**3. Mechanical properties**

Zens et al. [11] conducted a biomechanical analysis of the ALatL to determine its mechanical properties allowing for a better understand of its role. Four specimens were investigated in the study. When a load was applied, it was found that all four specimens showed an inter-ligamentous failure at approximately one third of the ALatL's length, distal from the femoral insertion site. The mean ultimate load to failure was 49.90 (±14.62) N, ultimate tension of 32.78 N/mm2 and the mean ultimate extension distance of 11.89 (±1.56) mm, hence, resulting in a mean extensional stiffness of 2.60 (±0.93) N.

Results from a study conducted in 2015 discovered that the average maximum load that the ALatL was able to handle during a pull-to-failure test was 175 N with a mean stiffness of 20 N/mm [5]. Failure of the ligament occurred through several mechanisms including ligamentous tear at the femoral or tibial origin, mid-substance tear and bony avulsion of the tibial attachment.

Helito et al. [10] also investigated the strength and stiffness of the ALatL of the knee through completing a biomechanical study. The methodology of testing involved 14 knee specimens of which the ALatL was tested for its tensile strength. Throughout testing the strength at the maximum resistance limit, deformation and stiffness were all measured. The mean maximum strength of the ALatL was found to be 204.8 (±114.9) N. The stiffness was 41.9 (±25.7) N/mm and the deformation of the ALatL was 10.3 (±3.5) mm [10]. **Table 1** shows a summary of the findings from the various studies discussed.

The mean maximum strength of the ALatL varied quite significantly between studies with Zens et al. [11] recording a much smaller strength value compared to other sources. Helito et al. [10] had a large variance in strength values from 89.9– 319.7 N outlining how much it can vary between specimens. Zens et al. [11] however detailed that the ACL has been proven to have a higher ultimate tensile strength in


#### **Table 1.**

*Comparison between mechanical properties measured.*

younger patients by a factor of 2.5 times. Considering that the previously presented loads of failure are based on specimens of mean age 86.5 ± 1.7 years, there is the possibility that the ALatL ultimate tension may be around 125 N in younger specimens if the same trend follows. The size of the ALatL is expected to reduce with age, hence the possibility for higher ultimate tension in younger specimens. This is more like the range of maximum strength found by other sources. The stiffness of the ligament was found to also differ between Kennedy et al. [5] and Helito et al. [10]. Zens et al. [11] and Helito et al. [10] agreed on the deformation of the ALatL to be around 10–12 mm. Hence, it can therefore be concluded from these studies that the ALatL has approximately the following mechanical properties: maximum strength of 50–200 N, stiffness of 20–42 N/mm, deformation of 30% of its length and tension of 33 N/mm<sup>2</sup> . These values and ranges for the mechanical properties of the ALatL were also supported by Patel and Brophy [12].

Drews et al. [13] conducted an investigation to assess the function of the ALatL. This research tested the response of the ALatL through recording the ligaments activity while completing flexion of the knee and a number of rotations and translations. The testing involved eight specimens with the three conditions of: a normal knee with both ACL and ALatL intact, ACL resected (ACLres) and ACL and ALatL resected (ALatLres) to be compared. During the flexion testing under unloaded conditions there was no significant difference in internal rotation between the ACLres and ALatLres specimens. With an internal tibial torque of 1–4 Nm applied, internal rotation significantly increased between 60 and 120° in the ALatLres specimen. Anterior tibial translation was also significantly higher at 30° in the ALatLres specimen. When unloaded there were no ALatL strains, however adding different internal tibial torques led to strain of the ALatL starting at an angle of 60° of flexion with a 1 Nm internal torque applied and 15° flexion with 4 Nm internal torque in the intact ligaments. It was also found that the ACLres specimen also had significantly greater ALatL strains under low flexion angles than the intact specimen [13].

#### **4. Analysis of the anterolateral ligament**

#### **4.1 Function**

Due to the findings of these insertion and origin sites, Claes et al. [4] concluded that given its anatomical location at the anterolateral edge of the knee, it is hypothesised that the ALatL functions as a stabiliser for internal rotation. Dissections found the ALatL to become tense with forced internal rotation between 30 and 90° of knee flexion, as seen in **Figure 3**, however further kinematic analysis is needed to confirm this hypothesis formally. Therefore, research is needed to establish the function of the ALatL and to determine its role in clinical knee joint injuries [4].

