Biomechanical Deviations During Level Walking Associated ...

Biomechanical Deviations During Level WalkingAssociated With Knee Osteoarthritis: A SystematicReview and Meta-AnalysisKATHRYN MILLS,1 MICHAEL A. HUNT,2 AND REED FERBER1

Objective. To identify which gait deviations are consistently associated with knee osteoarthritis (KOA) and how these areinfluenced by disease severity, the involved compartment, and sex.Methods. Five electronic databases and reference lists of publications were searched. Cross-sectional, observationalstudies comparing temporospatial variables, joint kinematics, and joint moments between individuals with KOA andhealthy controls or between KOA subgroups were considered for review. Only publications scoring >50% on a modifiedmethodology quality index were included. Because of the number of gait deviations examined, only biomechanicalvariables reported by >4 publications were further analyzed. Where possible, a meta-analysis was performed using effectsizes (ES) calculated from discrete variables.Results. In total, 41 publications examining 20 variables were included. The majority of consistent gait deviationsassociated with KOA were exhibited by those with severe disease in the temporospatial domain. Individuals with severeKOA exhibited greater stride duration than controls (ES 1.35 [95% confidence interval (95% CI) 1.03, 1.67]) and a decreasein cadence (ES �0.75 [95% CI �1.12, �0.39]) compared with controls. The evidence for kinematic and joint momentchange was primarily limited or conflicting. There was a lack of evidence for alterations in the external knee adductionmoment.Conclusion. Individuals with KOA exhibit a range of gait deviations compared with controls. Despite its common usagein KOA gait studies, we did not find consistent evidence that knee adduction moment differs between those with andwithout KOA or between disease severity levels. Further research examining the reasons for a lack of difference in manygait variables in those with knee OA is needed.

INTRODUCTION

Knee osteoarthritis (KOA) is a common, chronic joint dis-ease where alterations in gait biomechanics are frequentlyobserved. Disease characteristics such as joint pain andswelling as well as muscle dysfunction are potential fac-tors commonly cited as associated with these gait altera-tions (1,2). The large number of cross-sectional studiesinvestigating biomechanical changes during gait havedemonstrated that individuals with KOA adopt a wide

variety of patterns of locomotion depending on their dis-ease severity, sex, or which compartment is primarily af-fected (3–5). This diversity underlines the need for syn-thesis of evidence to inform clinicians which gaitalterations they can primarily expect their KOA patients toexhibit. To examine the type and magnitude of biome-chanical gait deviations associated with KOA during levelwalking, we reviewed cross-sectional observational stud-ies comparing individuals with KOA with matched orsimilar healthy controls. To examine the influence of dis-ease severity, the involved compartment, and sex on suchgait deviations, we reviewed cross-sectional studies com-paring differing KOA subgroups. Our aim was to identifywhich gait deviations are consistently associated withKOA.

MATERIALS AND METHODS

Literature search strategy. A literature search strategywas devised for electronic databases (Medline, CINAHL,SPORTDiscus, PubMed, and Embase) with no publication,

Dr. Mills’ work was supported by the Alberta InnovatesHealth Solutions Team in Osteoarthritis (award 200700596).

1Kathryn Mills, PhD, Reed Ferber, PhD, CAT(C), ATC:University of Calgary, Calgary, Alberta, Canada; 2MichaelA. Hunt, PhD: University of British Columbia, Vancouver,British Columbia, Canada.

Address correspondence to Reed Ferber, PhD, CAT(C),ATC, Faculties of Kinesiology and Nursing, University ofCalgary, 2500 University Drive NW, Calgary, Alberta, T2N1N4 Canada. E-mail: [email protected].

Submitted for publication October 24, 2012; accepted inrevised form March 20, 2013.

Arthritis Care & ResearchVol. 65, No. 10, October 2013, pp 1643–1665DOI 10.1002/acr.22015© 2013, American College of Rheumatology

ORIGINAL ARTICLE

1643

language, or date restrictions, with the last search con-ducted on June 10, 2012. The search strategy was as fol-lows (identical for all databases): 1) ‘knee osteoarthr*’ orgonarthr*, 2) gait or walking, 3) 1 and 2 and kinematics, 4)1 and 2 and kinetics, 5) 1 and 2 and load, 6) 1 and 2 andmechanics or biomechanics, 7) 6 and leg or lower limb,and 8) 6 and trunk. Titles and abstracts were screened inthe initial search, with the full text of publications meetingthe initial inclusion criteria retrieved for further screening.Reference lists of all publications considered for inclusionwere hand searched recursively until no additional eligi-ble publications were identified. One reviewer conductedthe literature search (KM) and 2 reviewers (KM and MAH)determined the final eligibility of the selected publica-tions.

Selection criteria. Cross-sectional, human-based obser-vational studies comparing level walking biomechanics ofindividuals with KOA with healthy controls or betweendiffering KOA subgroups (e.g., disease severity, the in-volved compartment, sex, etc.) were considered for inclu-sion. No restriction was placed on disease severity, sex, orthe involved compartment. Studies permitting partici-pants to walk with walking aids or including participantswith confirmed OA in lower extremity joints other thanthe knee or participants who had undergone total jointarthroplasty were excluded. Similarly, because biome-chanical changes in gait can occur as part of the normalaging process (6), comparisons between individuals withKOA and healthy controls where the average between-group age discrepancies exceeded 30 years were excluded.Studies were also excluded if biomechanical comparisonswere not the main focus or if they utilized mathematicalmodeling or 2-dimensional motion analysis. The lattercriterion was due to movement in the frontal plane being

strongly affected by alignment of the foot in the transverseplane (7).

To avoid bias that can be introduced through duplicatedata, all publications were juxtaposed for author names,affiliations, and participant characteristics. Where identi-cal authors, outcome variables, and exact participant num-ber, age, weight, and sex ratio occurred, the results ofpublications with the lower methodologic quality scorewere excluded from further analysis.

Methodology quality. Publications that met the inclu-sion criteria were assessed for methodologic bias by 2independent reviewers (KM and MAH), one of whom wasblinded to the author, title, affiliation, and journal. Be-cause only observational studies were assessed, a modifiedversion (8) of a quality index for nonrandomized trials (9)was used. This version contains 16 items (items 1–3, 5–7,10–12, 15, 16, 18, 20–22, and 25 of the original index)assessing reporting (items 1–3, 5–7, and 10), external va-lidity (items 11 and 12), and internal validity (bias andconfounding; items 15, 16, 18, 20–22, and 25). The mod-ified version does not include items related to the validityof the intervention (items 4, 8, 9, 13, 14, 17, 19, 23, 24, 26,and 27), but still includes items detailing the blinding ofobservers. The quality index awards a point for each item,with the exception of item 5, which awards 2 points for“yes.” For negative items or items unable to be deter-mined, no points are awarded. The maximum score for themodified index is 17 points. The agreement between re-viewers was assessed using a kappa statistic, referenced toHopkins’ criteria of very small (0 to 0.1), small (0.11 to0.3), moderate (0.31 to 0.5), high (0.51 to 0.7), very high(0.71 to 0.9), and almost perfect to perfect (0.91 to 1.0) (10).Disagreements were discussed at a consensus meeting.Publications scoring �50% on the quality index were ex-cluded from further analysis (11) (Table 1).

Data synthesis. One reviewer (KM) extracted groupmeans, SDs, and sample sizes directly from publicationsand all reviewers checked the extracted data. These datawere used to calculate point estimates of effect size (ES)and 95% confidence intervals (95% CIs; ES � mean dif-ference/pooled SD). ES magnitudes were interpreted basedon Hopkins’ criteria (12) as trivial (0 to 0.2), small (0.21 to0.6), moderate (0.61 to 1.2), and large (�1.2). Findingsfrom principle component or principal pattern analysiswere also extracted. When data were presented as themedian and range, the mean and variability were esti-mated using methods described by Hozo et al (13). Authorsof publications that did not provide data in an extractableform were contacted.

Based on the search strategy, biomechanical compari-sons were categorized as temporospatial variables, jointkinematics, or joint moments. Within these categories,comparisons were divided into those comparing KOA co-horts and healthy controls and those comparing differentKOA subgroups. KOA cohorts were further subdividedbased on varus malalignment and disease severity. Inclu-sion in the varus malalignment subgroup was based on theKOA group exhibiting a significantly greater mechanical

Significance & Innovations● This review presents the first systematic synthesis

of available literature for the purpose of identify-ing consistent temporospatial, kinematic, and jointmoment gait alterations exhibited by individualswith knee osteoarthritis.

● This review indicates that most consistent gait de-viations occur in people with more severe diseaseand that changes in the spatiotemporal character-istics of gait are common.

● A significant finding of this review is that the ex-ternal knee adduction moment is not consistentlyincreased in individuals with knee osteoarthritisregardless of their disease severity or lower ex-tremity alignment.

● This review highlights the need for a standardizedknee osteoarthritis classification system that en-compasses radiographic, clinical, and mechanicalalignment measures in order to facilitate furthercomparisons between studies.

