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Is adiposity an under-recognized risk factor for tendinopathy A systematic review.

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Arthritis & Rheumatism (Arthritis Care & Research)
Vol. 61, No. 6, June 15, 2009, pp 840 – 849
DOI 10.1002/art.24518
© 2009, American College of Rheumatology
ORIGINAL ARTICLE
Is Adiposity an Under-Recognized Risk Factor for
Tendinopathy? A Systematic Review
JAMES E. GAIDA,1 MAUREEN C. ASHE,2 SHONA L. BASS,1
AND
JILL L. COOK1
Objective. Tendon injuries have been reported to occur more frequently in individuals with increased adiposity.
Treatment also appears to have poorer outcomes among these individuals. Our objective was to examine the extent and
consistency of associations between adiposity and tendinopathy.
Methods. A systematic review of observational studies was conducted. Eight electronic databases were searched (Allied
and Complementary Medicine, Biological Abstracts, CINAHL, Current Contents, EMBase, Medline, SPORTDiscus, and
Web of Science) and citation tracking was performed on included reports. Studies were included if they compared
adiposity between subjects with and without tendon injury or examined adiposity as a predictor of conservative treatment
success.
Results. Four longitudinal cohorts, 14 cross-sectional studies, 8 case– control studies, and 2 interventional studies (28 in
total) met the inclusion criteria, providing a total of 19,949 individuals. Forty-two subpopulations were identified, 18 of
which showed elevated adiposity to be associated with tendon injury (43%). Sensitivity analyses indicated a clustering
of positive findings among studies that included clinical patients (81% positive) and among case– control studies (77%
positive).
Conclusion. Elevated adiposity is frequently associated with tendon injury. Published reports suggest that elevated
adiposity is a risk factor for tendon injury, although this association appears to vary depending on aspects of study design
and measurement. Adiposity is of particular interest in tendon research because, unlike a number of other reported risk
factors for tendon injury, it is somewhat preventable and modifiable. Further research is required to determine if reducing
adiposity will reduce the risk of tendon injury or improve the results of treatment.
INTRODUCTION
Increased adiposity is a well-recognized risk factor for
many diseases, including cardiovascular disease (CVD)
(1), chronic kidney disease (2), and type 2 diabetes mellitus (DM) (3). It is only recently that musculoskeletal manifestations of adiposity have been acknowledged. Musculoskeletal problems associated with increased adiposity
are often attributed to increased mechanical loading, but
some authors suggest that this may be overly simplistic (4).
One particular type of musculoskeletal symptom, tendon
injury, is increasingly recognized as a major cause of morbidity in the work force (5), as well as in active (6) and
inactive people (7). Whether or not increased adiposity is
1
James E. Gaida, BPhysio(Hons), Shona L. Bass, PhD,
MSc, BSc, Jill L. Cook, PhD, BAppSci(Phty): School of Exercise and Nutrition Sciences, Deakin University, Melbourne, Victoria, Australia; 2Maureen C. Ashe, PhD, MSc,
BSc(PT): School of Rehabilitation Sciences, University of
British Columbia, Vancouver, British Columbia, Canada.
Address correspondence to James E. Gaida, BPhysio(Hons),
Deakin University, 221 Burwood Highway, Melbourne, Victoria, 3125, Australia. E-mail: jega@deakin.edu.au.
Submitted for publication July 2, 2008; accepted in revised form February 17, 2009.
840
associated with tendon injury has received very little research attention. Clinical texts have not yet reported increased adiposity (or obesity) as a risk factor for tendon
injury.
There is a growing body of evidence showing that increased adiposity (referred to as obesity in pronounced
cases) promotes a chronic low-grade microvascular inflammation, and this mechanism underpins the wellknown associations with CVD, chronic kidney disease,
and type 2 DM (8,9). Similar systemic mechanisms may
also contribute to musculoskeletal symptoms that develop
in the presence of increased adiposity, tendon pain (tendinopathy) and tendon rupture potentially being 2 such
injuries.
Tendon injury is a problem that causes substantial morbidity in a broad cross-section of populations. Cross-sectional data suggest that individuals with tendon injury
have either higher adiposity levels (10,11) or distribute
adipose tissue around the body in a different manner
(12,13), whereas intervention data suggest that treatment
for tendinopathy may be less effective among patients with
high adiposity levels (14). In addition, elevated adiposity
is associated with high cytokine levels (8,9), and several
mechanisms exist whereby elevated cytokine levels may
Association of Elevated Adiposity and Risk of Tendinopathy
either directly or indirectly affect tendon structure (15).