**99**

**Figure 4.**

**Figure 3.**

*The Biomechanics of the Anterolateral Ligament DOI: http://dx.doi.org/10.5772/intechopen.92055*

Kosy et al. [9] concluded from their study that given the orientation of fibres in the ALatL and the tightening of this structure during internal rotation of the tibia as pictured in **Figure 4**, the structure plays a role in restraining this abnormal movement. Conclusions from the study of Drews et al. [13] were that the ALatL does not have a function under passive motion as there was no change in tibial rotation when the ALatL was removed from the specimen. When extrinsic loads are applied, the ALatL had a slight stabilising effect against anterior tibial shear at low flexion angles. Therefore, it is suggested that the ALatL is supporting the ACL

*Anatomical drawing of the anterolateral ligament on the lateral aspect of the human knee. (A) Knee in full extension. (B) Knee in 90° of flexion. ALatL = anterolateral ligament; GT = Gerdy's tubercle; LCL = lateral* 

*Photographs demonstrating the tightening of the anterolateral ligament (labelled ALL) between a - a neutral position and b - with internal rotation of the tibia reprinted from, Kosy et al. [9]. Please see the following link* 

*for the creative commons licence: http://creativecommons.org/licenses/by/4.0/.*

*collateral ligament; and LFE = lateral femoral epicondyle.*

*The Biomechanics of the Anterolateral Ligament DOI: http://dx.doi.org/10.5772/intechopen.92055*

Kosy et al. [9] concluded from their study that given the orientation of fibres in the ALatL and the tightening of this structure during internal rotation of the tibia as pictured in **Figure 4**, the structure plays a role in restraining this abnormal movement. Conclusions from the study of Drews et al. [13] were that the ALatL does not have a function under passive motion as there was no change in tibial rotation when the ALatL was removed from the specimen. When extrinsic loads are applied, the ALatL had a slight stabilising effect against anterior tibial shear at low flexion angles. Therefore, it is suggested that the ALatL is supporting the ACL

#### **Figure 3.**

*Recent Advances in Biomechanics*

Kennedy et al. [5]

**Table 1.**

**Max. Strength (N)**

*Comparison between mechanical properties measured.*

and tension of 33 N/mm<sup>2</sup>

specimen [13].

**4.1 Function**

the ALatL were also supported by Patel and Brophy [12].

**4. Analysis of the anterolateral ligament**

younger patients by a factor of 2.5 times. Considering that the previously presented loads of failure are based on specimens of mean age 86.5 ± 1.7 years, there is the possibility that the ALatL ultimate tension may be around 125 N in younger specimens if the same trend follows. The size of the ALatL is expected to reduce with age, hence the possibility for higher ultimate tension in younger specimens. This is more like the range of maximum strength found by other sources. The stiffness of the ligament was found to also differ between Kennedy et al. [5] and Helito et al. [10]. Zens et al. [11] and Helito et al. [10] agreed on the deformation of the ALatL to be around 10–12 mm. Hence, it can therefore be concluded from these studies that the ALatL has approximately the following mechanical properties: maximum strength of 50–200 N, stiffness of 20–42 N/mm, deformation of 30% of its length

**Stiffness (N/mm)**

Helito et al. [10] 204.8 (±114.9) 41.9 (±25.7) 10.3 (±3.5) —

Zens et al. [11] 49.90 (±14.62) — 11.89 (±1.56) 32.78 N/mm2

Drews et al. [13] conducted an investigation to assess the function of the ALatL. This research tested the response of the ALatL through recording the ligaments activity while completing flexion of the knee and a number of rotations and translations. The testing involved eight specimens with the three conditions of: a normal knee with both ACL and ALatL intact, ACL resected (ACLres) and ACL and ALatL resected (ALatLres) to be compared. During the flexion testing under unloaded conditions there was no significant difference in internal rotation between the ACLres and ALatLres specimens. With an internal tibial torque of 1–4 Nm applied, internal rotation significantly increased between 60 and 120° in the ALatLres specimen. Anterior tibial translation was also significantly higher at 30° in the ALatLres specimen. When unloaded there were no ALatL strains, however adding different internal tibial torques led to strain of the ALatL starting at an angle of 60° of flexion with a 1 Nm internal torque applied and 15° flexion with 4 Nm internal torque in the intact ligaments. It was also found that the ACLres specimen also had significantly greater ALatL strains under low flexion angles than the intact

