Journal of Diabetes and Its Complications 30 (2016) 944950

Contents lists available at ScienceDirect

Journal of Diabetes and Its Complications

j o u r n a l h o m e p a g e : W W W. J D C J O U R N A L . C O M

Type 2 diabetes and osteoarthritis: a systematic review and

meta-analysis
Mia F. Williams a, Daniel A. London b, Elaine M. Husni c, Sankar Navaneethan c, Sangeeta R. Kashyap c,
a
b
c

University of California San Francisco, Internal Medicine Residency, 505 Parnassus Avenue, San Francisco, CA 94143-0119
5 East 98th Street, Box 1188, New York, NY 10029
Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195

a r t i c l e

i n f o

Article history:
Received 5 November 2015
Received in revised form 15 February 2016
Accepted 18 February 2016
Available online 2 March 2016
Keywords:
Type 2 diabetes
Obesity
Osteoarthritis
Meta-analysis
Prediabetes

a b s t r a c t
Background: Observational studies have reported an association between type 2 diabetes and osteoarthritis
(OA) development and progression. However no systematic review of the literature exists assessing whether
this association is consistently true. We aimed to systematically review the association between type 2
diabetes and the presence, development, and progression of OA.
Methods: We searched MEDLINE, SCOPUS, EMBASE, the Web of Science, and Grey Literature (through August
2014) for prospective cohort, cross-sectional, and casecontrol studies with condence intervals (CI) that
reported an association between type 2 diabetes and impaired glucose tolerance (IGT) and the development
or presence of OA of any joint.
Results: Ten studies and fourteen ratios were included in the analysis. The pooled population size in our
meta-regression was 16,742 patients. Type 2 diabetes was signicantly associated with the development or
presence of OA (OR; 1 21, 95% CI: 1 021 41). In the subset of 7 studies that did control for weight or BMI
there was an increased odds of OA associated with type 2 diabetes was (OR: 1 25, 95% CI: 1 051 46)
from a smaller pool of patients (n = 7156).
Conclusions: Type 2 diabetes is associated with the development and presence of radiographic and
symptomatic OA even when controlling for body mass index and weight.
2016 Elsevier Inc. All rights reserved.

1. Introduction
In the United States, osteoarthritis (OA) is estimated to affect
26 9 million Americans with a mean cost of over $2000 per patient
per year (Gabriel, Crowson, Campion, & OFallon, 1997; Lawrence,
Felson, Helmick, et al., 2008). OA is historically considered a
non-inammatory arthritis whose development is primarily associated with age and weight, but a growing body of literature has shed
light on the role of inammation and type 2 diabetes mellitus in the
development of the disease (Berenbaum, 2011). The independent
prevalence of both conditions has risen in the United States as the
population ages and struggles with the obesity epidemic (Deshpande,
2008; Gregg, Beckles, Williamson, et al., 2000; National Diabetes Fact
Sheet, 2011; Risk Factors for Non-Insulin Dependent Diabetes).
Among patients with type 2 diabetes, the prevalence of OA is
signicantly higher than in those without the condition (Cheng et al.,
2012; Puenpatom & Victor, 2009). Recent studies have found that the
Conicts of interest: None.
Funding: None.
Corresponding author at: Cleveland Clinic Main Campus, Mail Code F20, 9500 Euclid
Avenue, Cleveland, OH 44195. Tel.: +1 216 445 2679.
E-mail address: kashyas@ccf.org (S.R. Kashyap).
http://dx.doi.org/10.1016/j.jdiacomp.2016.02.016
1056-8727/ 2016 Elsevier Inc. All rights reserved.

association between the two conditions exists even when controlling

for identied risk factors such as age and sex (Nieves-Plaza,
Castro-Santana, Font, Mayor, & Vil, 2013; Yoshimura, Muraki, Oka,
et al., 2012). When controlling for other common risk factors such as
weight or body mass index, results have been heterogeneous
regarding whether a statistically signicant association exists between OA and type 2 diabetes (Bagge, Bjelle, Edn, & Svanborg, 1991;
Nieves-Plaza et al., 2013; Schett, Kleyer, Perricone, et al., 2013;
Yoshimura et al., 2012). Furthermore, there is only limited longitudinal data regarding an association between these two diseases. A
relationship between the two conditions would have clinical
implications for diabetes management, as early diabetes management
thru lifestyle modication and pharmacotherapy may favorably
impact OA progression and severity. Moreover, guidelines for physical
activity, the cornerstone for diabetes prevention and treatment, may
need to be modied to avoid joint damage in those at risk.
As such, there is a need to clarify the association of these disease
entities and critically examine the literature for whether existing
reports consider the possible interaction between type 2 diabetes, OA,
and obesity. In this systematic review and meta-analysis, we aimed to
examine the associations between type 2 diabetes and OA even after
adjusting for body weight and body mass index (BMI).

