ARTHRITIS & RHEUMATISM
Vol. 52, No. 8, August 2005, pp 2343–2349
DOI 10.1002/art.21277
© 2005, American College of Rheumatology
The Natural History of Anteroposterior Laxity and
Its Role in Knee Osteoarthritis Progression
Nimesh Dayal, Alison Chang, Dorothy Dunlop, Karen Hayes, Rowland Chang,
September Cahue, Jing Song, Leah Torres, and Leena Sharma
Objective. To test the hypotheses that 1) osteoar-
thritic (OA) knees at more advanced stages have less
anteroposterior (AP) laxity compared with OA knees at
milder stages, 2) AP laxity decreases over time, and 3)
the absence of a decrease in AP laxity is associated with
greater progression of medial tibiofemoral OA.
Methods. The study group comprised 230 patients
with knee OA (75% women, mean age 64 years, mean
body mass index [BMI] 30 kg/m2). At baseline and 18
months, AP laxity was measured (in millimeters of tibial
translation, under AP shear loading), and semiflexed
AP knee radiographs (with knee position confirmed by
fluoroscopy) were obtained. Osteophytes were graded
for each compartment, using a scale of 0–4. Disease
progression was measured as the amount of medial joint
space loss between baseline and followup, using linear
regression with generalized estimating equations.
Results. At baseline, measurements of AP laxity
were lower in knees with a Kellgren/Lawrence (K/L)
score of 4 (mean ⴞ SD 5.0 ⴞ 2.1 mm) than in those with
a K/L score of 0–1 (mean ⴞ SD 7.1 ⴞ 2.6 mm). There
was a weak negative correlation between osteophyte
grade and AP laxity. In knees with a K/L score of 0–2,
AP laxity was slightly lower at 18 months than at
baseline. AP laxity at baseline was not a predictor of
progression of OA. Knees without a decrease in AP
laxity had a greater loss of medial joint space (0.22 mm
Supported by the NIH (grants P60-AR-48098 and AR-48478
from the National Institute of Arthritis and Musculoskeletal and Skin
Diseases) and the Arthritis Foundation.
Nimesh Dayal, MD, Alison Chang, MS, Dorothy Dunlop,
PhD, Karen Hayes, PhD, Rowland Chang, MD, MPH, September
Cahue, BS, Jing Song, Leah Torres, BS, Leena Sharma, MD: Feinberg
School of Medicine, Northwestern University, Chicago, Illinois.
Address correspondence and reprint requests to Leena
Sharma, MD, 240 East Huron, Suite 2300, Feinberg School of Medi-
cine, Northwestern University, Chicago, IL 60611. E-mail: L-Sharma@
northwestern.edu.
Submitted for publication December 8, 2004; accepted in
revised form April 29, 2005.
2343
greater, after adjusting for age, sex, and BMI) than did
knees in which laxity decreased.
Conclusion. AP laxity at baseline is not predictive
of progression of OA. Although knees with a K/L score
of 4 had less AP laxity than those with a K/L score of
0–1, most of this difference was attributable to the
significant difference in AP laxity between knees with a
K/L score of 0–1 and knees with a K/L score of 2 (i.e.,
definite osteophytes). Knees in which AP laxity de-
creased had less medial joint space loss than did knees
without a decrease in AP laxity. The knee joint may
successfully compensate for AP laxity; the absence of
such compensation may have a deleterious effect.
Stability is a critical component of healthy joint
mechanics. At the knee, stability is provided by the
ligaments, capsule, bony geometry of the joint surfaces,
and tibiofemoral contact forces generated by muscle
activity and gravitational forces (1). Knee instability or
laxity is broadly defined as abnormal displacement or
rotation of the tibia with respect to the femur. Knee
laxity is associated with greater and more abrupt motion
of joint surfaces, as well as contact between poorly fitting
joint surfaces, which has the potential to damage artic-
ular cartilage and contribute to the progression of
osteoarthritis (OA).
