Literature Review

LIGAMENT INJURY AND REPAIR: CURRENT CONCEPTS

Gabriel Y.F. Ng, PhD, PT

Abstract: Ligament injuries have multiple causes. The most usual injury mechanism in sports is abrupt tensile
loading that exceeds the strength limit of the ligaments. Injuries should be accurately diagnosed and properly
managed in the acute phase to facilitate favourable healing. Different ligaments have unique healing potentials,
and for those that have poor natural healing potential, surgical repair or reconstruction may be indicated. Previous
studies have revealed that the biomechanical performance of ligament grafts is inferior to normal tissue even
with long-term follow-up. Prolonged immobilization of joints has a detrimental effect on the physical properties
of ligaments and it takes a long time to recondition ligaments after immobilization. Appropriate exercise training
has been shown to strengthen ligaments, and there is evidence to suggest that therapeutic ultrasound or laser
can hasten ligament healing after injury, but the optimal parameters for these treatments are yet to be determined.

Key words: ligament, injury, healing, reconstruction, physiotherapy

Introduction collagen and GAGs than tendons. In general, ligaments

The word ligament is derived from the Latin ligare,
which means binding [1]. According to Snook [2], the
Smith Papyrus in 3000 BC had already described a
symptom similar to joint sprain, and around 400 BC,
Hippocrates described treatments for ligament injuries.
In 100 BC, Hegator provided the first anatomical defini-
tion of a ligament, but the first correct description of a
ligament came from Galen in 130 AD. Before that,
ligaments were generally considered similar to nerves
but with a vague contractile function.
Traditionally, tendons and ligaments are both re-
garded as dense parallel connective tissues with very
similar structures [3, 4]. Sometimes, the terms ligament
and tendon are intermingled in the literature [5, 6].
However, biochemical analysis of ligaments and ten-
dons reveals subtle differences between these structures
[7]. Ligaments contain about two-thirds water by weight.
The remaining one-third consists of collagen, elastin,
glycosaminoglycans (GAGs), fibroblasts, and other bio-
chemical substances. Ligaments contain more protein,
less total collagen, and greater proportions of type III
are more metabolically active than tendons.
According to Frank and Shrive [8], the major func-
tions of skeletal ligaments are to attach bones to one
another across a joint, guide joint movement, maintain
joint congruency, and act as position sensors for joints.
With these roles, ligament injury has a significant impact
on functional performance.
Ligament injury
The mechanisms of ligament injury are multifactorial
and can be classified into seven categories: contact or
direct trauma, dynamic loading, repetitive overuse, struc-
tural vulnerability, poor flexibility, muscle imbalance,
and rapid growth [9]. In sports-related injuries, the
principal mechanism is mechanical loading character-
ized by the magnitude, location, direction, duration,
frequency, variability, and rate of the load [10].
Injury to a ligament will compromise its joint stabiliz-
ing function and ability to control movement. It will also
reduce the proprioceptive acuity and lengthen the liga-
ment-muscle reflex time of the joint [1116]. Ligament
injury can happen with a single load that exceeds its

Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Kowloon, Hong Kong.
Received: 7 March 2002. Accepted: 10 May 2002.
Reprint requests and correspondence to: Dr. Gabriel Ng, Department of Rehabilitation Sciences, The Hong Kong Polytechnic
University, Hung Hom, Kowloon, Hong Kong.
E-mail: rsgng@polyu.edu.hk

22 Hong Kong Physiotherapy Journal Volume 20 2002

maximum strength, or from cumulative overload
(repetitive sprains) with insufficient recovery time so Inflammation
that these chronic insults set the stage for an acute rupture. phase
Repair Remodelling
Knowing the extent of injury is vital to determine Injury phase phase
optimal management. Minor ligament sprains may only

