Anterior Cruciate Ligament Injury: Current Understanding of Risk Factors-JuniperPublishers
Orthopedics & Rheumatology-Juniper Publishers
Abstract
Reconstruction of the anterior cruciate ligament
(ACL) is a common surgical procedure with an estimated 50,000 procedures
in the US annually. Injury of the ACL often requires costly treatment,
extensive rehabilitation, and results in early osteoarthritis. While ACL
ruptures occur secondary to a complex interplay of multiple variables, a
number of risk factors have been identified that increase risk of ACL
rupture. We will analyze a variety of identified risk factors including
anatomic, neuromuscular control, hormonal, genetic, and external
variables.
In terms of intrinsic risk factors, multiple recent
studies have identified neuromuscular risk factors that put the ACL at
risk for injury. These studies show differences in neuromuscular control
of knee joint mechanics, hamstring muscle strength and core stability
in patients who sustain ACL injury.
Anatomical variants between individuals, genders and
races have also been implicated as risk factors for ACL injury. These
risk factors include femoral intercondylar notch width, tibial slope
geometry, ACL dimensions, and generalized ligamentous laxity. Studies
have sought to evaluate the interactions between absolute femoral notch
width, notch width index, and intercondylar notch shape and how these
factors relate to ACL injury risk. Postulating that an increased
anteriordirected shear force on the tibia correlates with higher
incidence of ACL injury, studies have identified an increased
posteriorinferior directed tibial slope and shallow medial depth of the
tibial plateau, as significant risk factors for ACL injury. Newer
research suggests that meniscal geometry factors into this equation as
well. Other studies have suggested that decreased ACL volume is a
contributing factor, while further studies propose that ACL injury risk
can be predicted as a factor of generalized joint laxity. Lastly, prior
ACL injury and reconstruction have been implicated as risk factors for
future knee injury. Patients undergoing ACL reconstruction are at higher
risk for contralateral ACL injury and ACL rerupture postreconstruction
compared to individuals without prior ACL injury.
Additionally, hormonal and genetic factors have been
connected to ACL injury. After estrogen and progesterone receptor sites
were found on the ACL, multiple studies have analyzed hormone levels and
ACL rupture risk. Overall, the results of these studies are varied and
controversial, but suggest an increased risk in the preovulatory
menstrual cycle phase. Genetic studies have shown specific mutations
that place patients at risk for ACL injury and other tendon injury.
Also, a study has shown that patients with an ACL rupture were more than
4 times as likely to have a relative with history of ligament injury. External variables for ACL injury include cleat
design, drier weather conditions and certain playing surfaces, that have
been shown to contribute to increased incidence of ACL injuries.
Neuromuscular Control
25 y/o Male who has a significant history of multiple
reconstructive surgeries for residual clubfoot. Patient continues to
have severe pain due to nerve entrapment and neuritis that has been
confirmed with segmental nerve conduction velocity examinations of the
superficial peroneal nerve. Entrapment was identified approximately 6 cm
above the lateral malleolus. Patient has been unresponsive to
conservative treatment. Patient continues to have difficulty ambulating
due to pain. Patient has failed conservative treatment and understands
that this procedure is a salvage attempt to relieve the constant pain.
Anterior cruciate ligament loading and failure is a
well studied phenomenon with numerous cadaveric models, computer models,
and observational studies aiding our understanding. The majority of ACL
injuries are due to noncontact mechanisms. Video analysis of ACL
injuries show most of these injuries occur with knee extension during a
deceleration or landing maneuver [1]. Other analyses have shown lateral
trunk motion and posterior weight distribution as other risk factors for
ACL injury. These observations are confirmed by cadaveric studies
showing high ACL strain with the coupling of knee rotation, tibial
compression, and knee abduction [2-4].
Given that ACL injuries appear to occur following a
common mechanism further studies have analyzed neuromuscular control to
see if individuals at risk for injury can be identified, if
neuromuscular control may explain the sex based differences in ACL
injury and if neuromuscular training can be used to reduce at risk
motions and ultimately ACL injury.
A number of motions have been assessed to predict ACL
injury. [5] and Hewett et al have shown lateral trunk motion as an
independent risk factor, but only in female athletes [5-7]. Valgus
collapse of the knee has been identified as a risk factor in both male
and female athletes [8,9]. However, female athletes appear to land with
more knee and hip flexion as well as considerably more valgus collapse
than male players [9]. An electromyography study further supported these
sex related differences showing decreased knee flexion, hip flexion,
hip abduction, and increased quadriceps activation during landing in
female subjects [10]. These landing characteristics may be partially
explaining the increased rate of ACL rupture in females.
