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A Neuromuscular Mechanism of Posttraumatic Osteoarthritis Associated with ACL Injury

Palmieri-Smith, Riann M.1,2,3; Thomas, Abbey C.1

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Exercise and Sport Sciences Reviews: July 2009 - Volume 37 - Issue 3 - p 147-153
doi: 10.1097/JES.0b013e3181aa6669
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Tibiofemoral osteoarthritis (OA), the most common cause of disability in the United States, affects 30% of Americans older than 55 yr, yet little is known regarding the mechanistic contributors to this disease. In recent years, overwhelming evidence has emerged that experiencing an anterior cruciate ligament (ACL) rupture, as well as other knee joint injuries, increases the risk of developing knee OA (23). Furthermore, OA secondary to ACL injury tends to afflict a younger population. Current estimates indicate that rupturing the ACL leads to OA 5-20 yr after injury, "aging" the knee by approximately 30 yr (23). When considering these estimations and keeping in mind that ACL injury primarily affects teenagers and young adults, this suggests that symptomatic OA may begin presenting in adults in their 20s and 30s, a time when high demands are still placed on the joints for work and physical activity. The early onset of OA after ACL injury presents a clinical conundrum, as treatment strategies used for older adults with idiopathic OA (e.g., joint replacement, restriction of activity) are not appropriate or acceptable for the younger patient. Thus, it is imperative that we, as 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 the disease.

Quadriceps weakness is ubiquitous after ACL rupture and is often persistent despite restitution of static stability through ACL reconstruction and aggressive rehabilitation (34). Although surgical intervention and subsequent rehabilitation are deemed successful in many cases, full quadriceps strength is often never achieved. In fact, quadriceps weakness can persist for years after injury and/or reconstruction (17). Lingering quadriceps weakness may be detrimental to knee joint tissues because of its importance as a shock attenuator and its function to help distribute loads across the knee. Quadriceps weakness results in loads being transmitted at higher rates and magnitudes up the lower limbs, and thus, maintaining strength of this muscle group is considered a vital neuromuscular protective mechanism. The inability of ACL patients to restore complete quadriceps strength may help explain the development of early-onset posttraumatic OA (32). In this article, we provide evidence supporting the hypothesis that quadriceps weakness may result in posttraumatic OA. Furthermore, we suggest a possible mechanism through which quadriceps weakness manifests after ACL injury/reconstruction. Finally, we provide suggestions for future research that will help prove or disprove the hypotheses put forward.


Quadriceps weakness is well accepted as a consequence of knee OA, but less accepted is the notion that it is directly responsible for the development and/or progression of the disease. Although available data in humans cannot prove that quadriceps weakness contributes to the onset of OA, the data do strongly suggest that quadriceps weakness may be a risk factor predisposing persons to develop idiopathic knee OA.

Initial evidence to support that quadriceps weakness is related to the onset of OA comes from a cross-sectional investigation that found quadriceps strength was a significant predictor of symptomatic idiopathic tibiofemoral OA (this was significant despite adjustments for age, sex, and body weight) (28). A prospective study conducted in 300 subjects confirmed the above-referenced findings (29). Quadriceps weakness relative to body weight was found to be a predictor for the occurrence of OA at a 30-month follow-up. Women who developed OA had 18% lower quadriceps strength, whereas men who developed OA had 15% lower quadriceps strength at baseline compared with those who did not develop OA. These findings were further supported by Baker et al. (2), who found using a large cross-sectional investigation that there was a strong relationship between quadriceps weakness and combined tibiofemoral and patellofemoral OA in both men and women and between quadriceps weakness and isolated patellofemoral and tibiofemoral OA in women. In a recent investigation examining 148 patients, the fewer number of straight leg raises performed, which would be related to quadriceps strength and endurance, was capable of predicting incident radiographic OA 5 yr later (odds ratio, 2.6) (33).

