ARTICLE

A Neuromuscular Mechanism of Posttraumatic

Osteoarthritis Associated with ACL Injury
Riann M. Palmieri-Smith1,2,3 and Abbey C. Thomas1
1
School of Kinesiology, University of Michigan; 2Department of Orthopaedic Surgery, and 3Bone and Joint Injury
Prevention and Rehabilitation Center, University of Michigan, Ann Arbor, MI

PALMIERI-SMITH, R.M. and A.C. THOMAS. A neuromuscular mechanism of posttraumatic osteoarthritis associated with
ACL injury. Exerc. Sport Sci. Rev., Vol. 37, No. 3, pp. 147Y153, 2009. Anterior cruciate ligament (ACL) injury leads to early-onset
osteoarthritis. Quadriceps weakness is a consequence of ACL injury and is considered to result from arthrogenic inhibition (AMI). AMI is the
neurological ‘‘shutdown’’ of muscles surrounding an injured joint, preventing full activation, reducing strength, and promoting atrophy. As
quadriceps function is critical for energy absorption, its dysfunction may contribute to posttraumatic osteoarthritis. Key Words: arthrogenic
inhibition, muscle, knee injury, quadriceps, strength

INTRODUCTION Quadriceps weakness is ubiquitous after ACL rupture and

is often persistent despite restitution of static stability
Tibiofemoral osteoarthritis (OA), the most common cause through ACL reconstruction and aggressive rehabilitation
of disability in the United States, affects 30% of Americans (34). Although surgical intervention and subsequent reha-
older than 55 yr, yet little is known regarding the mechanistic bilitation are deemed successful in many cases, full quad-
contributors to this disease. In recent years, overwhelming riceps strength is often never achieved. In fact, quadriceps
evidence has emerged that experiencing an anterior cruciate weakness can persist for years after injury and/or reconstruc-
ligament (ACL) rupture, as well as other knee joint injuries, tion (17). Lingering quadriceps weakness may be detrimental
increases the risk of developing knee OA (23). Furthermore, to knee joint tissues because of its importance as a shock
OA secondary to ACL injury tends to afflict a younger attenuator and its function to help distribute loads across the
population. Current estimates indicate that rupturing the knee. Quadriceps weakness results in loads being transmitted at
ACL leads to OA 5Y20 yr after injury, ‘‘aging’’ the knee by higher rates and magnitudes up the lower limbs, and thus,
approximately 30 yr (23). When considering these estimations maintaining strength of this muscle group is considered a vital
and keeping in mind that ACL injury primarily affects neuromuscular protective mechanism. The inability of ACL
teenagers and young adults, this suggests that symptomatic patients to restore complete quadriceps strength may help
OA may begin presenting in adults in their 20s and 30s, a explain the development of early-onset posttraumatic OA (32).
time when high demands are still placed on the joints for In this article, we provide evidence supporting the hypothesis
work and physical activity. The early onset of OA after ACL that quadriceps weakness may result in posttraumatic OA.
injury presents a clinical conundrum, as treatment strategies Furthermore, we suggest a possible mechanism through which
used for older adults with idiopathic OA (e.g., joint replace- quadriceps weakness manifests after ACL injury/reconstruc-
ment, restriction of activity) are not appropriate or acceptable tion. Finally, we provide suggestions for future research that
for the younger patient. Thus, it is imperative that we, as will help prove or disprove the hypotheses put forward.
scientists, identify the mechanisms leading to the genesis of
OA after ACL rupture so that effective methods can be
developed to prevent or delay the onset and/or progression of ASSOCIATION BETWEEN QUADRICEPS WEAKNESS
the disease. AND JOINT DEGENERATION

Address for correspondence: Riann M. Palmieri-Smith, Ph.D., A.T.C., Athletic

Quadriceps weakness is well accepted as a consequence of
Training, Movement Science, and Orthopaedics, 4745G CCRB, 401 Washtenaw knee OA, but less accepted is the notion that it is directly
Ave., Division of Kinesiology, University of Michigan, Ann Arbor, MI 48109 responsible for the development and/or progression of the
(E-mail: [email protected]). disease. Although available data in humans cannot prove
Accepted for publication: March 16, 2009.
Associate Editor: Daniel P. Ferris, Ph.D. that quadriceps weakness contributes to the onset of OA,
the data do strongly suggest that quadriceps weakness may
0091-6331/3703/147Y153 be a risk factor predisposing persons to develop idiopathic
Exercise and Sport Sciences Reviews
Copyright * 2009 by the American College of Sports Medicine knee OA.

