knee osteoarthritis_ muscle weakness, sensory dysfunction and exercise friendly)

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CME Information

CME Released: 11/30/2010; Valid for credit through 11/30/2011

Target Audience

This activity is intended for primary care clinicians, rheumatologists, orthopaedists, and other health professionals caring for patientsat risk for knee OA.

Goal

The goal of this activity is to describe the risk factors for knee OA and suitable exercise interventions for at-risk patients.

Learning Objectives

Upon completion of this activity, participants will be able to:

Describe the association of muscle weakness with risk for knee OA1.

Describe the association of afferent sensory dysfunction with risk for knee OA2.Describe suitable exercise training interventions for persons at risk for knee OA3.

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Author(s)

Ewa M. Roos, PhD

Professor; Leader of the Multi-Professional Research Unit for Musculoskeletal Function and Physiotherapy, University of Southern

Denmark, Odense, Denmark

Disclosure: Ewa M. Roos, PhD, has disclosed no relevant financial relationships.

Walter Herzog, PhD

Director, Human Performance Lab, University of Calgary; Canada Research Chair; Killam Fellow for Molecular and Cellular

Biomechanics, Calgary, Alberta, Canada

Disclosure: Walter Herzog, PhD, has disclosed no relevant financial relationships.

Joel A. Block, MD

Willard L. Wood MD Chair in Rheumatology; Professor of Medicine, Rheumatology, and Biochemistry; Director, Section of

Rheumatology, Rush Medical College, Chicago, Illinois


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From Nature Reviews Rheumatology

Abstract and Introduction

Lower-extremity muscle strength and afferent sensory dysfunction, such as reduced proprioceptive acuity, are potentially modifiable

putative risk factors for knee osteoarthritis (OA). Findings from current studies suggest that muscle weakness is a predictor of knee

OA onset, while there is conflicting evidence regarding the role of muscle weakness in OA progression. In contrast, the literature

suggests a role for afferent sensory dysfunction in OA progression but not necessarily in OA onset. The few pilot exercise studies

performed in patients who are at risk of incident OA indicate a possibility for achieving preventive structure or load modifications. In

contrast, large randomized controlled trials of patients with established OA have failed to demonstrate beneficial effects of

strengthening exercises. Subgroups of individuals who are at increased risk of knee OA (such as those with previous knee injuries)

are easily identified, and may benefit from exercise interventions to prevent or delay OA onset.

Disclosure: Joel A. Block, MD, has disclosed no relevant financial relationships.

Kim L. Bennell, PhD

Professor; Director, Centre for Health, Exercise and Sports Medicine, Department of Physiotherapy, University of Melbourne,

Melbourne, Australia; Australian Research Council Future Fellow

Disclosure: Kim L. Bennell, PhD, has disclosed no relevant financial relationships.

Editor(s)

Jenny Buckland

Chief Editor, Nature Reviews Rheumatology

Disclosure: Jenny Buckland has disclosed no relevant financial relationships.

CME Author(s)

Laurie Barclay, MD

Freelance writer and reviewer, Medscape, LLC

Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.

CME Reviewer( s)

Sarah Fleischman

CME Program Manager, Medscape, LLC

Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.

Laurie E. Scudder, DNP, NP

CME Accreditation Coordinator, Medscape, LLC

Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.

CME

Ewa M. Roos, PhD; Walter Herzog, PhD; Joel A. Block, MD; Kim L. Bennell, PhD

CME Released: 11/30/2010; Valid for credit through 11/30/2011


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Introduction

Patients with knee osteoarthritis (OA) seek medical care as a result of joint pain and functional loss. The structural hallmarks of OA

are cartilage loss (seen as joint-space narrowing on radiography) and bone changes (manifesting as osteophytes and subchondral

sclerosis). However, as cartilage is aneural, these structural changes are poorly related to the perceived joint pain. OA is also

associated with changes in other intra-articular and extra-articular joint structures, such as the synovium, menisci, ligaments, muscles

and the afferent sensory system. Research interest has increased into whether muscle function and the afferent sensory system are

risk factors for OA development and progression. Muscle function is more closely associated with joint pain than is joint-space

narrowing, and, as muscle function is easily modifiable, it is a potential therapeutic target in patients with this disease.