1644 Mills et al

axis alignment (or other validated alignment measure)than controls. Disease severity was extracted directly frompublications based on Kellgren/Lawrence (K/L) grades.The criteria for data pooling were met when publicationsincluded a range of severities within a single KOA cohort

(i.e., general KOA) or when participants were the sameacross varus malalignment and disease severity. Compar-isons were also made between unilateral and bilateraldisease, medial and lateral compartment KOA, symptom-atic and asymptomatic individuals, and males and fe-

Table 1. Quality index*

Author, year (ref.)

Reporting item

Externalvalidity

itemInternal validity:

bias item

Internalvalidity:

confoundingitem

1 2 3 5† 6 7 10 11 12 15 16 18 20 21 22 25Total(17)

Astephen et al, 2008 (16) 1 1 1 2 1 1 0 0 0 0 1 0 1 0 0 0 9Baliunas et al, 2002 (41) 1 1 1 1 1 1 1 0 0 0 1 0 1 0 0 1 10Bejek et al, 2005 (31) 1 1 1 2 1 1 0 0 0 0 1 0 1 0 0 0 9Butler et al, 2011 (21) 1 1 1 1 1 1 1 0 0 0 1 1 1 0 0 1 11Chen et al, 2003 (17) 1 1 0 1 1 1 0 0 0 0 1 1 1 1 0 0 9Childs et al, 2004 (56) 1 1 1 2 1 1 1 0 0 0 1 1 0 0 0 0 10Creaby et al, 2012 (42) 1 1 1 2 1 1 1 0 0 0 1 1 1 1 0 1 13Deluzio and Astephen, 2007 (32) 1 1 1 0 1 1 1 0 0 0 1 1 1 0 0 0 9Gok et al, 2002 (38) 1 1 1 1 1 1 1 0 0 0 1 0 1 1 0 0 10Heiden et al, 2009 (22) 1 1 1 1 1 1 1 0 0 0 1 1 1 0 0 1 11Huang et al, 2008 (18) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 0 1 12Hubley-Kozey et al, 2006 (30) 1 1 1 2 1 1 1 0 0 0 1 1 1 1 0 0 12Hubley-Kozey et al, 2009 (26) 1 1 1 2 1 0 0 0 0 0 1 1 1 0 1 0 10Hunt et al, 2010 (19) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 0 1 12Hurwitz et al, 2002 (40) 1 1 1 2 1 0 1 0 0 0 1 1 1 0 0 1 11Kaufman et al, 2001 (45) 1 1 1 0 1 1 1 0 0 0 1 1 1 1 0 1 11Kean et al, 2012 (43) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 0 1 12Ko et al, 2011 (44) 1 1 1 0 1 0 1 0 0 0 1 1 1 1 1 1 11Krackow et al, 2011 (59) 1 1 1 1 1 1 1 0 0 0 1 1 1 0 0 1 11Landry et al, 2007 (34) 1 1 1 2 1 0 0 0 0 0 1 1 1 0 0 1 10Levinger et al, 2012 (23) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 0 1 12Lewek et al, 2004 (20) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 0 1 12Lewek et al, 2006 (29) 1 1 1 2 1 1 1 0 0 0 1 0 1 0 0 1 11Liikavainio et al, 2010 (60) 1 1 1 2 1 1 0 0 0 0 1 1 0 1 0 1 11Linley et al, 2010 (35) 1 1 1 2 1 1 1 0 0 0 1 0 1 1 0 0 11Manetta et al, 2002 (24) 1 1 1 1 1 1 1 0 0 0 1 1 1 1 0 0 11McGibbon and Krebs, 2002 (61) 1 1 1 0 1 1 0 0 0 0 1 1 1 0 0 1 9McKean et al, 2007 (36) 1 1 1 1 0 1 1 0 0 0 1 1 1 0 0 0 9Messier et al, 2005 (47) 1 1 1 1 1 1 1 0 0 0 1 1 1 0 0 1 11Mundermann et al, 2005 (33) 1 1 1 1 1 0 1 0 0 0 1 1 1 0 0 1 10Rudolph et al, 2007 (6) 1 1 1 1 1 1 1 0 0 0 1 1 1 0 0 1 11Rutherford et al, 2008 (25) 1 1 1 2 1 0 0 0 0 0 1 1 1 1 1 1 12Rutherford et al, 2011 (27) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 1 1 13Sahai et al, 2003 (46) 1 1 1 1 0 1 1 0 0 0 1 1 1 1 0 0 10Schmitt and Rudolph, 2007 (39) 1 1 1 2 1 1 1 0 0 0 1 1 1 1 0 0 12Sims et al, 2009 (4) 1 1 1 2 1 1 1 0 0 0 1 1 1 1 1 0 13Weidow et al, 2006 (5) 1 1 1 2 1 0 1 0 0 0 1 0 1 0 0 0 9Zeni and Higginson, 2009 (3) 1 1 1 2 1 1 1 0 0 0 1 1 1 0 0 1 12Zeni and Higginson, 2009 (37) 1 1 1 2 1 1 1 0 0 0 1 1 1 1 0 1 13Zeni et al, 2010 (28) 1 1 0 1 1 1 1 0 0 0 1 1 1 0 0 1 10Zeni and Higginson, 2011 (62) 1 1 1 2 1 1 1 0 0 0 1 1 1 1 0 1 13Frequency of “yes” 46 47 43 26 42 38 36 0 0 0 47 38 42 16 5 26Frequency of “unable to be

determined”0 0 0 17 0 0 0 47 47 47 0 6 3 21 39 5

Frequency of “no” 1 0 4 4 5 9 11 0 0 0 0 3 2 10 3 16

* Includes quality scores for publications that were subsequently excluded from further analysis.† This category was interpreted as the knee osteoarthritis diagnosis being clearly described with respect to radiographic severity, clinical severity, andmechanical alignment. If all 3 of the criteria were described, 2 points were awarded for “yes”; if 2 of the criteria were described, 1 point was awardedfor “partially.”

Biomechanical Changes Associated With Knee OA 1645

males. Data pooling for these further comparisons wasconducted only if the initial criteria of the same alignmentand severity were met.

Data pooling was performed in Cochrane Review Man-ager, version 5.1, using the ES in a fixed-effects model.Evidence of heterogeneity, or consistency, between pooledresults was assessed using the I2 index (14). Low, moder-ate, and high heterogeneity were assigned the thresholdsof 25%, 50%, and 75%, respectively (14). Because thisreview did not include randomized controlled trials, weadapted the levels of evidence proposed by van Tulder etal (15). Evidence of gait deviations associated with KOAwas interpreted as strong (large ES and low evidence ofheterogeneity), moderate (moderate ES and low evidence

of heterogeneity), limited (small ES with low heterogene-ity or moderate/large ES with moderate evidence of heter-ogeneity), conflicting (high evidence of heterogeneity), andno evidence (95% CI of ES crossed zero).

RESULTS

Search strategy. Forty-seven publications were re-trieved for consideration, and following quality assess-ment, 41 were eligible for review (Figure 1). Because thesepublications reported on 180 different biomechanical vari-ables, a further analysis only on variables that were re-

Figure 1. Flow chart of the study selection process. KOA � knee osteoarthritis.

1646 Mills et al

ported by �4 articles was conducted (Table 2). This re-duced the number of biomechanical variables to 20.

Methodologic quality. The initial agreement betweenreviewers in the present study was almost perfect (� �0.904) (10) and the reliability for individual items rangedfrom moderate (� � 0.483 for item 18) to perfect (items7–11 and 15). Consensus was reached for all items at theinitial discussion between the 2 reviewers, and the maxi-mum quality index score was 13 points, indicating publi-cations were generally of low to moderate methodologicquality.

Temporospatial variables. The temporospatial vari-ables examined were walking speed, stride length, strideduration, stance duration, and cadence. Twenty-sevenpublications examined differences in temporospatial vari-ables between KOA and comparators and 16 publicationsmade comparisons between KOA subgroups (Table 3 andFigure 2).

KOA versus controls. Data pooling was possible forwalking speed, stride length, stance duration, and cadence(Figure 2). The effect of KOA on these variables appearedto be dependent on disease severity. Strong evidence sug-gested that individuals with severe KOA exhibited greaterstride duration than controls (ES 1.35 [95% CI 1.03, 1.67],I2 � 19%) (3,16,17) and a moderate decrease in cadence(ES �0.75 [95% CI �1.12, �0.39], I2 � 0%) (3,5,17,18).There was conflicting evidence for deviations in walkingspeed and stride length associated with severe KOA. How-ever, this was most likely due to variations in ES magni-tude between pooled publications because most publica-tions showed a reduction in walking speed and stridelength.

Moderate evidence suggested that individuals withmoderate KOA and varus malalignment walked slowerthan controls (ES �0.87 [95% CI �1.23, �0.44], I2 � 0%)(6,19,20). For individuals with mild and moderate KOA aswell as those with severe KOA and varus malalignment,pooled data revealed conflicting evidence or a small ES.Interestingly, there was no evidence for walking speedalterations in general KOA cohorts compared with healthycontrols (21–24). Data from publications that did not meetthe criteria for pooling also indicated that the magnitude oftemporospatial gait deviations associated with KOA wasinfluenced by disease severity (3,18,19,25).