To predict ACL rupture, the Landing Error Scoring
System (LESS) has been developed. The LESS uses a scoring system based
on jump landing biomechanics to identify athletes at risk for
lowerextremity injury. In youth soccer players the system has been shown
to predict noncontact injury [11,12]. However, the LESS has not
predicted injury in all studies [13] and will require future research to
determine its predictive capacity across all age groups.
Lastly, preventative training exercises have been
developed to reduce neuromuscular factors contributing to ACL injury.
These exercises appear to reduce ACL injury rates in females, but
require a considerable time commitment (23 times/week) [14-18]. Further
research is needed to determine their protective
ability in male athletes.
ACL Dimensions
Inferences that smaller sized ACLs correlate with greater
likelihood of noncontact
injury have led researchers to
investigate the ligament’s overall dimensions and its effect on
injury rates. Several studies have evaluated, using MRI analysis,
the contralateral ACL of patients with noncontact
ACL injuries
and compared it to a group of matched controls. Using MRIbased
volume calculations, one study demonstrated a significantly
decreased ACL volume in the injured population compared to
the control group [19]. Another study yielded similar findings
that were limited exclusively to the male group, suggesting
variations in the anatomic features that predispose each gender
to injury [20].
Femoral Intercondylar Notch Geometry
The intercondylar notch of the femur houses a portion of the
ACL, and from as early as 1936, it has been speculated that injury
to the ligament results, in part, from entrapment of the ACL at
the notch during the course of specific motions. Researchers
have studied the interplay between several variables related
to femoral notch dimensions and identified characteristics that
place an individual at increased risk for sustaining a noncontact
ACL injury.
Femoral notch width is a wellstudied
anatomic feature that
has shown to be variable across genders and races, and may offer
a partial explanation for differences in ACL injury rates between
the groups [21]. Although conflicting studies exist, recent metaanalyses
reveal that smaller notch widths, on average 2.15 mm
or less, are correlated with increased rates of ACL injury. It has
been suggested that stenotic intercondylar notches increase the
vulnerability of the ACL to stretching over the medial border
lateral femoral condyle particularly during valgus loading of the
knee [22].
Notch width index (NWI) is a more specific measurement
with similar implications for ACL injury. Initially described
by Souryal, NWI is defined as the ratio of the width of the
intercondylar notch at the level of the popliteal groove, to the
femoral bicondylar width taken at the same level [23]. His initial
study implicated a decreased NWI as a risk factor for bilateral
ACL injuries when compared to matched controls. A subsequent
study defined notch stenosis as NWI less than 0.20 mm, and
identified it as a threshold for increased injury risk. Multiple
studies have evaluated similar variables, and come up with
different definitions of notch stenosis. Although several trials
have not found similar correlations, [22] performed a metaanalysis
evaluating 16 studies, concluding that such a correlation
exists [22].
More recently, variations in notch morphology have been
identified as potential sources for ACL impingement and injury.
Using MRI analysis, [24]. evaluated three potential shapes of
femoral intercondylar notches, and retrospectively evaluated
the risks of ACL injury for each, as well as for NWI [24]. Type
A notches are defined as narrow from base to apex, Type U
notches do not narrow past the midsection, and Type W notches
are similar to U’s but with a bifid apex. The study showed a
significant association between Ashaped
notches and ACL injury,
and found no association between smaller NWI and injury.
Tibial Plateau Geometry
The geometry of the tibial plateau, specifically the depth and
slope, is a more recently discovered risk factor with significant
implications on ACL injury. As the tibial plateau is a complex
geometrical surface, with numerous variables factoring into
its motion, studies have sought to model and identify which
features have the greatest impact on noncontact
ACL injuries.
In the most essential sense, the posterior tibial slope describes
the angle between a line tangential to the tibial plateau surface,
in the anteriorposterior
direction, and a line perpendicular to
the lengthwise axis of the tibia. Averages have been reported as
10° ± 3°, with deviations altering the kinematics of the swing
and stance phases of the knee joint [25]. Using MRI analysis [26],
identified increased posterior inferior directed tibial slopes and
shallow medial tibial plateau depth as an anatomic variant found
more commonly in the ACL injured population [27]. Further,
they began to identify differences in risk factors for each gender,
which will be highlighted in a later section.