147

Copyright @ 2009 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
 Initial evidence to support that quadriceps weakness is re- the use of quadriceps strengthening to prevent the incidence
lated to the onset of OA comes from a cross-sectional in- and progression of OA.
vestigation that found quadriceps strength was a significant
predictor of symptomatic idiopathic tibiofemoral OA (this was ALTERED JOINT LOADING: HOW QUADRICEPS
significant despite adjustments for age, sex, and body weight) WEAKNESS MAY RESULT IN POSTTRAUMATIC OA
(28). A prospective study conducted in 300 subjects con-
firmed the above-referenced findings (29). Quadriceps weak- Muscle forces are a major determinant of how loads are
ness relative to body weight was found to be a predictor for distributed across a joint’s surface. Altering the muscle forces
the occurrence of OA at a 30-month follow-up. Women who acting about the knee joint complex as a result of ACL
developed OA had 18% lower quadriceps strength, whereas injury will ultimately affect loading conditions. Because OA
men who developed OA had 15% lower quadriceps strength is considered to be a mechanically driven disease, altered
at baseline compared with those who did not develop OA. joint loads are likely a requirement for its development and
These findings were further supported by Baker et al. (2), who progression.
found using a large cross-sectional investigation that there Traditional thought surrounding what biomechanical/
was a strong relationship between quadriceps weakness and neuromuscular alterations possibly result in OA is centered
combined tibiofemoral and patellofemoral OA in both on muscle weakness leading to increased joint loading and
men and women and between quadriceps weakness and eventually OA. Intuitively, this makes sense, as the quad-
isolated patellofemoral and tibiofemoral OA in women. In a riceps has a protective function serving as a shock absorber
recent investigation examining 148 patients, the fewer capable of dampening loads during activity. Failure to
number of straight leg raises performed, which would be adequately absorb energy about the knee can cause greater
related to quadriceps strength and endurance, was capable dynamic loads to be placed on the articular cartilage,
of predicting incident radiographic OA 5 yr later (odds resulting in progressive degeneration. Radin et al. (21) have
ratio, 2.6) (33). shown that repetitive impulse loading in the hind limb of
The idea that quadriceps weakness is capable of causing rabbits results in rapid degeneration of articular cartilage
OA associated with ACL injury is interesting because it when the load was delivered quickly, even if the load was
suggests that the joint degeneration can be prevented. At not excessive. However, if a load of a similar or a greater
this point, no data are available to make a direct connection magnitude was provided gradually, articular surfaces re-
between the quadriceps strengthening after knee injury and mained normal as the muscles (primarily the quadriceps)
the prevention or delay of OA. Furthermore, no evidence is were able to absorb the energy via eccentric contraction.
available connecting quadriceps weakness after ACL rupture Mikesky et al. (14) found that the rate of loading during
to OA. Our hypothesis is based on the literature in the walking among women with higher quadriceps strength was
idiopathic OA population, which suggests quadriceps weak- significantly slower when compared with those with lower
ness is related to knee OA. Thus, if there is a cause-and- quadriceps strength. These data support the hypothesis that
effect relationship between quadriceps weakness and OA, it quadriceps weakness can overload the knee joint and seems
would be logical that restoring quadriceps strength will delay to be capable of causing joint degeneration.
or prevent the onset of OA. As the vast majority of OA associated with ACL injury
A recent randomized clinical trial that examined the seems to afflict the medial tibiofemoral compartment,
effects of a 12-month quadriceps/hamstring strengthening or loading in the frontal plane would seem to be critical to
a range of motion (control) program on the incidence and the onset of posttraumatic OA. Although the quadriceps
progression of OA in older adults, in part, supports our musculature has only a small moment arm to render it
hypothesis (13). Results demonstrated that persons in both capable of controlling adduction/abduction loading, it still is
groups actually lost strength for 30 months but that the important in this regard. Quadriceps and hamstring cocon-
subjects in the strength training group who had established traction has been shown to provide the majority of support
knee OA at baseline displayed 37% less mean loss in joint for the knee adduction moment during walking (27) and is
space width, suggesting that thigh muscle strengthening may also vital for frontal plane stabilization during sporting tasks.
slow the rate of progression of knee OA. Contrary to these Larger than normal external knee adduction moments,
findings where strengthening seemed to be beneficial, the which are indicative of greater joint loading in the medial
same study demonstrated that persons without established compartment, have been associated with the incidence (3),
OA at baseline who participated in strength training were severity (26), and the progression (15) of tibiofemoral OA.
more likely to demonstrate joint space narrowing than those ACL-reconstructed patients display larger-than-expected
in the control group (34% vs 19%, respectively). However, adduction moments during gait walking (4), although the
the data were unable to demonstrate an association between relationship between quadriceps weakness and the adduction
quadriceps strength and joint space width, making it difficult moment in this population is unknown. Recent evidence,
to implicate strength training as the cause of the narrowing. however, has emerged in postmeniscectomy patients, a
Furthermore, there is evidence from other studies to suggest population at risk for posttraumatic OA, demonstrating that
that strength training is not harmful to the osteoarthritic patients with weaker quadriceps had higher knee adduction
knee (5) and may be beneficial to articular cartilage in moments than those with stronger quadriceps (31). Further
persons after a partial meniscectomy (24). work is necessary to establish a relationship or lack thereof
It is clear that more research, ideally in the form of between quadriceps weakness after ACL injury and frontal
randomized controlled trials, is needed to better understand plane loading.