M.F. Williams et al. / Journal of Diabetes and Its Complications 30 (2016) 944950

2. Methods
We followed Meta-analysis of Observational Studies in Epidemiology (MOOSE) guidelines during the conduct of this systematic
review.
2.1. Data Sources and Searches
MEDLINE, SCOPUS, Web of Science, and EMBASE were searched in
July 2013 using optimally sensitive search strategies for relevant studies
with key search terms osteoarthritis and diabetes (and their acronyms
such as OA and DM). Authors were updated regarding publications
meeting the original search parameters through August 2014. We
reviewed the references of included studies for any further potential
studies. The authors of studies that assessed the association between OA
and type 2 diabetes but did not include a hazard ratio (HR), relative risk
(RR), or odds ratio (OR) were contacted for further information by
electronic and traditional mail. Inquiries were made as to whether
analyses pertinent to the association of interest were performed, as well
as details of their study design and patient population.
2.2. Study Selection
Two reviewers (M.F.W. and D.A.L.) independently analyzed the
search results and came to a consensus regarding which studies
contained pertinent data. CaseControl, cross-sectional, and prospective
cohort studies that reported the presence, development, or progression
of OA of weight bearing and non-weight bearing joints were included in
the study. Non-English language studies' abstracts were excluded.
Studies were included if the outcome was the presence or development
of OA of any joint. This was dened radiographically (Kellgren-Lawrence
Scale or Atlas of Rheumatology), clinically (American College of
Rheumatology criteria for diagnosis of OA), symptomatically (WOMAC
score), by outcome (requiring arthroplasty) or by diagnosis codes.
Studies that included hyperglycemic states including impaired fasting
glucose and type 2 diabetes as an independent variable were included if
it was dened by patient history, laboratory value denitions (i.e. fasting

945

glucose values and glycated hemoglobin), or ICD-9 diagnosis codes. In

our initial analysis we chose to include impaired fasting glucose based
on the sensitivity of these lab tests for identifying those patients with
hyperglycemia and possible early type 2 diabetes given the considerable
overlap between pre-diabetes and type 2 diabetes. In particular,
impaired fasting glucose does not preclude type 2 diabetes since the
gold standard test (ie. oral glucose tolerance test) was not performed.
Excess body weight and BMI are drivers for both type 2 diabetes
and osteoarthritis development. However, it also acts as a potential
confounder in the relationship between type 2 diabetes and
osteoarthritis. Therefore, our strategy was to include the full breadth
of articles on the topic of type 2 diabetes and osteoarthritis including
those that did not control for BMI and perform a subsequent subset
analysis in which BMI was controlled for.
2.3. Data Extraction and Quality Assessment
Data pertaining to study design (country of origin, years of study,
study type, and follow-up duration), participant characteristics (age,
gender, and race), and outcome measures (development or presence
of osteoarthritis as dened above) were independently extracted by
the reviewers. The authors of the included studies were contacted
when necessary for additional details regarding study design.
Study quality was assessed using the validated Newcastle-Ottawa
Scale for assessment of non-randomized and observational studies as
discussed in the MOOSE guidelines. Study quality measures were
divided into subgroups of cohort, cross-sectional, and case-report
studies. Studies were evaluated based on subject selection, comparability of study groups, and assessment of the outcome and exposure.
Authors were contacted when necessary for further information in
order to assess study quality.
2.4. Data Synthesis and Analysis
All outcomes assessed in the study were dichotomous (yes/no)
and included development or presence of osteoarthritis through the
denitions outlined above. The adjusted risk estimates (HR/RR/OR)

Fig. 1. Study ow diagram.