These reports, and a background of increasing adiposity
levels in the community, led us to perform a systematic
review examining these associations.
MATERIALS AND METHODS
A systematic review aims to comprehensively compile and
synthesize evidence to answer an explicit research question using reproducible methods, and is often applied to
randomized controlled trials. However, when the question
of interest concerns etiology, randomized controlled trials
are not only problematic to implement, they are often
unethical (16). The study of etiology is therefore typically
conducted using observational designs such as cross-sectional studies, case– control studies, or cohort studies,
with systematic reviews increasingly being used to summarize these results (16). This systematic review of observational studies asks the question, “Is elevated general or
regional adiposity related to tendon injury?”
Our outcomes of interest were 1) a clinical diagnosis of
tendinopathy or tendon rupture and 2) abnormal tendon
imaging on ultrasound or magnetic resonance imaging
(MRI). The exposures of interest were 1) increased overall
adiposity and 2) altered body fat distribution. Populationbased studies typically use body mass index (BMI) to
measure adiposity, and the World Health Organization
defines overweight as a BMI between 25.0 and 29.9 kg/m2
and obesity as a BMI of ⱖ30 kg/m2 (17). Anthropometric
measures such as waist circumference and waist to hip
ratio are often used to quantify body fat distribution. Body
composition can also be quantified using imaging methods. Modalities that distinguish fat from bone and lean
tissue include MRI, computed tomography (CT), and dual
x-ray absorptiometry (DXA). For reasons of expense, time,
access, and radiation exposure (CT and DXA), these techniques are often limited to smaller studies. For clarity, we
used adiposity throughout this report to describe increased adiposity or altered body fat distribution measured by any of these methods.
Identification and selection of the studies. One author
(JEG) conducted an electronic literature search in March
2007 using multiple databases (Allied and Complementary
Medicine [1985 to March 2007], Biological Abstracts [1985
to February 2007], CINAHL [1982 to March week 1, 2007],
Current Contents [week 27, 1993 to week 12, 2007], EMBase [1988 to week 10, 2007], Medline [1950 to February
week 4, 2007], SPORTDiscus [1830 to November 2006],
and Web of Science [1945 to March 13, 2007]) to identify
studies examining associations between adiposity and tendon injury in humans. No limitation was applied regarding publication year, although only studies published in
English were considered. The medical subject headings
used included Tendons, Tendon Injuries, Tendinopathy,
Tendinitis, Adiposity, Obesity, Body Mass Index, Anthropometry, Body Fat Distribution, and Adipose Tissue. Plain
text searching was also used in combination with wildcards and truncation (18). Terms used for plain text
searching included tend#nopath$, tend#nos#s, achil?o-
841
dynia, obesity, adiposity, body composition, fat distribution, anthropometry, waist circumference, hip circumference, (waist adj2 hip) AND ratio, (abdominal OR visceral)
adj5 adipose (for full details, see Supplemental Appendix
A, available in the online version of this article at http://
www3.interscience.wiley.com/journal/77005015/home).
Electronic searches with broad scope (tendon AND obesity, tendon AND body composition, tendon AND adiposity) were conducted using the Google and Google Scholar
search engines. The first 200 records for each search were
screened for relevance by title.
Hand searching supplemented the electronic searches.
Two authors (JEG, JLC) independently searched the reference lists of included articles for relevant studies. Additionally, 5 articles considered to be of key relevance
(10,11,13,14,19) were identified on PubMed and the “Related Articles” function was selected. Both authors independently assessed the first 100 citations linked to each of
the 5 key articles.
Records were imported into Endnote, version 9.0.0 for
Macintosh (Thompson, Stamford, CT). Letters, conference
proceedings, and duplicates were excluded. Two authors
(JEG, JLC) then independently applied the predefined inclusion criteria to the titles and abstracts of the retrieved
references. If both authors included the study or if there
was disagreement, the full-text article was obtained and
checked for eligibility. Disagreement regarding inclusion
was resolved by discussion between the 2 authors.