Additional studies have corroborated these findings and
expanded on the postulated mechanisms for this risk [28,29].
Cadaveric studies have demonstrated that artificially created
increases in the tibial slope correlate with increased anterior
translation forces on the tibia relative to the femur [30]. As the
ACL is the primary restraint to such forces, it is believed that
increased strain is experienced with such anatomic variants
in vivo. The depth of the tibial plateau has been thought of as
a general indicator of motion constraint across the joint, and a
shallow medial plateau surface has been suggested to contribute
to an increase in the internal rotation forces experienced by the
tibia during compressive loading.
These forces have been shown to be a product of the tibial
bony surface as well as the overlying articular cartilage, and
surrounding tissues [31]. It is important to recognize that
following ACL injury, the articular cartilage of the tibial plateau
has been demonstrated to undergo morphologic changes,
specifically flattening in the medial compartment and increased
posterior sloping in the lateral compartment, when compared to
the contralateral knee. As such, the majority of studies analyze the geometry of the uninjured knee when evaluating articular
morphology. Beynnon et al. analyzed the cartilaginous profile of
the ACL injured population compared to a matched uninjured
cohort and found that similarly, an increased posteriorinferior
slope along the lengthwise axis of the tibial plateau was
associated with an increased risk for ACL injury [32]. Several
studies have even implicated variations in menisceal geometry
as potential risk factors for ACL injury. A similar effect of
increased anterior tibial translation has been demonstrated in
individuals with increased lateral meniscal slopes, which was
previously shown to correlate with increased ACL injury.
Body Mass Index
Perhaps the only modifiable risk factor, the role of body
mass index (BMI) has been evaluated with regards to noncontact
ACL injury. In two studies evaluating ACL injury in
military populations, BMI was shown to be a risk factor, although
not universally. A retrospective evaluation of 2,345 U.S Naval
Academy midshipmen suggested that a BMI 1 standard deviation
above the gender specific mean, in conjunction with a decreased
femoral notch width, was a significant risk factor for ACL injury
in both genders, while independently neither notch width nor
BMI was significant [33]. A similar study evaluating cadets
from the United States Military Academy found that BMI was
a significant independent risk factor in females, but not males
[34]. Comparably, this effect was amplified when combined
with a narrow femoral notch width. Although the reasoning
isn’t as straightforward, BMI’s influence on ACL injury can play
an important role identifying at risk individuals and starting
possible interventions.
Ligamentous laxity
Ligamentous laxity, both generalized and kneespecific,
has been explored as a potential risk factor for ACL injury. The
Beighton hypermobility score is a ninepoint
scale used to assess
generalized joint laxity and ligamentous hypermobility. Several
studies have examined the relationship between increased
Beighton scores and ACL injury rates, and identified generalized
joint laxity as a risk factor for ACL injury in both male and
female populations [35,36]. Knee specific laxity measurements,
evaluated using a KT1000
arthrometer, or goniometer for the
presence of genu recurvatum, have yielded similar associations
for ACL injury [34,36]. As females have been shown to have
greater amounts of knee and generalized joint laxity, these
findings may offer partial explanation as to why the overall
incidence of ACL injury is greater in the female gender.
Composite/Gender Variability
It is important to recognize that significant variability
exists between male and female knee morphology, even when
controlling for disparities in height and weight. Features such
as narrower femoral notch widths, increased posteriorinferior
tibial plateau slopes and decreased ACL width have been
shown to more prevalent in the female population than in their
male counterparts [27,37]. As such, overall rates and specific
combinations of anatomical variants have been shown to differ
between the genders.
In an MRI analysis of firsttime,
noncontact
ACL injuries in both
male and female participants, compared to a sample of uninjured
matched controls, [20]. identified differing combinations of knee
joint geometry that put members of each gender at increased risk
for injury. While males with smaller ACL volumes, medial tibial
spines, and decreased lateral compartment posterior menisceal
angles were at a significantly higher risk for injury, the best
fitting model of injury for females included decreased femoral
notch width and increased posteriorinferior
directed lateral
compartment tibial cartilaginous slopes [20]. Although these
findings may seemingly muddle an already complicated issue,
they serve to highlight the important fact that combinations of
features, rather than individual morphological differences, are
the most likely explanation for variable susceptibility to ACL
injury between individuals.