148 Exercise and Sport Sciences Reviews www.acsm-essr.org

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 The quadriceps musculature also supports sagittal plane hamstrings) contraction, rather than from a restriction in
loads during static and dynamic conditions (11,16). ACL- joint motion. Furthermore, early signs of OA were noted in
deficient or ACL-reconstructed patients with weak quad- rabbits after induced quadriceps muscle weakness that led to
riceps musculature display diminished external knee flexion a reduction in ground reaction forces (6).
moments and reduced knee flexion angles (11,25). Further- It seems from the data available that alterations (increases
more, the external knee flexion moments in ACL-deficient and/or decreases) in loading patterns across a joint can result
limbs seem to be related to quadriceps strength, with weaker in OA. As quadriceps muscle weakness is indeed capable of
quadriceps muscles being associated with smaller external changing joint loads, it seems plausible that it may contrib-
flexion moments (25). We have shown in our laboratory that ute to the pathogenesis of OA.
isolated quadriceps weakness, induced by an experimental
knee effusion, is capable of altering dynamic loading ARTHROGENIC MUSCLE INHIBITION: AN
conditions as evidenced by increased vertical ground reac- EXPLANATION FOR QUADRICEPS WEAKNESS
tion forces and smaller external knee flexion moments and
flexion angles (16). These findings have been suggested to Muscle weakness associated with ACL injury is typically
preclude the knee from adequately absorbing shock during attributed to disuse atrophy; however, this is unlikely due to the
gait and, therefore, may cause greater dynamic loads to be near instantaneous presentation of the weakness and the failure
placed on the articular cartilage, resulting in progressive of the muscle to recover after undergoing rigorous strengthen-
degeneration. Although no direct link has been made ing exercises as a part of postoperative rehabilitation. In recent
between sagittal plane loading and the development of years, arthrogenic muscle inhibition (AMI), the inability to
OA, it seems plausible that altered loading in this plane completely voluntarily activate a muscle, has been implicated
could result in degenerative changes to the knee. as a potential factor contributing to the quadriceps weakness
According to Andriacchi and colleagues (1), initiation of associated with ACL rupture. AMI is an ongoing reflex
OA is related to shifts in ambulatory loading applied to inhibition that results in a diminished motor drive to muscles
articular cartilage, whereby regions of cartilage that were not surrounding an injured joint (8) and is considered to be a
previously loaded become newly loaded or areas that were natural response designed to protect the injured knee by
loaded become unloaded. These newly loaded or unloaded discouraging its use, likely helping to prevent painful and
areas are unable to adapt to the new mechanical environ- potentially detrimental movements. This protective mecha-
ment, and thus, the development of OA begins. Although nism comes at a high cost; however, as it results in weakness
not in line with traditional thought, the premise suggested by and wasting of the nearby musculature, which often cannot be
Andriacchi et al. (1), that unloading joint tissue can be overcome in the traditional rehabilitation process.
detrimental, is supported by research. Immobilizing the hind AMI has been identified almost universally in studies
limb of a dog results in degradation of articular cartilage (e.g., examining quadriceps activation in patients after ACL
cartilage thinning, decreased proteoglycan synthesis and rupture, although the magnitude of the reported activation
concentration). Data by Palmoski et al. (20) suggest that deficits vary, ranging anywhere from 8% to 45%. Data have
cartilage degeneration that results from immobilization is begun to emerge providing evidence that AMI presents
primarily the result of a lack of normal muscle (quadriceps/ bilaterally after unilateral ACL rupture, with the degree of