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M.F. Williams et al. / Journal of Diabetes and Its Complications 30 (2016) 944950

were pooled from individual studies. Only the adjusted risk estimates
that were most similar across studies were extracted and included in
the analysis. The pooled risk estimate was reported using the random
effects model because of anticipated statistical heterogeneity. A
sensitivity analysis was conducted using the risk estimates that
controlled for weight or BMI to assess whether statistical signicance
persisted in the presence of this potential confounder. Heterogeneity
was analyzed using a chi-squared test of N-1 degrees of freedom, with
the I2 test, and with an alpha of 0 05 dening statistical signicance
(Higgins, Thompson, Deeks, & Altman, 2003). Analyses were performed
using Comprehensive Meta-analysis (Biostat, Englewood, NJ) and
STATA/SE 10 1 (Stata Corporation, College Station, TX) software.

3. Results
3.1. Search Results
Our systematic review of the literature through August 2014
identied 1079 records that t our broad search strategy and a review
of their references resulted in an additional 42 abstracts of interest for
a total of 1121 abstracts (Fig. 1). After removal of duplicates and
reviewing the abstracts manually, 820 unique records remained. The
majority of records (n = 739) were excluded because only a title, but
no abstract or publication, could be obtained in English, or the
abstracts did not contain information pertaining to the disease entities

Table 1
Studies Included in Meta-Analysis.
Study

Cohort studies
Bagge et al.
(1991)

Sample size of
Recruitment source
study population
analyzed in
meta-analysis
340

Diabetes denition

Joint
involvement

Outcome

Group
analyzed

Pertinent
ratio

Factors
adjusted

Community, 30% sample all Serum glucose

70 year old followed
reading of 149.5
mg/dl or use of
antidiabetic
medication

Hand (DIP, PIP,

IP MCP, II-V,
MCP I, CMC I),
Knee

Kellgren
Lawrence &
Symptoms

Total (n =
340)
Male

Age, sex &

BMI

DIP, PIP, MCP

and thumb base
joints

OA development
via Kellgren
Lawrence &
Symptoms
Kellgren
Lawrence &
Symptoms
Knee
replacement

Total

1.22
(0.722.07)
1.08
(0.512.28)
1.44
(0.543.00)
(0.351.14)

Total

(1.374.27)

Age, sex,
BMI

Total

(1.113.84)

Age, sex,
BMI, prior
joint
replacement

Knee

Kellgren
Lawrence 2 &
Symptoms

Female

Physician diagnosis
or use of oral
antihypergly-cemics
or insulin
Diagnosis by doctor
or on medications

Hip, hand, knee

Kellgren
Lawrence &
Symptoms

Hip, hand, knee

Blood glucose N100

mg/dL

DIP, PIP, MCP,

CMC

Symptomatic OA
conrmed with
ACR criteria &
Radiographs
Kellgren
Lawrence &
Symptoms

Female

Haugen et al.
(2011 abstract)

522

Framingham OA Study
Offspring Cohort, USA

Elevated blood
glucose

Yoshimura et al.
(2012)

1384

Schett et al.
(2013)

927

ROAD study cohort,

Nationwide from Japan
over 3 years
Bruneck cohort;
Bolzano,Italy

IGT as fasting glucose Knee

110 mg/dL or
HbA1c 5.5%
Serum glucose N126 Hip and knee
mg/dL or diagnosis or
medication for
diabetes)

United States First National

Health and Nutrition
Examination Survey of
19711975 (HANES I)
4 major hospitals in SW
Germany

Questionnaire
regarding previous
diagnosis

Cross sectional studies

Anderson and
2765
Felson (1988)

Strmer et al.
(2001)

171

Andrianakos et al.
(2006)

547

Community based study

in Greece

Dahaghin et al.
(2007)

3585

Community cohort.
Erasmus Medical Centre,
Rotterdam

Reid et al. (2010)

6299

CaseControl studies
Nieves-Plaza et al. 202
(2013)

Diagnosis Code
of OA

Southern Califronia
American Indian Health
Clinics Database

Diabetes diagnosed
by diagnosis code

Unclear based
on diagnosis
codes

Endocrinology clinics,
University of Puerto Rico's
Medical Sciences Campus

Plasma glucose
concentration,
fasting plasma,
2-hour plasma

Hand (MCP,DIP) ACR criteria

and knee

Indicates model included further adjustments beyond those included in gure.

Excluded from nal metanalysis, see text for details.

Included risk ratios obtained through correspondence with author.