To ensure the validity of the included data, only full and
original articles from peer-reviewed journals were considered for inclusion. To be eligible, a study had to compare
adiposity between individuals with and without tendon
injury or examine the influence of adiposity on recovery
from tendon injury. In both cases, the statistical methods
had to be appropriate to the study design. Factors predicting successful outcome after surgical intervention for tendon injuries were excluded. Studies examining conservative management of tendon injury, however, were
included if treatment was standardized. Carpal tunnel syndrome was excluded a priori because it differs from other
tendon injuries in several fundamental aspects. Appropriate assessment of adiposity was considered to include
height to weight ratios (e.g., BMI), waist circumference,
waist to hip ratio, and adipose tissue volumes or crosssectional areas as measured by CT, MRI, or DXA. Reporting body weight without adjusting for height is not a valid
measure of adiposity and these studies were excluded.
The published version of each study was examined for
methodologic quality using the checklist by Downs and
Black (20). Two items suggested by the Centre for Reviews
and Dissemination (21) were added. Two authors (JEG,
MCA) marked each study, with a third author (JLC) making
the final decision in the case of disagreement.
Data were extracted from each eligible study by 2 of the
authors (JEG, MCA). The items were chosen for their ability to highlight the important aspects of study design, the
demographics of the studied population, and the definition of disease. The methods used to measure adiposity
were noted, as was the use of cutoffs (e.g., BMI ⬎30 kg/
m2). The association between adiposity and tendon injury
was either recorded as an odds ratio or as an effect size
842
(22), and the P value was recorded as calculated from
presented data (23).
In circumstances where it was not possible to extract
these data from the published manuscript, corresponding
authors were contacted for the required information. Nine
of the 14 corresponding authors contacted supplied the
requested data, 2 stated that the data were no longer available, 2 responded but did not provide the requested data,
and one author could not be contacted. In one case, all data
were available except for the SD of BMI in the tendinopathy group (24). To allow interpretation, a conservative
estimate (mean ⫹ 2 SDs) was calculated from the reported
SD of BMI in the other studies. If more than one data point
was missing, no values were substituted.
Because a single study may often report results for multiple groups (e.g., men with upper extremity tendinopathy,
women with upper extremity tendinopathy, men with
lower extremity tendinopathy, etc.), it was considered important to maintain these subpopulations for the purposes
of this review. In contrast, where studies used multiple
measures of adiposity (e.g., BMI, waist circumference, and
waist to hip ratio) or examined the effect of different cutoffs (e.g., BMI ⬎30 kg/m2 versus BMI ⬎35 kg/m2) to report
the results from a single subpopulation, it was important
that these results were grouped together and only counted
once. Similarly, where data for individuals with unilateral
and bilateral tendinopathy were reported separately, online tools were used to combine the 2 groups (25). These
tools allowed the input of means and SDs from 2 groups
and then calculated the mean and SD of the 2 groups
combined. This was performed for the variables of interest
(i.e., age, BMI, waist circumference, and waist to hip ratio).
Any person participating in an included study was referred to as an individual. This term was further qualified
according to whether they were an individual with a tendon injury (tendinopathy group) or an individual without
a tendon injury (control group). Individuals recruited
through their participation in organized sports were referred to as athletes, whereas those recruited through their
place of employment were known as workers. Finally,
those presenting to their health care practitioner for the
management of tendon pain were referred to as patients.
Of note is that athletes and workers (and those in the
general community) often do not seek treatment for tendon
pain and so, for example, a group of workers with tendon
injuries was not always synonymous with a clinical patient group.
Statistical analysis. Where a study showed that individuals with a tendon injury had significantly greater levels of adiposity than controls, it was reported as a significant positive association. This term was also used when
individuals had significantly greater abdominal adiposity
(defined by elevated waist circumference or waist to hip
ratio), because this distribution pattern is associated with
increased incidence of CVD, chronic kidney disease, and
type 2 DM (9). Conversely, when the opposite was shown
(decreased general or abdominal adiposity), it was described as a significant negative association.
Sensitivity analyses were conducted based on 6 vari-
Gaida et al
Figure 1. Flow chart describing the source of included articles.
BMI ⫽ body mass index.
ables: sex (men, women, combined), population (athletes,
patients, workers), injury location (upper extremity, lower
extremity, not specified), adiposity measure (BMI, circumferences, other), study design (longitudinal, cross-sectional, case– control), and quality score (above middle
rank, below middle rank). The effect of each of these
grouping scenarios was tested with a chi-square test
(SPSS, version 15.0.1 for Windows; SPSS, Chicago, IL). P
values less than 0.05 were considered significant.
RESULTS
A total of 245 unique records were retrieved using the
citation databases. The application of inclusion criteria to
abstracts reduced the count to 47. Of the 47 potentially
applicable studies, 29 were excluded (for full details, see
Supplemental Appendix B, available in the online version
of this article at http://www3.interscience.wiley.com/journal/77005015/home). Therefore, 18 articles met the inclusion criteria and were included in the review (10 –12,14,
19,24,26 –37) (Figure 1).
