Post on 12-May-2023
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: rferber@ucalgary.ca.
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-
Biomechanical Changes Associated With Knee OA 1647
Tab
le2.
Det
ails
ofth
ein
clu
ded
stu
die
s*
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
Ast
eph
enet
al,
2008
(16)
Mod
erat
e:n
�60
,M
/F40
/20,
age
58.3
2�
9.31
year
s,B
MI
30.9
1�
5.17
kg/m
2
Sev
ere:
n�
61,
M/F
28/3
3,ag
e64
.49
�7.
75ye
ars,
BM
I32
.05
�5.
48kg
/m2
WO
MA
CM
oder
ate:
mil
dS
ever
e:m
oder
ate
Pre
dom
inan
tly
med
ial
com
par
tmen
t
Mod
erat
eS
ever
eN
�60
,M
/F23
/37,
age
50.2
7�
10.0
9ye
ars,
BM
I25
.45
�4.
04kg
/m2
Bal
iun
aset
al,
2002
(41)
N�
31,
M/F
13/1
8,ag
e65
�9
year
s,h
eigh
t1.
68�
0.09
m,
mas
s76
�12
kg
AC
Rcr
iter
ia,
HS
Sfu
nct
ion
alkn
eeev
alu
atio
n
Mil
dto
seve
reU
nil
ater
ald
isea
seM
edia
lco
mp
artm
ent
OA
(var
us)
N�
31,
M/F
13/1
8,ag
e62
�9
year
s,h
eigh
t1.
68�
12m
,m
ass
74�
16kg
Var
us
alig
nm
ent
7°�
4°B
ejek
etal
,20
05(3
1)N
�20
,M
/F8/
12,
age
68.2
�7.
1ye
ars,
hei
ght
1.69
�0.
11m
,m
ass
71.1
�11
.9kg
HS
Skn
eesc
orin
gsy
stem
Sev
ere
Bil
ater
al:
mos
tsy
mp
tom
atic
knee
Sev
ere
N�
20,
M/F
8/12
,ag
e68
.8�
9.1
year
s,h
eigh
t1.
69�
0.19
m,
mas
s73
.3�
11.4
kgB
utl
eret
al,
2011
(21)
Med
ial
OA
:n
�15
,ag
e66
.2�
7.9
year
s,B
MI
32.2
�7.
9kg
/m2
Pai
nV
AS
Mil
dto
seve
reU
nil
ater
alM
edia
lan
dla
tera
lco
mp
artm
ents
OA
N�
15,
age
56.3
�10
.7ye
ars,
BM
I27
.8�
5.7
kg/m
2
Lat
eral
OA
:n
�15
,ag
e65
.7�
6.4
year
s,B
MI
30.4
�7.
5kg
/m2
Ch
enet
al,
2003
(17)
N�
20,
M/F
0/20
,ag
e65
.5�
9.3
year
s,h
eigh
t1.
56�
0.7
m,
wei
ght
63.2
�10
.6kg
Ah
lbac
kgr
ade:
mod
erat
ean
dse
vere
chan
ges
Bil
ater
ald
isea
seM
oder
ate
tose
vere
N�
15,
M/F
0/15
,ag
e63
.5�
11.3
year
s,h
eigh
t1.
59�
0.9
m,
mas
s62
.6�
8.2
kgC
hil
ds
etal
,20
04(5
6)N
�24
,M
/F10
/14,
age
62�
10ye
ars,
BM
I30
�7
kg/m
2A
CR
clin
ical
crit
eria
,W
OM
AC
,K
OS
�M
ild
Un
ilat
eral
dis
ease
All
com
par
tmen
tsM
oder
ate
N�
24,
M/F
10/1
4,ag
e62
�10
year
s,B
MI
27�
6kg
/m2
Cre
aby
etal
,20
12(4
2)U
nil
ater
alp
ain
/un
ilat
eral
rad
iogr
aph
:n
�11
,M
/F6/
5,ag
e64
.5�
7.6
year
s,B
MI
31.1
�3.
8kg
/m2
Un
ilat
eral
pai
n/b
ilat
eral
rad
iogr
aph
:n
�22
,M
/F10
/12,
age
65.1
�9.
4ye
ars,
BM
I26
.8�
5kg
/m2
Bil
ater
alp
ain
/bil
ater
alra
dio
grap
h:
n�
56,
M/F
29/2
4,ag
e64
.5�
8ye
ars,
BM
I29
.9�
4.1
kg/m
2
Pai
nV
AS
All
grou
ps
varu
sal
ign
ed(i
.e.,
�18
2°)
Mil
d,
mod
erat
e,an
dse
vere
Un
ilat
eral
/bil
ater
ald
isea
seO
A(v
aru
s)N
�31
,M
/F11
/20,
age
63.8
�8
year
s,h
eigh
t1.