1.02
(0.522.00)
Male
2.14
(0.924.96)
Generalized 0.97
OA
(0.50 1.86)

Age & sex

Age & sex

stratied

Age, sex,
BMI

Knee OR

1.26
(0.981.63)

Age, sex,
obesity

Total

1.20
(0.901.60)
1.90
(1.003.8)

Age
stratied,
sex, BMI

5562
years
62.168.7
years
N68.8
years
3544
years
4554
years
5564
years
N65 years

1.10
(0.701.8)
0.90
(0.601.4)
1.90
(1.063.40)
1.62
(1.092.42)
1.31
(0.811.99)
1.25
(0.801.94)

Total

2.18
(1.124.24)

Age
stratied, sex

Age, sex,
BMI

M.F. Williams et al. / Journal of Diabetes and Its Complications 30 (2016) 944950

947

of interest. Eighty one full-text records were assessed. The majority of

these (n = 64) were excluded either because the studies did not
evaluate the association between OA and type 2 diabetes (n = 53) or
they did assess the association between the two conditions but the
statistics presented did not include an OR/HR/RR (n = 11).

Sarzi-Puttini, Scarpa, et al., 2005). The risk ratios from the Andrianakos
and Sturmer studies were updated following communication with those
authors. Finally, there were two publications from the ROAD study: the
one study that only included prevalence data was excluded, while the
publication with incidence data was included (Yoshimura et al., 2012).

3.2. Study characteristics

3.3. Odds of type 2 diabetes in OA

Regarding those studies that assessed the association but did not
include a pertinent ratio, 2 found a statistically signicant positive
association between OA and type 2 diabetes (Puenpatom & Victor,
2009; Silveri, Brecciaroli, Argentati, & Cervini, 1994), 1 found a
statistically signicant negative association (Horn et al., 1992), 1
failed to show an association (Magar et al., 1989), while 1 varied
between a positive or no association depending on the joint analyzed
(Waine, Nevinny, Rosenthal, & Joffe, 1961). An additional 4 studies did
not analyze the association beyond prevalence in a population of
diabetics. The nal 2 studies discussed pertinent analyses, with one
failing to show a signicant statistical relationship while the other
found no signicant difference; however, the publications did not
discuss further details, and the authors could not be reached (Carman,
Sowers, Hawthorne, & Weissfeld, 1994; Frey, Barrett-Connor, Sledge,
Schneider, & Weisman, 1996). Notable amongst these 11 rejected
studies are two publications that were foundational in presenting the
question of an association between type 2 diabetes and OA
(Silberberg, Frank, Jarrett, & Silberberg, 1959; Waine et al., 1961).
Seventeen studies were included in the qualitative analysis but 5
were excluded from the nal quantitative synthesis. Two studies were
excluded as their primary outcome related to mortality (Gabriel,
Crowson, & OFallon, 1999; Nesch et al., 2011). A study from the
AMICA cohort had proxy outcomes of pain on the visual analog scale and
use of non-steroidal anti-inammatory drugs, while the Horn study
employed osteophytes as their outcome. Given that these outcomes did
not meet our inclusion criteria they were excluded (Cimmino,

Ultimately, there were 12 studies that we attempted to include in

the meta analysis. These were comprised of 4 cohort studies (33 3%)
(Bagge et al., 1991; Haugen, Englund, Aliabadi, et al., 2011; Schett et
al., 2013; Yoshimura et al., 2012), 6 cross-sectional studies (50%)
(Anderson & Felson, 1988; Andrianakos, Kontelis, Karamitsos, et al.,
2006; Dahaghin, Bierma-Zeinstra, Koes, Hazes, & Pols, 2007; Marshall
et al., 2013; Reid et al., 2010; Strmer, Brenner, Brenner, & Gnther,
2001), and 2 case-control studies (16 7%) (Cooper, McAlindon,
Snow, et al., 1994; Nieves-Plaza et al., 2013) that met the inclusion
criteria. However, 2 studies and 1 subgroup analysis were unable to be
included in the nal analysis secondary to the large range of the
condence intervals thus making them inappropriate for our
statistical software (Anderson & Felson, 1988; Cooper et al., 1994;
Marshall et al., 2013). While excluded from the nal analysis all three
of the odds ratios generated by these studies showed a positive, albeit
not statistically signicant, association between the conditions.
Additionally, while the outcome in the ROAD study classied a
group as having impaired glucose tolerance this study was included
because subjects with type 2 diabetes were included in this cohort.
Thus, the pertinent risk estimates of 10 studies were included in
our nal analysis (Table 1). Only one association per study was
included in order to not confound the data with overlapping groups
from those studies that reported separate associations for each joint
analyzed (Andrianakos et al., 2006; Strmer et al., 2001). Given
stratication across pertinent risk factors, 2 studies contributed more
than one independent risk estimate to the meta-analysis (Bagge et al.,
1991; Reid et al., 2010). This resulted in 14 separate HR/RR/OR
included in the meta-analysis. Overall the studies used for the analysis
included 12 positive associations (5 statistically signicant) and 2
negative associations (neither of which were statistically signicant).