Between KOA subgroups. Data pooling between moder-ate and severe KOA subgroups was possible for walkingspeed, stride length, and stride duration. The pooled re-sults revealed moderate evidence that those with severeKOA exhibited longer stride duration (ES �0.99 [95% CI�1.32, �0.65], I2 � 0%) (3,16) and conflicting evidence ofreduced walking speed (ES �1.14 [95% CI �1.39, �0.89],I2 � 85%) (3,16,26–28) and stride length (ES �0.99 [95%CI �1.24, �0.74], I2 � 81%) (3,16,26,27) (Figure 2).

It was not possible to pool data for comparisons betweenmild and severe, unilateral and bilateral involvement, andmedial and lateral compartment subgroups. No consistenteffects were observed between any subgroups for walkingspeed, cadence, and stride length; however, Zeni and Hig-

ginson (3) reported a moderate reduction in stride durationin individuals with severe KOA compared with those withmoderate KOA during fast walking (Table 3).

Joint kinematics. Twenty-five publications reported ki-nematic alterations associated with KOA during gait. Lat-eral trunk lean, hip adduction, knee flexion at initial con-tact (IC), knee flexion (peak and excursion during loading,stance, and stride), knee range of motion, and knee exten-sion were included in this review. Twenty-eight publica-tions compared KOA kinematics with healthy controls,while 10 compared kinematics between KOA subgroups(Table 3 and Figure 3).

KOA versus controls. The criteria for data pooling weremet for comparisons investigating peak hip adduction,knee flexion at IC, knee flexion excursion during loading,and peak knee flexion. There was moderate evidence in-dicating that individuals with moderate KOA and varusmalalignment exhibited reduced knee flexion excursionduring loading (ES �1.12 [95% CI �1.59, �0.66], I2 � 0%)(6,20,29) and that normally aligned individuals with mod-erate KOA had reduced peak knee flexion (ES �0.63 [95%CI �0.92, �0.34], I2 � 0%) (16,30). Limited evidence sug-gested that general KOA cohorts also exhibited reducedknee flexion excursion during loading and increased flex-ion at IC compared with controls. Large pooled ES and ahigh evidence of heterogeneity were observed for peak hipadduction comparisons between individuals with severeKOA and controls, indicating conflicting evidence; how-ever, this was most likely due to variations in the magni-tude of effect between pooled publications.

The largest ES from nonpooled data indicating the great-est differences from healthy controls involved individualswith severe KOA (Table 3). Specifically, large reductionswere reported in peak hip adduction during stance (19),knee range of motion (31,32), and knee flexion (peak, ex-cursion, and during loading) (16,18,31). Contrasting re-sults were reported for knee extension, with Bejek et al(31) reporting large reductions at several different walkingspeeds between individuals with severe KOA and varusmalalignment and controls, while Mundermann et al (33)reported no differences. A large increase was reported inlateral trunk lean in individuals with severe KOA andvarus malalignment (19), whereas a moderate increase wasobserved in those with moderate KOA and varus malalign-ment. Multiple studies reported no difference in lateraltrunk lean angle between individuals with mild KOA andcontrols (19,34,35), and there was no difference found inknee motion between those with mild KOA and controls(34).

Between KOA subgroups. The criteria for pooling werenot met for any kinematic comparisons between KOA sub-groups. Nonpooled comparisons, however, were made be-tween mild, moderate, and severe KOA, medial and lateralcompartment involvement, males and females with KOA,and symptomatic and nonsymptomatic individuals (Table3). Significant differences were observed in lateral trunklean (19) and knee extension (33) between individualswith mild and severe KOA. Significant and large increasesin lateral trunk lean and knee flexion (peak and excur-


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1648 Mills et al

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kg/m

2

Gok

etal

,20

02(3

8)N

�13

,M

/F0/

13,

age

58�

11ye

ars,

hei

ght

1.57

�4.

7m

,w

eigh

t72

�12

kg

AC

Rcl

inic

alcr

iter

iaA

hlb

ack

grad

e:jo

int

nar

row

ing

(mil

dch

ange

s)

Med

ial

com

par

tmen

tM

ild

N�

13,

M/F

0/12

,ag

e57

�8

year

s,h

eigh

t1.

57�

7.2

m,

wei

ght

77�

12kg

Hei

den

etal

,20

09(2

2)N

�54

,M

/F24

/30,

age

65�

8ye

ars,

hei

ght

1.7

�0.

09m

,m

ass

81.4

�14

.2kg

KO

OS

and

SF

-36

Bil

ater

alO

AN

�30

,M

/F11

/19,

age

64�

6ye

ars,

hei

ght

1.7

�0.

09m

,m

ass

81.4

�14

.2kg

Hu

ang

etal

,20

08(1

8)M

ild

:n

�15

,M

/F6/

9,ag

e63

.1�

11.9

year

s,h

eigh

t1.

62�

0.06

m,

mas

s68

.4�

10.3

kgS

ever

e:n

�15

,M

/F2/

13,

age

63.1

�8.

2ye

ars,

hei

ght

1.56

�0.

09m

,m

ass

64�

8.5

kg

VA

San

dS

F-3

6M

ild

:m

ild

Sev

ere:

mod

erat

ean

dse

vere

Bil

ater

al:

mos

tsy

mp

tom

atic

knee

Med

ial

com

par

tmen

t

Mil

dS

ever

eN

�15

,M

/F6/

9,ag

e63

.2�

9.9

year

s,h

eigh

t1.

59�

0.08

m,

mas

s60

.5�

8.5

kg

Hu

bley

-Koz

eyet

al,

2006

(30)

N�

40,

M/F

29/1

1,ag

e58

.9�

8.07

year

s,B

MI

29.9

4�

4.86

kg/m

2

WO

MA

C,

SF

-36,

clin

ical

exam

inat

ion

Mil

dto

mod

erat

eU

nil

ater

ald

isea

seM

oder

ate

N�

38,

M/F

17/2

1,ag

e51

.08

�9.

99ye

ars,

BM

I24

.74

�4.

25kg

/m2

Hu

bley

-Koz

eyet

al,

2009

(26)

Mod

erat

e:n

�56

,ag

e58

.0�

8.7

year

s,B

MI

30.8

�5.

5kg

/m2

Sev

ere:

n�

48,

age

63.7

�8.

2ye

ars,

BM

I31

.8�

5.3

kg/m

2

Cli

nic

alex

amin

atio

nS

ever

egr

oup

sch

edu

led

for

tota

ljo

int

arth

rop

last

y

Mod

erat

e:m

oder

ate

Sev

ere:

seve

re

Pre

dom

inan

tly

med

ial

com

par

tmen

t

Mod

erat

eS

ever

eN

�63

,ag

e49

.2�

9.7

year

s,B

MI

25.1

�4.

2kg

/m2

Hu

nt

etal

,20

10(1

9)M

ild

:n

�25

,M

/F10

/15,

age

61.2

�7.

7ye

ars,

hei

ght

1.65

�0.

08m

,m

ass

73.7

�14

kgM

oder

ate:

n�

25,

M/F

14/1

1,ag

e63

.6�

8.4

year

s,h

eigh

t1.

67�

0.08

m,

mas

s78

.4�

14.8

kgS

ever

e:n

�25

,M

/F13

/12,

age

68�

6.6

year

s,h

eigh

t1.

68�

0.09

m,

mas

s81

.7�

20.2

kg

WO

MA

C,

11-p

oin

tkn

eep

ain

scal

eA

llgr

oup

sva

rus

alig

ned

(i.e

.,�

182°

)

Mil

dM

oder

ate

Sev

ere

Med

ial

com

par

tmen

tM

ild

(var

us)

Mod

erat

e(v

aru

s)S

ever

e(v

aru

s)

N�

20,

M/F

5/15

,ag

e63

.2�

12.4

year

s,h

eigh

t1.

65�

0.06

m,

mas

s69

.3�

12.1

kg

(con

tin

ued

)


Tab

le2.

(Con

t’d

)

Au

thor

,ye

ar(r

ef.)

OA

coh

ort

Cli

nic

alm

easu

res

Rad

iogr

aph

icch

ange

s†O

Ad

escr

ipti

onS

ever

ity

Com

par

ator

coh

ort

Hu

rwit

zet

al,

2002

(40)

N�

62,

M/F

32/3

0,ag

e62

�10

year

s,h

eigh

t1.

71�

0.11

m,

mas

s79

�12

kg

Var

us

alig

nm

ent

�9°

to15

°M

ild

tose

vere

Bil

ater

al:

mos

tsy

mp

tom

atic

knee

Pri

mar

ily

med

ial

com

par

tmen

t

OA

(var

us)

N�

49,

M/F

24/2

5,ag

e59

�10

year

s,h

eigh

t1.

7�

0.1

m,

mas

s76

�16

kg

Kau

fman

etal

,20

01(4

5)N

�92

,M

/F0/

92C

lin

ical

exam

inat

ion

Dia

gnos

isco

nfi

rmed

byra

dio

grap

hs;

no

det

ails

pro

vid

edre

gard

ing

seve

rity

ofch

ange

s

Bil

ater

al:

mos

tsy

mp

tom

atic

knee

OA

N�

47,

M/F

47/0

Kea

net

al,

2012

(43)

Mil

d:

n�

87,

age

62.3

�7.