Due to the findings of these insertion and origin sites, Claes et al. [4] concluded that given its anatomical location at the anterolateral edge of the knee, it is hypothesised that the ALatL functions as a stabiliser for internal rotation. Dissections found the ALatL to become tense with forced internal rotation between 30 and 90° of knee flexion, as seen in **Figure 3**, however further kinematic analysis is needed to confirm this hypothesis formally. Therefore, research is needed to establish the function of the ALatL and to determine its role in clinical knee joint injuries [4].

. These values and ranges for the mechanical properties of

**Deformation (mm)**

175 20 — —

**Ultimate Tension (N/mm2 )**

**98**

*Anatomical drawing of the anterolateral ligament on the lateral aspect of the human knee. (A) Knee in full extension. (B) Knee in 90° of flexion. ALatL = anterolateral ligament; GT = Gerdy's tubercle; LCL = lateral collateral ligament; and LFE = lateral femoral epicondyle.*

#### **Figure 4.**

*Photographs demonstrating the tightening of the anterolateral ligament (labelled ALL) between a - a neutral position and b - with internal rotation of the tibia reprinted from, Kosy et al. [9]. Please see the following link for the creative commons licence: http://creativecommons.org/licenses/by/4.0/.*

against internal tibial loads to a slight degree. Hence all three sources were in support that the ALatL plays a role in restricting internal tibial rotations [4, 9, 13].

#### **4.2 Kinematics of the anterior cruciate (ACL) and anterolateral (ALatL) ligaments**

#### *4.2.1 The anterior cruciate ligament*

The largest kinematic difference resulting from ACL deficiency is a substantial increase in anterior tibial translation on application of anterior tibial force [14], which has led to the clinical tests that employ anterior tibial force, for example the Lachman test, where pulling the leg forwards at the knee can result in an increase in translation in the horizontal plane [15].

Surgical replacement of the ACL, or reconstruction, reduces anterior tibial translation to (near-) normal levels, but in some knees there is a rotational instability remaining [16]. This residual instability is thought to lead to the accelerated osteoarthritis seen in the years following ACL rupture and reconstruction [17], and residual rotational instability, diagnosed through the pivot shift test, is associated with poorer outcomes following surgery [18].

In vivo studies of knee joint kinematics following ACL rupture and reconstruction can give a partial view into the ligament's function and its functional loss, but with the potential confounding influence of concurrent injuries to other structures. Further information can be drawn from in vitro laboratory experiments, where damage can be limited to the individual structures. Anterior tibial translation clearly is increased [19–22], but there is contention around rotation in the same plane. Internal tibial rotation as a response to internal tibial torque, defined to occur about a centrally-located axis [23], has been found to be unchanged [24, 25], or slightly increased [22, 26] following ACL ablation, but there has been doubt expressed as to whether this is sufficient to cause clinical problems [22].

The residual rotational instability that is sometimes seen following reconstruction is found during the pivot shift test [27], which involves coupling of internal rotation torque with abduction torque in the frontal plane. Application of these combined loads in the ACL deficient knee leads to normal [19] or slightly increased [28, 29] internal rotation but increased anterior translation [19, 30–32]. This finding has led some researchers to recommend that rotational instability be observed by increased translation [19].