Table 2
Assessment of Study Quality Using the Moose Criteria.
Cohort studies
Study

Selection Comparability Outcome Total stars

(maximum score 9)

3.4. Risk of bias assessment

Bagge et al. (1991)

Haugen et al.
(2011)
Yoshimura et al.
(2012)
Schett et al. (2013)

****
****

**
**

***
**

9
8

****

**

***

****

**

***

Study quality was assessed using the MOOSE and modied-MOOSE

criteria (Table 2). Using the Newcastle-Ottawa scoring system the
majority of studies presented a low risk for study bias as assessed by
representativeness and selection of the cohort. Furthermore, all studies
included in the nal analysis controlled for the important risk factor of
age and at least one other known risk factor, which is included in the
scoring of Comparability of the studies. In terms of ascertainment of
outcome, only 1 of the included studies did not use secure medical
records to determine whether the outcome was achieved. While the
majority of studies did independently assess the outcome, 4 either used
records or patient self-reports; they thus received a lower score for the
Selection component of the Newcastle-Ottawa score.

Cross-sectional studies
Study

Selection Comparability Outcome Total stars

(maximum score 6)

Anderson and
Felson (1988)
Strmer et al.
(2001)
Andrianakos et al.
(2006)
Dahaghin et al.
(2007)
Reid et al. (2010)

***

**

**

**

**

***

**

**

**

CaseControl study
Study

Selection Comparability Outcome Total stars

(maximum score 9)

Nieves-Plaza et al. **
(2013)

***

**

* indicates a number indicating study quality according to Moose Criteria. The greater
number of * indicates higher quality.

3.5. Meta-analysis
Using the random effects model, we found a statistically signicant
increased odds ratio of OA associated with the presence or
development of type 2 diabetes of 1 21 (95% CI 1 021 41)
from a pooled sample of 16,742 patients (Fig. 2). The heterogeneity
detected in these studies generated an I 2 value of 26% indicating mild
to moderate heterogeneity between the results of the studies. The
sensitivity analysis performed to assess whether the odds of the
association between type 2 diabetes and OA remained the same when
controlling for weight and BMI showed a consistent result to the
overall analysis.

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M.F. Williams et al. / Journal of Diabetes and Its Complications 30 (2016) 944950

Study Name

Bagge 1991 Males

Bagge 1991 Females
Haugen 2011
Yoshimura 2012
Schett 2013
Anderson 1988 Female
Sturmer 2001
Andrianakos 2006
Dahaghin 2007
Reid 2010a
Reid 2010b
Reid 2010c
Reid 2010d
Nieves-Plaza

Point Estimate and 95% CI

Point
Estimate

Standard
Error

1.080
1.440
0.640
2.420
2.060
1.020
0.970
1.260
1.200
1.900
1.620
1.310
1.250
2.180
1.215

0.273
0.628
0.202
0.740
0.696
0.378
0.347
0.163
0.179
0.597
0.339
0.301
0.291
0.967
0.099
-2.00

-1.00

Does Not Favor

Association

0.00

1.00

2.00

Favors
Association

Fig. 2. Association between type 2 diabetes & OA.

