Obesity and Musculoskeletal System

REVIEW

The impact of obesity on the musculoskeletal system

A Anandacoomarasamy1, I Caterson2, P Sambrook1, M Fransen3 and L March1

1Institute of Bone and Joint Research, Kolling Institute, Royal North Shore Hospital, University of Sydney, Sydney, New SouthWales, Australia; 2Boden Professor of Human Nutrition, University of Sydney, Sydney, New South Wales, Australia and3Musculoskeletal Program, The George Institute, University of Sydney, Sydney, New South Wales, Australia

Obesity is associated with a range of disabling musculoskeletal conditions in adults. As the prevalence of obesity increases, thesocietal burden of these chronic musculosketelal conditions, in terms of disability, health-related quality of life, and health-carecosts, also increases. Research exploring the nature and strength of the associations between obesity and musculoskeletalconditions is accumulating, providing a better understanding of underlying mechanisms. Weight reduction is important inameliorating some of the manifestations of musculoskeletal disease and improving function.

International Journal of Obesity (2008) 32, 211–222; doi:10.1038/sj.ijo.0803715; published online 11 September 2007

Keywords: musculoskeletal; arthritis; disability; function

Introduction

Obesity represents a major public health problem and carries

with it the risk of developing significant medical problems.

The global burden of obesity is rising at an alarming rate. The

World Health Organization estimates that more than one

billion people are overweight and of these, 300 million are

obese.1 In Australia, about 20% of the population is obese

(approximately 2.6 million).2 In addition, the levels of

extreme obesity (obesity grade 3, body mass index (BMI)

X40) are also escalating.3 Recently, McTigue et al.3 reported

that weight-related health risk, specifically all-cause mortal-

ity, varies with degree of excess weight with those in the

obesity grade 3 range faring significantly worse than

individuals of normal weight or a lower grade of obesity.3

Concurrently, in part due to the aging population, the

burden of arthritis and musculoskeletal conditions as causes

of pain and disability continues to increase. In Australia,

these conditions have been identified as the third largest

contributor to direct health expenditure (behind cardiovas-

cular disease and neurological disorders).4 ‘Arthritis and

related disorders’ were the most common cause of disability

in Australia in a recent population survey,5 the second most

common reason for general practitioner (GP) visits and also

the cause of a large number of hospital separations.6 In an

analysis of the direct costs of obesity, it was estimated that the

cost of osteoarthritis (some $300 million) was second only to

the cost of diabetes in obesity-associated conditions.

There is a significant positive association between musculo-

skeletal disorders and the level of obesity.7 The Centre for

Disease Control recently reported that in the United States,

more than 31% of obese adults reported a doctor diagnosis of

arthritis compared to only 16% of non-obese people.8 The

nature and extent of the impact of obesity on the

musculoskeletal system and the spectrum of conditions

implicated is not well appreciated. This is surprising

considering the high prevalence of chronic musculoskeletal

conditions in a rapidly aging population and the associated

significant societal burden of lost productivity and direct

health-care costs. In addition, the chronic pain and disability

associated with musculoskeletal conditions not only signifi-

cantly affect an individual’s quality of life but often result in

the early uptake of a sedentary lifestyle associated with

various serious comorbidities.

Obesity has been implicated in the development or

progression of a wide variety of musculoskeletal conditions.

These are summarized in Table 1. Obesity is also associated

with increased operative risks in the surgical management of

some of these conditions.9 The aim of this study is to provide

a comprehensive overview of the specific musculoskeletal

conditions associated with obesity and present the evidence

underpinning the association between obesity and these

musculoskeletal conditions. The possible impact of obesity

on therapy is also explored. A literature search (Medline and

Pubmed) was conducted from January 1966 to December

2006. Articles assessing the effect of obesity or weight loss on

musculoskeletal conditions were reviewed.Received 27 February 2007; revised 1 August 2007; accepted 1 August 2007;

published online 11 September 2007

Correspondence: Dr A Anandacoomarasamy, Institute of Bone and Joint

Research, Royal North Shore Hospital, St Leonard’s, New South Wales 2065,

Australia.