The idea that quadriceps weakness is capable of causing OA associated with ACL injury is interesting because it suggests that the joint degeneration can be prevented. At this point, no data are available to make a direct connection between the quadriceps strengthening after knee injury and the prevention or delay of OA. Furthermore, no evidence is available connecting quadriceps weakness after ACL rupture to OA. Our hypothesis is based on the literature in the idiopathic OA population, which suggests quadriceps weakness is related to knee OA. Thus, if there is a cause-and-effect relationship between quadriceps weakness and OA, it would be logical that restoring quadriceps strength will delay or prevent the onset of OA.

A recent randomized clinical trial that examined the effects of a 12-month quadriceps/hamstring strengthening or a range of motion (control) program on the incidence and progression of OA in older adults, in part, supports our hypothesis (13). Results demonstrated that persons in both groups actually lost strength for 30 months but that the subjects in the strength training group who had established knee OA at baseline displayed 37% less mean loss in joint space width, suggesting that thigh muscle strengthening may slow the rate of progression of knee OA. Contrary to these findings where strengthening seemed to be beneficial, the same study demonstrated that persons without established OA at baseline who participated in strength training were more likely to demonstrate joint space narrowing than those in the control group (34% vs 19%, respectively). However, the data were unable to demonstrate an association between quadriceps strength and joint space width, making it difficult to implicate strength training as the cause of the narrowing. Furthermore, there is evidence from other studies to suggest that strength training is not harmful to the osteoarthritic knee (5) and may be beneficial to articular cartilage in persons after a partial meniscectomy (24).

It is clear that more research, ideally in the form of randomized controlled trials, is needed to better understand the use of quadriceps strengthening to prevent the incidence and progression of OA.


Muscle forces are a major determinant of how loads are distributed across a joint's surface. Altering the muscle forces acting about the knee joint complex as a result of ACL injury will ultimately affect loading conditions. Because OA is considered to be a mechanically driven disease, altered joint loads are likely a requirement for its development and progression.

Traditional thought surrounding what biomechanical/neuromuscular alterations possibly result in OA is centered on muscle weakness leading to increased joint loading and eventually OA. Intuitively, this makes sense, as the quadriceps has a protective function serving as a shock absorber capable of dampening loads during activity. Failure to adequately absorb energy about the knee can cause greater dynamic loads to be placed on the articular cartilage, resulting in progressive degeneration. Radin et al. (21) have shown that repetitive impulse loading in the hind limb of rabbits results in rapid degeneration of articular cartilage when the load was delivered quickly, even if the load was not excessive. However, if a load of a similar or a greater magnitude was provided gradually, articular surfaces remained normal as the muscles (primarily the quadriceps) were able to absorb the energy via eccentric contraction. Mikesky et al. (14) found that the rate of loading during walking among women with higher quadriceps strength was significantly slower when compared with those with lower quadriceps strength. These data support the hypothesis that quadriceps weakness can overload the knee joint and seems to be capable of causing joint degeneration.

As the vast majority of OA associated with ACL injury seems to afflict the medial tibiofemoral compartment, loading in the frontal plane would seem to be critical to the onset of posttraumatic OA. Although the quadriceps musculature has only a small moment arm to render it capable of controlling adduction/abduction loading, it still is important in this regard. Quadriceps and hamstring cocontraction has been shown to provide the majority of support for the knee adduction moment during walking (27) and is also vital for frontal plane stabilization during sporting tasks.

Larger than normal external knee adduction moments, which are indicative of greater joint loading in the medial compartment, have been associated with the incidence (3), severity (26), and the progression (15) of tibiofemoral OA. ACL-reconstructed patients display larger-than-expected adduction moments during gait walking (4), although the relationship between quadriceps weakness and the adduction moment in this population is unknown. Recent evidence, however, has emerged in postmeniscectomy patients, a population at risk for posttraumatic OA, demonstrating that patients with weaker quadriceps had higher knee adduction moments than those with stronger quadriceps (31). Further work is necessary to establish a relationship or lack thereof between quadriceps weakness after ACL injury and frontal plane loading.