Citation tracking of these 18 articles yielded a further 6
unique records meeting the inclusion criteria (38 – 43),
tracking related articles using PubMed yielded 2 (44,45),
and contact with a tendinopathy expert (JLC) yielded an
Association of Elevated Adiposity and Risk of Tendinopathy
additional 2 (13,46). Using all of the reference tracking
techniques described, 28 original research reports meeting
the inclusion criteria were identified (Figure 1) and subsequently marked using the quality criteria. The included
studies had a combined total of 9,536 male individuals
and 10,413 female individuals.
Nineteen points were available from the 18 questions on
the quality assessment (one question is marked between 0
and 2). Included studies scored 18 (n ⫽ 5), 17 (n ⫽ 11), 16
(n ⫽ 6), 15 (n ⫽ 2), 13 (n ⫽ 1), 12 (n ⫽ 2), and 10 (n ⫽ 1)
out of 19. No studies were excluded on quality assessment.
Most points were deducted for an inadequate description
of potential confounding variables (n ⫽ 24; deduction of 1
or 2 points from each study), outcome assessors not
blinded to exposure (n ⫽ 19), failure to demonstrate that
the recruited population was comparable with the source
population (n ⫽ 9), non-precise reporting of P values (n ⫽
8), poorly described aim/hypothesis/objective of the study
(n ⫽ 3), failure to report estimates of random variability
(n ⫽ 3), cases and controls not recruited from the same
population (n ⫽ 3), and cases and controls not recruited
over the same time period (n ⫽ 3). Points were also lost for
an inadequate description of patient characteristics (n ⫽
2), inappropriate use of statistical techniques (n ⫽ 2), a
lack of an explicit case definition (n ⫽ 1), and failure to
establish accurate outcome measures (n ⫽ 1).
Six studies utilized a longitudinal cohort design to investigate risk factors for tendon injury. In 2 of these studies, followup data were not sufficiently detailed to allow
analysis (26,38). Therefore, only baseline data from these 2
studies were included, and consequently the research is
best described as cross-sectional for the purposes of this
review. Including these 2 cases, the cross-sectional design
was used 14 times. Eight studies were of case– control
design, while 2 interventional studies examined BMI as a
factor predicting treatment success.
Fourteen (50%) of the 28 included studies showed ⱖ1
significant positive association between increased adiposity and tendon injury (10 –14,24,26,30,31,34,36,37,44,46).
Interestingly, one of these 14 studies (24) identified a significant negative association in one subgroup (female runners with patellar tendinopathy), whereas all other subgroups in the study showed positive associations. The
remaining 14 studies found no significant association between adiposity and tendinopathy (19,27–29,32,33,35,38 –
43,45). Examination of the subpopulations (rather than the
studies as a whole) showed similar results: 18 positive
(43%), 23 no association, and 1 negative (Table 1). Effect
sizes (Figure 2) were not calculated if odds ratios (Figure 3)
were reported in the article.
Sensitivity analysis showed no deviation from chisquare distribution for groupings based on sex (␹2 ⫽ 0.257,
2 df, P ⫽ 0.879), location of injury (␹2 ⫽ 2.964, 2 df, P ⫽
0.227), adiposity measure (␹2 ⫽ 1.667, 2 df, P ⫽ 0.432), or
quality score (␹2 ⫽ 0.138, 1 df, P ⫽ 0.710). When grouped
according to the population studied (athletes versus patients versus workers: ␹2 ⫽ 9.051, 2 df, P ⫽ 0.011) and the
study design (longitudinal versus cross-sectional versus
case– control: ␹2 ⫽ 9.365, 2 df, P ⫽ 0.009), the distribution
of positive findings (compare negative and nonsignificant
combined) differed from that expected. A high proportion
843
of positive findings was noted for patients (13 [81%] of 16)
and case– control studies (10 [77%] of 13).
Importantly, there was no difference in the frequency of
significant results when comparing studies falling above
and below the median quality score rank. This suggests
that elevated adiposity in the study group did not affect
the decision to publish to a greater or lesser extent in the
articles with a lower quality score. This finding is an
indication that the pool of studies may not be affected by
publication bias. This is consistent with the observation
that only a small proportion of the included investigations
identified adiposity as a key factor of interest, and as such,
this factor would not be expected to affect the decision to
publish.
