongation and failure) but also by the “killer turn” effect on the posterior tibial cortex (tunnel inlet enlargement). In addition, the grafts in the low BMD group were more influenced by the “killer turn” effect on the posterior tibial cortex (tunnel inlet enlargement) than in the control group. As a result, as long as the transtibial technique was applied, the “double effect” of the “killer turn” would still be present and the effect on the bone would be enhanced under low BMD conditions.

Clinical Relevance

Due to the similar PCL anatomy of rabbits and humans, the findings in the present study are likely to translate into clinical practice. The clinical relevance of the present study is the emphasis on the “killer turn” in osteoporotic status. First, patients with low BMD, such as patients after multi‐ligament injury combined with fractures or vascular injuries, chronic insufficiency of cruciate ligament injury and revision surgery, would be more prone to residual laxity after transtibial PCL reconstruction. Second, if the transtibial technique must be applied in patients with low BMD, more caution should be paid or modifications should be made, such as a lower tunnel outlet, remnant preservation, and a conservative rehabilitation protocol, because of the “double effect” of the “killer turn30, 31, 32, 33.” Third, in a normal BMD state, the transtibial technique seems to be a relatively safe procedure with less tunnel inlet enlargement. Although there was still graft elongation, the magnitude was acceptable.

Limitations

There were some limitations in the present study. First, this is an in vitro study evaluating the biomechanical properties in an ideal osteoporotic model, although the model was tested and proved effective pathologically; second, there was no assessment of the anteroposterior laxity. Because the present study was in vitro, there seemed to be less reliability than for an in vivo study with muscles and capsule intact; third, the micro‐movement of bone bending and device deformation might be another source of bias.

Conclusion

We concluded that the low BMD group demonstrated an inferior biomechanical outcome than the control group with the ranstibial technique. In a low BMD state, the “killer turn” effect compromises the posterior tibial cortex by the enlarging the tunnel inlet.

Acknowledgement

We wish to thank Mr Jianfeng Tao for the help on biomechanical testing.

Disclosure: This work was supported by National Natural Science Foundation of China (Award Number: 81171733).

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