69ye

ars,

hei

ght

1.65

�0.

09m

,m

ass

75.5

�15

.3kg

WO

MA

Cp

ain

,av

erag

ew

alki

ng

pai

nM

ild

varu

s:18

2°�

2.4°

Sev

ere

varu

s:17

9.5°

�3.

0°

Mil

dS

ever

eM

edia

lco

mp

artm

ent

Mil

dS

ever

eS

ever

e:n

�82

,ag

e65

.7�

8.0

year

s,h

eigh

t1.

69�

0.09

m,

mas

s84

.6�

15.0

kg

Ko

etal

,20

11(4

4)S

ymp

tom

atic

:n

�17

,ag

e70

.24

�8.

49ye

ars,

BM

I28

.08

�4.

33kg

/m2

Asy

mp

tom

atic

:n

�24

,ag

e72

.33

�8.

47ye

ars,

BM

I27

.2�

4.31

kg/m

2

Cli

nic

alex

amin

atio

nm

odel

edon

AC

R

Dia

gnos

isco

nfi

rmed

byra

dio

grap

hs;

no

det

ails

pro

vid

edre

gard

ing

seve

rity

ofch

ange

s

OA

N�

112,

age

67.6

9�

9.31

year

s,B

MI

26.9

4�

4.34

kg/m

2

Kra

ckow

etal

,20

11(5

9)N

oto

rsio

nal

def

orm

ity:

n�

8,M

/F4/

4,ag

e59

�11

.34

year

s,h

eigh

t1.

74�

0.13

m,

mas

s10

1.5

�14

.75

kg,

BM

I33

.84

�6.

9kg

/m2

Tor

sion

ald

efor

mit

y:n

�6,

M/F

5/1,

age

61.8

3�

7.96

year

s,h

eigh

t1.

73�

0.1

m,

mas

s10

.2�

14.1

8kg

Sev

ere

Un

ilat

eral

/bil

ater

ald

isea

seM

edia

lco

mp

artm

ent

Sev

ere

N�

10,

M/F

5/5,

age

62.5

�4.

17ye

ars,

BM

I28

.44

�4.

23kg

/m2

Lan

dry

etal

,20

07(3

4)N

�41

,ag

e58

.2�

8.3

year

s,B

MI

30.3

�4.

5kg

/m2

On

wai

tin

gli

stfo

rar

thro

scop

icsu

rger

y

Med

ian

�m

ild

Mil

dN

�43

,ag

e50

.7�

10.2

year

s,B

MI

24.8

�3.

9kg

/m2

Lev

inge

ret

al,

2012

(23)

N�

50,

M/F

27/2

3,ag

e66

.4�

7.6

year

s,B

MI

29.6

�5.

1kg

/m2

WO

MA

C,

VA

Sp

ain

Au

thor

s’ow

ncr

iter

iaM

ild

tose

vere

OA

N�

28,

M/F

13/1

5,ag

e65

.1�

11.2

year

s,B

MI

25.7

�3.

9kg

/m2

Lew

eket

al,

2004

(20)

N�

12,

M/F

6/6,

age

50.3

�7.

4ye

ars

Sch

edu

led

for

hig

hti

bial

oste

otom

yK

OS

,w

eigh

t-be

arin

gli

ne

23.1

%�

10%

Con

firm

edjo

int

spac

en

arro

win

gin

med

ial

com

par

tmen

t

Med

ial

com

par

tmen

tM

oder

ate

(var

us)

N�

12,

M/F

6/6,

age

49.5

�6.

1ye

ars,

wei

ght-

bear

ing

lin

e46

%�

8.6%

(con

tin

ued

)

1650 Mills et al

Tab

le2.

(Con

t’d

)

Au

thor

,ye

ar(r

ef.)

OA

coh

ort

Cli

nic

alm

easu

res

Rad

iogr

aph

icch

ange

s†O

Ad

escr

ipti

onS

ever

ity

Com

par

ator

coh

ort

Lew

eket

al,

2006

(29)

N�

15,

M/F

9/6,

age

48.7

�7.

4ye

ars,

hei

ght

1.75

�0.

09m

,m

ass

91.9

�17

.4kg

KO

OS

,cl

inic

alex

amin

atio

nV

aru

sal

ign

men

t:w

eigh

t-be

arin

gli

ne

18.9

%�

12.7

%

Con

firm

edjo

int

spac

en

arro

win

gin

med

ial

com

par

tmen

t

Un

ilat

eral

dis

ease

Med

ial

com

par

tmen

tM

oder

ate

(var

us)

N�

15,

M/F

9/6,

age

48.4

�6.

3ye

ars,

hei

ght

1.71

�0.

9m

,m

ass

83.8

�17

.3kg

Wei

ght-

bear

ing

lin

e45

.1%

�8.

1%L

iika

vain

ioet

al,

2010

(60)

N�

54,

M/F

54/0

,ag

e59

�5.

3ye

ars,

BM

I29

.7�

4.7

kg/m

2

AC

Rcl

inic

alcr

iter

ia,

pai

nV

AS

Var

us

alig

nm

ent

5.2°

�3.

2°

Mil

dto

seve

reU

nil

ater

al/b

ilat

eral

:m

ore

sym

pto

mat

ickn

ee

OA

(var

us)

N�

53,

M/F

53/0

,ag

e59

.2�

4.7

year

s,B

MI

27.1

�3.

1kg

/m2,

alig

nm

ent

2.5°

�2.

0°L

inle

yet

al,

2010

(35)

N�

40,

M/F

17/2

3,ag

e63

�10

year

s,B

MI

27.4

�5.

5kg

/m2

WO

MA

Csc

ale

Med

ian

�m

ild

Un

ilat

eral

/bil

ater

al:

mor

esy

mp

tom

atic

knee

Med

ial

com

par

tmen

t

Mil

dN

�40

,M

/F17

/23,

age

64�

9ye

ars,

BM

I24

.0�

3.2

kg/m

2

Man

etta

etal

,20

02(2

4)N

�10

,M

/F10

/0,

age

68�

11ye

ars

WO

MA

CN

ora

dio

grap

hs

take

nO

AN

�10

,ag

e68

�11

year

s

McG

ibbo

nan

dK

rebs

,20

02(6

1)N

�13

,M

/F2/

11,

age

72.9

�8.

9ye

ars

Not

rep

orte

dU

nil

ater

ald

isea

seO

AN

�10

,M

/F4/

6,ag

e73

.3�

4.6

year

sM

cKea

net

al,

2007

(36)

N�

39,

M/F

24/1

5W

omen

:ag

e58

.32

�9.

31ye

ars,

BM

I31

.5�

5.2

kg/m

2

Men

:ag

e55

.1�

12.8

year

s,B

MI

29.7

�4.

6kg

/m2

WO

MA

C,

clin

ical

exam

inat

ion

Mil

dto

mod

erat

eM

oder

ate

N�

42,

M/F

18/2

4W

omen

:ag

e48

.7�

10.3

year

s,B

MI

24.4

�3.

6kg

/m2

Men

:ag

e52

.2�

10.1

year

s,B

MI

24.7

�3.

2kg

/m2

Mes

sier

etal

,20

05(4

7)N

�10

,M

/F1/

9,ag

e74

.1�

1.49

year

s,m

ass

65.1

�2.

61kg

AC

Rcl

inic

alcr

iter

iaM

ild

tose

vere

All

com

par

tmen

tsO

AN

�10

,M

/F1/

9,ag

e73

�1.

61ye

ars,

mas

s58

.3�

2.74

kgM

un

der

man

net

al,

2005

(33)

Mil

d:

n�

19,

M/F

6/13

,ag

e65

.2�

12.5

year

s,B

MI

26.9

�3.

1kg

/m2

Sev

ere:

n�

23,

M/F

13/1

0,ag

e65

�8

year

s,B

MI

27.8

�4.

8kg

/m2

WO

MA

CM

ild

:va

rus

alig

nm

ent

0.3°

Sev

ere:

varu

sal

ign

men

t5.

7°

Mil

d:

mil

dS

ever

e:m

oder

ate

tose

vere

Bil

ater

al:

mor

esy

mp

tom

atic

knee

Med

ial

com

par

tmen

t

Mil

dS

ever

e(v

aru

s)L

ess

seve

reco

ntr

ols:

n�

19,

M/F

6/13

,ag

e61

.7�

12.3

year

s,B

MI

26.1

�2.

6kg

/m2

Mor

ese

vere

con

trol

s:n

�23

,M

/F13

/10,

age

63.7

�9.

2ye

ars,

BM

I27

.1�

4kg

/m2

Ru

dol

ph

etal

,20

07(6

)N

�15

,M

/F8/

7,ag

e49

.2�

4.5

year

s,B

MI

30.7

�4.

8kg

/m2

Sch

edu

led

for

hig

hti

bial

oste

otom

yA

CR

clin

ical

crit

eria

KO

SV

aru

sal

ign

men

t6.

33°

�2.

39°

Rad

iogr

aph

sta

ken

but

not

rep

orte

dB

ilat

eral

:m

ore

sym

pto

mat

ickn

eeM

edia

lco

mp

artm

ent

Mod

erat

e(v

aru

s)N

�15

,M

/F8/

7,ag

e49

.2�

4.25

year

s,B

MI

28.7

�5.