The quadriceps musculature also supports sagittal plane loads during static and dynamic conditions (11,16). ACL-deficient or ACL-reconstructed patients with weak quadriceps musculature display diminished external knee flexion moments and reduced knee flexion angles (11,25). Furthermore, the external knee flexion moments in ACL-deficient limbs seem to be related to quadriceps strength, with weaker quadriceps muscles being associated with smaller external flexion moments (25). We have shown in our laboratory that isolated quadriceps weakness, induced by an experimental knee effusion, is capable of altering dynamic loading conditions as evidenced by increased vertical ground reaction forces and smaller external knee flexion moments and flexion angles (16). These findings have been suggested to preclude the knee from adequately absorbing shock during gait and, therefore, may cause greater dynamic loads to be placed on the articular cartilage, resulting in progressive degeneration. Although no direct link has been made between sagittal plane loading and the development of OA, it seems plausible that altered loading in this plane could result in degenerative changes to the knee.

According to Andriacchi and colleagues (1), initiation of OA is related to shifts in ambulatory loading applied to articular cartilage, whereby regions of cartilage that were not previously loaded become newly loaded or areas that were loaded become unloaded. These newly loaded or unloaded areas are unable to adapt to the new mechanical environment, and thus, the development of OA begins. Although not in line with traditional thought, the premise suggested by Andriacchi et al. (1), that unloading joint tissue can be detrimental, is supported by research. Immobilizing the hind limb of a dog results in degradation of articular cartilage (e.g., cartilage thinning, decreased proteoglycan synthesis and concentration). Data by Palmoski et al. (20) suggest that cartilage degeneration that results from immobilization is primarily the result of a lack of normal muscle (quadriceps/hamstrings) contraction, rather than from a restriction in joint motion. Furthermore, early signs of OA were noted in rabbits after induced quadriceps muscle weakness that led to a reduction in ground reaction forces (6).

It seems from the data available that alterations (increases and/or decreases) in loading patterns across a joint can result in OA. As quadriceps muscle weakness is indeed capable of changing joint loads, it seems plausible that it may contribute to the pathogenesis of OA.


Muscle weakness associated with ACL injury is typically attributed to disuse atrophy; however, this is unlikely due to the near instantaneous presentation of the weakness and the failure of the muscle to recover after undergoing rigorous strengthening exercises as a part of postoperative rehabilitation. In recent years, arthrogenic muscle inhibition (AMI), the inability to completely voluntarily activate a muscle, has been implicated as a potential factor contributing to the quadriceps weakness associated with ACL rupture. AMI is an ongoing reflex inhibition that results in a diminished motor drive to muscles surrounding an injured joint (8) and is considered to be a natural response designed to protect the injured knee by discouraging its use, likely helping to prevent painful and potentially detrimental movements. This protective mechanism comes at a high cost; however, as it results in weakness and wasting of the nearby musculature, which often cannot be overcome in the traditional rehabilitation process.

AMI has been identified almost universally in studies examining quadriceps activation in patients after ACL rupture, although the magnitude of the reported activation deficits vary, ranging anywhere from 8% to 45%. Data have begun to emerge providing evidence that AMI presents bilaterally after unilateral ACL rupture, with the degree of inhibition in the uninjured limb falling between 7% and 26%. (34) Surprisingly, the quadriceps activation failure in the contralateral limb in some cases is reported to be equivalent to that present in the injured limb. ACL reconstruction (34) and subsequent rehabilitation (9,34) seem capable of 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 that, at 2 yr after reconstruction, the quadriceps muscles on the affected and unaffected legs were inhibited by approximately 15% and 16%, respectively (Fig. 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:1104-10.)

It should be noted that in addition to inhibition, a reflexively mediated facilitation of different muscles may accompany ACL injury. Specifically, there may be a facilitation of the knee and ankle flexors in addition to the quadriceps inhibition. This has not been well studied in an ACL injury model, but using effusion (18,19) or animal (22) models, facilitation of the hamstrings and soleus musculature has been noted. No available evidence exists to suggest whether a reflexive inhibition or facilitation occurs in the musculature acting at the hip (7), although hip muscle 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 quadriceps inhibition and OA, it should be considered that muscle dysfunction occurring throughout the lower extremity kinetic chain might contribute to knee joint degeneration.