67�
0.09
m,
mas
s71
.3�
12.6
kg,
BM
I25
.5�
3.7
kg/m
2
(con
tin
ued
)
1648 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
Del
uzi
oan
dA
step
hen
,20
07(3
2)N
�50
,ag
e70
�7.
8ye
ars,
mea
nB
MI
29.2
kg/m
2S
ched
ule
dfo
rkn
eere
pla
cem
ent
Sev
ere
N�
63,
age
65�
8.5
year
s,m
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2
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hei
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ater
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ang
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dS
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ild
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Sev
ere:
mod
erat
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vere
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ater
al:
mos
tsy
mp
tom
atic
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Med
ial
com
par
tmen
t
Mil
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ever
eN
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mas
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bley
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2006
(30)
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M/F
29/1
1,ag
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8.07
year
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MI
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4.86
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2
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MA
C,
SF
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clin
ical
exam
inat
ion
Mil
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mod
erat
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nil
ater
ald
isea
seM
oder
ate
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M/F
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99ye
ars,
BM
I24
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/m2
Hu
bley
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eyet
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2009
(26)
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erat
e:n
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8.7
year
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ere:
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age
63.7
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kg/m
2
Cli
nic
alex
amin
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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
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9.7
year
s,B
MI
25.1
�4.
2kg
/m2
Hu
nt
etal
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9)M
ild
:n
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age
61.2
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hei
ght
1.65
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kgM
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age
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year
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mas
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ned
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)
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)
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M/F
5/15
,ag
e63
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12.4
year
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m,
mas
s69
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12.1
kg
(con
tin
ued
)
Biomechanical Changes Associated With Knee OA 1649
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
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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
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69ye
ars,
hei
ght
1.65
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09m
,m
ass
75.5
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WO
MA
Cp
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erag
ew
alki
ng
pai
nM
ild
varu
s:18
2°�
2.4°
Sev
ere
varu
s:17
9.5°
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0°
Mil
dS
ever
eM
edia
lco
mp
artm
ent
Mil
dS
ever
eS
ever
e:n
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s,h
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0.09
m,
mas
s84
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15.0
kg
Ko
etal
,20
11(4
4)S
ymp
tom
atic
:n
�17
,ag
e70
.24
�8.
49ye
ars,
BM
I28
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�4.
33kg
/m2
Asy
mp
tom
atic
:n
�24
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e72
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�8.
47ye
ars,
BM
I27
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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
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4�
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kg/m
2
Kra
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etal
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11(5
9)N
oto
rsio
nal
def
orm
ity:
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4,ag
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year
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mas
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kg,
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Tor
sion
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mit
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M/F
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age
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year
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eigh
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m,
mas
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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
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�4.
23kg
/m2
Lan
dry
etal
,20
07(3
4)N
�41
,ag
e58
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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
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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
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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
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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
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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
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,ag
e68
�11
year
s
McG
ibbo
nan
dK
rebs
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02(6
1)N
�13
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/F2/
11,
age
72.9
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ars
Not
rep
orte
dU
nil
ater
ald
isea
seO
AN
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6,ag
e73
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4.6
year
sM
cKea
net
al,
2007
(36)
N�
39,
M/F
24/1
5W
omen
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e58
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31ye
ars,
BM
I31
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5.2
kg/m
2
Men
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e55
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12.8
year
s,B
MI
29.7
�4.
6kg
/m2
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MA
C,
clin
ical
exam
inat
ion
Mil
dto
mod
erat
eM
oder
ate
N�
42,
M/F
18/2
4W
omen
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e48
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10.3
year
s,B
MI
24.4
�3.
6kg
/m2
Men
:ag
e52
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10.1
year
s,B
MI
24.7
�3.
2kg
/m2
Mes
sier
etal
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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
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9,ag
e73
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61ye
ars,
mas
s58
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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
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12.3
year
s,B
MI
26.1
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6kg
/m2
Mor
ese
vere
con
trol
s:n
�23
,M
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age
63.7
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2ye
ars,
BM
I27
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4kg
/m2
Ru
dol
ph
etal
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07(6
)N
�15
,M
/F8/
7,ag
e49
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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
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ore
sym
pto
mat
ickn
eeM
edia
lco
mp
artm
ent
Mod
erat
e(v
aru
s)N
�15
,M
/F8/
7,ag
e49
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4.25
year
s,B
MI
28.7
�5.
5kg
/m2
(con
tin
ued
)
Biomechanical Changes Associated With Knee OA 1651
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
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,M
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age
53�
10ye
ars,
BM
I26
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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
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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
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�16
.16
kg
Kn
eela
xity
asse
ssed
Var
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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
le2.
(Con
t’d
)
Au
thor
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ar(r
ef.)