DISCUSSION
To our knowledge, this is the first time a systematic review
has examined the association between tendon injury and
adiposity. The results show that individuals with tendon
abnormality, tendon pain, tendon rupture, or failure to
respond to conservative management have significantly
higher adiposity levels than their respective controls
nearly half of the time.
This review suggests that individuals with tendinopathy
often have higher adiposity, because adiposity is an intrinsic risk factor for this condition. The mechanism linking
adiposity and tendinopathy may be mechanical or systemic. The mechanical hypothesis is that weight-bearing
tendons are exposed to higher loads with increasing adiposity, and the higher loads then lead to tendinopathy.
Studies that report associations between lower extremity
tendinopathy and BMI could support this hypothesis.
The systemic hypothesis maintains that bioactive peptides released by adipose tissue may influence tendon
structure (direct mechanism). Alternately, systemic metabolic alterations associated with elevated adiposity may
affect tendon structure (indirect mechanism). Many of the
studies in this review support the systemic hypothesis.
Recent work has demonstrated a strong association between tendon abnormality and abdominal adiposity in
male athletes (13). In this study, the athlete’s waist circumference was able to discriminate normal from abnormal
tendons, whereas body weight, match schedule, and training volume did not. These elite volleyball players had full
match and training schedules and thus did not have an
opportunity to increase their level of adiposity secondary
to a reduction in physical activity. However, longitudinal
data are required to confirm that tendon injury develops
secondary to elevated adiposity.
Additional support for a systemic mechanism comes
from the sensitivity analysis, which highlighted equivalent distributions of positive and negative findings according to whether the affected tendon was in the upper or
lower extremity. Because only the tendons of the lower
extremity are weight bearing, this finding supports the
earlier suggestion that the association between adiposity
and tendinopathy cannot be adequately explained by increased tendon loading. That is, if adiposity increases the
risk of tendinopathy predominantly through loading, a
10
12
15
13
US
US
Sweden
France
Holmes et al,
1991 (40)
Holmes and
Mann, 1992
(31)
Jacobsson et al,
1992 (32)
Leclerc et al,
2001 (41)
12
US
Holmes and
Lin, 2006
(30)
15
16
Sweden
Australia
17
Sweden
Gaida et al,
2004 (12)**
16
Sweden
Fahlström et al,
2002 (28)
Fahlström et al,
2002 (29)
Fahlström et al,
2003 (14)
16
17
Australia
France
17
Denmark
Quality
Country score
Descatha et al,
2003 (38)
Bonde et al,
2003 (26)
Cook et al,
2004 (27)**
Author,
year (ref.)
General
population
Workers
Patients
Patients
Patients
Sporting
Patients
Sporting
Sporting
Workers
Industrial
workers
Sporting
Population
Crosssectional
Cohort
Retrospective
case–control
Case–control
Retrospective
case–control
Crosssectional
Crosssectional
Crosssectional
Intervention
Crosssectional
Crosssectional
Crosssectional
Study design
Symptomatic
Symptomatic
Rupture
Rupture
Symptomatic
Imaging
Treatment
response
Symptomatic
Symptomatic
Symptomatic
Imaging
Symptomatic
Case
definition