5kg

/m2

(con

tin

ued

)


Tab

le2.

(Con

t’d

)

Au

thor

,ye

ar(r

ef.)

OA

coh

ort

Cli

nic

alm

easu

res

Rad

iogr

aph

icch

ange

s†O

Ad

escr

ipti

onS

ever

ity

Com

par

ator

coh

ort

Ru

ther

ford

etal

,20

08(2

5)M

ild

tom

oder

ate:

n�

46,

M/F

20/2

6,ag

e60

�9

year

s,B

MI

31�

5kg

/m2

Sev

ere:

n�

44,

M/F

20/2

4,ag

e67

�8

year

s,B

MI

32�

5kg

/m2

Fu

nct

ion

alte

stin

gM

ild

tom

oder

ate:

mil

dto

mod

erat

eS

ever

e:m

oder

ate

tose

vere

Pre

dom

inan

tly

med

ial

com

par

tmen

t

Mil

dto

mod

erat

eS

ever

eN

�50

,M

/F32

/18,

age

53�

10ye

ars,

BM

I26

�4

kg/m

2

Ru

ther

ford

etal

,20

11(2

7)M

oder

ate:

n�

16,

M/F

8/8,

age

61�

6ye

ars,

BM

I31

.3�

3.6

kg/m

2

Sev

ere:

n�

15,

M/F

10/5

,ag

e61

�9

year

s,B

MI

30.7

�5.

4kg

/m2

Sev

ere

grou

psc

hed

ule

dfo

rto

tal

join

tar

thro

pla

sty

WO

MA

C

Mod

erat

e:m

oder

ate

Sev

ere:

seve

reP

red

omin

antl

ym

edia

lco

mp

artm

ent

Mod

erat

eS

ever

eN

�16

,M

/F8/

8,ag

e56

�6

year

s,B

MI

24.6

�3.

9kg

/m2

Sah

aiet

al,

2003

(46)

N�

15,

M/F

15/0

,ag

e68

�11

year

sW

OM

AC

No

rad

iogr

aph

sta

ken

Bil

ater

al:

aver

age

ofex

trem

itie

san

alyz

ed

OA

N�

13,

M/F

13/0

,ag

e68

�11

year

s

Sch

mit

tan

dR

ud

olp

h,

2007

(39)

N�

28,

M/F

14/1

4,ag

e60

.4�

9.75

year

s,h

eigh

t1.

7�

0.11

m,

mas

s92

.91

�16

.16

kg

Kn

eela

xity

asse

ssed

Var

us

alig

nm

ent

174.

82°

�0.

6°(�

180°

�va

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1652 Mills et al

sions) were also observed in individuals with severe KOAcompared with those with moderate KOA (16,19). Individ-uals with medial compartment involvement exhibited re-duced peak hip adduction compared with individualswith lateral compartment KOA (5,21). A waveform analy-sis of sagittal plane knee motion revealed that greater changesoccurred in females with KOA compared with males (36);however, this was not supported by a study examining dis-crete variables between females and males (4).

Joint moments. The most common peak external jointmoments reported were hip adduction, abduction, andinternal rotation moments, and knee flexion, adductionand internal rotation moments. Twenty publications com-pared KOA with healthy controls, while 19 compared jointmoments between KOA subgroups (Table 3 and Figure 3).

KOA versus controls. Comparisons involving individu-als with severe KOA most frequently met the criteria fordata pooling (Figure 3). Moderate evidence suggested thatindividuals with severe KOA with or without varus mal-alignment exhibited reduced hip adduction moments (ES�0.96 [95% CI �1.4, �0.52], I2 � 7% [19,33] and ES �0.73[95% CI �1.06, �0.4], I2 � 0% [5,16], respectively). Incontrast, pooled data revealed limited evidence of an in-crease in peak hip abduction moment values (19,33) forthose with severe disease and varus malalignment andconflicting evidence regarding hip internal rotation mo-ment in those with severe nonvarus KOA compared withhealthy controls (5,16). Regarding knee moments, the evi-dence of alteration in the knee adduction moment associ-ated with mild KOA was conflicting, although the pooledES suggested small increases. For more severe and generalKOA cohorts, there was no evidence of a change in kneeadduction moment compared with healthy controls basedon 8 different studies. Similarly, evidence of alterations inknee flexion and internal rotation moments in individualswith severe KOA was conflicting. However, this was mostlikely due to a difference in magnitude of ES of pooledstudies because both Astephen et al (16) and Weidow et al(5) reported reductions.

Significant results of nonpooled comparisons betweenKOA and controls indicated that individuals with moder-ate KOA exhibited a moderate reduction in peak hip ad-duction moment (16,19) and small reductions in peak hipinternal rotation, knee internal rotation, and knee flexionmoments (16,37). Those with mild KOA also exhibited areduction in peak knee flexion moment (38), althoughthere was no difference between individuals with mildKOA and varus malalignment and controls (39). Thesefindings were confirmed in waveform comparisons(32,34,36) (Table 3). An analysis of waveforms also re-vealed a larger knee adduction moment throughout stancefor individuals with mild (34) and moderate KOA (36)compared with healthy controls. This finding was sup-ported by 2 publications comparing general KOA cohortsand healthy controls that did not provide enough data tocalculate ES (40,41), but was in contrast to other non-pooled data (25,37,42). Deluzio and Astephen (32) re-ported that individuals with severe KOA exhibited anincreased average knee adduction moment throughout

Tab

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Table 3. Results of nonpooled data*

Authors Outcome Study group ComparatorMean difference

(95% CI) ES

TemporospatialButler et al, 2011

(21)Walking speed,

m/secondLateralMedial

ControlLateral

�0.1 (�0.26, 0.06)0.00 (�0.72, 0.72)

0.440.0

Creaby et al, 2012(42)

Walking speed,m/second

UnilateralBilateral

ControlControl

�0.27 (�0.37, 0.17)�0.22 (�0.30, �0.14)

1.591.3

Unilateral pain,bilateral OA

Control �0.14 (�0.25, �0.03) 0.7

Unilateral Bilateral �0.05 (�0.13, 0.03) 0.32Unilateral pain,

bilateral OABilateral 0.08 (�0.02, 0.18) 0.44

Unilateral Unilateral pain,bilateral OA

�0.13 (�0.25, 0.01) 0.66

Gok et al, 2002 (38) Stride duration,seconds

Mild Control 0.1 (�0.2, 0.22) 0.61

Huang et al, 2008(18)

Cadence,steps/minute

Mild Severe 4.3 (�4.20, 12.80) 0.35

Stride length,% leg length

Mild Severe 0.03 (�0.11, 0.17) 0.15

Walking speed,% height

Mild Severe 0.11 (�0.01, 0.23) 0.65

Hunt et al, 2010(19)


Mild (varus)Mild (varus)

ControlSevere (varus)

�0.1 (�0.2, 0.0)0.11 (0.02, 0.2)

0.60.68

Moderate (varus) Severe (varus) 0.04 (�0.05, 0.13) 0.24Kaufman et al, 2001

(45)Walking speed,

m/secondFemales Males �0.09 (�0.18, �0.52) 0.17

Ko et al, 2011 (44) Walking speed,m/second

Symptomatic OAAsymptomatic

ControlControl

P � 0.153P � 0.076

Symptomatic OA Asymptomatic P � 0.99†Krackow et al, 2011

(59)Walking speed,

m/secondSevere (tibial torsion)Severe

ControlSevere

(tibial torsion)

�0.36 (�0.57, �0.15)0.1 (�0.11, 0.31)

1.540.46

Landry et al, 2007(34)

Stance duration (FW),seconds

Mild Control 0.02 (�0.01, 0.05) 0.3

Stride duration (FW),seconds

0.01 (�0.03, 0.05) 0.1

Stride length (FW), m 0.0 (�0.06, 0.06) 0.0Walking speed (FW),

m/second�0.03 (�0.13, 0.07) 0.12

Levinger et al, 2012(23)

Stride length OA Control �0.2 (�0.25, �0.15) 1.98

Liikavainio et al,2010 (60)

Stride length(1.2 m/second)

OA (varus) Control 0.02 (�0.01, 0.05) 0.28


OA (varus) Control 0.0 (�0.03, 0.03) 0.0


OA (varus) Control 0.01 (�0.02, 0.04) 0.11

Mundermann et al,2005 (33)


Mild Severe (varus) 0.01 (�0.13, 0.15) 0.04

Rutherford et al,2008 (25)


Mild to moderateMild to moderate

ControlSevere

�0.07 (�0.15, 0.01)0.37 (0.27, 0.47)

0.351.6

Sahai et al, 2003(46)


OA Control �0.34 (�0.53, �0.15) 1.29

Sims et al, 2009 (4) Stride length, %height

Females Males 0.03 (�0.03, 0.05) 0.26


Females Males 0.06 (�0.05, 0.17) 0.28

(continued)

1654 Mills et al

Table 3. (Cont’d)


(95% CI) ES

Weidow et al, 2006(5)

Cadence, strides/minute

LateralMedial

ControlLateral

�23.1 (�34.41, �11.79)6.4 (�6.13, 18.93)