The anterior and posterior cruciate ligaments of
the knee make a major contribution to anteroposterior
(AP) stability (2). In the canine model, anterior cruciate
ligament (ACL) transection leads to pathologic changes
of OA (3,4). According to results of retrospective studies
in humans (5–9), as many as 60–90% of knees sustaining
ACL rupture develop radiographic changes of OA
within 15 years of injury.
Evidence of ACL damage may be more common
in persons with idiopathic knee OA (i.e., the commonest
form of OA, which is not secondary to ACL tear) than in
age-matched controls (10), but it is unclear whether this
2344
abnormal ACL anatomy accelerates OA progression.
This has been examined in one study, in which the
presence of an ACL tear on magnetic resonance imaging
(MRI) did not increase the odds of joint space loss as
determined by radiography (11) but was predictive of
tibiofemoral cartilage loss on MRI (12).
AP knee instability may be directly assessed and
has been examined in patients with knee OA in a small
number of cross-sectional studies. Results of these stud-
ies suggest that greater disease severity is associated with
less AP laxity, despite the presence of ACL pathology in
the advanced stages of OA (13,14). Brage et al theorized
that AP laxity decreases over time in OA knees due to
osteophyte growth and soft tissue contracture (14).
Changes in AP laxity over time in patients with knee OA
has not as yet been reported.
A decrease in AP laxity over time in OA knees
would suggest that joint tissues compensate for the
instability. With successful compensation, it is likely that
neither ACL status nor AP laxity at one time point
would be a predictor of progression of knee OA. How-
ever, a lack of compensation, as reflected by the absence
of a decrease in AP laxity, may be associated with a
greater likelihood of OA progression.
The medial tibiofemoral compartment may be at
greater risk for OA progression due to AP laxity. During
walking in healthy knees, 60–80% of load passes through
the medial tibiofemoral compartment, making it more
vulnerable to factors that increase load across the knee,
including AP laxity. Posttraumatic ACL tears were predic-
tive of greater OA changes in the medial compartment
than in the lateral compartment (5,8,9), and change in
AP laxity in the setting of ACL injury was a predictor of
major meniscal tears more often in the medial compart-
ment than in the lateral compartment (15).
We tested the following hypotheses in patients
with knee OA: 1) the degree of AP laxity is lower at
more advanced stages of knee OA than at mild stages, 2)
AP laxity is decreased in knees with a higher osteophyte
grade, 3) AP laxity decreases over time in OA knees, and
4) a lack of decrease in AP laxity over time is associated
with a greater likelihood of medial tibiofemoral OA
progression.
PATIENTS AND METHODS
Participants. The Mechanical Factors in Arthritis of
the Knee (MAK) study is a longitudinal study of the contribu-
tion of mechanical factors to disease progression and func-
tional decrease in knee OA. Participants were recruited from
the community through advertising in periodicals target-
ing elderly persons, neighborhood organizations, letters to
DAYAL ET AL
members of the registry of the Beuhler Center on Aging at
Northwestern University, and via local medical center
referrals.
Inclusion and exclusion criteria were based on Na-
tional Institute of Arthritis and Musculoskeletal and Skin
Diseases/National Institute on Aging–sponsored multidisci-
plinary workshop recommendations for knee OA progression
studies (16). Inclusion criteria were definite tibiofemoral os-
teophyte presence (Kellgren/Lawrence [K/L] radiographic
score ⱖ2) (17) in 1 or both knees and at least some difficulty
with knee-requiring activity. Exclusion criteria were cortico-
steroid injection within the previous 3 months or history of
avascular necrosis, rheumatoid or other inflammatory arthritis,
periarticular fracture, Paget’s disease, villonodular synovitis,
joint infection, ochronosis, neuropathic arthropathy, acromeg-
aly, hemachromatosis, gout, pseudogout, or osteopetrosis.
Approval was obtained from the Office for the Protection of
Research Subjects–Institutional Review Board of Northwest-
ern University. Written consent was obtained from all partic-
ipants.