#### *4.2.2 The anterolateral ligament*

Injury to the ALatL may cause residual instability in the knee after the ACL has been reconstructed. In a retrospective study of ACL reconstruction patients, those who were diagnosed as also suffering an ALatL tear, by MRI, showed a greater tendency to instability by the pivot shift test following reconstruction [33]. But the picture in relation to the pivot shift test, or in combined internal/valgus torque, is far from clear. What clarity studies of the ALatL provide will therefore be of great interest. Kennedy et al. [34] claimed that "residual rotatory laxity that may be seen clinically following ACL reconstruction may be attributable to an associated anterolateral structure injury". Considering this proposition when looking at ALatL-related kinematics will help to shed light on this issue.

Studies have mostly investigated the ALatL's contribution to kinematics in the ACL-deficient or -reconstructed knee, reflecting the ligament's role as a secondary stabiliser, i.e., having a lesser role than the ACL, and serving that function in the ACL-deficient knee. As knee flexion angle can affect the results of these

**101**

and Zens et al. [11].

*The Biomechanics of the Anterolateral Ligament DOI: http://dx.doi.org/10.5772/intechopen.92055*

following ACL reconstruction (with the ALatL intact).

**4.3 Grafts for the anterolateral ligament**

of flexion.

appears not significant.

investigations, the findings of the following studies relate to results found at 30°

Application of an 88 N anterior tibial force produced an additional increase in anterior translation after cutting the ALatL in the ACL-deficient knee [35]. This was supported by Tavlo and co-workers [36]. Knees with ACL reconstruction showed no change in anterior translation with an 88 N anterior force after cutting the ALatL, or after reconstructing the ALatL [37]. Thus the role of the ALatL in restraining anterior translation in the presence of either an intact or a reconstructed ACL

ALatL-deficient knees showed an increase in internal rotation on application of 5 Nm internal rotation torque to ACL-deficient knees [35]. Knees with ACL reconstruction showed an increase in internal rotation, compared with the intact state, on internal torque of 5 Nm, and this was increased on cutting the ALatL; rotation in turn decreased to intact levels with ALatL reconstruction [37]. Although Tavlo et al. found that ALatL deficiency led to greater internal rotation in ACL-deficient knees than with ACL deficiency alone, there was no such increase in internal rotation

A 5 Nm internal rotation torque in combination with a 10 Nm valgus torque increased both anterior translation and internal rotation in ALatL- and ACLdeficient knees, when compared with only ACL-deficiency [35]. On application of a combined loading of 4 Nm internal rotation torque and 8 Nm of valgus torque, sectioning of the ACL increased anterior translation and internal rotation, and

Nitri et al. [37] found that at 30 degrees, anterior translation on combined internal torque (5 Nm) and valgus torque (10 Nm) was not increased after ACL reconstruction, and this was not further changed with ALatL deficiency or reconstruction. In contrast, internal rotation was increased on combination loading in the ACLreconstructed knee, further increased with ALatL deficiency, and reduced to intact levels following ALatL reconstruction. While loss of the ALatL amplifies the rotational instability of ACL deficiency, where rotational instability has remained after ACL reconstruction, loss/reconstruction of the ALatL increases/alleviates instability.

Providing a surgeon was to undertake an ALatL reconstruction it would be important to determine the correct method of operation and in particular select the correct replacement graft. Kennedy et al. [5] suggests a graft of the gracilis tendon for an anatomical repair of the ALatL. Mechanical properties of several ligaments as measured by Zens et al. [11] are displayed in **Table 2**. All structures listed are able to provide a sufficient load to failure to replace the ALatL due to the low strength properties of the ligament, however the ultimate tension of the gracilis tendon matches the ALatL the least, with a much higher tension. Based on the data found through the study of Zens et al. [11] other possible graft options, such as the iliotibial band (ITB) or semitendinosis tendon would be a more suitable choice. Kennedy et al. [5] also investigated the best tissue structure to use as a replacement for the ALatL during reconstruction, identifying the semitendinosis tendon and gracilis tendon as appropriate graft selections. This selection was based on their mechanical strength properties and supported choices of both Kennedy et al. [5]

As well as choosing an appropriate graft for reconstruction of the ALatL, the development of a suitable surgical technique is also important. Kennedy et al. [5] suggested that reconstruction should follow similar techniques as used for other

knee reconstructions with grafts used of similar length and properties.

sectioning the ALatL increased translation and rotation further [38].