1.420.36

Stride length, m Lateral Control �0.18 (�0.30, �0.06) 1.02Medial Lateral 0.00 (�0.13, 0.13) 0.00


LateralMedial

ControlLateral

�0.43 (�0.60, �0.26)0.12 (�0.02, 0.26)

1.780.6

Zeni and Higginson,2009 (3)

Cadence (FW), steps/minute

ModerateSevere

ControlControl

�9.45 (�17.86, �1.04)�10.09 (�22.92, 2.74)

0.650.58

Moderate Severe 0.64 (�11.67, 12.95) 0.04Cadence (SS),

steps/minuteModerateModerate

ControlSevere

�4.83 (�11.87, 2.21)3.1 (�9.72, 15.92)

0.40.19

Cadence (1.0 m/second),steps/minute

ModerateSevere

ControlControl

�1.28 (�6.36, 3.80)4.01 (�2.23, 10.25)

0.150.41

Moderate Severe �5.29 (�10.95, 0.37) 0.54Stride duration (FW),

secondsModerateSevere

ControlControl

0.04 (�0.01, 0.09)0.1 (0.05, 0.15)

0.491.32

Moderate Severe �0.06 (�0.11, �0.01) 0.79Stride duration (1.0 m/

second), secondsModerateSevere

ControlControl

�0.02 (�0.07, 0.03)�0.01 (�0.07, 0.05)

0.230.12

Moderate Severe �0.01 (�0.07, 0.05) 0.11Stride length (FW),

secondsModerateSevere

ControlControl

�19.57 (�30.38, �8.76)�25.19 (�40.73, �9.65)

1.051.19

Moderate Severe 5.62 (�9.6, 20.84) 0.28Stride length (1.0 m/

second), cmModerateSevere

ControlControl

�6.18 (�12.00, �0.36)0.51 (�9.51, 10.53)

0.620.04

Moderate Severe �6.69 (�16.12, 2.74) 0.58Walking speed (FW),

m/secondModerateSevere

ControlControl

�0.22 (�0.34, �0.1)�0.32 (�0.47, �0.17)

1.051.49

Moderate Severe 0.1 (�0.05, 0.25) 0.48Zeni et al, 2010 (28) Walking speed (FW),

m/secondModerateSevere

ControlControl

�0.22 (�0.36, �0.08)�0.35 (�0.53, �0.17)

1.021.56

Moderate Severe 0.13 (�0.05, 0.31) 0.62Zeni and Higginson,

2011 (62)Walking speed (FW),

m/secondModerate Control �0.33 (�0.47, �0.19) 1.47

Kinematics†Astephen et al, 2008

(16)Knee flexion peak

during stanceSevereModerate

ControlSevere

�10.68 (�13.09, �8.27)5.98 (3.6, 8.36)

1.570.89

Knee flexion excursion Moderate Control �2.5 (�4.91, �0.09) 0.37Severe Control �18.6 (�22.92, �14.28) 1.52Moderate Severe 16.1 (11.65, 20.55) 1.28

Knee peak flexion Moderate Control �2.7 (�5.2, �0.2) 0.38Severe Control �18.1 (�22.25, �13.95) 1.53Moderate Severe 15.4 (11.05, 19.75) 1.25

Baliunas et al, 2002(41)

Knee extensionKnee range of motion

OA (varus) Control �3.0 (�5.25, �0.75)�6.0 (�9.03, �2.97)

0.650.97

Knee peak flexion �3.0 (�6.25, 0.25) 0.45Bejek et al, 2005

(31)Knee extension (1.0 m/

second)Severe Control �7.4 (�8.35, 6.45) 4.74

Knee extension (2.0 m/second)

�8.5 (�9.38, �7.62) 5.89

Knee extension (3.0 m/second)

�8.7 (�9.38, �7.62) 4.87

Knee peak flexion(1.0 m/second)

�18.0 (�22.70, �13.3) 2.33


�23.1 (�26.42, �19.78) 4.22


�28.0 (�31.57, �24.43) 4.77

(continued)


Table 3. (Cont’d)


(95% CI) ES

Knee range of motion(1.0 m/second)

�25.4 (�30.95, �19.85) 2.78


�31.5 (�36.75, �26.25) 3.64


�37.0 (�42.35, �31.65) 4.87

Butler et al, 2011(21)

Hip peak adduction MedialLateral

ControlControl

�1.5 (�3.60, 0.60)1.4 (�1.0, 3.8)

0.50.41

Medial Lateral �2.9 (�5.04, �0.76) 0.95Creaby et al, 2012

(42)Lateral trunk lean

(average)UnilateralUnilateral pain,

bilateral OA

ControlControl

3.0 (2.53, 3.47)2.20 (1.85, 2.55)

5.294.46

Bilateral Control 2.14 (1.88, 2.4) 5.11Unilateral Bilateral 0.86 (0.41, 1.31) 1.99Unilateral pain,



0.8 (0.31, 1.29) 1.31

Knee peak flexion Unilateral Control �4.61 (�5.91, �3.31) 2.94Unilateral pain,

bilateral OAControl �6.71 (�7.67, �5.75) 4.88

Bilateral Control �6.44 (�6.96, �5.92) 5.89Unilateral Bilateral 1.83 (0.59, 3.07) 1.54Unilateral pain,

bilateral OABilateral �0.27 (�0.92, 0.38) 0.24


1.23 (0.44, 2.02) 0.21

Gok et al, 2002(38)

Knee flexion peakduring stance

Mild Control �4.0 (�7.73, �0.27) 0.8

Deluzio andAstephen, 2007(32)

Knee range of motionKnee peak flexion

Severe Control PCA: OA patients hadless range of motion

PCA: knees of OApatients were lessflexed throughout thegait cycle

Huang et al, 2008(18)

Hip peak adduction MildMild

ControlSevere

�1.55 (�4.96, 1.86)1.48 (�1.65, 4.61)

0.320.33

Knee flexion duringloading (excursion)

MildSevere

ControlControl

�2.21 (�8.18, 3.76)�7.48 (�13.08, �1.88)

0.260.93

Mild Severe 5.27 (0.22, 10.32) 0.73Hunt et al, 2010

(19)Lateral trunk lean

(peak)Mild (varus)Moderate (varus)

ControlControl

0.7 (�0.61, 2.01)1.5 (0.19, 2.81)

0.310.67

Severe (varus) Control 3.4 (2.04, 4.76) 1.46Mild (varus) Moderate (varus) �0.8 (�1.91, 0.31) 0.39Mild (varus) Severe (varus) �2.7 (�3.87, �1.53) 1.26Moderate (varus) Severe (varus) �1.9 (�3.07, �0.73) 0.89

Hip peak adduction Mild (varus) Control �0.8 (�2.79, 1.19) 0.23Moderate (varus) Control �3.0 (�5.07, �0.93) 0.81Severe (varus) Control �4.4 (�6.45, �2.35) 1.21Mild (varus) Moderate (varus) 2.2 (0.06, 4.34) 0.56Mild (varus) Severe (varus) 3.6 (1.49, 5.71) 0.93Moderate (varus) Severe (varus) 1.4 (�0.79, 3.59) 0.35

Ko et al, 2011 (44) Knee range of motion Symptomatic OA Control P � 0.403Asymptomatic Control P � 0.207Symptomatic OA Asymptomatic P � 0.987§

(continued)

1656 Mills et al

Table 3. (Cont’d)


(95% CI) ES


Knee range of motion(FW)

Knee range of motion(SS)

Mild Control PCA: walking fasterincreased knee rangeof motion and phase-shifted anglesthroughout the stridein both groups. Nodifference betweengroups

Linley et al, 2010(35)

Lateral trunk lean(peak)

Mild Control 0.0 (�0.79, 0.79) 0.00

Manetta et al, 2002(24)

Knee flexion duringloading (peak)

OA Control �3.1 (�8.8, 2.6) 0.46

McGibbon andKrebs, 2002 (61)

Knee range of motion OA Control PCA: OA patientsextended knee inmid to late stanceand flexed knee lessin swing

McKean et al, 2007(36)

Knee flexionexcursion

Mild to moderate Control PCA: OA patientsexhibited smallerknee flexion anglesthroughout the entiregait cycle

Knee range of motion Females Controls andmales

PCA: females with OAexhibited less rangeof motion duringstance phase thancontrols and maleswith OA


Knee extension MildSevere (varus)

ControlControl

�4.09 (�6.48, �1.70)2.32 (�3.91, 8.55)

1.070.21

Mild Severe (varus) �4.66 (�7.72, �1.60) 0.87Knee flexion at initial

contactMildSevere (varus)

ControlControl

�7.08 (�11.93, �2.23)�3.75 (�9.61, 2.09)

0.910.5

Mild Severe (varus) �2.68 (�4.83, �0.53) 0.74Rudolph et al,

2007 (6)Knee flexion at initial

contactModerate (varus) Control 1.09 (�2.6, 4.78) 0.21

Schmitt andRudolph, 2007(39)

Knee flexionexcursion

Mild (varus) Control �2.6 (�4.98, �0.22) 0.57

Sims et al, 2009 (4) Knee range of motion Females Males 0.94 (�2.37, 4.25) 0.15Weidow et al,