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coh
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Cli
nic
alm
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res
Rad
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Biomechanical Changes Associated With Knee OA 1653
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)
Walking speed,m/second
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
Stride length(1.5 m/second)
OA (varus) Control 0.0 (�0.03, 0.03) 0.0
Stride length(1.7 m/second)
OA (varus) Control 0.01 (�0.02, 0.04) 0.11
Mundermann et al,2005 (33)
Walking speed,m/second
Mild Severe (varus) 0.01 (�0.13, 0.15) 0.04
Rutherford et al,2008 (25)
Walking speed,m/second
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)
Walking speed,m/second
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
Walking speed,m/second
Females Males 0.06 (�0.05, 0.17) 0.28
(continued)
1654 Mills et al
Table 3. (Cont’d)
Authors Outcome Study group ComparatorMean difference
(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
Walking speed,m/second
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
Knee peak flexion(2.0 m/second)
�23.1 (�26.42, �19.78) 4.22
Knee peak flexion(3.0 m/second)
�28.0 (�31.57, �24.43) 4.77
(continued)
Biomechanical Changes Associated With Knee OA 1655
Table 3. (Cont’d)
Authors Outcome Study group ComparatorMean difference
(95% CI) ES
Knee range of motion(1.0 m/second)
�25.4 (�30.95, �19.85) 2.78
Knee range of motion(2.0 m/second)
�31.5 (�36.75, �26.25) 3.64
Knee range of motion(3.0 m/second)
�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,
bilateral OABilateral 0.06 (�1.17, 1.29) 0.15
Unilateral Unilateral pain,bilateral OA
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
Unilateral Unilateral pain,bilateral OA
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)
Authors Outcome Study group ComparatorMean difference
(95% CI) ES
Landry et al, 2007(34)
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
Mundermann et al,2005 (33)
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)
Biomechanical Changes Associated With Knee OA 1657
Table 3. (Cont’d)
Authors Outcome Study group ComparatorMean difference
(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
Knee peak adductionmoment, Nm/kgand m
LateralMedial
ControlLateral
�0.14 (�0.21, �0.07)0.23 (0.16, 0.3)
1.422.33
Creaby et al, 2012(42)
Knee peak adductionmoment, Nm/kgand m
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,
bilateral OABilateral 0.16 (�0.07, 0.25) 1.01
Unilateral Unilateral pain,bilateral OA
�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
Unilateral Unilateral pain,bilateral OA
0.39 (0.14, 0.64) 1.23
Gok et al, 2002(38)
Knee peak flexionmoment, Nm/kg
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
Knee peak flexionmoment, Nm/kg
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)
Hip peak adductionmoment, Nm/kgand m
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
Knee peak adductionmoment, Nm/kgand m
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)
Authors Outcome Study group ComparatorMean difference
(95% CI) ES
Hurwitz et al, 2002(40)
Knee peak adductionmoment, Nm/kgand m
OA (varus) Control OA group wassignificantly higher(P � 0.027)
Kaufman et al,2001 (45)
Knee peak adductionmoment, Nm/kgand m
Females Males �0.08 (�0.2, 0.36) 0.1
Knee peak flexionmoment, Nm/kgand m
�0.16 (�0.42, 0.1) 0.22
Knee peak internalrotation moment,Nm/kg and m
0.09 (�0.02, 0.2) 0.3
Landry et al, 2007(34)
Knee peak adductionmoment, Nm/kg
Mild Control PCA: OA patientsexhibited largeroverall adductionmoments duringstance in both fastwalking andpreferred speeds
Knee peak flexionmoment, Nm/kg
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
Knee peak adductionmoment, Nm/kg
Females Controls andmales
PCA: OA femalesexhibited lowermagnitude thancontrols and OAmales
Knee peak flexionmoment, Nm/kg
Females Controls andmales
PCA: OA femalesexhibited lowermoment thancontrols and OAmales
Knee internal rotationmoment, Nm/kg
Females Controls andmales
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
Mundermann et al,2005 (33)
Hip peak adductionmoment, Nm/kgand m
MildMild
ControlSevere (varus)
�0.13 (�0.66, 0.40)0.52 (�0.06, 1.10)
0.150.54
Hip peak abductionmoment, Nm/kgand m
MildMild
ControlSevere (varus)
0.97 (0.14, 1.81)�0.57 (�1.45, 0.31)
0.730.41
Knee peak adductionmoment, Nm/kgand m
Mild Severe (varus) �0.79 (�1.28, �0.40) 1.17
(continued)
Biomechanical Changes Associated With Knee OA 1659
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)
Authors Outcome Study group ComparatorMean difference
(95% CI) ES
Rutherford et al,2008 (25)
Knee peak adductionmoment, Nm/kg
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)
Knee peak flexionmoment, Nm/kgand m
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
Knee peak adductionmoment, Nm/kg
�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
Knee peak adductionmoment, Nm/kg
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,
Knee peak adductionmoment, Nm/kg
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.
Biomechanical Changes Associated With Knee OA 1661
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.
Biomechanical Changes Associated With Knee OA 1663
Study conception and design. Mills, Hunt, Ferber.Acquisition of data. Mills, Ferber.Analysis and interpretation of data. Mills, Hunt.
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