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Variables associated with the progression of hip osteoarthritisA systematic review.

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Arthritis & Rheumatism (Arthritis Care & Research)
Vol. 61, No. 7, July 15, 2009, pp 925–936
DOI 10.1002/art.24641
© 2009, American College of Rheumatology
ORIGINAL ARTICLE
Variables Associated With the Progression of Hip
Osteoarthritis: A Systematic Review
ALEXIS A. WRIGHT,1 CHAD COOK,2
AND
J. HAXBY ABBOTT1
Objective. As populations age and the prevalence of hip osteoarthritis (OA) increases, health care providers must
manage increasing demands for services. Evidence regarding the progression of hip OA can assist health care practitioners in determining expected patient prognosis and planning care. This systematic review of prospective cohort studies
examines prognostic variables in patients with hip OA.
Methods. Articles were selected following a comprehensive search of Medline, EMBase, CINAHL, and Allied and
Complementary Medicine from database inception to October 2008 and hand searches of the reference lists of retrieved
articles. Inclusion criteria involved 1) estimates of the association between prognostic variables and progression of OA,
2) prospective cohort design, 3) patients diagnosed with hip OA based on established criteria, 4) at least 1 year of
followup, and 5) access to the full published text. Two independent reviewers assessed the methodologic quality of each
study and the association between prognostic variables and OA progression.
Results. Eighteen articles met the inclusion criteria; 17 were considered to be of high quality. Strong evidence of
progression was associated with age, joint space width at entry, femoral head migration, femoral osteophytes, bony
sclerosis, Kellgren/Lawrence hip grade 3, baseline hip pain, and Lequesne index score >10. Strong evidence of no
association with progression was associated with acetabular osteophytes. Evidence was weak or inconclusive regarding
associations between various other radiographic or clinical variables, molecular biomarkers, or use of nonsteroidal
inflammatory drugs.
Conclusion. Overall, few variables were found to be strongly associated with the progression of hip OA, and a variety of
other variables were weakly predictive of outcome.
INTRODUCTION
Osteoarthritis (OA) is the most common form of arthropathy (1), and is second only to heart disease as the predominant cause of functional decline in the elderly (2). OA of
the hip affects approximately 5% of the population age
⬎65 years, resulting in nearly 200,000 total hip replacements per year in the US (1). It has been estimated that the
aging population will give rise to a higher prevalence of
disabling OA because the number of people age ⬎60 years
is expected to increase by 20 –33% by 2030 (3). An aging
population, along with escalations in obesity and physical
Dr. Wright’s work was supported by a grant from the
Health Research Council of New Zealand.
1
Alexis A. Wright, PT, DPT, J. Haxby Abbott, PhD, MScPT,
FNZCP: University of Otago, Dunedin, New Zealand; 2Chad
Cook, PT, PhD, MBA, FAAOMPT: Duke University Medical
Center, Durham, North Carolina.
Address correspondence to Alexis A. Wright, PT, DPT,
School of Physiotherapy, University of Otago, Post Office
Box 56, Dunedin, New Zealand 9054. E-mail: lexie.wright@
gmail.com.
Submitted for publication January 26, 2009; accepted in
revised form April 3, 2009.
inactivity (4,5), would increase the economic burden to
society of disablement due to OA. It has been estimated
that loss of consumer and occupational productivity, diagnostic services, pharmacologic and nonpharmacologic
therapies, and surgical interventions due to OA cost approximately 0.7% of the US gross domestic product (5,6).
OA is a chronic disease that manifests inconsistently in
those afflicted. Recent prognostic studies have investigated variables that are associated with accelerated or delayed progression of joint destruction or functional loss
due to OA (7–9). Prognostic studies provide patients, physicians, and third-party payers with expectations in regard
to the course of symptoms, and help distinguish between
patients who are at high risk for worsening pain and
disability versus those with a more favorable clinical
course.
The objective of this study was to systematically review
the evidence regarding useful prognostic variables associated with the progression of hip OA. This review involved
a systematic review of available articles using contemporary methods of identification and assessment of the available evidence (10,11). The findings may assist in outlining
effective diagnostic and intervention strategies for patients
with OA.
925
926
Wright et al
Table 1. Criteria list for the methodologic quality assessment of studies on prognostic
factors in patients with hip osteoarthritis
Criteria
Study population
A
B
C
Response
D
Followup
E
F
G
H
Treatment
I
Prognostic factors
J
K
L
Outcome
M
N
O
Data presentation
P
Q
R
Methodologic quality
Score*
Inception cohort
Description of study population
Description of inclusion and exclusion criteria
⫹/⫺/?
⫹/⫺/?
⫹/⫺/?
Response of ⱖ75% for cohorts and controls
⫹/⫺/?
Followup of at least 12 months
Dropouts/loss to followup ⬍20%
Information completers vs. loss to followup/dropouts
Prospective data collection
⫹/⫺/?
⫹/⫺/?
⫹/⫺/?
⫹/⫺/?
Treatment in cohort is fully described/standardized
⫹/⫺/?
Clinically relevant potential prognostic factors
Standardized or valid measurements
Data presentation of the most important prognostic factors
⫹/⫺/?
⫹/⫺/?
⫹/⫺/?
Clinically relevant outcome measures
Standardized or valid measurements
Data presentation of the most important outcome
measures
⫹/⫺/?
⫹/⫺/?
⫹/⫺/?