#### *The Biomechanics of the Anterolateral Ligament DOI: http://dx.doi.org/10.5772/intechopen.92055*

*Recent Advances in Biomechanics*

*4.2.1 The anterior cruciate ligament*

translation in the horizontal plane [15].

with poorer outcomes following surgery [18].

increased translation [19].

*4.2.2 The anterolateral ligament*

**ligaments**

against internal tibial loads to a slight degree. Hence all three sources were in support that the ALatL plays a role in restricting internal tibial rotations [4, 9, 13].

The largest kinematic difference resulting from ACL deficiency is a substantial increase in anterior tibial translation on application of anterior tibial force [14], which has led to the clinical tests that employ anterior tibial force, for example the Lachman test, where pulling the leg forwards at the knee can result in an increase in

Surgical replacement of the ACL, or reconstruction, reduces anterior tibial translation to (near-) normal levels, but in some knees there is a rotational instability remaining [16]. This residual instability is thought to lead to the accelerated osteoarthritis seen in the years following ACL rupture and reconstruction [17], and residual rotational instability, diagnosed through the pivot shift test, is associated

In vivo studies of knee joint kinematics following ACL rupture and reconstruction can give a partial view into the ligament's function and its functional loss, but with the potential confounding influence of concurrent injuries to other structures. Further information can be drawn from in vitro laboratory experiments, where damage can be limited to the individual structures. Anterior tibial translation clearly is increased [19–22], but there is contention around rotation in the same plane. Internal tibial rotation as a response to internal tibial torque, defined to occur about a centrally-located axis [23], has been found to be unchanged [24, 25], or slightly increased [22, 26] following ACL ablation, but there has been doubt expressed as to whether this is sufficient to cause clinical problems [22].

The residual rotational instability that is sometimes seen following reconstruction is found during the pivot shift test [27], which involves coupling of internal rotation torque with abduction torque in the frontal plane. Application of these combined loads in the ACL deficient knee leads to normal [19] or slightly increased [28, 29] internal rotation but increased anterior translation [19, 30–32]. This finding has led some researchers to recommend that rotational instability be observed by

Injury to the ALatL may cause residual instability in the knee after the ACL has been reconstructed. In a retrospective study of ACL reconstruction patients, those who were diagnosed as also suffering an ALatL tear, by MRI, showed a greater tendency to instability by the pivot shift test following reconstruction [33]. But the picture in relation to the pivot shift test, or in combined internal/valgus torque, is far from clear. What clarity studies of the ALatL provide will therefore be of great interest. Kennedy et al. [34] claimed that "residual rotatory laxity that may be seen clinically following ACL reconstruction may be attributable to an associated anterolateral structure injury". Considering this proposition when looking at

Studies have mostly investigated the ALatL's contribution to kinematics in the ACL-deficient or -reconstructed knee, reflecting the ligament's role as a secondary stabiliser, i.e., having a lesser role than the ACL, and serving that function in the ACL-deficient knee. As knee flexion angle can affect the results of these

ALatL-related kinematics will help to shed light on this issue.

**4.2 Kinematics of the anterior cruciate (ACL) and anterolateral (ALatL)** 

**100**

investigations, the findings of the following studies relate to results found at 30° of flexion.

Application of an 88 N anterior tibial force produced an additional increase in anterior translation after cutting the ALatL in the ACL-deficient knee [35]. This was supported by Tavlo and co-workers [36]. Knees with ACL reconstruction showed no change in anterior translation with an 88 N anterior force after cutting the ALatL, or after reconstructing the ALatL [37]. Thus the role of the ALatL in restraining anterior translation in the presence of either an intact or a reconstructed ACL appears not significant.

ALatL-deficient knees showed an increase in internal rotation on application of 5 Nm internal rotation torque to ACL-deficient knees [35]. Knees with ACL reconstruction showed an increase in internal rotation, compared with the intact state, on internal torque of 5 Nm, and this was increased on cutting the ALatL; rotation in turn decreased to intact levels with ALatL reconstruction [37]. Although Tavlo et al. found that ALatL deficiency led to greater internal rotation in ACL-deficient knees than with ACL deficiency alone, there was no such increase in internal rotation following ACL reconstruction (with the ALatL intact).