of response
cause annoyance and minimal functional loss, but if

ignored and with repetitive loading, these minor injuries
can progress. Increasingly severe ligament sprains will
lead to more functional loss requiring a longer time to
heal.
Every ligament injury is unique despite similarities in
the biomechanical events and subsequent biological
responses. The severity of ligament injury is graded
using various clinical classifications. The most typical is
a three-level system that quantifies structural
involvement, signs, and functional loss (Table 1) [9].
Natural healing process
Healing after injury is structure specific. Some ligaments,
such as the medial collateral ligament (MCL), have good
healing potential, whereas others, such as the anterior
cruciate ligament (ACL), have a poor chance of healing
after total rupture because the failed ends are likely to be
exposed to joint fluid that does not favour healing [17
20]. Generally, the biological responses following liga-
ment injury can be summarized into three phases: bleed-
ing and inflammation, active repair with proliferation of
bridging materials, and remodelling (Figure 1) [21].
If the injury is not managed appropriately in the early
phase with adequate RICE (rest, ice, compression, and
elevation), it will result in uncontrolled bleeding and
oedema, causing abnormal arrangement of collagen
fibres so that the resultant scar becomes hypertrophic,
stiff, and painful [22].
In the repair phase, water content remains high. The
rate of collagen synthesis reaches its peak about 3 weeks
after injury [23]. Studies with quantitative collagen fibril
analysis have indicated that early mobilization in the
first 3 weeks could be detrimental to collagen orientation,
but after this period, mobilization increases the tensile
strength of the repairing ligament [22].
Intensity
0 3 411 days 6 weeks 6 months
Fig 1. The three phases of healing and the cells involved.
Adapted from Oakes [22].
The remodelling phase starts from week 6 onwards
and lasts for up to 1 year. The water content returns to
normal and total collagen content remains slightly
increased. Scar tissues continue to mature slowly and
approximate the properties of normal tissue. In our
study of ACL repair in goats with a 3-year follow-up
period, we induced surgical transection injuries to the
posterolateral bundle of the ligament and kept the
anteromedial bundle intact as an internal splint [24]. We
found that the repaired tissues attained 75% of the
normal ultimate tensile strength at 1 year. At 3 years, the
strength surpassed that of the normal ligament by 28%.
The structural stiffness also improved with time and
achieved 97% of the normal value at 3 years. However,
the material properties (Youngs modulus) of the re-
paired tissue did not parallel its structural properties and
only achieved 72% of the normal value at 3 years.
Electron microscopy of the repaired tissue revealed that
the collagen fibrils at 3 years were mainly small (< 100
nm in diameter), with only very few large fibrils (> 100
nm) scattered in the matrix. Furthermore, the cross-
sectional area of the repaired bundle increased by about
50% at 3 years [25].
These findings indicate two important points. Under
favourable conditions such as spontaneous incomplete
injury with close approximation of the ruptured ends,

Table: Classification of ligament injury modified from Leadbetter [9]

Grade Severity Degree Structural involvement Exam Performance deficit

1 Mild First Negligible No visible injury, Minimal to a few days

locally
tender only, joint stable
2 Moderate Second Partial Visible swelling, Up to 6 weeks (may be
marked tenderness, modified by protective
stability bracing)
3 Severe Third Complete Gross swelling, Indefinite, minimum
marked tenderness, of 68 weeks
antalgic posture, unstable

Hong Kong Physiotherapy Journal Volume 20 2002 23

 A B

D
C

Fig. 2. Transverse sections through collagen fibrils of A) normal patellar tendon (PT) of goat; B) anterior cruciate
ligament (ACL)-PT graft at 12 weeks; C) ACL-PT graft at 1 year; and D) ACL-PT graft at 3 years. The collagen fibrils
size remained small in the graft in all time points. Some large fibrils repopulated the graft at 3 years, but the
orientation of the fibrils is still not parallel even at 3 years. (x 20,000).

healing of the ACL is possible. With enough time, the
repaired tissue can simulate the structural strength of a
normal ligament. This is in keeping with reports using
different animal models and ligaments [19, 26]. The
material properties of the repaired ACL remain inferior
to the normal tissue even 3 years after injury. The good
ultimate tensile strength and stiffness of the repaired
ligament is due to hypertrophy of the scar. Although the
hypertrophic scar can increase the structural strength, it
will occupy more space, especially for intra-articular
ligaments. This may cause impingement of the joint
structures and, hence, degenerative changes.
Ligament reconstruction
Ligament grafts, in particular ACL reconstruction, have
attracted much attention in clinical and basic science
research in the past two decades. Since the first reported
case of ACL graft by Hey Groves [27], there have been
significant advances in surgical procedures, postopera-
tive management, and rehabilitation. Generally, ACL
reconstruction is the preferred choice of management
for the following patient groups: young and athletic
people, chronic cases with knee instability, and com-
bined ligament and meniscal injuries [2831].
There is evidence to suggest that ACL reconstruction
should not be performed in the acute phase due to
increased risk of arthrofibrosis [32, 33]. The operation
should be delayed for 2 to 3 weeks, during which time
patients should undergo an aggressive rehabilitation
programme to help improve the joint range and resolve
any swelling. The success of ACL reconstruction de-
pends on the biological responses of the graft tissue and
surgical precision in maintaining graft isometry per se
[29]. The selection of graft has been a subject of interest
for a long time. Hitherto, three main types of grafts have
been used: bone-patellar tendon (PT)-bone autograft,
quadruple looped semitendinosus autograft, and bone-
PT-bone allograft.
Ng studied ACL-PT autograft in goats and found that
most endogenous large collagen fibrils (> 100 nm
diameter) in the original PT graft disappeared by 6 weeks
after surgery [25]. The collagen fibril sizes remained
small throughout the first year. At 3 years, some large
collagen fibrils were scattered inside the graft, but the
packing density and orientations of the collagen fibrils
were still inferior to the normal tissue (Figure 2).
Examination of the biomechanical strength and bio-
chemical cross-link density of the ACL graft at different