Figure 1. Percent voluntary activation before anterior cruciate ligament (ACL) reconstruction and 2 yr after reconstruction. Results demonstrate that
ACL reconstruction and rehabilitation are capable of improving quadriceps activation (i.e., decreasing arthrogenic muscle inhibition (AMI)) but are unable
to restore it to 100%. (Data from Urbach D, Nebelung W, Becker R, Awiszus F. Effects of reconstruction of the anterior cruciate ligament on voluntary
activation of quadriceps femoris. A prospective twitch interpolation study. J. Bone Joint Surg. 2001; 83-B:1104Y10.)

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inhibition in the uninjured limb falling between 7% and work by Konishi et al. (10) suggests that AMI is the result
26%. (34) Surprisingly, the quadriceps activation failure in of dysfunction in the gamma loop (Fig. 3). It is most
the contralateral limb in some cases is reported to be equiv- likely that AMI results from a combination of mechanisms
alent to that present in the injured limb. ACL reconstruction including those described above as well as others currently
(34) and subsequent rehabilitation (9,34) seem capable of unknown.
diminishing the amount of quadriceps AMI, but are not
capable of preventing it from persisting for several years after
surgery (34). Urbach and colleagues (34), for example, found THEORETICAL MODEL FOR HOW AMI INITIATES OA
that, at 2 yr after reconstruction, the quadriceps muscles
on the affected and unaffected legs were inhibited by It is our premise that ACL injury results in AMI that
approximately 15% and 16%, respectively (Fig. 1). causes lingering quadriceps weakness that is not overcome
It should be noted that in addition to inhibition, a during traditional rehabilitation and initiates processes
reflexively mediated facilitation of different muscles may ultimately resulting in knee joint degeneration. After ACL
accompany ACL injury. Specifically, there may be a facili- injury, altered afferent feedback resulting from damage to
tation of the knee and ankle flexors in addition to the joint mechanoreceptors, pain, inflammation, and effusion
quadriceps inhibition. This has not been well studied in an leads to inhibition of the quadriceps alpha motoneuron pool
ACL injury model, but using effusion (18,19) or animal (22) or AMI. AMI limits the ability to voluntarily activate the
models, facilitation of the hamstrings and soleus musculature quadriceps musculature, which in turns creates weakness,
has been noted. No available evidence exists to suggest wasting, and altered dynamic neuromuscular activation
whether a reflexive inhibition or facilitation occurs in the patterns. The impaired quadriceps activation alters lower
musculature acting at the hip (7), although hip muscle extremity kinematics and kinetics causing load distribution
strength has been shown to be diminished after ACL injury
and might be attributable to AMI. Thus, while this article
attempts to establish a potential relationship between quad-
riceps inhibition and OA, it should be considered that muscle
dysfunction occurring throughout the lower extremity kinetic
chain might contribute to knee joint degeneration.