As AMI may contribute to the onset of posttraumatic 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 mechanical 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 the quadriceps alpha motoneuron pool (i.e., AMI). This altered afferent input may stem from stimulation of mechanoreceptors, via joint effusion or excessive movement, nociceptors, as a result of pain or excessive movement, as well as the loss of joint mechanoreceptors from within the ruptured ligament.

Although it is well accepted that afferent input is involved in AMI (8), little is known about the central nervous system pathways that modulate the afference from the periphery eventually causing inhibition of the alpha motoneurons and the decreased motor output seen in the quadriceps after ACL injury. Data from our laboratory suggest that quadriceps inhibition, associated with a joint effusion, originates from both presynaptic and postsynaptic spinal mechanisms directly affecting alpha motoneurons (18,19) (Fig. 2), whereas work by Konishi et al. (10) suggests that AMI is the result of dysfunction in the gamma loop (Fig. 3). It is most likely that AMI results from a combination of mechanisms including those described above as well as others currently unknown.

Simplified schematic demonstrating how arthrogenic muscle inhibition (AMI) may result from pre-synaptic and recurrent (postsynaptic) inhibition. Abnormal afference (dashed arrows) is conveyed from mechanoreceptors or nociceptors about the knee joint to the spinal neurons (e.g., motoneurons (MN) and interneurons (IN)). For presynaptic inhibition, afferent information transmitted via Ia afferents is modulated before synapsing on the quadriceps alpha MN. So, before the action potential reaches the alpha MN, GABAergic IN, thought to control presynaptic inhibition, make an inhibitory synapse (•) on the Ia afferent terminal, either reducing the amplitude of the incoming action potentials or blocking the action potential from arriving at the primary afferent terminal, prohibiting the affected alpha MN from firing. With recurrent inhibition, the action potentials generated from the knee joint receptors reach the alpha MN resulting in depolarization. The action potential then travels down the motor axon and activates the recurrent collateral axon (dashed line) and the Renshaw cell it connects to, causing an inhibitory signal to be sent from the Renshaw cell, to the alpha MN, to the muscle. The supraspinal centers may also have a direct impact on the alpha MN. ACL indicates anterior cruciate ligament.
Schematic illustrating how arthrogenic muscle inhibition (AMI) may result from gamma loop dysfunction (10). Dashed lines from anterior cruciate ligament (ACL) to alpha and gamma motoneurons (MN) represent attenuation of afferent feedback from ACL. Attenuated afferent feedback from the ACL results in a decline of gamma-motor neuron activation (dashed line from gamma MN to intrafusal muscle fiber). Reduced gamma motor neuron activation results in attenuation of Ia afferents (dotted line) as a result of the reduced sensitivity of muscle spindles. As the Ia afferents are necessary for the recruitment of high-threshold motor units (HTMU), recruitment of such units are hindered. Low-threshold motor units (LTMU) recruitment remains unaffected, recruited even when Ia afferent feedback is attenuated. [Adapted from Konishi Y, Fukubayashi T, Takeshita D. Mechanism of quadriceps femoris muscle weakness in patients with anterior cruciate ligament reconstruction. Scand. J. Med. Sci. Sports 2002; 12:371-5. Copyright © 2002 Wiley-Blackwell. Used with permission].


It is our premise that ACL injury results in AMI that causes lingering quadriceps weakness that is not overcome during traditional rehabilitation and initiates processes ultimately resulting in knee joint degeneration. After ACL injury, altered afferent feedback resulting from damage to joint mechanoreceptors, pain, inflammation, and effusion leads to inhibition of the quadriceps alpha motoneuron pool or AMI. AMI limits the ability to voluntarily activate the quadriceps musculature, which in turns creates weakness, wasting, and altered dynamic neuromuscular activation patterns. The impaired quadriceps activation alters lower extremity kinematics and kinetics causing load distribution across the knee to be affected. Cartilage begins experiencing uncharacteristic stress because of the newly developed neuromechanical strategy, which will lead to pain, disability, degeneration, and ultimately early onset of OA (Fig. 4).