Muscles are critical for maintaining joint mobility, stability and function,[1] as they aid in shock absorption and proper force transfer

across the joint2 and provide dynamic stability to the normal and injured joint.[3-5] Muscle weakness has been associated with OA

onset and progression[6,7] by adversely affecting the ability to control joint movements accurately. [2,8] Muscle weakness is thought to

be one of the earliest and most frequent findings in patients with OA, [7] and is a better predictor of disability than either joint space

narrowing or pain.[7,9] While obesity, age, sex and joint injury have all been shown to be significant risk factors for OA,[10] the precise

nature by which they contribute to joint-degenerative changes remains speculative. Muscle weakness might be a unifying feature

explaining these risk factors (Figure 1), as muscle strength is lower in women than in men, is reduced following injury, decreases

with age and is lower relative to overall body mass in obese individuals. [11,12] However, while muscle weakness and atrophy

accompany OA,[13,14] it is not clear whether this weakness is caused by OA or precedes it, and, thus, whether it represents an

independent risk factor for disease onset and rate of progression. In this Review, we describe the roles of muscle weakness,

afferent sensory dysfunction and exercise in the development and progression of knee OA.

Figure 1. Joint Injury, Obesity, Age and Sex are Associated With Muscle Weakness and Af ferent Sensory Dysfunction.

Addressing muscle weakness and afferent sensory dysfunction with strength and neuromuscular training in patients either at

risk of or with knee OA can be evaluated using various techniques for assessing structural outcomes. Abbreviation: OA,

osteoarthritis.

Muscle Weakness

Relevance of Animal Models to Human OA


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Muscle weakness is easily studied in animal models of knee OA. Anterior cruciate ligament (ACL) transection is a frequently used

method to induce post-traumatic OA in a variety of animals. Following ACL loss, the quadriceps muscles atrophy and become

weaker.[15] In addition, forces across the knee are reduced during locomotion,[3] quadriceps activation is interrupted during stance

rather than being continuous (as found in the intact joint),[3] and hamstring muscles are activated at paw contact to prevent anterior

sliding of the tibia relative to the femur in cats,[3 as has also been observed in ACL-deficient dogs and humans.[16] Consequently,

load transfer across the joint is altered following ACL loss, and the associated instability of the knee, the loss of smooth control of

agonist and antagonist muscle interaction and the subsequent atrophy of the quadriceps muscles are thought to accelerate

degeneration of the joint.[1,17]

In an effort to study the effects of controlled muscle weakness on OA onset, Longino et al.[18] developed an animal model in which

quadriceps strength was reduced through injections of botulinum toxin A into the musculature. This technique induced muscle

weakness and atrophy, while locomotion remained relatively unaffected.[19] After 4 weeks of muscle weakness, retropatellar

cartilage degeneration, as evaluated histologically, was greater in the experimental rabbits compared to control rabbits, while the

tibiofemoral joint cartilage remained unaffected.[20] These results suggest that quadriceps weakness is an independent risk factor

for the onset of OA in the patellofemoral but not the tibiofemoral joints in rabbits.

The role of muscle weakness in OA onset and progression is less established in humans, as direct interventions to control muscle

weakness are difficult to perform. However, as observed in animal models, ACL loss in humans is associated with muscle

inhibition[21] and atrophy,[22] changes in activation patterns and gait kinematics,[23] and an increased risk of OA onset and

progression.[24] Furthermore, observational evidence links muscle weakness to increased radiographic joint disease and pain, [7,9]

and to an increased rate of OA development in elderly community-dwelling women. [25] Decreased isokinetic quadriceps strength in

women has also been found to be indicative of an increased rate of lower limb loading during locomotion,[2] and prolonged,

repetitive rapid loading of joints has been associated with both the initiation and progression of OA. [26,27] Although observational,

these studies support evidence obtained in animal models suggesting that muscle weakness is an independent risk factor for OA

and might provide a link between other risk factors such as age, sex, obesity and joint injury.