24 Hong Kong Physiotherapy Journal Volume 20 2002

time intervals revealed that the rate of load-relaxation in
the graft was significantly faster than normal at less than
1 year. After the first year, the load-relaxation rate
slowed down. The strength and stiffness of the graft
dropped in the first 3 months and then gradually
improved, but only reached 43% and 48%, respectively,
of the normal values at 3 years. There was a concomitant
change in hydroxypyridinium cross-link density in the
graft, which was significantly correlated with the Youngs
modulus of the graft [34, 35]. This implies that
hydroxypyridinium cross-links in collagen may be a
determining factor of the material strength of the re-
paired tissue.
These studies of ACL grafts reveal that graft remod-
elling is a long and continuing process. The long time (3
years) involved in our goat studies and the persistently
poor biomechanical performance of the grafts imply that
grafts may never achieve the physical properties of
normal tissue. Our findings are in agreement with other
animal studies that the ultimate strength of the grafts at
1 or 2 years after reconstruction was less than 50% of the
normal value [29]. In contrast, a biomechanical study by
Beynnon et al with a human ACL graft revealed that the
graft achieved 87% strength compared to the control
side at 8 months after surgery [36]. The discrepancy of
this human study from the findings of animal studies
could be due to inter-species difference or success of the
rehabilitation programme in people after ACL
reconstruction. However, Beynnon et al only had one
subject in their study and the strength of the normal ACL
of that subject was only 1,015 N [36], substantially lower
than the normal values of 1,730 N and 2,160 N reported
in the literature [37, 38]. Therefore, caution must be
exercised in interpreting the result of that single-case
human study.
Nonoperative management for ligament injury
Surgical treatment for ligament injury may not be ap-
propriate for all patients. In nonsurgical management,
success is dependent on the physiotherapy rehabilita-
tion programme and future goals of the patient. In
general, when a ligament heals, it forms scar tissue that
may gradually mature and strengthen to resemble the
normal tissue. However, research findings from our
group [24] and others [21, 23] have shown that scar
tissue remains mechanically inferior to normal tissue for
a long time after injury. The rehabilitation programme
should, therefore, aim to facilitate muscle function and
proprioception to provide active support for the joint.
In a survey by Beard and Fergusson [39], 80% of
centres in England had no defined rehabilitation proto-
col for nonsurgical ACL cases. Most respondents were
not aware of the important role of hamstrings in these
patients and there was also a large variation in the
objectives and treatment protocols among hospitals. In a
local survey [40], we found that most hospitals and
Hong Kong Physiotherapy Journal Volume 20 2002
centres in Hong Kong had a well-defined rehabilitation
protocol for ACL surgical cases, but very few had such a
protocol for nonsurgical cases. Furthermore, most clini-
cians did not aim to help patients return to their pre-
injury sports in their treatment goal, which could have
a significant negative impact on the quality of life of
patients. Since our survey was conducted more than 5
years ago [40], it is hoped that the approach of local
clinicians might have changed, but this needs to be
verified with another similar study.
Effects of immobilization versus exercise
Ligaments are sensitive to training and disuse. One of the
original studies in this area, by Noyes et al [41], demon-
strated that in primates, 8 weeks of cast immobilization
of the lower limb resulted in substantial loss of strength
in the ACL. With a reconditioning programme, it took
close to 1 year for the ligament to attain 91% normal
strength and 98% normal stiffness.
From the metabolic perspective, Amiel et al analysed
the collagen turnover rate in rabbit MCL following 12
weeks of knee immobilization [42]. They found that the
collagen mass of the ligament decreased by about 30%
due to degradation of the collagen. In a later study,
Amiel and co-workers further demonstrated a close
relationship between joint stiffness induced by immobi-
lization and a decrease in GAGs in joint tissues [43]. Woo
et al reported similar findings of ligament atrophy with
immobilization [44].
The beneficial effects of exercise on ligaments have
been thoroughly reported by various researchers [45
47]. The early work of Tipton et al revealed that the MCL
of dogs that had been subjected to 6 weeks of strenuous
exercise training were significantly stronger and stiffer
than those of the control group [47]. Woo et al demon-
strated that an enforced exercise programme could has-