Simplified schematic illustrating our hypothesis of how arthrogenic muscle inhibition (AMI) may lead to osteoarthritis (OA). After anterior cruciate ligament (ACL) injury, AMI afflicts the quadriceps musculature of the involved and uninvolved limbs. AMI leads to weakness, wasting, and altered neuromuscular activation strategies, which result in impaired movement strategies (e.g., changes in kinematics) and altered loading patterns (e.g., increases/decreases in loading or the rate of loading). These gross biomechanical changes will afflict the loading of the articular cartilage, either increasing the stress in areas not previously loaded or reducing/removing stress applied to previously loaded areas. These loading adaptations will lead to pain, disability, degeneration, and ultimately, joint failure.


Current ACL rehabilitation programs focus on restoring quadriceps strength by means of active exercise. Although inclusion of exercise in postoperative strengthening programs is absolutely warranted and appropriate, these measures alone are unlikely to result in patients resuming full quadriceps activation. Clinicians must keep in mind the mechanisms leading to the quadriceps strength deficits when designing treatment strategies. Based on the literature presented above, AMI seems to be present after ACL injury and subsequent reconstruction, and its removal/reversal must be a rehabilitation goal. As AMI prevents full voluntary activation of the quadriceps, the use of traditional rehabilitation exercises, whereby patients voluntarily activate their muscles, will prove to be ineffective in restoring muscle strength. It is our contention that failure to directly target AMI is the 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%-45%) respond poorly to standard ACL rehabilitation, displaying minimal improvements 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 - 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 strength. Furthermore, an assessment of the magnitude of quadriceps AMI should be made, if possible, as more aggressive rehabilitation strategies may be necessary to remove AMI and restore quadriceps strength in patients with greater amounts of inhibition.

Currently, no treatment approach has been shown to universally remove quadriceps AMI associated with ACL injury, although several interventions seem promising. For example, transcutaneous electrical nerve stimulation (TENS) has been shown to modulate presynaptic inhibition, which we have shown (19) is involved in the genesis of AMI. Application of TENS while patients complete active exercises may allow for more motoneurons to be recruited during the voluntary contraction promoting more complete restoration of strength. Other interventions aimed at removing inhibition such as cryotherapy also have been proposed and maybe effective in removing AMI (17). Rather than turning off the inhibitory processes causing AMI, another 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 shown to diminish AMI in an ACL population (30).


Scientific advances related to the mechanism of posttraumatic OA are desperately needed if we are to prevent its onset and progression. At this point in time, very little concrete evidence exists as to how ACL injury results in joint degeneration, despite the fact that many hypotheses outlining potential mechanistic contributors exist (12). Several research endeavors must be undertaken to advance the hypothesis that quadriceps AMI associated with ACL injury leads to the early onset of OA. Below, we provide future research directions that may aid in advancing the premise put forth in the current article:

  • Prospective, longitudinal studies examining the association between quadriceps AMI after ACL trauma and joint space width narrowing in both the tibiofemoral and patellofemoral joints. Furthermore, the association between quadriceps AMI and actual cartilage loss, as assessed by magnetic resonance imaging, are required.
  • Research identifying interventions capable of combating AMI are necessary so that randomized clinical trials can be performed. A longitudinal study, wherein one group is randomized to receive an intervention proven to combat AMI and a second group is randomized to receive standard ACL rehabilitation, should be conducted, and the participants should be followed to examine the development of cartilage loss over time.
  • Cross-sectional studies that examine whether joint contact patterns are different in persons with quadriceps weakness compared with matched controls. These descriptive studies seem warranted to ascertain whether quadriceps weakness is capable of altering subtle local joint kinematics (i.e., bony motion) before longitudinal studies in ACL patients are undertaken.
  • Modeling studies that compare if lower versus higher quadriceps forces lead to altered joint contact patterns and cartilage thinning.


AMI results in the quadriceps weakness associated with ACL injury. We hypothesize that AMI is not overcome during standard rehabilitation protocol and prohibits complete 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 posttraumatic OA.


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


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arthrogenic inhibition; muscle; knee injury; quadriceps; strength

©2009 The American College of Sports Medicine