Appropriate analysis techniques
Prognostic model is presented
Sufficient numbers
⫹/⫺/?
⫹/⫺/?
⫹/⫺/?
* ⫹ ⫽ positive (sufficient information and a positive assessment); ⫺ ⫽ negative (sufficient information,
but potential bias due to inadequate design or conduct); ? ⫽ unclear (insufficient information).
MATERIALS AND METHODS
Identification and selection of the literature. We conducted a systematic, computerized search of the literature
based on recommendations by Wilczynski and Haynes
(10,11) in Medline (1950 to October 2008), EMBase (1988
to October 2008), CINAHL (1951 to October 2008), and
Allied and Complementary Medicine (AMED) (1985 to
October 2008) (the search strategy is shown in Supplementary Appendix A, available in the online version of this
article at http://www3.interscience.wiley.com/journal/
77005015/home). The reference lists of all selected publications were checked to retrieve relevant publications
that were not identified in the computerized search. To
identify relevant articles, titles and abstracts of all identified citations were independently screened by 2 reviewers
(AAW, JHA). Full-text articles were retrieved if the abstract provided insufficient information to establish eligibility or if the article had passed the first eligibility
screening.
Selection criteria. An article was eligible if it met all of
the following criteria: 1) the statistical association of at
least 1 prognostic variable with the outcome of interest
reported, 2) derived from a prospective cohort of subjects,
3) included radiographic or clinical evidence of hip OA
based on established criteria, 4) the outcome of interest
was radiologic and/or clinical progression of hip OA, 5)
the followup period was at least 1 year, and 6) the article
was available in full text. No language restrictions were
imposed.
An article was excluded if 1) the study population principally included patients with secondary OA, including
major congenital or developmental diseases and bone dysplasias; metabolic diseases associated with joint disease
such as hemochromatosis, rheumatoid arthritis, tuberculosis, ankylosing spondylitis, sickle cell disease, and
Cushing’s syndrome; infection; other bone diseases such
as Perthes disease and osteochondritis; femoral head necrosis; and trauma (fractures); or 2) the article discussed
prognosis following joint replacement surgery, osteotomy,
or other specific surgery.
All criteria were independently applied by 2 reviewers
(AAW, JHA) to the full text of the articles that passed the
first eligibility screening. In case of disagreement, a consensus method was used to discuss and solve the disagreement.
Quality assessment. The methodologic quality of each
of the studies was independently assessed by the same 2
reviewers (AAW, JHA). Reviewers were not masked to trial
identifiers such as author and journal names. To our
knowledge, there is presently no consensus standard for
the assessment of prognostic studies; therefore, we used a
modified version of checklists used in other systematic
reviews of prognostic variables in musculoskeletal disor-
Systematic Review of the Progression of Hip OA
927
Table 2. Levels of evidence for prognostic factors on
hip osteoarthritis
1.
2.
3.
4.
5.
Evidence obtained from high-quality cohort studies
Evidence obtained from lesser-quality cohort studies
Case–controlled or retrospective studies
Case series
Expert opinion
ders (12–14) that reflected the important methodologic
aspects (15). The final checklist consisted of 18 items
(Table 1), with each having a “yes”/“no”/“don’t know”
answer option. A “yes” score indicated sufficient information and a positive assessment, with bias considered unlikely. A “no” score indicated sufficient information, but
with potential bias from inadequate design or conduct. A
“don’t know” score indicated that insufficient information
was provided in the article or the methodology was unclear. Disagreements among the reviewers were discussed
during a consensus meeting and, where unresolved, were
resolved by a third reviewer (CC). A detailed explanation
of each of the criteria is available from the corresponding
author.
The maximum attainable score on the criteria list was
18. The total score was the count of all of the criteria that
scored “yes.” “No” and “don’t know” scores carried a zero
score value. For each study, a total quality score was given
based on the information from all of the available publications. A priori, we chose to consider a study to be of high
quality if it scored ⱖ12 points (ⱖ66.6% of the maximum
attainable score), and of low quality if its score was ⬍12
points. The cut point score was arbitrary but similar to
other previously mentioned systematic reviews on prognosis (13,14).
Data abstraction. One reviewer (AAW) independently
extracted information and data regarding study population, setting, outcome measures, prognostic variables, and
strength of association statistics associated with the prognostic variables. Another reviewer (JHA) reviewed and
confirmed the abstracted results. The second reviewer
(JHA) was not blinded to the results abstracted by the first
reviewer (AAW).
Statistical analysis. Interobserver agreement of quality
assessment was assessed using kappa statistics. Because
unadjusted kappa can provide misleading results when
the sample size is small (16) or if the data are highly
symmetric or unbalanced, despite high observed agreement (17), we calculated an adjusted kappa. The adjusted
kappa was calculated from the unadjusted kappa divided
by the maximum kappa (16).
We tabulated the available evidence for each prognostic
variable by reporting the number of articles evaluating
each variable, the methodologic quality of the articles, and
the strength and grade of the available evidence. The
strength of evidence for prognostic variables associated
with progression of OA of the hip was assessed by defining
4 levels of evidence based on those by Phillips et al (18)
(Tables 2 and 3). Findings were reported as relative risks,
odds ratios, hazard ratios, or P values.