MECHANISMS OF AMI

As AMI may contribute to the onset of posttrau-

matic OA, it seems critical to develop an understanding
of the peripheral and central mechanisms that cause it so
that treatment strategies directed at targeting AMI can be
formulated.
The primary function of the ACL is to serve as a me-
chanical restraint to tibiofemoral movement; however, it
also has a significant function as a neural organ. The
mechanoreceptors populated within the ACL provide
sensory information from the knee joint to the spinal
cord and supraspinal centers regarding joint movement,
position, and loads. After an ACL rupture, abnormal
afferent information is transmitted to the central nervous
system ultimately resulting in a decrease in the excitability of Figure 2. Simplified schematic demonstrating how arthrogenic muscle
the quadriceps alpha motoneuron pool (i.e., AMI). inhibition (AMI) may result from pre-synaptic and recurrent (postsynaptic)
This altered afferent input may stem from stimulation inhibition. Abnormal afference (dashed arrows) is conveyed from
mechanoreceptors or nociceptors about the knee joint to the spinal
of mechanoreceptors, via joint effusion or excessive move- neurons (e.g., motoneurons (MN) and interneurons (IN)). For presynaptic
ment, nociceptors, as a result of pain or excessive move- inhibition, afferent information transmitted via Ia afferents is modulated
ment, as well as the loss of joint mechanoreceptors from before synapsing on the quadriceps alpha MN. So, before the action
within the ruptured ligament. potential reaches the alpha MN, GABAergic IN, thought to control
Although it is well accepted that afferent input is involved &
presynaptic inhibition, make an inhibitory synapse ( ) on the Ia afferent
terminal, either reducing the amplitude of the incoming action potentials
in AMI (8), little is known about the central nervous system or blocking the action potential from arriving at the primary afferent
pathways that modulate the afference from the periphery terminal, prohibiting the affected alpha MN from firing. With recurrent
eventually causing inhibition of the alpha motoneurons and inhibition, the action potentials generated from the knee joint receptors
the decreased motor output seen in the quadriceps after ACL reach the alpha MN resulting in depolarization. The action potential then
injury. Data from our laboratory suggest that quadriceps travels down the motor axon and activates the recurrent collateral axon
(dashed line) and the Renshaw cell it connects to, causing an inhibitory
inhibition, associated with a joint effusion, originates from signal to be sent from the Renshaw cell, to the alpha MN, to the muscle.
both presynaptic and postsynaptic spinal mechanisms directly The supraspinal centers may also have a direct impact on the alpha MN.
affecting alpha motoneurons (18,19) (Fig. 2), whereas ACL indicates anterior cruciate ligament.

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 reason that ACL rehabilitation protocols are ineffective in
recovering quadriceps strength. Available data support this
idea. Hurley and colleagues (9) found that patients with a
large magnitude of inhibition (30%Y45%) respond poorly to
standard ACL rehabilitation, displaying minimal improve-
ments in knee extensor strength and muscle inhibition.
Hurley and colleagues (9) also noted that patients with
greater amounts of joint damage (e.g., ACL rupture plus
meniscus tears, ruptured collateral ligaments V the typical
ACL injured patient) had a greater magnitude of quadriceps
inhibition compared with patients with isolated ACL injury.
Together, these results suggest that patients with extensive
damage to the knee will display greater amounts of inhibition
initially and will likely not respond well to typical ACL
rehabilitation programs.