An Additional Risk Factor for Knee OA

Muscle weakness may be an important additional risk factor in groups of individuals who have a propensity for knee OA

development and progression. Obesity is a well characterized risk factor for the onset of knee OA,[10] and has been associated with

alterations in mechanical loading of the knee.[28] Furthermore, overweight individuals have a decreased percentage of lean body

mass, and thus reduced muscle strength relative to body size. Knee malalignment also increases knee load during walking (Figure

2a),[29] and can mediate the effects of other risk factors such as obesity.[30] While there is considerable evidence to support an

increased risk of OA progression in those with knee malalignment,[31,32]

the relationship between malalignment and OA onset isless clear and has given rise to contradictory findings.[33-36]

Figure 2. The Effects of Knee Malalignment on Knee Loading. a | Knee alignment can be categorized as genu valgum

(knock-knee), normal or genu varum (bow legged). A knock-knee will transfer more load to the outer compartment and a bow

knee will transfer more load to the inner compartment. b | Knee adduction moment represents the tendency to apply a varus


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torque on the knee, forcing the knee laterally and compressing the medial compartment during the stance phase of walking. It

is created because the ground reaction force vector passes medial to the knee joint centre. The higher the adduction moment,

the greater the load on the medial compartment.

Neuromuscular Training

Patients who have experienced previous knee injury have an increased risk of developing OA. Up to 50% of all people with an ACL

injuryeither isolated or combined with meniscal injury, with or without surgical reconstruction, or patients having meniscal surgery

only develop OA within 10-15 years.[37,38] Muscle function is rarely fully restored in ACL-deficient patients, regardless of whether

they undergo surgical reconstruction,[39,40] and so is considered a potential contributor to OA development. An exception to this

trend is described in a prospective cohort study of 100 ACL-deficient patients who were treated using supervised neuromuscular

training and activity level modification.[41] Neuromuscular training programs aim to improve sensorimotor control and achieve

compensatory functional stability. Functional, weight-bearing exercises are designed to resemble conditions of daily life, with some

more-strenuous activities also included. The main emphases are on the knee-over-foot position and the quality of the patient's

performance in each exercise, with the level and progression of training intensity guided by the patient's neuromuscular function. [42]

The patients in this study showed a remarkably low rate of OA onset (16%) and few meniscal injuries after 15 years' follow-up. [24]

They also displayed good muscle function at 3 and 15 years, with the injured leg performing at 95-103% of the capacity of the

non-injured contralateral leg in tests of functional performance and isometric strength.[41] Strong muscles and good neuromuscular

function may be more relevant in ACL-deficient and meniscectomized individuals compared to those with normal knees, as

increased muscle strength and neuromuscular control is needed to absorb the altered knee load seen is patients with these defects.[43,44]

Muscle Strengthening and Exercise Training

Protective Effects Against Onset of Knee OA. Evidence suggests that quadriceps weakness precedes the onset of knee OA,

thereby increasing the risk of disease developmentpossibly to a greater extent in women than in men. [25,45,46] The first

longitudinal study to investigate this connection, performed over a decade ago, found lower baseline quadriceps strength in women

who developed incident radiographic knee OA than in those who did not. [25] The most recent cohort study, which included over

2,000 individuals, showed that greater knee extensor strength protected against development of incident symptomatic knee OA in

both sexes.[46]

The implication of these longitudinal results is that lower-limb strengthening, particularly of the quadriceps, may be an effective

strategy to help prevent knee OA. Strength training programs usually involve non-weight-bearing exercises, which selectively train

isolated muscles. Weight-bearing exercises, which involve multiple joints, are also sometimes used. The emphasis is on the quantity

of muscle output, and the level of training and progression is guided by the patient's one-repetition maximum. [47] To date, the

effects of lower-limb strengthening on OA onset have only been investigated in one clinical trial.[48] A protective effect ofstrengthening on radiographic disease onset was not demonstrated; however, adherence was low, the drop-out rate was high and

even the trained group lost lower-extremity muscle strength over the 30-month experimental period. Further studies are needed to

clarify the effects of increased muscle strength on OA onset.

Radiographic changes associated with OA onset and progression take years to develop, which makes this a problematic outcome

measure in exercise studies. Pilot studies using medial-compartment knee loading and cartilage glycosaminoglycan content as

proxies for structural modification in at-risk knees and in early disease have shown positive effects of exercise on joint health, and

might represent more-feasible study end points.[49-51]

4 months of physiotherapist-supervised neuromuscular training has been shown to increase glycosaminoglycan content in the

weight-bearing cartilage of the medial knee compartment in middle-aged meniscectomized patients, indicating that neuromuscular

training may have a role in preventing deleterious structural modifications of cartilage in this group of high-risk individuals.[50]

Patientsin this study showed improved performance in functional tasks that require sensorimotor control, but did not improve quadriceps

strength or aerobic capacity,[52] lending further support to the importance of the neuromuscular component of the training program.