RESULTS
Selection of studies. Initially, the search yielded 3,018
citations (Medline 1,298, EMBase 1,530, CINAHL 124, and
AMED 66). Of these, 363 duplicates were deleted, leaving
2,655 titles with abstracts for review. After the first screening, the full-text studies of 40 potentially eligible citations
were retrieved. Following a consensus meeting, a total of
18 studies were included in the review (7–9,19 –33) (Figure 1). Reference checking did not provide any additional
studies.
Methodologic quality. The 2 primary reviewers (AAW,
JHA) required clarification from a third reviewer (CC) for
the interpretation of 2 quality assessment criteria (item A
and item R). Following clarification, the adjusted interobserver agreement was ␬ ⫽ 0.68, calculated from the unadjusted ␬ ⫽ 0.51 and maximum ␬ ⫽ 0.75. This finding
represents substantial agreement (34). Items E and H were
not included because all studies scored “yes” based on our
inclusion criteria.
Disagreements occurred mainly because of reading errors and misinterpretation of the methodologic criteria list
and were readily resolved, with only 1 disagreement persisting (item I: Ledingham et al [33]). The third reviewer
Table 3. Grades of evidence for prognostic factors on hip osteoarthritis*
Grades of recommendation
A. Strong evidence
B. Moderate evidence
C. Weak evidence
D. Conflicting evidence
E. Theoretical/foundational evidence
F. Expert opinion
Consistent findings (ⱖ75%) in ⱖ2 high-quality cohort
studies
Consistent findings (ⱖ75%) in 1 high-quality cohort
and ⱖ1 low-quality cohort
Findings in 1 high-quality cohort study or consistent
findings (ⱖ75%) in ⱖ3 low-quality cohorts
Inconsistent or inconclusive studies of any level or 1
low-quality study
No data presented
No data presented
* Modified from the Oxford Centre for Evidence-Based Medicine (18).
928
Wright et al
Most methodologic shortcomings concerned the following items: description of inception cohort, failure to describe response rate, failure to report numbers lost to followup, failure to provide information on completers
versus those lost to followup, and failure to determine a
collection of prognostic variables with the highest prognostic value using multivariate techniques.
Study characteristics. Supplementary Appendix B outlines the characteristics of the articles, including study
population, outcome measures, followup, prognostic variables, and the strength of association with outcome (estimates and 95% confidence intervals) (Supplementary Appendix B, available in the online version of this article
at http://www3.interscience.wiley.com/journal/77005015/
home). We found that several studies were conducted in a
common cohort of subjects, and so grouped according to
the study cohorts (Evaluation of the Chondromodulating
Effect of Diacerein in Osteoarthritis of the Hip [7,8,19,
20,22], Study of Osteoporotic Fractures [9,24,25,27,32,35],
and the Rotterdam Study [28 –31]). Of the 18 different
articles, 7 included patients referred from rheumatologists,
10 from the general population, and 1 from both rheumatology and orthopedic clinics.
There was considerable variation among the studies
with respect to sample size, length of followup, diagnostic
criteria, and definition of progression. The sample size
ranged from 48 to 1,904, with 12 studies enrolling ⬎300
subjects and 4 enrolling ⬎1,000 subjects (28 –31). The
length of followup ranged from 12 months to 8 years. OA
diagnosis at baseline was determined based on 3 different
criteria: American College of Rheumatology (36), Croft
summary grade, and Kellgren/Lawrence (K/L) grade. Four
studies defined the progression of OA as joint space narrowing (JSN) alone, although the studies varied in their
definition of progression (0.5, 0.6, 1.0, or 1.5 mm/year).
Two studies defined OA progression as total hip arthroplasty (THA) alone, and 3 used a combination of JSN or
Figure 1. Retrieval of studies for the review.
(CC) made the final decision in this case. The results of the
quality assessment are shown in Table 4. The studies are
ranked in descending order by methodologic quality score.
The overall quality score ranged from 10 to 17 points and
17 studies were classified as high-quality studies. The
median score was 13 points (72.2%).
Table 4. Results of the methodologic assessment
Author, year (ref.)
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
Quality
score
Mazieres et al, 2006 (7)
Dougados et al, 1996 (19)
Dougados et al, 1997 (20)
Dougados et al, 1999 (8)
Gossec et al, 2005 (21)
Maillefert et al, 2003 (22)
Conrozier et al, 1998 (23)
Beattie et al, 2005 (24)
Chaganti et al, 2008 (25)
Kelman et al, 2006 (26)
Lane et al, 2004 (9)
Lane et al, 2007 (27)
Reijman et al, 2004 (28)
Reijman et al, 2005 (29)
Reijman et al, 2007 (30)
Reijman et al, 2005 (31)
Hochberg 2004 (32)
Ledingham et al, 1993 (33)
1
1
1
1
1
1
0
0
0
0
0
0
0
0
0
0
1
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
0
0
0
1
0
1
1
1
1
0
1
0
0
0
0
0
0
0
0
1
0
0
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
1
1
1
0
1
1
0
0
0
0
0
0
0
0
0
0
0
1
0
0
1
1
0
1
0
0
0
0
0
1
0
0
0
0
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
0
0
1
1
1
1
1
1
1
1
1
1
1
1
1
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
0
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
1
1
1
1
1
1
1
0
1
1
1
1
1
1
1
1
1
1
1
1
0
0
0
1
0
0
0
0
0
0
0
0
1
0
0
0
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
0
17
15
15
15
15
15
14
13
13
13
13
13
13
13
13
12
12
10
Systematic Review of the Progression of Hip OA
929
THA. The remaining 9 studies used a combination of JSN,
THA, increased osteophyte score, bony sclerosis, or an
increase in a Croft summary grade or K/L grade to define
OA progression. The percentage lost to followup varied
between 0% and 40%. The most frequently reported prognostic variables were age, sex, and joint space width (JSW).
erance (33). One variable, male sex (33), demonstrated
inconclusive (Level 2D) evidence for no progression of hip
OA. Intermediate bone response (33) demonstrated inconclusive (Level 2D) evidence for no association with the
progression of hip OA.