Treatment Approaches to Combat AMI

Rehabilitation after ACL injury and reconstruction
requires clinicians to appreciate the involvement of AMI in
causing quadriceps weakness and use treatment strategies
directed at removing inhibition rather than just improving
Figure 3. Schematic illustrating how arthrogenic muscle inhibition strength. Furthermore, an assessment of the magnitude of
(AMI) may result from gamma loop dysfunction (10). Dashed lines from quadriceps AMI should be made, if possible, as more
anterior cruciate ligament (ACL) to alpha and gamma motoneurons (MN) aggressive rehabilitation strategies may be necessary to
represent attenuation of afferent feedback from ACL. Attenuated remove AMI and restore quadriceps strength in patients
afferent feedback from the ACL results in a decline of gamma-motor
neuron activation (dashed line from gamma MN to intrafusal muscle with greater amounts of inhibition.
fiber). Reduced gamma motor neuron activation results in attenuation of Currently, no treatment approach has been shown to
Ia afferents (dotted line) as a result of the reduced sensitivity of muscle universally remove quadriceps AMI associated with ACL
spindles. As the Ia afferents are necessary for the recruitment of high- injury, although several interventions seem promising. For
threshold motor units (HTMU), recruitment of such units are hindered.
example, transcutaneous electrical nerve stimulation
Low-threshold motor units (LTMU) recruitment remains unaffected,
recruited even when Ia afferent feedback is attenuated. [Adapted from (TENS) has been shown to modulate presynaptic inhibition,
Konishi Y, Fukubayashi T, Takeshita D. Mechanism of quadriceps femoris which we have shown (19) is involved in the genesis of
muscle weakness in patients with anterior cruciate ligament reconstruc- AMI. Application of TENS while patients complete active
tion. Scand. J. Med. Sci. Sports 2002; 12:371Y5. Copyright * 2002 exercises may allow for more motoneurons to be recruited
Wiley-Blackwell. Used with permission].
during the voluntary contraction promoting more complete
restoration of strength. Other interventions aimed at remov-
across the knee to be affected. Cartilage begins experiencing ing inhibition such as cryotherapy also have been proposed
uncharacteristic stress because of the newly developed and maybe effective in removing AMI (17). Rather than
neuromechanical strategy, which will lead to pain, disability, turning off the inhibitory processes causing AMI, another
degeneration, and ultimately early onset of OA (Fig. 4). approach to combat its effects would be to directly activate
the motor axons that are inhibited. Neuromuscular electrical
stimulation should be effective in this regard and has been
IMPLICATIONS OF AMI FOR ACL REHABILITATION shown to diminish AMI in an ACL population (30).

Current ACL rehabilitation programs focus on restoring

quadriceps strength by means of active exercise. Although WHERE DO WE GO FROM HERE: ADVANCING THE
inclusion of exercise in postoperative strengthening programs HYPOTHESIS
is absolutely warranted and appropriate, these measures alone
are unlikely to result in patients resuming full quadriceps Scientific advances related to the mechanism of post-
activation. Clinicians must keep in mind the mechanisms traumatic OA are desperately needed if we are to prevent its
leading to the quadriceps strength deficits when designing onset and progression. At this point in time, very little
treatment strategies. Based on the literature presented above, concrete evidence exists as to how ACL injury results in
AMI seems to be present after ACL injury and subsequent joint degeneration, despite the fact that many hypotheses
reconstruction, and its removal/reversal must be a rehabil- outlining potential mechanistic contributors exist (12).
itation goal. As AMI prevents full voluntary activation of Several research endeavors must be undertaken to advance
the quadriceps, the use of traditional rehabilitation exercises, the hypothesis that quadriceps AMI associated with ACL
whereby patients voluntarily activate their muscles, will injury leads to the early onset of OA. Below, we provide
prove to be ineffective in restoring muscle strength. It is future research directions that may aid in advancing the
our contention that failure to directly target AMI is the premise put forth in the current article:

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 SUMMARY

AMI results in the quadriceps weakness associated with

ACL injury. We hypothesize that AMI is not overcome
during standard rehabilitation protocol and prohibits com-
plete restoration of strength. Although more evidence is still
needed, we further hypothesize that the lingering weakness
resulting from ineffective ACL rehabilitation alters loading
conditions about the knee and ultimately leads to post-
traumatic OA.

Acknowledgments
The authors would like recognize the work of other researchers that could
not be cited because of the reference limitations.

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Volume 37 c
Number 3 c
July 2009 Quadriceps and Posttraumatic Osteoarthritis 153

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