Given the above stated heterogeneity we performed following

sensitivity analyses to conrm the primary ndings (controlling for
weight and BMI, excluding those with impaired glucose tolerance
etc). In this subset of 7 studies that did control for weight or BMI, the
increased odds of the increased severity, presence or development of
OA associated with type 2 diabetes was 1 25 (95% CI 1 051 46)
from a smaller pool of patients (n = 7156) (Fig. 3).
4. Discussion
This systematic review and meta-analysis estimated the odds ratio of
type 2 diabetes and the presence or development of OA from 10 studies
having a combined 16,742 patients. While including patients with varying
OA joint involvement from various ethnic groups, we found that the
presence of type 2 diabetes was signicantly associated with the
development or presence of OA with an OR of 1 21 (95% CI 1 02
1 41) and this associations persisted even after adjusting for their
weight/BMI. These ndings have clinical implication for diabetes management, which includes modulating types of physical activity in those at risk.
Our meta-analysis revealed the limited number of studies that have
fully assessed the risk of the presence of or developing OA in patients
with type 2 diabetes. While the concept of a connection between the
two diseases is long-standing, it is only recently that studies have
pursued more sophisticated statistical analyses that adjust for BMI and
weight as risk factors, as well as for possible confounding between
obesity, diabetes, and OA. We found that even when limiting analysis to
those studies that controlled for weight/BMI and obesity, a statistically
signicant relationship between type 2 diabetes and OA remained.
These results in particular strengthen the thought of an independent
association between type 2 diabetes and OA.
Beyond epidemiological associations noted in this analysis, there
are a variety of postulated mechanisms regarding the impact of type 2
diabetes on the progression of OA including advanced glycation
end-products (AGEs). Data suggest that metabolic factors such as
hyperglycemia may contribute to joint vulnerability through the
formation of AGEs in cartilage (Saudek & Kay, 2003). The accumulation of AGEs leads to increasing stiffness and brittleness of collagen,
thereby causing the joint to be more vulnerable to mechanical stress
(DeGroot, Verzijl, Wenting-van Wijk, et al., 2004; Verzijl, DeGroot,
Ben, et al., 2002). AGEs are also implicated in altering the synthesis
and degradation of collagen and likely compromising the integrity of

cartilage (DeGroot, Verzijl, Jacobs, et al., 2001; Steenvoorden,

Huizinga, Verzijl, et al., 2006).
With the increasing prevalence of diabetes internationally, our
ndings of an increased risk of having or developing OA in patients with
type 2 diabetes is particularly relevant. This is especially true as studies
have found that OA, as well as type 2 diabetes, is underdiagnosed
(Falagas, Vardakas, & Vergidis, 2007). Without a clinical diagnosis and
appropriate education, patients are at risk for not understanding OA or
the wide-range of therapies available for its management. (Hill & Bird,
2007) Sharing this information is vital, as physical activity is a
cornerstone of lifestyle interventions recommended for patients with
type 2 diabetes. By not adequately recognizing and treating patients'
pain and limitation of daily activities caused by OA, we may be limiting
treatment of their metabolic disease.
The strength of this meta-analysis is that it is based on a pre-specied
study protocol that included a systematic search of MEDLINE, SCOPUS,
EMBASE, and Web of Science databases, as well as Grey Literature, to
obtain pertinent studies. Our ndings were strengthened in that we also
reached out to authors who had noted type 2 diabetes being included in
their analysis, but did not include these data in their publication. As such,
our pool of included studies was broader than those in existing review
studies. The main limitation of this analysis is that it involves individual
observational studies and that the majority of these studies were not
prospective cohort studies. As such, the studies may be subject to
unknown confounding factors, selection bias, and attrition bias.
However, overall study quality was high.
We acknowledge the mild to moderate heterogeneity noted in the
analysis. These could be attributed to the differences in the following
aspects of the studies: a) differences in the study population- mean age
and race, b) differences among the joints assessed to diagnose OA, tools
used to assess OA and differences in the study duration. Unfortunately
we lacked the adequate number of studies to conduct meta-regression
analysis to explore the reasons for the observed heterogeneity.
Results of this systematic review and meta-analysis demonstrate a
positive association between type 2 diabetes and OA, although the
individual condence intervals were non-signicant. However, when
individual risk estimates were pooled, we found a statically signicant
association between type 2 diabetes and the presence or development
of OA. Our results emphasize the need to identify individuals with
type 2 diabetes and educate them on the increased risk of OA
progression and severity, as well as consider appropriate referral for

M.F. Williams et al. / Journal of Diabetes and Its Complications 30 (2016) 944950

1.250

949

0.101

Fig. 3. Association between type 2 diabetes & OA in studies controlling for weight and bmi.

more aggressive risk factor modication and management by a

primary care physician or rheumatologist.

Acknowledgements
We thank Marian Simonson of the Cleveland Clinic Alumni Library
for her assistance in approaching the systematic review of the
literature.
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