Prognostic variables. Table 5 shows a summary of the
evidence for the prognostic variables reported with regard
to each associated outcome and overall level of evidence.
Level 1A evidence: strong. Eight variables demonstrated
the strongest level of evidence (Level 1A) and were predictive of the progression of hip OA: age (7,8,19,29), JSW
at entry (7,8,19,20,29), femoral head migration (7–9,19,20,
32,33,35), femoral osteophytes (9,32,35), bony sclerosis
(9,20), K/L hip grade 3 (8,21,33), baseline hip pain
(8,9,29,32,33,35), and Lequesne index score ⱖ10 (8,19).
Acetabular osteophytes (9,20,32,35) demonstrated
strong (Level 1A) evidence for no association with the
progression of hip OA.
Level 1C evidence: weak. The following variables were
assigned the score of Level 1C because each was reported
in only 1 high-quality study: acetabular and femoral osteophytes (9), K/L hip grade ⱖ2 (29), K/L hip grade ⱖ2 plus
hip pain (29), K/L hip grade 4 (21), a combination of
radiographic grade 3 or 4 plus previous nonsteroidal antiinflammatory drug (NSAID) use and global assessment
above the median (21), functional impairment ⱖ2 (7),
mean global patient assessment ⬎47 over the first 6
months (21), disability index score ⱖ0.5 (29), restricted
flexion ⬎20% (29), molecular biomarker C-terminal
crosslinking telopeptide of type II collagen (CTX-II) ⬎346
ng/mmoles of urinary creatinine (7), molecular biomarker
serum hyaluronic acid ⬎137 mg/ml (7), CTX-II ⬎346 ng/
mmoles of urinary creatinine plus serum hyaluronic acid
⬎137 mg/ml (7), and baseline hip pain plus diclofenac
⬎180 days (31) are predictive of the progression of hip OA.
Body mass index (30), the presence of cysts (9), molecular biomarker CTX-II (28), molecular biomarker Frizzledrelated protein (27), baseline serum N-telopeptide crosslinks (NTX) (26), percent change in serum NTX (25), statin
user (24), previous NSAID intake (21), ibuprofen (⬎30
days) (31), naproxen (⬎30 days) (31), diclofenac (⬎30
days) (31), and piroxicam (⬎30 days) (31) demonstrated
weak (Level 1C) evidence of no association with the progression of hip OA.
Molecular biomarker Dkk-1 (27) and percent change in
serum cartilage oligomeric matrix protein (COMP) (25)
demonstrated weak (Level 1C) evidence of reduced progression of hip OA.
Level 1D evidence: inconclusive. There is inconclusive
(Level 1D) evidence that female sex (7,8,19,22,29,33) and
baseline serum COMP (23,26) are associated with the progression of hip OA.
Level 2D evidence: inconclusive. Seven variables demonstrated inconclusive (Level 2D) evidence and were predictive for the progression of hip OA: atrophic bone response (33), mild OA (33), any radiographic change (33),
rapid radiographic change (33), night pain (33), patient
assessment of change (33), and a decrease in exercise tol-
DISCUSSION
This systematic review has summarized the results of 18
prospective cohort studies reporting the prognostic value
of various variables for the progression of radiographic JSN
or THA. The evidence is weak or inconclusive on most
prognostic variables because of inconsistencies in the way
data is collected and measured, dissimilar outcome measures, and when variables were reported in few articles.
Heterogeneity in diagnostic criteria, definitions of progression, and variations in the definitions of the prognostic
variables themselves prevent us from performing a metaanalysis; therefore, each article must be described separately. This resulted in weak or inconclusive evidence for
many variables. However, there was strong evidence that
age, JSW at entry, femoral head migration, femoral osteophytes, bony sclerosis, K/L hip grade 3, baseline hip pain,
and Lequesne index score ⱖ10 are predictive of poorer
outcome or progression of hip OA. Similarly, there was
strong evidence that acetabular osteophytes demonstrate
no association with the progression of hip OA.
Our findings updated those reported in an earlier review
performed in 2002 (12). In contrast to the previously reported review, we did not restrict our search by publication language, we used the search strategy guidelines by
Wilczynski and Haynes (10,11), and we used contemporary methods for the identification and assessment of
available evidence. In contrast to the findings of Lievense
et al (12), we found a higher age at baseline assessment and
JSW at entry to demonstrate strong evidence of poorer
outcome or progression of hip OA. We could not confirm
the strong prognostic value of atrophic bone response for
progression. Furthermore, we found that body mass index
demonstrated weak (Level 1C) versus strong evidence for
no association with progression. These discrepancies are
likely associated with the more recently available evidence and our inclusion and exclusion criteria, which
included only prospective study designs and excluded
patients with congenital or developmental bone dysplasias. We only included studies with a prospective study
design because this is considered to be the optimal design
to minimize bias in the association between prognostic
variables and outcome. We believed that a followup period
of ⬎1 year was needed in order to study the course of
chronic hip OA. Therefore, some otherwise relevant studies (37,38) were not eligible for our review.