Measurement of AP laxity. AP laxity was evaluated
with the KT1000 arthrometer (MEDmetric Corporation, San
Diego, CA). This system reproducibly measures the anterior
and posterior displacement of the tibia that results from known
forces (18–22) and is used to assess anterior stability of the
knee before and after ACL reconstruction. The arthrometer is
strapped to the leg, and tibial translations are recorded relative
to the femur during AP shear loading.
Specifically, a thigh-support platform was placed under
both legs proximal to the popliteal space to maintain an angle
of 35° of knee flexion and establish the patella in the trochlea.
The patient’s heels were placed on a platform such that the
lateral malleoli rested proximal to upright components of the
platform, preventing external rotation. The arthrometer was
placed on the anterior tibia so that the patellar pad was on the
patella and completely proximal to the patellar tendon. A
distal Velcro strap was applied firmly around the calf to
stabilize the arthrometer. The examiner stabilized the patella
and pulled the force handle smoothly and slowly until tones
sounded at 15N and 20N. One examiner made all measure-
ments of AP translation. The intersession reliability for mea-
surements obtained by this examiner, who was testing subjects
of varying body habitus who had knee OA, was high (intraclass
correlation coefficients [ICCs] 0.95–0.99).
Acquisition of knee radiographs. In all participants,
bilateral, weight-bearing knee radiographs were obtained at
baseline and at 18 months, following the Buckland-Wright
protocol (23). According to this protocol, knee position, crite-
ria for beam alignment relative to the knee center, radiopaque
markers to account for magnification, and measurement land-
marks were specified.
The standing semiflexed view of the knee in this
protocol enhances the accuracy and reliability of medial joint
space assessment because it achieves superimposition of the
anterior and posterior tibial plateau lines. Specifically, the
knee was flexed until the tibial plateau was horizontal, parallel
to the beam and perpendicular to the film. To control for
rotation, the heel was fixed and the foot rotated until the tibial
spines were central within the femoral notch. Knee position
was confirmed by fluoroscopy before films were obtained. Foot
AP LAXITY AND PROGRESSION OF KNEE OA 2345

maps made at baseline were used to standardize repositioning

at 18 months.
Radiographic assessments and definition of progres-
sion. The K/L grading system was used to measure global
radiographic severity. According to this system, 0 ⫽ normal
(no osteophytes), 1 ⫽ possible osteophytes, 2 ⫽ definite
osteophytes and possible joint space narrowing, 3 ⫽ moderate/
multiple osteophytes, definite joint space narrowing, some
sclerosis, and possible attrition, and 4 ⫽ large osteophytes,
marked joint space narrowing, severe sclerosis, and definite
attrition. Osteophytes were graded separately for each com-
partment on a scale of 0–4, where 0 ⫽ none, 1 ⫽ possible, 2 ⫽
small, 3 ⫽ moderate, and 4 ⫽ large. The highest osteophyte
grade for a given knee within either the tibiofemoral or Figure 2. Anteroposterior (AP) laxity, anterior laxity, and posterior
patellofemoral compartment was determined. To assess me- laxity according to highest osteophyte grade per knee at baseline.
dial tibiofemoral OA progression, joint space was measured at
the narrowest point in the medial compartment, using calipers
with electronic readout, according to a previously described were used to examine the relationship between medial space
measurement protocol (24). Progression was defined as the loss and the absence of a baseline–to–18-month decrease in
loss of medial joint space between baseline and 18 months. AP laxity (defined as a decrease of ⱖ5% and, in further
Reliability for the single reader (LS) was very good for grading analyses, as a decrease of ⱖ10%).
(␬ ⫽ 0.85–0.86) and measurement (ICC 0.95–0.98). The
examiner who measured AP laxity and the radiograph reader RESULTS
were blinded to the results obtained by each other.