2006 (5)Hip peak adduction Lateral

MedialControlLateral

3.46 (2.15, 4.77)�9.53 (�10.78, �8.28)

1.835.29

Knee peak extension Medial Control 5.67 (�8.3, �3.04) 1.5Lateral Control �5.0 (�7.39, �2.61) 1.46Medial Lateral �0.67 (�3.19, 1.85) 0.19

Knee peak flexion Medial Control �9.4 (�12.79, �6.01) 1.93Lateral Control �10.87 (�14.18, �7.56) 2.29Medial Lateral 1.47 (�3.00, 5.94) 0.23

Joint moments‡Astephen et al,

2008 (16)Hip peak adduction

moment stance,Nm/kg

ModerateModerate

ControlSevere

�0.18 (�0.28, �0.08)0.03 (�0.08, 0.14)

0.660.1

Hip peak internalrotation moment,Nm/kg

ModerateModerate

ControlSevere

�0.04 (�0.07, 0.00)0.04 (0.02, 0.07)

0.40.62

Knee peak flexionmoment, Nm/kg

ModerateModerate

ControlSevere

�0.12 (�0.21, �0.03)0.07 (�0.00, 0.14)

0.460.33

Knee peak internalrotation moment,Nm/kg

ModerateModerate

ControlSevere

�0.02 (�0.04, 0.00)0.07 (0.04, 0.1)

0.320.92

(continued)


Table 3. (Cont’d)


(95% CI) ES

Baliunas et al,2002 (41)

Knee peak adductionmoment, Nm/kgand m

OA (varus) Control OA group wassignificantly higher(P � 0.003)

Butler et al, 2011(21)

Hip peak adductionmoment, Nm/kgand m

MedialLateralMedial

ControlControlLateral

0.00 (�0.72, 0.72)0.03 (�0.05, 0.11)

�0.03 (�0.12, 0.06)

0.000.250.24


LateralMedial

ControlLateral

�0.14 (�0.21, �0.07)0.23 (0.16, 0.3)

1.422.33

Creaby et al, 2012(42)


UnilateralUnilateral pain,

bilateral OA

ControlControl

�0.19 (�0.38, 0.0)�0.1 (�0.21, 0.0)

0.840.5

Bilateral Control �0.26 (�0.34, �0.18) 1.67Unilateral Bilateral 0.07 (�0.11, 0.25) 0.41Unilateral pain,



�0.09 (�0.29, 0.11) 0.36

Knee peak flexionmoment, Nm/kgand m

Unilateral pain,bilateral OA

Bilateral

Control

Control

�1.97 (�2.11, �1.83)

�2.09 (�2.19, �1.99)

7.51

10.26Unilateral Bilateral 0.51 (�0.28, 0.74) 2.33Unilateral pain,

bilateral OABilateral 0.12 (0.0, 0.24) 0.59


0.39 (0.14, 0.64) 1.23

Gok et al, 2002(38)


Mild Control �0.21 (�0.38, �0.04) 0.9

Deluzio andAstephen, 2007(32)

Knee peak adductionmoment, Nm/kg

Severe Control PCA: OA patientsexhibited a higheraverage moment, buta lower momentduring early stance


PCA: OA patientsexhibited an overalllower magnitude offlexion momentduring stance, lowerpositive flexionmoment during thefirst half of stance,and lower absolutemagnitude ofnegative flexionmoment

Hunt et al, 2010(19)


Mild (varus)Moderate (varus)Mild (varus)

ControlControlModerate (varus)

�0.43 (�0.94, 0.08)�0.71 (�1.26, �0.16)

0.28 (�0.3, 0.86)

0.460.700.26

Mild (varus) Severe (varus) 0.69 (0.16, 1.22) 0.71Moderate (varus) Severe (varus) 0.41 (�0.16, 0.98) 0.39

Hip peak abductionmoment, Nm/kgand m

Mild (varus)Moderate (varus)Mild (varus)

ControlControlModerate (varus)

0.28 (�0.39, 0.95)0.37 (�0.34, 1.08)

�0.09 (�0.8, 0.62)

0.230.280.07

Mild (varus) Severe (varus) �0.62 (�1.48, 0.24) 0.39Moderate (varus) Severe (varus) �0.53 (�1.42, 0.36) 0.32


Mild (varus)Moderate (varus)

Moderate (varus)Severe (varus)

�0.04 (�0.61, 0.53)�0.14 (�0.7, 0.42)

0.040.14

(continued)

1658 Mills et al

Table 3. (Cont’d)


(95% CI) ES

Hurwitz et al, 2002(40)


OA (varus) Control OA group wassignificantly higher(P � 0.027)

Kaufman et al,2001 (45)


Females Males �0.08 (�0.2, 0.36) 0.1


�0.16 (�0.42, 0.1) 0.22

Knee peak internalrotation moment,Nm/kg and m

0.09 (�0.02, 0.2) 0.3



Mild Control PCA: OA patientsexhibited largeroverall adductionmoments duringstance in both fastwalking andpreferred speeds


PCA: OA patientsexhibited smallerflexion moments atboth fast andpreferred speeds

Linley et al, 2010(35)

Hip peak adductionmoment, Nm/kg

Mild Control 0.02 (�0.03, 0.07) 0.17

McKean et al, 2007(36)

Hip peak internalrotation moment,Nm/kg

Moderate Control PCA: OA patientswalked with asmallerinternal/externalrotation moment andmore internallyrotated hip


Females Controls andmales

PCA: OA femalesexhibited lowermagnitude thancontrols and OAmales



PCA: OA femalesexhibited lowermoment thancontrols and OAmales

Knee internal rotationmoment, Nm/kg


PCA: OA femalesexhibited lower kneeinternal rotationmoment duringstance than controlsand OA males

Messier et al, 2005(47)

Knee peak internalrotation moment

OA Control �0.03 (�0.05, 0.01) 1.44



MildMild


�0.13 (�0.66, 0.40)0.52 (�0.06, 1.10)

0.150.54

Hip peak abductionmoment, Nm/kgand m

MildMild


0.97 (0.14, 1.81)�0.57 (�1.45, 0.31)

0.730.41


Mild Severe (varus) �0.79 (�1.28, �0.40) 1.17

(continued)


stance, but this was reduced (compared with controls)during early stance. Rutherford et al (25) reported a changein shape of the knee adduction moment waveform in in-dividuals with severe KOA compared with controls andthose with moderate KOA, but reported no change in am-plitude.

Between KOA subgroups. The only data meeting criteriafor pooling indicated no difference in knee adduction mo-

ment between individuals with mild and severe KOA withvarus malalignment (19,43) (Figure 3). Similar findingshave been reported when comparing individuals withmild KOA and varus malalignment with those with mod-erate KOA and varus malalignment as well as those withmoderate and severe disease and varus malalignment (19).Significant increases in knee adduction moment were re-ported in individuals with primarily medial compartment

Table 3. (Cont’d)


(95% CI) ES

Rutherford et al,2008 (25)


Mild to moderateSevere

ControlControl

PCA: the mild tomoderate OA andcontrol groupsdisplayed 2 distinctpeaks in the moment.The first peak wasdelayed by 7% of thegait cycle in thesevere group and thesecond peak was noteasily distinguished.There appeared to beno difference inamplitude betweenthe groups

Schmitt andRudolph, 2007(39)


Mild (varus) Control 0.00 (�0.53, 0.53) 0.00

Sims et al, 2009 (4) Hip peak abductionmoment, Nm/kg

Females Males 0.04 (�0.08, 0.17) 0.18


�0.13 (�0.22, �0.03) 0.7

Weidow et al, 2006(5)

Hip peak adductionmoment, Nm/kg

LateralMedial

ControlLateral

�0.18 (�0.28, �0.08)0.05 (�0.05, 0.15)

1.290.34

Hip peak abductionmoment, Nm/kg

MedialLateral

ControlControl

0.02 (�0.06, 0.1)0.13 (0.07, 0.19)

0.171.45

Medial Lateral �0.11 (�0.17, �0.05) 1.33Hip peak internal

rotation moment,Nm/kg

LateralMedial

ControlLateral

0.03 (�0.02, 0.08)�0.05 (�0.1, 0.00)

0.450.65


MedialLateral

ControlControl

0.18 (0.06, 0.30)�0.32 (�0.42, �0.21)

1.092.32

Medial Lateral 0.50 (0.42, 0.58) 4.52Knee peak flexion

moment, Nm/kgLateralMedial

ControlLateral

�0.21 (�0.34, �0.08)�0.08 (�0.20, 0.04)

1.140.46

Knee peak internal Lateral Control �0.01 (�0.02, 0.00) 0.49rotation moment,Nm/kg

Medial Lateral 0.0 (�0.02, 0.02) 0.0

Zeni andHigginson,


ModerateSevere

Control No difference reportedNo difference reported

2011 (62) Knee peak flexionmoment, Nm/kg

Moderate At SS, there wassignificant reduction

Severe At both SS and FW,there were significantreductions

* 95% CI � 95% confidence interval; ES � effect size; OA � osteoarthritis; FW � fast walking; SS � self-selected speed; PCA � principle componentsanalysis.† Authors did not provide estimates of variability.‡ All kinematic measurements are in degrees. All joint moments are external moments.§ Authors did not provide measures of variance.