A 5 Nm internal rotation torque in combination with a 10 Nm valgus torque increased both anterior translation and internal rotation in ALatL- and ACLdeficient knees, when compared with only ACL-deficiency [35]. On application of a combined loading of 4 Nm internal rotation torque and 8 Nm of valgus torque, sectioning of the ACL increased anterior translation and internal rotation, and sectioning the ALatL increased translation and rotation further [38].

Nitri et al. [37] found that at 30 degrees, anterior translation on combined internal torque (5 Nm) and valgus torque (10 Nm) was not increased after ACL reconstruction, and this was not further changed with ALatL deficiency or reconstruction. In contrast, internal rotation was increased on combination loading in the ACLreconstructed knee, further increased with ALatL deficiency, and reduced to intact levels following ALatL reconstruction. While loss of the ALatL amplifies the rotational instability of ACL deficiency, where rotational instability has remained after ACL reconstruction, loss/reconstruction of the ALatL increases/alleviates instability.

#### **4.3 Grafts for the anterolateral ligament**

Providing a surgeon was to undertake an ALatL reconstruction it would be important to determine the correct method of operation and in particular select the correct replacement graft. Kennedy et al. [5] suggests a graft of the gracilis tendon for an anatomical repair of the ALatL. Mechanical properties of several ligaments as measured by Zens et al. [11] are displayed in **Table 2**. All structures listed are able to provide a sufficient load to failure to replace the ALatL due to the low strength properties of the ligament, however the ultimate tension of the gracilis tendon matches the ALatL the least, with a much higher tension. Based on the data found through the study of Zens et al. [11] other possible graft options, such as the iliotibial band (ITB) or semitendinosis tendon would be a more suitable choice. Kennedy et al. [5] also investigated the best tissue structure to use as a replacement for the ALatL during reconstruction, identifying the semitendinosis tendon and gracilis tendon as appropriate graft selections. This selection was based on their mechanical strength properties and supported choices of both Kennedy et al. [5] and Zens et al. [11].

As well as choosing an appropriate graft for reconstruction of the ALatL, the development of a suitable surgical technique is also important. Kennedy et al. [5] suggested that reconstruction should follow similar techniques as used for other knee reconstructions with grafts used of similar length and properties.


*ALatL = anterior lateral ligament; ACL = anterior crutiate ligament; PCL = posterior crutiate ligament; MCL = medial collataeral ligament; sMCL = (superficial) medial collateral ligament; POL = posterior oblique ligament; LCL = lateral collateral ligament; PFLC = popliteofibular ligament complex; ITB = iliotibial band.*

#### **Table 2.**

*Ultimate tension and ultimate load to failure of the ALatL in comparison to other ligaments and possible grafts as researched by Zens et al. [11].*

#### **4.4 Discussion**

To summarise the results of the ALatL studies described, ALatL-deficiency makes the pattern of ACL deficiency (specifically anterior tibial translation and internal rotation) worse, as there is a greater range of movement with application of a load. In the ACL-reconstructed knee, ALatL-deficiency does not increase anterior tibial translation, but does increase internal rotation, an increase that is reversed after reconstructing the ALatL.

However, the results of ALatL studies cannot simply be superimposed on a background of solid agreement of ACL-related kinematics. While anterior tibial translation on the Lachman test is taken as read, not all researchers have found rotational laxity when applying internal rotation torque, and the pivot shift test may show rotational instability through an increase in translation.

The position and alignment of the ALatL make it logical that it would restrain internal rotation to a degree at least, but that degree aside, it is not always clear what a restraint of internal rotation might be useful for.