Of the 237 persons at risk for OA progression in
Statistical analysis. All descriptive and univariate sta-
tistical analyses examined measurements of AP, anterior, and at least 1 knee, 7 (3%) did not return at 18 months (5
posterior laxity in 1 knee per person (the right knee). Differ- died, and 2 could not be reached). Among the 230
ences in AP laxity related to the K/L score were analyzed using participants, 172 (75%) were women. The mean ⫾ SD
t-tests. The 95% confidence interval (95% CI) was calculated age of the participants was 64 ⫾ 11 years, and the
for the difference in AP laxity at baseline according to K/L
mean ⫾ SD BMI was 30 ⫾ 6 kg/m2. At baseline, the
score. Correlation coefficients and associated 95% CIs were
calculated for the association between the highest osteophyte distribution of disease severity (among right knees) was
grade and measures of AP laxity. The mean change in laxity as follows: 15 knees had a K/L score of 0–1, 108 knees
measures and 95% CIs between baseline and 18 months were had a K/L score of 2, 71 knees had a K/L score of 3, and
calculated. 36 knees had a K/L score of 4. At baseline, the mean ⫾
In knee-based analyses (i.e., using both knees), the
SD AP laxity was 5.7 ⫾ 2.2 mm and did not differ
relationship between baseline AP laxity measures and subse-
quent medial joint space loss (from baseline to 18 months), between men (5.5 ⫾ 2.0 mm) and women (5.8 ⫾ 2.3
adjusting for potentially influential factors (i.e., age, sex, body mm). AP laxity did not correlate with age (R ⫽ 0.02) in
mass index [BMI], baseline disease severity), was examined these individuals with established knee OA.
using multiple regression analysis with generalized estimating Baseline AP laxity. As shown in Figure 1, less AP
equations (GEE) to account for the correlation between knees
laxity was observed in knees with a K/L score of 4 than
within an individual patient (25). Multiple regression analyses

Figure 1. Anteroposterior (AP) laxity, anterior laxity, and posterior Figure 3. Change in anteroposterior (AP) laxity between baseline and
laxity according to Kellgren/Lawrence (K/L) score at baseline. 18 months, according to Kellgren/Lawrence (K/L) score.
2346 DAYAL ET AL

Figure 4. Change in anteroposterior (AP) laxity between baseline and 18 months,

according to highest osteophyte grade per knee.

in knees with a K/L score of 0–1 (5.0 ⫾ 2.1 mm versus
7.1 ⫾ 2.6 mm [95% CI 0.6, 3.4]). The difference in AP
laxity between knees with a K/L score of 0–1 and those
with a K/L score of 2–3 was significant (mean difference
1.3 [95% CI 0.04, 2.6]). The difference in AP laxity
between knees with a K/L score of 2–3 and those with a
K/L score of 4 was not significant (mean difference 0.7
[95% CI ⫺0.1, 1.5]).
For all K/L scores, anterior laxity was higher than
posterior laxity; both anterior and posterior laxity ap-
peared to be lower in knees with a K/L score of 4 than in
those with a K/L score of 0–1 (Figure 1). Figure 2 shows
AP laxity, anterior laxity, and posterior laxity according
to the maximum osteophyte grade, with a pattern of
distribution similar to that shown for AP laxity according
to K/L score. Weak negative correlations were observed
between the highest osteophyte grade and AP laxity
(R ⫽ ⫺0.20, P ⫽ 0.003), anterior laxity (R ⫽ ⫺0.13, P ⫽
0.04), and posterior laxity (R ⫽ ⫺0.16, P ⫽ 0.01) at the
baseline visit.
Change in AP laxity between baseline and 18
months. Next, we examined the course of AP laxity over
time. In all right knees without advanced OA, the level
of AP laxity was lower at 18 months than at baseline.