Prior ACL Injury or Reconstruction
Individuals who have undergone ACL reconstruction
previously have been shown to be at an increased risk for graft
reinjury
and contralateral knee injury. In one study evaluating
professional Swedish soccer players, a prior ACL injury was
identified as a significant risk factor for sustaining a new knee
injury of any kind. This risk did not extend to other lower
extremity injuries or total body injuries [38]. Interestingly
another study found a significant correlation between prior ACL
reconstruction and increased risk of is pilateral ankle injury. In
an Australian study evaluating football players, [39]. found that
prior ACL reconstruction put a player at a significantly increased
risk for both ispilateral and contralateral knee injury, with the
effects being most prominent in the first 12 months following
injury (12.3 times more likely) but still significant for ACL
injuries sustained greater than 12 months prior (4.4 times more
likely) [39]. It has been suggested that scar tissue, decreased
range of motion and alterations in proprioception may provide
explanation for these trends.
Hormonal Risk Factors
Sex hormones have been postulated to play a role in ACL
pathogenesis after hormone receptors for estrogen, testosterone,
relaxin and progesterone were localized to the ACL. It is known
that female athletes have a two to eightfold greater incidence of
ACL injury compared to male athletes [41-43]. This increased
female incidence is likely a result of multiple sex related factors
including anatomic, strength, and laxity differences. However,
sex hormones may also play a role. Supporting this hypothesis,
multiple hormone receptors have been identified on the ACL and
there also appear to be sexrelated
differences in expression of
these receptors.
Relaxin is a peptide hormone found in the serum of both
pregnant and nonpregnant
females thought to be responsible
for connective tissue remodeling during pregnancy [44]. It is
known to have collagenolytic effects secondary to MMP release
[45,46]. Relaxin receptors have been identified on the ACL and
with their potential collagenolytic effects have been proposed
as a potential risk factor for rupture [47]. Animal models show
increased laxity and strength in pregnant females with ACLs
[48]. Dragoo et al analyzed ACL sections from both men and
women with ACL ruptures for relaxin receptors. This is further
supported by [49]. who found higher rates of relaxin binding
in injured female ACL specimens. However, she did find relaxin binding in ⅕ of the male ACL specimens [49]. Dragoo et al. [50]
also elevated levels of relaxin in female NCAA athletes with ACL
injury versus noninjured
controls [50]. Given these findings, he
concluded relaxin may play a role in ACL rupture in females.
Relaxin expression is believed to be regulated by estrogen
as there appears to be upregulation of relaxin receptors after
pretreatment
with estrogen in animal models [51]. Estrogen
itself may also play a role in ACL pathogenesis. Liu et al. [52]
identified progesterone and estrogen receptors on synoviocytes,
fibroblasts, and blood cells of injured ACLs in both females and
males [52]. In a rabbit animal model, ACL strength decreased
after exposure to pregnancy levels of estrogen [53]. In a rodent
model, human relaxin caused decreased collagen accumulation
[54] and in another caused changes to collagen structure [27].
Sciore et al. [55] localized estrogen and progesterone receptors
to the ACL and via reverse transcriptionpolymerase
chain
reaction showed differences in expression after sex hormone
binding between sexes [55]. However, estrogen effects on ACL
fibroblasts has been studied in vitro with varying results: Yu
et al. [56] found inhibition of collagen synthesis with estrogen
while Seneviratne et al. [57] found no direct effect on ACL
fibroblasts [57,58].
Given these findings that estrogen may participate in
ACL pathogenesis, research into the effect of these hormones
throughout the menstrual cycle was undertaken. The effects
of the menstrual cycle on the ACL remain controversial. The
menstrual cycle has varying stages of hormone release with a
gradual increase in estrogen during the follicular phase followed
by a relative decrease in estrogen production and increased
progesterone until the late phase of the luteal phase. Across the
menstrual cycle, Shultz et al. [59] has shown alterations in knee
joint laxity as well as changes in serum collagen breakdown
and production markers [59]. However, Karageanes et al. [60]
followed female high school athletes over an 8 week period using
questionnaires to report menstrual phase and an arthrometer to
measure laxity and found no variation in ACL laxity throughout
the menstrual cycle [60].