Protective Effects Against OA Progression? The relationship between quadriceps muscle strength and structural disease

progression in those with established knee OA is currently controversial. Two longitudinal cohort studies failed to find a significant

relationship between quadriceps strength and cartilage loss at the tibiofemoral joint,[53,54] while a controversial finding of increased

risk of disease progression in those with greater quadriceps strength and malaligned or lax knees[55] could not be replicated.[53]

Increased quadriceps strength might protect against cartilage degeneration in the lateral aspect of the patellofemoral

compartment,[53] suggesting that strength effects may depend upon the knee compartment involved.

Whether quadriceps-strengthening exercise could be a disease-modifying intervention is unclear, and further long-term studies are


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needed before recommendations can be made. In a randomized controlled trial, the effects of a 12-week quadriceps-strengthening

program were compared in patients with medial knee OA with or without varus malalignment.[56] Despite strength increases in both

patient groups, quadriceps strengthening did not significantly alter the knee adduction moment during walkingan indicator of

medial knee load[57] and, importantly, a biomechanical factor that is thought to predict disease progression (Figure 2b).[58] In the

limited number of published clinical trials that directly measured joint structure,[48,59,60] there was no significant effect of lower-limb

strengthening on radiographic OA progression; however, a trend towards a beneficial effect was noted in the only study where

disease progression was the primary outcome.[48]

While the emphasis in the studies described above has been on quadriceps muscle strength, findings from a longitudinal cohort

study by Chang et at.[61] introduced the premise that the hip abductors might influence knee OA disease progression. Participants

with a lower hip adduction moment during walking (presumed to indicate hip abductor weakness) demonstrated more-rapid knee OA

progression. Patients with knee OA seem to have substantial weakness of the hip muscles, [62] but a large clinical trial published in

2010 did not support a role for hip-muscle strengthening in providing structural benefits. [63] A 12-week hip abductor strength

program was associated with significant increases in hip muscle strength but no change in hip adduction and knee adduction

moments during walking.[63] While hip-muscle strengthening may not be beneficial for slowing progression of well-established

disease, it has been shown to relieve pain and improve function in patients with knee OA. [51,63,64] For symptomatic benefits, then, it

seems the emphasis should be on strength training of the whole lower extremity and not only the quadriceps.

Afferent Somatosensory Dysfunction

Symptomatic OA is preceded by a prolonged sub-clinical phase. As OA onset and progression are mediated by aberrant

biomechanical joint loading,[65] subtle biomechanical aberrations that persist for years or decades may have important structural

consequences. The maintenance of efficient responses to forces generated during normal activity requires both intact

somatosensory afferents and functional musculoskeletal effectors. The afferent system includes pain, temperature, soft touch,

proprioception and vibration, among others (Figure 3). Proprioception is a complex sensation derived from multiple inputs that

provide the conscious and subconscious perception of position and motion in space, and includes the perception of joint position

and movement, muscle force, stretching and body position, as well as the unconscious regulation of postural response to positional

perturbations. Aside f rom visual, vestibular and auditory inputs, proprioception depends on afferent receptors in the muscles,

ligaments, synovial capsule and skin.[66,67]

Figure 3. The afferent somatosensory system comprises the receptors, afferent neurons and central processing centers that

permit the detection of a diverse range of environmental sensory inputs, including the tactile sense (touch), proprioception,

temperature and nociception (pain). Proprioception, including the sense of position in space, underlies the ability to maintain

erect posture, control joint movements and respond to perturbations. Hence, subtle dysfunction of the somatosensory afferent

system may alter dynamic loading of joints and alter the ability to protect joint tissue during motion.

Role of Proprioception in OA

As with the assessment of any aspect of the somato-sensory system, testing of proprioceptive acuity may focus on any of its

multiple inputs, and at various levels in the nervous system. However, in musculoskeletal diseases, joint position sense, assessed


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by the ability to reproduce knee f lexion to fixed angles, and the threshold of perception of passive motion are most commonly

assessed.[68] Using these techniques, it has been established that proprioceptive acuity declines with normal aging, [69,70] and that

patients with knee OA have significantly worse proprioceptive capacities than age-matched, normal individuals.[68,70,71] Moreover,

evaluation of the canine ACL transection model of OA has demonstrated that afferent denervation, either at the dorsal root ganglion

or the ipsilateral peripheral nerves, dramatically accelerates the development of OA. [72,73] Interestingly, the model is dependent on

joint destabilization, as denervation without ligament transection does not induce degenerative changes.[72,73] These observations,

in addition to the role that afferent innervation has in normal ambulation and posture, suggest that somatosensory dysfunction,

especially proprioceptive acuity, may be pathophysiologically important in OA.