The mean change was a 0.4-mm decrease (95% CI 0.2,
0.7 [P ⫽ 0.002 for the difference between visits]). This
change was predominantly attributable to a decrease in
anterior laxity. The mean change in anterior laxity was
an 0.8-mm decrease (from 4.4 mm to 3.6 mm; 95% CI
0.6, 1.0 [P ⬍ 0.0001]). The mean change in posterior
laxity was a 0.4-mm increase (from 1.4 to 1.8 mm) (95%
CI 0.2, 0.5 [P ⬍ 0.0001]).
The change in AP laxity over time according to
K/L score is shown in Figure 3, and the change in AP

Figure 5. Change in anterior laxity between baseline and 18 months, according to

Kellgren/Lawrence (K/L) score.
AP LAXITY AND PROGRESSION OF KNEE OA
Figure 6. Change in posterior laxity between baseline and 18 months, according to
Kellgren/Lawrence (K/L) score.
laxity according to the highest osteophyte grade in
shown in Figure 4. The changes in anterior and posterior
laxity according to K/L score are shown in Figures 5 and
6, respectively. In knees with a K/L score of ⬍3, AP
laxity decreased slightly (Figure 3). Anterior laxity de-
creased slightly in knees with a K/L score of ⱕ3 (Figure
5). In knees with a K/L score of 4, AP laxity increased
slightly, and anterior laxity did not change. Posterior
laxity appeared to increase slightly in all knees, although
to a lesser degree in knees with a K/L score of 4 (Figure
6). Results for AP, anterior, and posterior laxity change
according to highest osteophyte grade were similar to
those determined according to the K/L score.
AP laxity and OA progression. The relationship
of AP, anterior, and posterior laxity to the loss of medial
joint space between baseline and 18 months was exam-
ined via multiple regression analysis using GEE. As
shown in Table 1, no measure of baseline AP laxity was
Table 1. Relationship between AP laxity and loss of medial joint
space over 18 months*
Coefficient (95% confidence interval)
Age-, sex-, and
Risk factor Unadjusted BMI-adjusted
AP laxity at baseline ⫺0.03 (⫺0.08, 0.008) ⫺0.03 (⫺0.07, 0.008)
Anterior laxity at ⫺0.02 (⫺0.07, 0.02) ⫺0.03 (⫺0.07, 0.02)
baseline
Posterior laxity at ⫺0.07 (⫺0.15, 0.006) ⫺0.57 (⫺0.13, 0.02)
baseline
Lack of decrease in 0.18 (0.01, 0.35) 0.22 (0.06, 0.38)
AP laxity
* Loss of medial joint space was the dependent variable. When the
95% confidence interval (95% CI) excluded 0, the coefficient was
significant. AP ⫽ anteroposterior; BMI ⫽ body mass index.
2347
predictive of medial joint space loss in either adjusted or
unadjusted analyses.
In knees in which AP laxity did not decrease, the
mean loss of medial joint space was 0.21 mm, compared
with a mean loss of 0.03 mm in knees in which AP laxity
decreased. This unadjusted difference (0.18) was statis-
tically significant (95% CI 0.01, 0.35) and persisted after
adjustment for age, sex, and BMI (Table 1). The ad-
justed coefficient of 0.22 indicates that knees in which
AP laxity did not decrease had an additional 0.22-mm
loss of joint space compared with the loss in knees in
which AP laxity did decrease. Further adjustment for
disease severity at baseline minimally affected the result
(the age-, sex-, BMI-, and disease severity–adjusted
coefficient was 0.19 [95% CI 0.03, 0.35]). The findings
were similar when an alternative definition of what
constituted a decrease in AP laxity (i.e., at least 10%)
was applied.
DISCUSSION
AP laxity was greater in knees with no or only
possible osteophytes than in knees with definite osteo-
phytes. In knees without advanced OA, there was a small
decrease in AP and anterior laxity between baseline and
18 months. AP, anterior, or posterior laxity at baseline
were not predictive of progression of OA between
baseline and 18 months. A lack of decrease in laxity
between baseline and 18 months was associated with a
greater loss of medial joint space.