Of greater importance in this context is whether instability following ACL reconstruction can be attributed to ALatL injury. Nitri et al. [37] claimed that residual instability on the pivot shift test following ACL reconstruction "reaffirms the theory that tears of secondary restraints… should be properly recognized and treated". Although tears to secondary structures may be responsible for residual instability, it is clear from their results that residual instability results from ACL reconstruction in the presence of an intact ALatL, so at least part of the residual instability is likely to result from the simple fact that ACL reconstruction does not completely restore rotational stability to ACL intact levels. This supports the hypothesis that ACL reconstruction does not completely reproduce ACL-intact

**103**

*The Biomechanics of the Anterolateral Ligament DOI: http://dx.doi.org/10.5772/intechopen.92055*

reduce post-ACL reconstruction instability.

anterolateral ligament injuries is less clear.

its length and tension of 33 N/mm2

properties compared to other structures of the knee.

structing it.

**5. Summary**

kinematics, but given an ALatL lesion its reconstruction could be expected to

Such a conclusion though is theoretically more difficult to support under in vivo conditions. Less than complete restoration of normal stability appears to be typical following ACL reconstruction, and even with a reliable method of diagnosing ALatL injury, the confounding factor of imperfect ACL reconstruction would still cast uncertainty of the role of the ALatL and the clinical wisdom of recon-

Within these studies, ALatL reconstruction reverses the rotational deficits seen after ACL reconstruction when the ALatL is deficient. However, in the wider world of ACL research, where the pattern of rotational instability is controversial, and where translation may be a bigger problem, the benefit of recognising and repairing

The anterolateral ligament (ALatL) of the knee is an under investigated soft tissue structure with its existence within the body mostly unknown to the layperson. It was determined the ALatL has a femoral origin which is either anterior and distal, or posterior and proximal to the origin of the lateral collateral ligament, varying depending on the specimen being investigated. It is not clear exactly why there is such variation. The tibial attachment site was commonly found as midway between Gerdy's tubercle and the fibular head. These origin and attachment sites result in the ALatL running from the lateral femur to the anterior tibia with average physical properties of the ALatL; length of 40–42 mm, width 4–7 mm and thickness 0.8–1.3 mm. The ALatL was found to have mechanical properties on average of; maximum strength of 50–200 N, stiffness of 20–42 N/mm, deformation of 30% of

tension during internal rotations of the knee and therefore acts a stabiliser during internal tibial rotation. All studies presented the issue of lateral instability remaining after patients have undergone isolated ACL reconstruction and had the common belief that this is due to damage caused to lateral soft tissue structures on the knee. Findings of many studies have not been conclusive enough to confidently suggest ALatL reconstruction as a viable option due to the lower maximum mechanical

While there have been several studies recently conducted investigating the function of the ALatL of the knee through analysing a number of different factors including origin and insertion along with both physical and mechanical properties, there is still much mystery surrounding this ligament. Hence, further research should be conducted to accurately quantify the importance of the anterolateral ligament to internal tibial rotation stability, and the effect that a damaged ALatL can have on the stresses experienced by surrounding soft tissue structures of the knee.

. Studies conducted found that the ALatL is in

#### *The Biomechanics of the Anterolateral Ligament DOI: http://dx.doi.org/10.5772/intechopen.92055*

kinematics, but given an ALatL lesion its reconstruction could be expected to reduce post-ACL reconstruction instability.

Such a conclusion though is theoretically more difficult to support under in vivo conditions. Less than complete restoration of normal stability appears to be typical following ACL reconstruction, and even with a reliable method of diagnosing ALatL injury, the confounding factor of imperfect ACL reconstruction would still cast uncertainty of the role of the ALatL and the clinical wisdom of reconstructing it.

Within these studies, ALatL reconstruction reverses the rotational deficits seen after ACL reconstruction when the ALatL is deficient. However, in the wider world of ACL research, where the pattern of rotational instability is controversial, and where translation may be a bigger problem, the benefit of recognising and repairing anterolateral ligament injuries is less clear.