If there is a higher risk phase of the menstrual cycle, the
exact phase remains controversial. Myklebust et al. [61] carried
out a prospective study on female handball players and found
a higher incidence of ACL injury in the late luteal phase [61].
However, the majority of studies suggest the preovulatory phase
is the highest risk phase [62-66]. Only two of the six referenced
studies measured hormone levels as the other four studies relied
on questionnaires for determination of menstrual phase. Further
controversy exists regarding the relationship oral contraceptives
have on ACL injury with Arendt et al showing a significant
relationship and Ruedi et al. [64] showing no increased risk of
injury with oral contraceptive use [64,65]. Additional studies
are needed in to more precisely determine the exact role of each
hormone and determine how these hormones exert their effects
throughout the menstrual cycle.
Genetic Risk Factors
Genetic risk factors for ACL rupture remains an area of
ongoing study. Two research groups have shown familial
predisposition toward ACL rupture. Harner et al. [67] carried
out a matched casecontrol
study and found patients with ACL
tears had a significant difference in family history of ACL rupture
[67]. This was further supported by a matched casecontrol
study
analyzing familial predisposition toward ACL rupture. Matching
was based on age, gender, and primary sport. They found
patients with an ACL tear were over 2 times as likely to have
another family member with an ACL tear. Posthumus et al. [68]
found a similar family association with ACL rupture [68].
Differences in gene expression also may explain the
increased incidence of ACL pathogenesis in females. Johnson et
al have shown upregulation of aggrecan (important extracellular
matrix component) and fibromodulin (controls collagen fibril
synthesis) and downregulation of WNT1 inducible signaling
pathway protein 2 (regulates collagen homeostasis) in females
with injured ACLs versus males [69].
At this point there are a number of casecontrol
studies showing association between specific gene variants and ACL
rupture. Many of these studies focus on collagen related genes
as Type I collagen comprises 7080% of dry ligament weight [70]. Some of these genes also appear to confer increased risk of
Achilles tendinopathy and rupture. Khoschnau et al. [71] analyzed
type 1 collagen polymorphisms in a matched case control
study. Specifically, they studied single gene polymorphisms
in the promoter region of COL1A1 (a regulator of type 1
collagen production). They found significant decrease in ACL
rupture risk and shoulder dislocations in patients with certain
polymorphisms [71]. This was followed with a number of case
control studies by a South African research group lead by Michael
Posthumus, to look at other collagen related genes. Notably, this
research group has included only Caucasian participants. In
2009, Posthumus et al. [72] analyzed the COL1A1 gene, but this
time used gender matched controls as opposed to Khoschnau
who used female controls with both female and males in the
injury group. Posthumus et al [72] found a rare TT genotype of
COL1A1 that was significantly underrepresented
in participants with ACL ruptures suggesting it was protective against rupture
[72]. Posthumus et al. [72] carried out a similar study analyzing
COL5A1 in female athletes and found a specific CC genotype
that was significantly underrepresented
in participants with ACL rupture again suggesting a possible protective role for that
genotype [72]. Further study turned to COL12A1 which encodes
for type XII collagen believed to regulate collagen fibril diameter
[73]. Posthumus et al. [74] showed an association between
a specific COL12A1 AA genotype and ACL rupture in females
[74]. Four matrix metalloproteinases (MMPs) on chromosome
11q22 have also been analyzed. These MMPs are responsible for
extracellular matrix degradation and remodeling and therefore
play an important role in ligament homeostasis. Posthumus
et al. [75] found that AG and GG genotypes of MMP12 were
significantly underrepresented suggesting a possible protective
role conferred by these genotypes [75]. Growth factors like
MMPs also play a role in ligament homeostasis. A variant of
growth differentiation factor 5 (GDF5) is known to stimulate
production of type 1 collagen in rabbit ACL models [76]. Given
these findings, it was hypothesized that the GDF5 rs143383
variant would provide a possible protective effect for ACL
rupture. However, Raleigh et al. showed in a matched casecontrol
with Caucasian males and females there were no association between the GDF5 rs143383 variant and ACL rupture. Lastly,
the most recently published research in genetics and ACL
pathology reports an association with a specific GG genotype of
fibrillin2 (FBN2) and ACL rupture in a casecontrol
study [77]. Fibrillins are glycoproteins present in the extracellular matrix of
ligaments and tendons [78]. Fibrillin 2 specifically plays a role in
the composition of elastic fibers [79].