ten the return of mechanical strength in ligaments that
had been weakened by immobilization [44]. Oakes and
Parker studied the collagen fibril diameters of ACL and
posterior cruciate ligament (PCL) in rats after 4 weeks of
treadmill running and swimming [48]. They found that
the exercised rats had more collagen fibrils per unit area
than the control rats. Interestingly, they found a de-
crease in mean fibril diameter in the exercised rats,
which they explained as related to the change in the type
of GAGs in response to loading, which mediated the
collagen fibril size.
We have recently completed a study to compare the
anteroposterior laxity, stiffness, and rate of change of
stiffness in the knee joint of athletes involved in basketball,
running, and swimming and in sedentary subjects [49].
We found that swimmers had the lowest laxity and
highest stiffness in their knees followed by the basketball
athletes, runners, and then control subjects. This could
be due to the different loading of these activities on the
knee joint structures and the biomechanical response of
25
these structures to loading. If this response also happens
in ligaments under repair, it will have clinical implica-
tions for the choice of rehabilitation exercises for sub-
jects after ligament injuries.
Notwithstanding, exercise may not always produce
beneficial effects on ligaments. Burroughs and Dahners
examined the effect of exercise dosage on rats with
different severity of injuries to the MCL, ACL, or medial
joint capsule [50]. They measured the tensile strength of
the repairing ligaments and laxity of the knee joint, and
found that exercise had a beneficial effect on the healing
MCL with no associated ACL injury. For joints that
demonstrated gross instability with combined injuries in
the MCL, ACL, and medial joint capsule, laxity in the
joint deteriorated and no increase in tensile strength of
repairing ligaments was found with exercise training.
Therefore, rehabilitation exercise programmes should
be carefully planned and monitored for subjects with
severe joint instability.
Efficacy of physical modalities on ligament repair
Therapeutic ultrasound (US) and laser are often used by
clinicians to hasten the natural healing process in soft
tissue injuries. Their effectiveness is summarized below.
Therapeutic ultrasound
US controls inflammation and regulates blood flow in
the acute phase of injury, stimulates fibroblastic actions
and promotes collagen formation in the active repair
phase, and improves collagen alignment and thus exten-
sibility of mature collagen such as in scar tissue in the
remodelling phase [5153]. An early survey by ter Haar
et al revealed a large degree of inconsistencies in the use
of US [54]. These include a lack of consensus in dosage,
choice of pulsed or continuous exposure, and lack of
scientific evidence on the effects and contraindications
of US. In a more recent review article [55], these ques-
tions remained unanswered and proof of clinical efficacy
of therapeutic US is still lacking. Although the anti-
inflammatory action of therapeutic US has been studied
in some depth by different researchers using different
approaches, their findings are equivocal.
An early study compared the anti-inflammatory ac-
tion of therapeutic US with flurbiprofen in the acute
phase of injury using a rat model [56]. Sponge cubes
containing irritants were implanted in the subcutaneous
tissues of rats and the animals were divided into three
groups: US, placebo US, and flurbiprofen. Their results
did not show any beneficial effect of US. However, their
injury model did not simulate the usual patterns of
ligament injuries. Furthermore, the presence of a for-
eign body in the tissues could cause significant reflection
of ultrasonic energy [57].
Since then, various researchers have examined the
effects of therapeutic US on tissue healing in animal
26
models or in vitro preparations. Enwemeka [58] and
Young and Dyson [59] demonstrated favourable results
with US for tissue healing in rabbits and rats. A few years
later, De Deyne and Kirsch-Volders examined the effects
of US on in vitro human fibroblastic activity [60]. They
found a dose-dependent increase in cellular activity
such that 30 and 60 seconds of exposure to US resulted
in more intense activity than 0 and 90 seconds of
exposure.
Recently, we studied the effects of US dosage on MCL
healing in rats by measuring the concentration of in-
flammation indicators, leukotriene B4 (LTB4) and pros-
taglandin E2 (PGE2), and a repair indicator, transforming
growth factor beta 1 (TGF1) [61]. LTB4 and PGE2 in the
high-intensity groups were increased by approximately
two-fold more than in the corresponding placebo US
group on post-injury Day 2. This suggests that US in-
creased inflammation in the acute phase of injury. On