#### **5. Summary**

*Recent Advances in Biomechanics*

**Structure Ultimate tension** 

**[MPa]**

**ALatL 32.78 ± 4.04 49.90 ± 14.62 100** ACL 37.80 ± 3.80 1725 ± 269 3457 PCL 35.90 ± 15.20 739–1627 1481 MCL 38.60 ± 4.80 1107 ± 126 2219 Distal sMCL — 557 ± 55 1116 Proximal sMCL — 88 ± 36 176 POL — 256 ± 30 513 Deep MCL — 101 ± 10 202 LCL — 309 ± 91 619 PFLC — 186 N ± 65 373 ITB 19.1 ± 2.9 769 ± 99 1541 Fascia lata 78.7 ± 4.6 628 ± 35 1259 Semitendinosus 88.5 ± 5.0 1216 ± 50 2437 Gracilis 111.5 ± 4.0 838 ± 30 1679 *ALatL = anterior lateral ligament; ACL = anterior crutiate ligament; PCL = posterior crutiate ligament; MCL = medial collataeral ligament; sMCL = (superficial) medial collateral ligament; POL = posterior oblique ligament; LCL = lateral collateral ligament; PFLC = popliteofibular ligament complex; ITB = iliotibial band.*

**Ultimate load to failure [N]**

**Relation to ALatL (load to failure) [%]**

**102**

**4.4 Discussion**

*as researched by Zens et al. [11].*

**Table 2.**

after reconstructing the ALatL.

To summarise the results of the ALatL studies described, ALatL-deficiency makes the pattern of ACL deficiency (specifically anterior tibial translation and internal rotation) worse, as there is a greater range of movement with application of a load. In the ACL-reconstructed knee, ALatL-deficiency does not increase anterior tibial translation, but does increase internal rotation, an increase that is reversed

*Ultimate tension and ultimate load to failure of the ALatL in comparison to other ligaments and possible grafts* 

However, the results of ALatL studies cannot simply be superimposed on a background of solid agreement of ACL-related kinematics. While anterior tibial translation on the Lachman test is taken as read, not all researchers have found rotational laxity when applying internal rotation torque, and the pivot shift test may

The position and alignment of the ALatL make it logical that it would restrain internal rotation to a degree at least, but that degree aside, it is not always clear what

Of greater importance in this context is whether instability following ACL reconstruction can be attributed to ALatL injury. Nitri et al. [37] claimed that residual instability on the pivot shift test following ACL reconstruction "reaffirms the theory that tears of secondary restraints… should be properly recognized and treated". Although tears to secondary structures may be responsible for residual instability, it is clear from their results that residual instability results from ACL reconstruction in the presence of an intact ALatL, so at least part of the residual instability is likely to result from the simple fact that ACL reconstruction does not completely restore rotational stability to ACL intact levels. This supports the hypothesis that ACL reconstruction does not completely reproduce ACL-intact

show rotational instability through an increase in translation.

a restraint of internal rotation might be useful for.

The anterolateral ligament (ALatL) of the knee is an under investigated soft tissue structure with its existence within the body mostly unknown to the layperson. It was determined the ALatL has a femoral origin which is either anterior and distal, or posterior and proximal to the origin of the lateral collateral ligament, varying depending on the specimen being investigated. It is not clear exactly why there is such variation. The tibial attachment site was commonly found as midway between Gerdy's tubercle and the fibular head. These origin and attachment sites result in the ALatL running from the lateral femur to the anterior tibia with average physical properties of the ALatL; length of 40–42 mm, width 4–7 mm and thickness 0.8–1.3 mm. The ALatL was found to have mechanical properties on average of; maximum strength of 50–200 N, stiffness of 20–42 N/mm, deformation of 30% of its length and tension of 33 N/mm2 . Studies conducted found that the ALatL is in tension during internal rotations of the knee and therefore acts a stabiliser during internal tibial rotation. All studies presented the issue of lateral instability remaining after patients have undergone isolated ACL reconstruction and had the common belief that this is due to damage caused to lateral soft tissue structures on the knee.

Findings of many studies have not been conclusive enough to confidently suggest ALatL reconstruction as a viable option due to the lower maximum mechanical properties compared to other structures of the knee.

While there have been several studies recently conducted investigating the function of the ALatL of the knee through analysing a number of different factors including origin and insertion along with both physical and mechanical properties, there is still much mystery surrounding this ligament. Hence, further research should be conducted to accurately quantify the importance of the anterolateral ligament to internal tibial rotation stability, and the effect that a damaged ALatL can have on the stresses experienced by surrounding soft tissue structures of the knee.

*Recent Advances in Biomechanics*