As you can see, genetics appears to play an important role
in ACL pathology. The number of genetic associations will likely
continue to grow and more diverse populations will go under
study.
Extrinsic Risk Factors
Extrinsic risk factors for ACL injury include weather
conditions, footwear and playing surface. These are not inherent
to the individual and therefore offer a more modifiable risk
source. As modern day athletics see continued innovations in
equipment and arena alike, studies evaluating these extrinsic
factors may serve as a viable foundation for future interventions.
Weathe
Weather conditions have been extensively studied in
regard to ACL injury incidence. As professional sports feature
performance athletes playing in highly documented conditions,
they offer ample material for risk factor analysis.
The National Football League is one such organization,
and several studies have evaluated the relationship between
weather conditions and ACL injuries in the league. In one
study analyzing a total of 5910 NFL games over 10 seasons,
the author’s identified significantly higher rates of ACL injury
in earlier parts of the season, associated with warmer weather
conditions, in comparison to later/cooler parts of the season, on
both artificial and grass playing surfaces [80]. Unsurprisingly,
this trend was no longer significant when artificial climates,
such as dome stadiums, were analyzed. It is postulated that
decreased amounts of shoesurface
traction in cooler months are
one component of this increased risk.
Specifically regarding climate, Walden et al. evaluated
regional differences between ACL injury rates in European
professional soccer players. Dividing teams into groups using
a standardized climate classification system, the researchers
found that noncontact
ACL injury rates were significantly less
in northern regions, an area associated with cooler winters and
the absence of a dry season. Interestingly, the opposite trend
was found for upper body, low back and Achilles tendinopathy
injuries [81].
Orchard et al published multiple studies evaluating the
risk factors for ACL injury in Australian footballers. One study
identified drier playing conditions: high water evaporation in
the previous month, and low rainfall the prior year, as significant
risk factors for player ACL injury [40]. In an attempt to provide
a direct correlation between ground hardness and ACL injury
rates, Orchard used readings from a penetrometer, a device that
measures surface hardness, and compared them to incidence of
ACL injury in AFL players [41]. Although no significant findings
were made, there was a trend supporting prior studies’ results
that matches in earlier months/warmer conditions play some
part in ACL injury risk.
Footwear
Few studies have evaluated the relationship between
footwear and ACL injury risk. In one prospective study, 3,119
high school level American football players were followed for 3
seasons and the incidence of ACL injury was measured, as well as
their playing footwear. It was found that edge design cleats, those
with longer cleats around the shoe’s periphery with shorter
inner cleats, produced higher amounts of torsional resistance
and were associated with significantly increased ACL injury rates
when compared to pivot disk, flat, and screw in designs [82].
Another study found that shoesurface
interactions vary with the
ambient temperature, and increased force is required to release
a shoe from an artificial turf surface at higher temperatures than
lower temperatures, a finding that may provide mechanism to
previously mentioned correlations [83].
Footwear
Playing surface represents an easily modifiable risk factor
for athletic teams that has unfortunately yielded mixed findings.
Numerous studies have been conducted to evaluate the difference
between artificial surfaces and grass regarding ACL injury risk.
While several studies have suggested have argued that there is
a significant difference between artificial and natural surfaces
[83,84], multiple others suggest that no significant difference
exists [80,86,87]. It is difficult to speculate on the nature behind
these mixed findings, but further analysis needs to be done if a
clear trend is to be discovered.
Interestingly, amongst different types of grass, variations in
ACL injury rates have been found. Orchard et al. [88] evaluated
4 different types of natural grass playing surfaces on Australian
Football fields and identified that Rye grass was associated with
significantly decreased rate of ACL injury when compared to
Bermuda grass. The authors speculate that this may be a result
of the thick thatch layer found in Bermuda grass, that likely
increases gripping between cleats and the playing surface [88].
Discussion
Anterior cruciate ligament rupture is an injury that often
results in costly treatment, extensive recovery and numerous
immediate and longterm
complications. The risk of ACL injury
is a complex interplay of factors both intrinsic to the individual
and extrinsic to the activity or playing conditions. Although
individual risk factors have been identified further research
is needed to determine the mechanics of ACL injury in all
population groups, the interplay between risk factors, and
ultimately further prevention of these injuries.
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