There were some limitations of this review. Of the 18
articles included, 15 were derived from 3 patient cohorts.
Therefore, we decided to evaluate and report the findings
from each individual article. Separate reporting may risk
bias resulting from statistical associations reported twice
from the same cohort. The lack of independent study cohorts highlights that prognostic research regarding variables associated with the progression of hip OA is under-
930
Wright et al
Table 5. Overall level of evidence for prognostic factors and their association with long-term outcome*
Prognostic factor
Studies
reporting
Level of
evidence
Demographic variables
Female
6
1D
Outcome
JSN
JSN or THA
THA
High-quality studies, association
(95% CI)†
OR 2.51 (1.49–4.23) at 1 year (19)
OR 2.34 (1.1–5.2) at 1 year (22)
Adj RR 1.20 (0.88–1.63) at 3 years (7)
Adj OR 1.8 (1.4–2.4) at 6.6 years (29)
RR 1.71 (1.11–2.62) at 3 years (8)
RR 1.26 (0.872–1.822) at 5 years (22)
Global assessment
of change
Male
1
2D
Global assessment
of change
Higher age at study
entry
4
1A
JSN
Low-quality studies,
association (95% CI)
OR 2.53 (0.91–7.41) for
rapid change at 1
year (33)
OR 2.33 (1.2–4.34) for
no change at 1 year
(33)
OR 1.90 (1.18–3.08) at 1 year (19)
JSN or THA
BMI, kg/m2
Radiographic variables
JSW at entry
1
1C
5
1A
Adj RR 1.21 (0.90–1.63) at 3 years (7)
Adj OR 1.06 (1.04–1.08) at 6.6 years
(29)
THA
RR 1.65 (1.06–2.56) at 3 years (8)
JSN ⱖ1 mm
Adj OR 0.9 (0.6–1.3) for BMI ⬎25–27.5
at 6.6 years (30)
Adj OR 0.9 (0.6–1.3) for BMI ⬎27.5 at
6.6 years (30)
JSN ⱖ1.5 mm
Adj OR 1.5 (0.6–3.8) for BMI ⬎25–27.5
at 6.6 years (30)
Adj OR 1.5 (0.6–3.7) for BMI ⬎27.5 at
6.6 years (30)
Increase of ⱖ1 in Adj OR 1.1 (0.8–1.6) for BMI ⬎25–27.5
K/L grade
at 6.6 years (30)
Adj OR 1.3 (0.9–1.8) for BMI ⬎27.5 at
6.6 years (30)
JSN
JSN or THA
Migration (lateral/
concentric,
superior, medial,
superolateral,
superomedial of
the femoral head)
7
1A
THA
JSN
JSN or THA
THA
Combination†
Global assessment
of change
OR 2.11 (1.30–3.44) at 1 year (19)
OR 1.8 (1.19–2.76) at 2 years (20)
Adj RR 1.36 (1.02–1.82) at 3 years (7)
Adj OR 1.9 (1.2–2.9) at 6.6 years (29)
RR 1.85 (1.18–2.90) at 3 years (8)
OR 4.25 (2.26–8.01) at 1 year (19)
OR 1.70 (1.10–2.63) at 2 years (20)
Adj RR 2.34 (1.66–3.30) at 3 years (7)
RR 1.96 (1.27–3.02) at 3 years (8)
Adj OR 2.6 for superolateral JSN ⫹ 2
at 8 years (P ⬍ 0.05) (32,35)‡
Adj OR 14.9 for superolateral JSN ⬎2
at 8 years (P ⬍ 0.01) (32,35)‡
Adj OR 1.7 for superomedial JSN ⫹ 2
at 8 years (not stated) (32,35)‡
Adj OR 5.0 for superomedial JSN ⬎2
at 8 years (P ⬍ 0.01) (32,35)‡
OR 0.7 (0.3–1.5) for concentric JSN at
8 years (9)
OR 1.9 (1.0–3.6) for superolateral JSN
at 8 years (9)
OR 0.7 (0.5–1.2) for superomedial JSN
at 8 years (9)
OR 3.71 (1.09–13.83)
for medial/axial
migration and no
change at 1 year (33)
(continued)
Systematic Review of the Progression of Hip OA
931
Table 5. (Cont’d)
Prognostic factor
Studies
reporting
Level of
evidence
Outcome
High-quality studies, association
(95% CI)†
Low-quality studies,
association (95% CI)
OR 11.41 (2.47–72.79)
for indeterminate
migration and no
change at 1 year (33)
OR 0.13 (0.05–0.35) for
superior migration
and no change at 1
year (33)
OR 9.00 (1.24–183.52)
for superior
migration and rapid
change at 1 year (33)
Acetabular
osteophytes only
3
1A
JSN
THA
Femoral osteophytes
only
2
1A
Combination†
Combination†
THA
Acetabular and
femoral
osteophytes
Bony sclerosis
present
K/L hip grade ⱖ2
K/L hip grade ⱖ2 ⫹
hip pain
K/L hip grade 3
1
1C
Combination†
2
1A
1
1
1C
1C
JSN
Combination†
JSN or THA
JSN or THA
3
1A
THA
OR 7.04 (0.91–54.35) at 2 years (20)