1660 Mills et al

involvement compared with those with lateral KOA (5,21)and in males with KOA compared with females (4,36)(Table 3).

Of the remaining comparisons between KOA cohorts,there was a moderately increased hip internal rotationmoment and knee internal rotation moment in individualswith moderate KOA when compared with severe KOA(16). Hunt et al (19) reported that individuals with mildKOA and varus malalignment exhibited a moderate in-crease in hip adduction moment compared with individ-uals with severe KOA and varus malalignment. However,this was not supported by the findings of Mundermann etal (33), whose mild KOA group exhibited normal align-ment. The hip abduction moment in individuals with me-

dial compartment KOA was larger than those with lateralcompartment involvement (5).

DISCUSSION

A comprehensive search of the literature revealed thatindividuals with KOA exhibited a variety of biomechani-cal alterations during gait compared with their healthycounterparts. However, the only gait alteration with strongand consistent evidence was increased stride duration forthose with severe KOA compared with healthy controls.Moderate evidence indicated that individuals with mod-erate KOA (varus malalignment only) exhibited reducedknee flexion excursion during loading, peak knee flexion,

Figure 2. Forest plot of data pooling for temporospatial variables. Open diamonds indicate the effect size and bars indicate the 95%confidence intervals (95% CIs). Solid diamonds represent pooled data. Contributing studies were weighted based on intersubjectvariability (i.e., width of CIs). OA � osteoarthritis; %BH � percentage of body height.


and walking speed, while individuals with severe KOA(varus malalignment only) reduced their cadence and hipadduction moment. Those with severe KOA also increasedtheir stride duration compared with those with moderatedisease. There was limited evidence for general KOA co-horts exhibiting reduced knee flexion excursion duringloading and increased knee flexion at IC compared withhealthy controls. Similarly, limited evidence indicatedthat individuals with moderate (nonvarus) KOA exhib-ited reduced walking speed (although faster than thosewith severe KOA) and individuals with severe KOA andvarus malalignment exhibited increased hip abductionmoments. The remaining pooled data resulted in conflict-ing or no evidence of biomechanical alterations.

A likely cause of conflicting evidence was the highamount of heterogeneity between pooled publications.While K/L grade was primarily used to determine diseaseseverity, the Ahlback scale (5,17,38) and magnetic reso-nance imaging (20,29) were also utilized. Furthermore, notall studies described the mechanical axis alignment oftheir cohorts. When classifying the severity of KOA co-

horts, some studies considered radiographic and clinicalfindings (3,26,30,32,37), while other studies solely refer-enced radiographic changes (19,33) and others used radio-graphs to confirm the presence of KOA but only reportedclinical findings (44–47). The lack of homogeneity in KOAdescription and classification schemes highlights the needfor standard classification systems to be used and reportedin future studies.

The key findings from nonpooled data indicated thattemporospatial and kinematic gait alterations associatedwith KOA increased in magnitude with increasing diseaseseverity. Therefore, individuals with severe KOA exhib-ited the greatest alterations, while there were few differ-ences observed between those with mild KOA and con-trols. There was insufficient evidence to support or refutethe influence of mechanical alignment, the involved com-partment, sex, and symptoms on most of the biomechani-cal variables examined. However, in joint moment com-parisons, larger moments were observed in milder KOAseverities, except for knee adduction moment, where therewere no differences between KOA subgroups. For knee

Figure 3. Forest plot of data pooling for joint kinematics and moments. Open diamonds indicate the effect size and bars indicate the 95%confidence intervals (95% CIs). Solid diamonds represent pooled data. Contributing studies were weighted based on intersubjectvariability (i.e., width of CIs). OA � osteoarthritis; Nm/kg*m � Nm/kg and meters; IC � initial contact.

1662 Mills et al

adduction moment, those with medial compartment in-volvement and males were reported to exhibit larger mo-ments.

It has been suggested that individuals with KOA adoptgait strategies that result in immediate reduction in kneejoint load, particularly medial compartment load (33,48).This is particularly pertinent for individuals with primar-ily medial compartment KOA, who constitute the majorityof individuals examined in the studies included in thisreview. The present data support this hypothesis becausethere was no evidence of increased knee adduction mo-ment, which is a proxy for medial knee joint load (49).Likewise, although pooled evidence was conflicting, kneeflexion and internal rotation moments were also reduced(more so in those with severe KOA). These moments havebeen correlated with the magnitude of adduction momentand compressive knee load in KOA (50,51).

The lack of evidence of alterations in knee adductionmoment is surprising (although similar to findings from aprevious systematic review examining knee adductionmoment [52]), given the importance of this variable in theprogression of KOA (53) and the large number of studiesthat have utilized knee adduction moment as a primaryoutcome. It is likely that alterations in knee adductionmoment are driven by alterations of known moment-mod-ifying gait characteristics. A recent systematic review re-ported that increased lateral trunk lean demonstrated thelargest reductions in early stance knee adduction moment(54), with other kinematic alterations such as foot progres-sion angle and walking speed also affecting knee adduc-tion moment magnitudes. In the current study, the magni-tude of trunk lean and resultant alterations at the hip(reduced hip adduction moment and increased hip abduc-tion moment and peak abduction) was greatest in thosewith severe KOA. Similarly, changes in temporospatialcharacteristics (i.e., walking speed, cadence, and stridelength) were also greatest in those with severe KOA. Suchchanges potentially decrease the ground reaction forces,moment arm, and cumulative load acting on the knee joint(55) and potentially explain why, unlike Foroughi et al(52), we did not find that the knee adduction momentincreased with severity of KOA. In contrast, those withmild KOA demonstrated the smallest number and magni-tude of kinematic and temporospatial alterations whiledemonstrating small increases in the knee adduction mo-ment. Therefore, this review demonstrates that differencesin knee adduction moment between individuals with KOAand healthy controls are not guaranteed and can poten-tially be explained by kinematic and temporospatial dif-ferences.

While some observed gait alterations might reflect at-tempts to reduce pain and protect the knee in the shortterm, they may have long-term adverse effects. Specifi-cally, it has been postulated that gait modification strate-gies that are successful in reducing joint loading and/orpain are attenuated by increased knee flexion excursion/angles (51). Childs et al (56) hypothesized that reducedknee motion stiffens the knee, making it less capable ofdissipating potentially harmful localized impact loads. Acaveat to these long-term effects is that this review waslimited to cross-sectional studies, meaning that the above

adverse effects are speculated. Longitudinal data are re-quired to make a causative statement regarding gait adap-tions and KOA progression, which is beyond the scope ofthis review.

Along with the lack of homogeneity in disease severityclassification and dearth of long-term studies, severalother methodologic factors influenced and limited thefindings of this review. The external and internal validityof the included publications was limited because the pub-lications did not provide sufficient information regardingparticipant recruitment and did not blind assessors togroup allocation/KOA diagnosis. It must be acknowledgedthat such limitations affect the validity of the findings ofthis review; however, this should be counterbalanced bythe increased precision gained from data synthesis. An-other limitation is that there is currently no consensusregarding an accepted standard reference frame for calcu-lating joint moments and no consensus on whether walk-ing speed is considered a confounding factor in publica-tions where participants set their own speed. Both of thesefactors have been shown to influence the magnitude ofjoint moments (16,57) and make comparisons across pub-lications difficult. Similarly, there is no standard for nor-malizing external joint moments. Normalizing momentsby height and body weight has the smallest residual effecton joint moments, but may also overcorrect data relative tonormalizing by body weight only due to the correlationbetween height and body weight (58). However, by choos-ing to pool data based on point estimates of effect ratherthan mean differences, such comparisons were possibleregardless of joint reference frame, walking speed, andnormalization protocol.

In summary, there is a range of evidence indicating thatindividuals with KOA exhibit altered gait biomechanicsduring gait compared with those without KOA. The ma-jority of strong and moderate evidence is for adaptationsoccurring in the temporospatial domain, whereas evidencefor kinematic and joint moment change is primarily lim-ited or conflicting. An interesting finding from the presentdata synthesis is the lack of evidence from pooled anddiscrete data for alterations in knee external adductionmoment. This was likely due to changes in known mo-ment-modifying gait characteristics such as lateral trunklean and temporospatial characteristics, all of which weremore altered in those with more severe KOA. However,some gait adaptations such as decreased knee motion aretheorized to have long-term adverse effects on the joint.Therefore, further research into the long-term effects ofconsistently occurring biomechanical gait adaptations, asidentified by this review, is needed. Such research wouldbenefit from a standardized KOA classification system thatencompasses radiographic and clinical findings and in-cludes measurement of mechanical axis alignment.

AUTHOR CONTRIBUTIONS

All authors were involved in drafting the article or revising itcritically for important intellectual content, and all authors ap-proved the final version to be published. Dr. Ferber had full accessto all of the data in the study and takes responsibility for theintegrity of the data and the accuracy of the data analysis.


Study conception and design. Mills, Hunt, Ferber.Acquisition of data. Mills, Ferber.Analysis and interpretation of data. Mills, Hunt.

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Biomechanical Deviations During Level Walking Associated ...

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