Unable to
determine
Unable to
determine
Unable to
determine
Waist††
WHR††
DXA¶¶
BMI ⬎30
BMI ⬎30
37.9 ⫾ 11.6
21 ⫾ 3.1
178:420
178:420
Wrist
254:248
16:51
39:19
BMI ⬎27 (men),
⬎26.5
(women)††
Increased BMI
ⱖ2††
BMI ⬎27 (men),
⬎26.5
(women)††
Increased BMI
ⱖ2††
37.7 ⫾ 8.3
(20–59)
37.7 ⫾ 8.3
(20–59)
BMI
20% over ideal
57.19 ⫾ 12.98
(19–87)
50–70
20% over ideal
41
51.3 (34–72)
BMI
46.1 ⫾ 9.5
0:44
Small††
Negligible††
Unable to
determine
BMI
44.2 ⫾ 5.9
49.5 (27–77)
Negligible††
BMI
23.4 ⫾ 4.3
2.2 (0.92–5.26)††
Unknown††
Unable to
determine††
Unable to
determine††
For††
Unknown††
Unknown††
Against
For¶
Unknown
For¶
For§§
Nil††
For¶
Against††
For¶
For¶
Against
Against
Against
Against
For
For¶
Direction
of effect
Unable to
determine††
Negligible
Medium
Medium
Small
Medium
0.89 (0.40–1.98)
BMI ⬎27 (men),
⬎26.5
(women)
BMI
Medium
Small
Skinfolds
16.6 ⫾ 1.1
(14–18)
16.3 ⫾ 1.0
(14–18)
38.1 ⫾ 9.3
(20–66)
Medium
Effect size
or OR
(95% CI)§
Skinfolds
BMI
Measure of
adiposity‡
38 ⫾ 10.7
Age,
years†
38:0
Lateral
elbow
Unspecified
Posterior
tibial
Achilles
Achilles
25:6
Distal
Achilles
Patellar
0:39
68:33
25:7
41:25
419:1,338
0:64
71:0
1,291:1,782
Sex, men:
women
Mid-Achilles
Mid-Achilles
Mid-Achilles
Medial
elbow
Patellar
Shoulder
Injury
location
Table 1. Summary of results from individual studies*
(continued)
⬍ 0.15††
⬎ 0.15††
⬎ 0.15††
⬎ 0.15††
0.681#
0.005
⬎ 0.05
⬍ 0.001
⬍ 0.05††
0.5591‡‡
⬍ 0.001
0.1597‡‡
⬍ 0.05
⬍ 0.01
0.4804#
0.1197#
0.1748#
0.0795#
0.0001#
P
844
Gaida et al
Tanaka et al,
2001 (45)
Sayana and
Maffulli,
2007 (35)
Seeger et al,
2006 (36)
Shiri et al,
2006 (37)
17
Finland
18
18
US
US
16
16
US
UK
Workers
18
Workers
Workers
Patients
Patients
Workers
Patients
Workers
17
Mokone et al,
2005 (34)
Ono et al,
1998 (42)
Ritz, 1995 (43)
17
Workers
Sporting
Military
Population
South
Africa
Japan
Finland
Miranda et al,
2005 (33)
17
17
Australia
France
18
Belgium
Quality
Country score
Melchior et al,
2006 (44)
Mahieu et al,
2006 (19)
Malliaras et al,
2007 (13)**
Author,
year (ref.)
Crosssectional
Crosssectional
Case–control
Crosssectional
Crosssectional
Intervention
Case–control
Crosssectional
Crosssectional
Crosssectional
Cohort
Study design
Symptomatic
Symptomatic
Rupture
Treatment
response
Symptomatic
0.90 (0.57–1.42)
1.42 (0.85–2.39)
1.01 (0.56–1.81)
Small
BMI ⬎30
BMI ⬎30
Shoulder
BMI ⬎30
BMI
3.5 (1.6–7.5)††
1.9 (1.0–3.7)††
1.4 (0.8–2.4)††
1.2 (0.7–2.1)††
1.3 (0.8–2.2)††
1.16 (0.77–1.76)
WHR ⬎0.95††
BMI ⬎30††
Waist ⬎100††
WHR ⬎0.95††
BMI ⬎30††
BMI ⬎25
46.3 ⫾ 9.6
(30–64)
2.3 (1.1–4.7)††
Waist ⬎100††
46.3 ⫾ 9.6
(30–64)
2.0 (1.2–3.1)
Obesity (ICD-9)
40.5 ⫾ 5.0
Negligible
1.0 (0.9–1.1)
Large
BMI
Ponderal index
BMI
BMI
47.3 ⫾ 23.7
(20–76)
49.6 ⫾ 4.6
(40–59)
46.2 (18–64)
44.7 ⫾ 8.4
(30–64)
44.2 ⫾ 8.8
(30–64)
40.1 ⫾ 12.0
14,647:15,427 18 to ⱖ65
2,245:2,453
Lateral
elbow
Distal upper
extremity
2,245:2,453
692:255
18:16
290:0
Medial
elbow
Achilles
Achilles
Elbow
0:575
163:78
0:1,795
0:1,107
1,945:0
38 ⫾ 10.3
(18–59)
Small
Medium††
Medium††
1.56 (1.07–2.27)
WHR††
BMI††
BMI 30
26.1 ⫾ 5.3
(19–43)
0:40
BMI
Large††
Large††
Small††
WHR††
BMI††
Waist††
38 ⫾ 10.3
(18–59)
Very large††
Waist††
26.1 ⫾ 5.3
(19–43)
69:0
Medium
Effect size
or OR
(95% CI)§
73:0
Measure of
adiposity‡
BMI
Age,
years†
18.40 ⫾ 1.29
Sex, men:
women
6 upper
1,549:0
extremity
diagnoses##
0:1,107
Shoulder
1,549:0