Adj OR 1.5 at 8 years (P value not
stated) (32,35)‡
OR 1.3 (0.8–2.2) at 8 years (9)
OR 4.9 (3.0–8.1) at 8 years (9)
Adj OR 2.7 at 8 years (P ⬍ 0.01)
(32,35)‡
OR 2.5 (1.4–4.6) at 8 years (9)
OR 1.68 (1.08–2.02) at 2 years (20)
OR 3.7 (2.6–5.2) at 8 years (9)
Adj OR 5.8 (4.0–8.4) at 6.6 years (29)
Adj OR 24.3 (11.3–52.1) at 6.6 years
(29)
RR 1.89 (1.21–2.96) at 3 years (8)
OR 3.3 (1.7–6.4) at 2 years (21)
Global assessment
of change
OR 2.88 (1.27–6.52) for
slow change at 1
year (33)
K/L hip grade 4
Mild OA (K/L hip
grade 2)
1
1
1C
2D
THA
OR 5.3 (2.6–10.8) at 2 years (21)
Global assessment
of change
Atrophic bone
response
1
2D
Global assessment
of change
THA
Intermediate bone
response
1
2D
Global assessment
of change
Cysts present
Any radiographic
change
Rapid radiographic
change
2 of 3 of radiographic
grade 3 or 4,
previous NSAID
intake, and global
assessment above
the median
3 of 3 of radiographic
grade 3 or 4,
previous NSAID
intake, and global
assessment above
the median
1
1
1C
2D
Combination†
THA
1
2D
THA
1
1C
THA
OR 3.0 (1.6–5.9) at 2 years (21)
1
1C
THA
OR 5.6 (2.6–12.2) at 2 years (21)
OR 15.05 (3.31–94.99)
for no change at 1
year (33)
OR 8.31 (3.18–21.98)
for rapid change at 1
year (33)
OR 3.13 (1.28–7.69) at
1 year (33)
OR 2.52 (0.97–6.77) for
slow change at 1
year (33)
OR 1.8 (1.0–3.3) at 8 years (9)
OR 2.19 (1.18–4.08) at
1 year (33)
OR 5.83 (1.90–19.11) at
1 year (33)
(continued)
932
Wright et al
Table 5. (Cont’d)
Prognostic factor
Clinical variables
Baseline hip pain
Studies
reporting
Level of
evidence
5
1A
THA
Disability score
change of ⱖ4 or
THA
JSN
JSN or THA
Increased Croft
summary score
ⱖ1
Increase in
osteophytes of
ⱖ2
Combination†
THA
Night pain
1
2D
Lequesne index ⱖ10
2
1A
Functional
impairment ⱖ2
Mean global patient
assessment ⬎47
over the first 6
months
Patient assessment
of change
Disability index
score ⱖ0.5
Decrease in exercise
tolerance
Restricted flexion
⬎20%
Molecular biomarkers
CTX-II
1
Outcome
RR 1.86 (1.23–2.83) at 3 years (8)
Adj OR 8.1 (4.2–15.4) at 8 years
(32,35)1 year (33)
Adj OR 2.93 (2.01–4.27) at 8 years (9)
Low-quality studies,
association (95% CI)
OR 2.80 (1.49–5.31) at
Adj OR 1.9 (1.4–2.6) at 8 years (32,35)
Adj OR 2.4 (1.7–3.5) at 6.6 years (29)
Adj OR 1.5 (1.0–2.1) at 8 years (32,35)
Adj OR 2.0 (1.4–2.9) at 8 years (32,35)
Adj OR 1.98 (1.5–2.7) at 8 years (9)
OR 2.73 (1.45–5.16) at
1 year (33)
1C
JSN
THA
JSN or THA
OR 2.66 (1.46–4.83) at 1 year (19)
RR 2.59 (1.73–3.88) at 3 years (8)
Adj RR 1.52 (1.10–2.07) at 3 years (7)
1
1C
THA
OR 2.2 (1.4–3.2) at 2 years (21)
1
2D
THA
1
1C
JSN or THA
1
2D
THA
1
1C
JSN or THA
Adj OR 3.1 (2.1–4.7) at 6.6 years (29)
1
1C
JSN ⱖ1 mm
OR 11.31 (5.24–24.73)
at 1 year (33)
Adj OR 1.9 (1.4–2.6) at 6.6 years (29)
OR 2.68 (1.29–5.60) at
1 year (33)
1
1C
JSN or THA
Adj OR 1.0 (0.4–2.4) for CTX-II 2.11–
2.25 at 6.6 years (28)
Adj OR 2.1 (0.9–4.6) for CTX-II 2.26–
2.39 at 6.6 years (28)
Adj OR 1.7 (0.7–4.0) for CTX-II ⱖ2.40
at 6.6 years (28)
Adj OR 3.9 (0.4–36.9) for CTX-II 2.11–
2.25 at 6.6 years (28)
Adj OR 8.3 (1.0–72.2) for CTX-II 2.26–
2.39 at 6.6 years (28)
Adj OR 8.4 (1.0–72.9) for CTX-II ⱖ2.40
at 6.6 years (28)
Adj RR 2.00 (1.49–2.70) at 3 years (7)
1
1C
JSN or THA
Adj RR 1.69 (1.25–2.27) at 3 years (7)
1
1C
JSN or THA
Adj RR 3.73 (2.48–5.61) at 3 years (7)
1
1C
Combination†
Adj OR 1.30 (0.67–2.51) for baseline
FRP ⬎53.1 (27)
JSN ⱖ1.5 mm
CTX-II ⬎346 ng/
mmoles of urinary
creatinine
Serum HA ⬎137
mg/ml
CTX-II ⬎346 ng/
mmoles of urinary
creatinine ⫹
serum HA ⬎137
mg/ml
FRP, ng/ml
High-quality studies, association
(95% CI)†
(continued)
Systematic Review of the Progression of Hip OA
933
Table 5. (Cont’d)