Knees with severe OA had less AP laxity at
baseline than did knees with mild OA. These results are
consistent with those reported by Brage et al, who, using
a different approach to measuring AP laxity (Genucom
2348
Knee Analysis System; FARO Technologies, Lake
Mary, FL), also observed greater AP laxity in knees with
mild OA (15.2 ⫾ 7.9 mm) than in knees with advanced
disease (6.6 ⫾ 6.4 mm) (14). Similarly, using the Genu-
com system, Wada et al observed greater AP laxity in
knees with mild OA than in knees with severe OA
(10.0 ⫾ 6.3 mm versus 6.2 ⫾ 3.4 mm), despite the
presence of partial or complete ACL rupture at the time
of arthroscopy in many patients with severe disease; they
observed no relationship between ACL status and AP
laxity (13).
Based on the presumption that osteophytes are
the specific elements responsible for the difference in
AP laxity between early and later stages of OA (14), we
also assessed AP laxity in knee subgroups that were
defined according to the highest osteophyte grade. AP
laxity was lower in knees with the highest osteophyte
grade than in those with the lowest grade and was
inversely correlated, though only weakly, with osteo-
phyte grade. The current results are consistent with a
previous finding that ACL damage at mild to moderate
stages of OA increased (albeit nonsignificantly) the odds
of osteophyte enlargement (11). It is noteworthy that in
our study the major decrease in AP laxity appeared
between K/L grades 0–1 and K/L grade 2 (definite
osteophytes), and there was no evidence of a further
decrease in AP laxity at K/L grades 3 or 4.
Brage et al theorized that osteophyte growth and
capsular changes may lead to a decrease in AP transla-
tion (14), and Buckwalter et al noted that, based on
clinical experience, some unstable knees become more
stable with time without signs of progression except,
perhaps, osteophyte growth (26). However, we were not
able to identify a longitudinal study in which AP laxity
was measured directly in persons with knee OA; neither
the change in AP laxity over time nor its impact on
disease progression is known. In the current study, we
observed a small decrease in AP laxity over time in
knees with mild to moderate knee OA (i.e., K/L score
ⱕ3). The source of this decrease was a decrease in
anterior, and not posterior, laxity. A difference in
change between anterior and posterior laxity could, in
theory, be attributable to the direction of osteophyte
growth and the location of capsular manifestations. No
decrease in AP laxity over time occurred in knees with a
K/L score of 4, suggesting a “floor” effect in these knees.
The lack of a decrease in AP laxity—and not AP
laxity at a single time point at baseline—was associated
with OA progression. Our constellation of findings imply
that the OA pathologic process can compensate for AP
laxity. It may be that a certain magnitude or increment
DAYAL ET AL
of compensation is necessary in order to prevent AP
laxity–associated progression. Osteophyte growth would
ultimately decrease AP laxity, although some of this
growth may take place after cartilage loss has already
occurred. In a theoretical paradigm, the first compensa-
tion may occur in very early OA: with AP laxity at its
greatest, small osteophytes develop and the joint capsule
starts to thicken, with a subsequent decrease in AP
laxity. Second, with the appearance of definite osteo-
phytes, AP laxity decreases further, limiting its potential
to add to articular cartilage damage. It is possible that if
AP laxity does not decrease by a specific amount over a
certain time period, OA progresses. At some point a
floor level of AP translation is reached, and other factors
are responsible for OA progression. Ultimately, the
osteophyte response in OA that occurs at advanced
stages will bring AP laxity to its floor level in any knees
in which this level has not already been reached.
We observed a link between a lack of decrease in
AP laxity and the loss of medial joint space. The greater
load distribution to the medial compartment, even in
healthy knees, may make the medial compartment more
vulnerable to impairments such as changes in AP laxity.