post-injury Day 11, there was a significant drop in LTB4
in all intensity groups but an increase in PGE2 in the
high-intensity group. We also observed that delaying US
treatment for 5 days after injury resulted in similar levels
of TGF1 to immediate treatment. This suggests that US
can enhance ligament healing, but the difference is not
obvious between early or delayed application.
Furthermore, early application of US may increase in-
flammation in the acute stage. However, this study only
focused on the biochemical aspect of ligament healing
and the findings need to be supported by functional or
biomechanical testing.
Laser
Clinicians often use low-energy laser in the treatment of
musculoskeletal conditions [6264]. Due to its
biostimulatory effects [65], low-energy laser therapy
has been found to be effective in the treatment of skin
wounds [63, 64], pain [66], and inflammatory condi-
tions [67]. Enwemeka et al found that repairing tissues
treated using laser therapy had smaller collagen fibres
than control tissues [68]. Furthermore, higher doses of
laser lead to significantly larger collagen fibrils than
lower doses. This finding suggests that collagen size in
repairing tissue is dependent on the dosage of laser
treatment.
In an ongoing study, we compared the effects of
different dosages of gallium-aluminium-arsenide laser
on healing of rat MCL by measuring the biomechanical
performance of the ligaments at 3 and 6 weeks after
injury. We tested four groups of rats; three groups had
their right MCL surgically cut and the other group
underwent a sham operation without MCL injury. Two
of the MCL-injured groups received a single dose of laser
directly to the ligament at either high or low intensity.
The biomechanical strength and stiffness of the MCL in
the sham and laser treatment groups were greater than
those in the MCL-injured control group [69]. The laser
Hong Kong Physiotherapy Journal Volume 20 2002
treatment groups had comparable strength to the sham
group, and all three groups had improved stiffness
between weeks 3 and 6. There was no difference be-
tween the high- or low-dosage groups.
Our results suggest that therapeutic laser hastens
MCL healing in rats. However, our mode of laser applica-
tion is different from the usual clinical approach because
we applied the laser treatment directly to the cut ends of
the ligament. It is not known whether transcutaneous
application of laser therapy would have the same effect,
so this should be examined in further studies.
Future directions
Studies of ligament healing have traditionally been
focused on surgical management and rehabilitation
programmes that include bracing and physical modalities.
Advances in surgical techniques, rehabilitation exercises,
and design of assistive devices result from a better
understanding of the biomechanical properties of liga-
ments and joints. In search of a biological solution for
soft tissue repair, researchers have found some positive
effects of the use of fibroblast growth factors on soft
tissue healing in animals [7072]. Despite the encourag-
ing results of animal studies, the use of growth factors in
humans is still in the experimental stage and it is likely
to be a long time before it becomes fully mature and safe.
Chinese medicine is becoming popular in many
areas of the world. New research findings have provided
solid scientific foundations to Chinese medicine and
unveiled the code of wisdom of the ancient Chinese
people. What had once been regarded as superstition or
cultural hypnosis in Chinese medical practice is now
being seriously studied and applied in many Western
countries. Preliminary findings of our group on the use
of Chinese herbal medicine in treating ligament injuries
are very positive [73]. We believe that the combined use
of Chinese and Western medicine in the treatment of
musculoskeletal injuries has good potential.
Conclusion
This paper presents the basic sciences of ligament injury
and repair. It is imperative for clinicians to understand
the way that ligaments behave after injury and what can
be done to hasten recovery. The rehabilitation pro-
gramme after ligament injury is one of the most impor-
tant determining factors in regaining function. Physi-
otherapists should follow closely the developments in basic
science research in soft tissue repair, clinical biomechanics,
and new orthopaedic surgical techniques to be able to
design the most appropriate rehabilitation protocol.
Acknowledgement
The author acknowledges the Hong Kong Research
Grants Council, The Hong Kong Polytechnic University
Hong Kong Physiotherapy Journal Volume 20 2002
Area of Strategic Development Grant, and Hong Kong
Sport Development Board Research Grant for financial
support of the studies reported in this paper.
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