Studies
reporting
Level of
evidence
Dkk-1, ng/ml
1
1C
Combination†
Baseline serum
COMP
2
1D
Combination†
1
1C
Yearly mean
narrowing of
JSW
Combination†
1
1C
Combination†
1
1C
Combination†
Adj OR 0.99 (0.80–1.23) for mean ⫾
SD NTX 24.9 ⫾ 11.9 (26)
Adj OR 1.41 (0.75–2.63) for NTX
⬎28.89 (26)
Adj OR 0.93 (0.73–1.19) at 8 years (25)
1
1
1C
1C
Combination†
THA
Adj OR 0.76 (0.41–1.40) at 8 years (24)
OR 1.5 (1.0–2.4) at 2 years (21)
1
1C
Combination†
Naproxen
1
1C
Combination†
Diclofenac
1
1C
Combination†
Piroxicam
1
1C
Combination†
Baseline hip pain ⫹
diclofenac ⬎180
days
1
1C
Combination†
Adj OR 0.7 (0.3–1.6) for users (31–80
days) at 6.6 years (31)
Adj OR 1.2 (0.4–3.5) for users (⬎180
days) at 6.6 years (31)
Adj OR 1.1 (0.5–2.7) for users (31–80
days) at 6.6 years (31)
Adj OR 0.8 (0.1–7.5) for users (⬎180
days) at 6.6 years (31)
Adj OR 1.2 (0.6–2.5) for users (31–80
days) at 6.6 years (31)
Adj OR 2.4 (1.0–6.2) for users (⬎180
days) at 6.6 years (31)
Adj OR 2.5 (0.5–13.4) for users (31–80
days) at 6.6 years (31)
Adj OR 1.7 (0.2–16.3) for users (⬎180
days) at 6.6 years (31)
Adj OR 228.1 (2.4–22,144.5) at 6.6
years (31)
Prognostic factor
% change in serum
COMP
Baseline serum
NTX, nM BCE
% change in serum
NTX
NSAIDs
Statin user
Previous NSAID
intake
Ibuprofen
Outcome
High-quality studies, association
(95% CI)†
Low-quality studies,
association (95% CI)
Adj OR 0.40 (0.21–0.77) for baseline
Dkk-1 25.79–31.48 at 8 years (27)
Adj OR 0.40 (0.21–0.76) for baseline
Dkk-1 ⱖ40.51 at 8 years (27)
Adj OR 0.44 (0.24–0.80) for baseline
Dkk-1 ⬎24.9 at 8 years (27)
Adj OR 1.21 (0.95–1.53) for mean ⫾
SD COMP 11.8 ⫾ 5.2 units/liter at 8
years (26)
Adj OR 1.64 (0.89–3.04) for COMP
⬎13.49 units/liter at 8 years (26)
P ⫽ 0.02 for higher rate of narrowing if
COMP ⬎8.5 ␮g/ml at 1 year (23)
Adj OR 0.74 (0.58–0.96) at 8 years (25)
* Values are the prognostic variables and their association with outcome. 95% CI ⫽ 95% confidence interval; 1D ⫽ inconclusive level 1 evidence;
JSN ⫽ joint space narrowing; OR ⫽ odds ratio; THA ⫽ total hip arthroplasty; Adj ⫽ adjusted; RR ⫽ relative risk; 2D ⫽ inconclusive level 2 evidence;
1A ⫽ strong level 1 evidence; BMI ⫽ body mass index; 1C ⫽ weak level 1 evidence; K/L ⫽ Kellgren/Lawrence; JSW ⫽ joint space width; NSAID ⫽
nonsteroidal antiinflammatory drug; CTX-II ⫽ C-terminal crosslinking telopeptide of collagen type II; HA ⫽ hyaluronic acid; FRP ⫽ Frizzled-related
protein; COMP ⫽ cartilage oligomeric matrix protein; NTX ⫽ N-telopeptide crosslinks; BCE ⫽ bone collagen equivalents.
† For association with a combination of either JSN, an increase in Croft summary grade, an increase of ⱖ2 in total osteophyte score, or THA unless
otherwise stated.
‡ 95% CI not reported.
934
studied and/or is a focus of few research teams. As a result,
we advise caution in interpreting the level of evidence for
the Lequesne index (8,19) and femoral osteophytes
(9,32,35). Furthermore, publications from common cohorts may receive higher-quality scores due to the reliability of information reported in earlier publications that may
have otherwise not been obtained within each individual
article.
Consensus on a validated methodologic quality checklist for prognostic studies is yet to be established, and
therefore our list was based on previous reviews and recommendations described by Scholten-Peeters et al (14),
Kuijpers et al (13), Hayden et al (39), and Altman (15).
Also, our cut point of ⱖ12 (66.6%) to define a high-quality
study was arbitrary. Although this is similar to or higher
than other prognostic studies, only one of the included
articles was rated as low quality.