Previous reports did not include a description of the
impact of AP laxity on OA progression but did describe
tibiofemoral compartment involvement with OA after
ACL injury. Although lateral tibiofemoral OA may
develop in a subset of knees with ACL insufficiency,
studies generally suggest that medial OA is more com-
mon (5,8,9). In 100 patients with functional AP instabil-
ity of the knee who had sustained a traumatic ACL
rupture 3 years previously, Irvine and Glasgow observed
that full-thickness tears were much more common in the
medial meniscus than in the lateral meniscus (15). The
greater prevalence of major tears medially may reflect
the relative immobility of the medial meniscus and its
action as a restraint to anterior tibial translation in the
cruciate-deficient knee (27).
Future studies should examine the lack of a
decrease in AP laxity in the period of time preceding
(and not concurrent with) the period of disease progres-
sion. In theory, it is biologically plausible that the lack of
a decline in AP laxity contributed to the progression of
OA. It is also possible that progression of medial OA
may contribute to the persistence of AP laxity via
cruciate ligament degeneration or may contribute to the
decline in AP laxity via osteophyte enlargement. A study
allowing serial examination of the periods of time during
which changes in and progression of AP laxity occur will
help to clarify the direction of the effect, and such a
study should be performed.
AP LAXITY AND PROGRESSION OF KNEE OA
We recognized that, in knees without a decrease
in AP laxity, more advanced OA at baseline could be
associated with both a faster rate of disease progression
and a floor effect for AP laxity. To address this possi-
bility, we excluded knees with advanced OA at baseline
and in the remaining knees adjusted for baseline disease
severity, and the results were not altered.
In summary, a higher osteophyte score was asso-
ciated with a lesser degree of AP laxity. Most of the
decrease in AP laxity occurred between K/L grade 0–1
and K/L grade 2 (the time at which definite osteophytes
appeared), with little decrease detected as osteophytes
enlarged further. AP laxity decreased a small amount
over time in knees without advanced OA. The severity of
AP laxity at a single time point was not a predictor of
OA progression. A lack of decrease in AP laxity was
associated with greater progression of medial tibiofemo-
ral OA.
REFERENCES
1. Markolf KL, Bargar WL, Shoemaker SC, Amstutz HC. The role of
joint load in knee stability. J Bone Joint Surg Am 1981;63:570–85.
2. Rosenberg A, Mikosz RP. Knee biomechanics. In: Scott WN,
editor. Ligament and extensor mechanism injuries of the knee. St.
Louis: Mosby; 1991. p. 33–58.
3. Pond MJ, Nuki G. Experimentally-induced osteoarthritis in the
dog. Ann Rheum Dis 1973;32:387–8.
4. Adams ME, Pelletier JP. Canine anterior cruciate ligament tran-
section model of osteoarthritis. In: Greenwald RA, Diamond HS,
editors. CRC handbook of animal models for the rheumatic
diseases. Boca Raton: CRC Press; 1988. p. 57–82.
5. Kannus P, Jarvinen M. Posttraumatic anterior cruciate ligament
insufficiency as a cause of osteoarthritis in a knee joint. Clin
Rheumatol 1989;8:251–60.
6. Jacobsen K. Osteoarthrosis following insufficiency of the cruciate
ligaments in man. Acta Orthop Scand 1977;48:520–6.
7. Dejour H, Walch G, Deschamps G, Champat P. Arthrosis of the
knee in chronic anterior cruciate laxity. Rev Chir Orthop
Reparatrice Appar Mot 1987;73:157–70.
8. Noyes FR, Mooar PA, Matthews DS, Butler DL. The symptomatic
anterior cruciate deficient knee. I. The long-term functional
disability in athletically active individuals. J Bone Joint Surg Am
1983;65:154–62.
9. McDaniel WJ, Dameron TB. The untreated anterior cruciate
ligament rupture. Clin Orthop 1983;172:158–63.
10. Hill CL, Seo GS, Gale D, Totterman S, Gale E, Felson DT. The
prevalence of cruciate ligament tears in osteoarthritis of the knee
and their association with disease severity and knee pain [abstract].