Patellar
Achilles
Injury
location
Symptomatic/ Achilles
rupture
Symptomatic Elbow
Symptomatic
Symptomatic
Imaging
Symptomatic
Case
definition
Table 1. (Cont’d)
For††
For††
For
For§§
For§§
For††
For§§
For¶
Against
Unknown
Nil
For¶
For
Nil
For
Against
For
For††
For††
For¶
For§§
For§§
For††
For§§
For
Direction
of effect
(continued)
0.7551#
⬎ 0.05
⬍ 0.001
⬎ 0.2
⬎ 0.2
0.48††
0.09††
⬍ 0.01††
⬍ 0.01††
0.13††
⬍ 0.01††
0.083
P
Association of Elevated Adiposity and Risk of Tendinopathy
845
17
US
Industrial
workers
Patients
Patients
Patients
Patients
Population
Cohort
Cohort
Case–control
Case–control
Retrospective
case–control
Study design
Patellar
Achilles
Injury
location
Symptomatic
Symptomatic
Upper
extremity
Medial or
lateral
elbow
Symptomatic/ Patellar
imaging
Surgery
Shoulder
Symptomatic
Case
definition
27:18
48
38.1 ⫾ 7.8
65.1 ⫾ 6.3
(55–74)
0:154
100:252
64.5 ⫾ 6.0
(55–74)
26.0 ⫾ 6.8
0:1,076
926:0
0:1,076
42:21
157:0
36.2 ⫾ 4.75
Age,
years†
926:0
Sex, men:
women
BMI
BMI ⬎30
BMI ⱖ35††
BMI 30–34.9††
BMI ⱖ35††
BMI 30–34.9††
BMI
BMI
BMI
BMI
BMI
Measure of
adiposity‡
Unable to
determine
1.86
(1.07–3.22)††
3.13
(1.29–7.61)††
2.43
(1.39–4.22)††
3.51
(1.80–6.85)††
1.93 (1.12–3.34)
Large
Negligible
Very large
Medium
Large
Effect size
or OR
(95% CI)§
For
For¶
For§§
For§§
For§§
For§§
For¶
For
Against¶
For¶
For¶
Direction
of effect
0.07¶¶¶
0.018§§§
⬍ 0.0001***
0.3814†††
⬍ 0.0001***
0.0047‡‡‡
⬍ 0.0001***
P
* OR ⫽ odds ratio; 95% CI ⫽ 95% confidence interval; BMI ⫽ body mass index; WHR ⫽ waist to hip ratio; DXA ⫽ dual x-ray absorptiometry; ICD-9 ⫽ International Classification of Diseases, Ninth
Revision.
† Values are the mean ⫾ SD, mean ⫾ SD (range), mean (range), mean, or range.
‡ BMI is measured in kg/m2.
§ Effect size calculated according to Hedges’ modification of Cohen’s d (also known as Hedges’ g) (22).
¶ Significant at P ⬍ 0.05.
# Calculated from provided data.
** Unilateral, bilateral, and tendinopathy groups combined for calculation of effect size.
†† Grouping where multiple outcome measures are used on the same subpopulation (see Materials and Methods for details).
‡‡ Calculated from provided data. Grouping where multiple outcome measures are used on the same subpopulation (see Materials and Methods for details).
§§ Significant at P ⬍ 0.05. Grouping where multiple outcome measures are used on the same subpopulation (see Materials and Methods for details).
¶¶ Trunk fat. Grouping where multiple outcome measures are used on the same subpopulation (see Materials and Methods for details).
## Six principal diagnoses: rotator cuff syndrome, epicondylitis, cubital tunnel syndrome, extensor/flexor tendonitis/tenosynovitis, de Quervain’s disease, and carpal tunnel syndrome.
*** Calculated from provided data. Factor was not retained in multiple logistic regression analysis. SD of BMI in the injured group was estimated (mean ⫹ 2 SDs) using a comparable measure across
the other studies.
††† Calculated from provided data. SD of BMI in the injured group was estimated (mean ⫹ 2 SDs) using a comparable measure across the other studies.
‡‡‡ Calculated from provided data. Factor was not retained in multiple logistic regression analysis.
§§§ Groups were compared with t-test in addition to logistic regression.
¶¶¶ Factor was not retained in multiple logistic regression analysis.