Items E (followup ⬎12 months) and H (prospective
study design) of our methodologic quality list were part of
our inclusion criteria, so perhaps they could have been
deleted from scoring. If these items had been excluded, 3
articles would have been below the 66.6% quality assessment cut point, and would therefore be rated as low quality. Eliminating items E and H would have downgraded
some of our conclusions, with NSAID variables then assigned inconclusive (Level 1D) evidence versus weak
(Level 1C) evidence, and femoral osteophytes assigned
moderate (Level 1B) evidence versus strong (Level 1A)
evidence. A higher cut point such as 75% would have had
a similar effect. However, our cut point was consistent
with other studies (13,14), and we reasoned that deleting
those methodologic quality items would have artificially
deflated the quality score because those studies included
earned the quality points of items E and H on merit. We
believe our quality assessment criteria were rigorous (12–
14) and our strict inclusion criteria strengthens our findings because retrospective studies, which carry a greater
risk of bias, were eliminated from the review.
Information about prognostic variables can guide physicians and other health care providers toward providing the
most appropriate treatment options. It has been recommended that clinicians conduct a holistic assessment of
patients and provide patients with information about the
condition, its management, and prognosis (40). The
knowledge that age, JSW at entry, femoral head migration,
femoral osteophytes, bony sclerosis, K/L hip grade 3, baseline hip pain, and Lequesne index score ⱖ10 are predictive of poorer outcome will help clinicians provide realistic, individually tailored advice, dispel myths, and better
plan care for their patients.
The results of our review suggest that patients with more
severe joint damage at study entry, hip pain at baseline,
and who report poorer function progress more rapidly.
These results are consistent with the contemporary understanding that loss of cartilage results in uneven and localized excess loading, which in turn accelerates damage to
the joint (41). Joint damage includes JSN, osteophytosis,
and malalignment, which can then lead to inflammation,
inhibition of muscle activity, and pain (41). This information may suggest a nonlinear relationship in the progres-
Wright et al
sion of hip OA, in that it is the additive effect of coexisting
features that lead to accelerated progression.
However, predicting outcome from hip pain and joint
damage at baseline remains inexact, because although
there is strong evidence that baseline pain and progressive
joint deterioration are associated, the strength of that association is modest in magnitude (Table 5). It is not uncommon for people with evidence of joint pathology to be
pain-free (41). Also relatively weak in magnitude was the
association of JSW at baseline with JSN at followup, which
is surprising in light of the potential circularity in using as
a predictive variable the same variable used to define
outcome. This form of incorporation bias may highlight
the consistent use of radiographic markers as predictors of
morbidity progression and demonstrates a need to avoid
confounding the relationship between the prognostic variables and the outcomes in research design. Adjusted odds
ratios from multivariate statistical models were seen in
disappointingly few of the included studies, and only 2
studies sought to estimate the incremental prognostic
power of combining radiographic data with other clinical
data (22,29).
JSN is considered the gold standard for monitoring the
progression of hip OA (42); however, given the variable
relationship between radiographic appearance, pain, and
function (41), better prognostic information may result
from a focus on what matters to patients, such as loss of
physical function and independence rather than simply
measures of joint structure damage. Botha-Scheepers et al
(43) suggest that in order to understand the entire impact
OA has on the lives of patients, a multiperspective approach is needed that evaluates not only the impairment of
body structures (JSW, JSN) but also the components of
body functions (pain, joint range of motion, muscle
strength), limitation of activities (walking, occupation),
and participation in societal activities (social involvement).
A variety of molecular biomarkers have been investigated for potential prognostic value; however, most have
been studied in only one cohort. Even in those that have
been studied in more than one cohort, such as CTX-II and
COMP, heterogeneous analysis methods and cut points, as
well as weak, inconclusive, and inconsistent evidence, fail
to demonstrate convincing prognostic value. It is possible
that other predictors exist, but at present evidence does
not exist to support this assumption. We found little or no
evidence regarding the prognostic value of common clinical information such as psychosocial variables, clinical
tests and measures such as strength and range of motion,
and physical performance measures.
The current understanding of prognostic variables influencing the clinical course and progression of hip OA is not
comprehensive. We suggest that further high-quality prognostic studies, i.e., prospective cohort studies with a followup period of at least 1 year, are needed to generate
valid and informative prognostic variables. Currently, the
available data are at risk of bias through multiple reports
from a few common cohorts, and the addition of one new
study can have a significant impact on the results. We
recommend that future studies investigate the predictive
value of psychosocial variables, clinical tests, and physical
Systematic Review of the Progression of Hip OA
performance measures such as range of motion, strength,
and flexibility, and address outcome in patient-centered
terms, such as physical function decline and health-related quality of life.
There is strong evidence that age, JSW at entry, femoral
head migration, femoral osteophytes, bony sclerosis, K/L
hip grade 3, baseline hip pain, and Lequesne index score
ⱖ10 are predictive of the progression of hip OA and that
acetabular osteophytes have no association with the progression of hip OA. There is weak or inconclusive evidence or no available high-quality evidence regarding the
prognostic value of a range of other potential prognostic
variables. These conclusions demonstrate a need for further high-quality research in the area of prognosis and hip
OA.
AUTHOR CONTRIBUTIONS
All authors were involved in drafting the article or revising it
critically for important intellectual content, and all authors approved the final version to be published. Dr. Wright had full
access to all of the data in the study and takes responsibility for
the integrity of the data and the accuracy of the data analysis.
Study conception and design. Wright, Abbott.
Acquisition of data. Wright.
Analysis and interpretation of data. Wright, Cook, Abbott.
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