Proprioceptive Acuity in OA Onset and Progression

The difficulty of determining whether proprioception has a potential role in OA pathophysiologydespite the clearly reduced

proprioceptive acuity among OA patientsis that, as noted above, proprioceptive acuity also declines with normal aging, [69,70] and

aging is the most important risk factor for developing OA. Moreover, the relationship between proprioception and OA pain is

complex: early cross-sectional observational studies failed to demonstrate an association,[74,75] but more-recent prospective,

longitudinal evaluations found significant, though modest, relationships between baseline proprioceptive acuity and the trajectory of

pain over time[76] and between improved proprioceptive acuity and pain palliation with exercise intervention.[77] Felson et al.[76]

confirmed the association between proprioceptive deficits (assessed by reproduction of knee flexion position) and knee pain, but

failed to identify a significant association with incident knee OA during 3 years of follow-up. Despite the short study duration relative

to the years of subclinical degeneration that often predate clinical OA, these findings do not support a clinically significant role for

proprioceptive deficits in the development of human OA.[78]

Important somatosensory deficits may be undetectable by conventional methodologies, as the high measurement errors yield large

minimal detectable dif ferences among OA patients.[79] Also, perceived pain, adherence to study protocol and distraction can

confound results. Alternative testing strategies with improved precision, such as vibratory perception threshold (vPT), permit

detection of subtle yet potentially important somato-sensory deficits. Proprioceptive and vibratory pathways are co-localized in the

dorsal columns,[80] but vPT assessment is not confounded by pain, mobility or strict subject attention,[81] suggesting that vPT is a

preferable readout to conventional proprioceptive measurements. Reports have confirmed the presence of significant vPT def icits

in patients with knee OA, similar to the observed deficits in proprioception; [81] however, unlike proprioception, VPT can be tested

throughout the body, and vibratory deficits have also been reported in patients with hip OA, thus implicating somatosensory deficits

as a more general component of the lower extremity OA phenotype. Furthermore, studies have shown diminished VPT in the hands

of patients with hip or knee OA[78] and impaired proprioception at the elbows in patients with knee OA,[82] suggesting that the

somatosensory dysfunction underlying lower extremity OA is systemic rather than local.

Conclusions

Findings from current studies suggest that muscle weakness is a predictor of knee OA onset, while evidence regarding the role of

muscle weakness in OA progression is conflicting. In contrast, the literature suggests a role for afferent sensory dysfunction in OA

progression but not necessarily in OA onset. The small number of published exercise studies involving structural or load

modification outcomes suggest that neuromuscular exercise may be beneficial, especially in patients who are already at risk of OA

or in those with early disease. Subgroups at increased risk of knee OA, including patients with prior knee injury, are easily identified

and may benefit from exercise interventions to delay OA onset.

Key Points

Muscle weakness is a predictor of knee osteoarthritis onsetAfferent sensory dysfunction is a predictor of osteoarthritis progression

Exercise training interventions should address both muscle weakness and afferent sensory dysfunction

Exercise regimens that aim to achieve modif ication of joint loading or cartilage structure seem to be more promising in at-risk

individuals or those with early disease

This article is a CME certified activity. To earn credit for this activity visit:http://www.medscape.org/viewarticle/733228

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Acknowledgments

L. Barclay, freelance writer and reviewer, is the author of and is solely responsible for the content of the learning objectives, questions and answers of theMedscapeCME-accredi ted continuing medical education activity associated with this article.

Reprint Address

Unit for Musculoskeletal Function and Physiotherapy, Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Campusvej 55,DK-5230 Odense, Denmark Ewa M. Roos, PhD [email protected]

Competing interests

The authors, the journal Chief Editor J. Buckland and the CME questions author L. Barclay declare no competing interests.

Nat Rev Rheumatol. 2010;6(12) 2010 Nature Publishing Group

This article is a CME certified activity. To earn credit for this activity visit:

http://www.medscape.org/viewarticle/733228


knee osteoarthritis_ muscle weakness, sensory dysfunction and exercise friendly)

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