16
US
17
US
et al,
(11)
et al,
(39)
18
Australia
Warden et al,
2007 (46)
Wendelboe et
al, 2004 (10)
Werner
2005
Werner
2005
17
Canada
Quality
Country score
Taunton et al,
2002 (24)
Author,
year (ref.)
Table 1. (Cont’d)
846
Gaida et al
Association of Elevated Adiposity and Risk of Tendinopathy
847
Figure 2. Effect sizes (Hedges’ modification of Cohen’s d) for
increased adiposity in the group with tendon injury (or failure to
respond to conservative treatment). Positive scores indicate increased adiposity. * Significant at P ⬍ 0.05. WC ⫽ waist circumference; WHR ⫽ waist to hip ratio; DXA ⫽ dual x-ray absorptiometry; BMI ⫽ body mass index.
characteristic nature that is diagnosed as arising from a
tendon may in fact be due to another structure with a
similar innervation pattern. Future investigations would
ideally confirm the clinical diagnosis of tendinopathy with
appropriate imaging and/or histopathology, where available.
Although the evidence linking adiposity and tendinopathy is not conclusive, unlike some other putative risk
factors (i.e., gene polymorphisms [34], prior history of
tendon rupture [47], sex, and age), elevated adiposity is
somewhat preventable and reversible (other modifiable
risk factors include medication exposure [fluoroquinolone
antibiotics (48), statins (49)] and unaccustomed, repetitive
tendon loading). If evidence in favor of this hypothesis
continues to accumulate, and cause and effect are established with longitudinal data, the next step will be to
determine how these factors are linked and through which
biologic pathways they act (50).
stronger association would be expected in the tendons of
the lower extremity in comparison with the tendons of the
upper extremity.
Some measures of adiposity also support the systemic
hypothesis. Although waist circumference and waist to
hip ratio cannot differentiate between lean and fat tissue,
they are considered valid surrogates of visceral adipose
tissue volume (waist circumference) and the ratio of central to peripheral fat storage (waist to hip ratio). A central
distribution of fat (large waist circumference) increases the
risk of CVD, with the mechanism thought to be low-level
inflammation promoted by the release of cytokines (9).
Perhaps these same cytokines influence tendon metabolism or response to injury and have a part to play in
explaining the findings described in this review.
This review may accentuate the association between
adiposity and tendinopathy because investigators in the
case– control studies often access pools of tendinopathy
patients through specialist centers on secondary or tertiary
referral. It can be speculated that these patients have not
responded quickly to conservative treatment with their
primary practitioner, which leads to referral. Therefore, in
the case– control studies, we may be seeing an interaction
of effects: adiposity as a risk factor for tendon injury,
adiposity as a consequence of tendon injury, and also
adiposity as a factor limiting recovery from tendon injury
(14). This is supported by the sensitivity analysis that
showed a clustering of positive findings among studies
investigating clinical patient populations (81%) and also
among studies using a case– control design (77%). It is
highly likely that these observations are closely linked,
because someone who seeks treatment for a condition (a
patient) is almost automatically defined as a case, and is
therefore likely to be included in a case– control study. A
clustering of positive results among the case– control studies is suggestive of selection bias (a well-recognized limitation of this design) influencing the findings. This finding
highlights the need for well-controlled longitudinal studies examining the relationship between adiposity and tendinopathy.
Finally, a limitation that should be kept in mind is the
use of symptoms to diagnose tendon pathology. Pain of a
Figure 3. Forest plot showing the relationship between adiposity
and tendon injury. Odds ratios are shown on a logarithmic scale,
with scores ⬎1 indicating increased adiposity among those with
tendon injury. Dx ⫽ diagnosis; WC ⫽ waist circumference;
WHR ⫽ waist to hip ratio; BMI ⫽ body mass index.
848
Gaida et al
AUTHOR CONTRIBUTIONS
Mr. Gaida 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 design. Gaida, Bass, Cook.
Acquisition of data. Gaida, Ashe, Cook.
Analysis and interpretation of data. Gaida.
Manuscript preparation. Gaida, Ashe, Bass, Cook.
Statistical analysis. Gaida.
17.
18.
19.
20.
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DOI 10.1002/art.24712
Submissions Invited for Themed Issue of Arthritis Care & Research:
Drug Safety in the Rheumatic Diseases
Arthritis Care & Research is soliciting manuscripts for a themed issue addressing drug safety in the treatment
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topics related to the major theme are invited; for example, update on safety issues related to a specific drug
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The issues will include regular submissions as well, but a certain number of pages will be reserved for
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