Arthritis Rheum 2003;48 Suppl 9:S78.
2349
11. Amin S, LaValley MP, Niu J, Seo GS, Hill CL, Gale D, et al.
Complete anterior cruciate ligament (ACL) tear and risk for
radiographic and symptom progression in subjects with knee
osteoarthritis [abstract]. Arthritis Rheum 2003;48 Suppl 9:S70.
12. Amin S, Guermazi A, LaValley M, Grigorian M, Hunter DJ, Gale
D, et al. Complete anterior cruciate ligament tear increases the
risk for cartilage loss in knee osteoarthritis [abstract]. Arthritis
Rheum 2004;50 Suppl 9:S142.
13. Wada M, Imura S, Baba H, Shimada S. Knee laxity in patients with
osteoarthritis and rheumatoid arthritis. Br J Rheumatol 1996;35:
560–3.
14. Brage ME, Draganich LF, Pottenger LA, Curran JJ. Knee laxity in
symptomatic osteoarthritis. Clin Orthop 1994;304:184–9.
15. Irvine GB, Glasgow MM. The natural history of the meniscus in
anterior cruciate insufficiency: arthroscopic analysis. J Bone Joint
Surg Br 1992;74:403–5.
16. Dieppe P, Altman R, Buckwalter JA, Felson DT, Hascall V,
Lohmander LS, et al. Standardization of methods used to assess
the progression of osteoarthritis of the hip or knee joints. In:
Kuettner KE, Goldberg VM, editors. Osteoarthritis disorders.
Rosemont (IL): American Academy of Orthopaedic Surgeons;
1995. p. 481–96.
17. Kellgren JH, Lawrence JS. Radiological assessment of osteoar-
throsis. Ann Rheum Dis 1957;16:494–501.
18. Daniel DM, Stone ML. KT1000 anterior-posterior displacement
measurements. In: Daniel DM, Akeson WA, O’Connor JJ, editors.
Knee ligaments: structure, function, injury and repair. New York:
Raven Press; 1990. p. 427–47.
19. Hanten WP, Pace MB. Reliability of measuring anterior laxity of
the knee joint using a knee ligament arthrometer. Phys Ther
1987;67:357–9.
20. Highgenboten CL, Jackson A, Meske NB. Genucom, KT1000, and
Stryker knee laxity measuring device comparisons: device repro-
ducibility and interdevice comparison in asymptomatic subjects.
Am J Sports Med 1989;17:743–6.
21. Wroble RR, van Ginkel LA, Grood ES, Noyes FR, Shaffer BL.
Repeatability of the KT-1000 arthrometer in a normal population.
Am J Sports Med 1990;18:396–9.
22. Malcolm LL, Daniel DM, Stone ML, Sachs R. The measurement
of anterior knee laxity after ACL reconstructive surgery. Clin
Orthop 1985;196:35–41.
23. Buckland-Wright C. Protocols for precise radio-anatomical posi-
tioning of the tibiofemoral and patellofemoral compartments of
the knee. Osteoarthritis Cartilage 1995;3 Suppl A:71–80.
24. Sharma L, Shamiyeh E, Felson DT, Cahue S, Song J, Dunlop DD.
The role of knee alignment in disease progression and functional
decline in knee osteoarthritis. JAMA 2001;286:188–95.
25. Zeger SL, Liang KY. Longitudinal data analysis for discrete and
continuous outcomes. Biometrics 1986;42:121–30.
26. Buckwalter JA, Lane NE, Gordon SL. Exercise as a cause of
osteoarthritis. In: Kuettner KE, Goldberg VM, editors. Osteoar-
thritis disorders. Rosemont (IL): American Academy of Ortho-
paedic Surgeons; 1995. p. 405–17.
27. Levy IM, Torzilli PA, Warren RF. The effect of medial meniscec-
tomy on anterior-posterior motion of the knee. J Bone Joint Surg
Am 1982;64:883–8.