E-mail: [email protected]

International Journal of Obesity (2008) 32, 211–222& 2008 Nature Publishing Group All rights reserved 0307-0565/08 $30.00

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http://dx.doi.org/10.1038/sj.ijo.0803715

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Osteoarthritis

Osteoarthritis (OA) is the most common form of arthritis and

the leading cause of chronic disability among older people.

Large longitudinal studies10–23 have demonstrated that

obesity is a significant risk factor for both the development

and progression of tibio-femoral knee OA (both symptomatic

and radiographic). An association, though modest, has also

been demonstrated between obesity and OA at other sites

such as the hip, hand and patello-femoral joint, suggesting

that both mechanical and metabolic factors may be

responsible for the link between OA and obesity.

Knee osteoarthritis

Prospective data from the Framingham population demon-

strated that obesity predates the development of knee OA,

and that obesity is an independent risk factor for incident

radiographic OA. The odds ratio (OR) per 5-U BMI increase

was 1.6.10 In the Chingford study of over 1000 women,

obesity was classified as the upper tertile of BMI (the

boundaries of the middle tertile were 23.4 and

26.4 kg m�2).24 The age-adjusted OR of unilateral and

bilateral radiological knee OA comparing the high and low

tertiles of BMI were 6.2 and 18, respectively, and the risk was

8.6 times higher for symptomatic disease. In the recent

MOST cohort, those with highest obesity were again at

highest risk of developing symptomatic and radiological

knee OA at 15 months (OR 3.4).25 A recent study on

ambulatory loads in overweight and obese subjects indicated

that cartilage thickness at the knee joint responds to loading

during gait in a similar manner to OA patients. These

findings suggest the possibility that increased weight

initiates a pathway of cartilage degeneration prior to the

emergence of OA symptoms.26

In a controlled study with twins, Cicuttini et al.19 showed

that each kilogram increase in body weight was associated

with an increased risk of radiographic features of OA at the

knee and carpometacarpal joint. The strong association

between high BMI and knee OA was confirmed in another

twin study and this association was found not likely to be

mediated by shared genetic factors.27 Obese patients with

knee OA have more joint space narrowing in the medial

and lateral tibio-femoral compartments than non-obese

patients.28

Obesity is also an important risk factor for the progression

of knee OA17 and has long-term detrimental effects on the

knee joint.29 Sharma et al.30 looked at the role of mechanical

factors, specifically malalignment, in mediating knee OA

severity or progression. In patients with knee OA, there was a

relationship between BMI and radiographic severity in those

with varus malalignment, but not in those with valgus

malalignment. BMI correlated positively with varus mala-

lignment. However, the partial correlation between BMI and

medial joint space width was reduced from 0.24 to 0.04 after

adjustment for malalignment, due to the strong positive

association between medial joint space width and varus

malalignment. It was found that varus malalignment may

explain, in part, the uniquely strong association between

BMI and OA at the knee compared to other lower extremity

sites. However, given the cross-sectional nature of the study,

it cannot be established whether varus malalignment is

causal or consequential in the relationship between obesity

and OA. Nevertheless, varus malalignment is an important

mediating factor in knee OA in the obese individual. Felson

et al.31 also found that the adverse effect of high BMI on knee

OA progression was limited to those patients with moderate

malalignment.

Although the strong association between knee OA and

obesity has been demonstrated, the factors underlying the

mechanism of the effect have not been entirely elucidated.

Age, serum lipids, serum uric acid, blood glucose or diabetes,

body fat distribution, blood pressure, smoking, chondrocal-

cinosis, hysterectomy or estrogen replacement therapy have

not been found to affect the obesity–OA relationship.30

However, being overweight is associated with increase in

cartilage turnover biomarkers. Cartilage oligomeric matrix

protein and collagen type 2 degradation products were

increased in those with high BMI.32,33

Another study examined the effects of measures of body

composition on the longitudinal change in tibial cartilage

volume using magnetic resonance imaging (MRI).34 Eighty-

six healthy adults underwent assessment of body composi-

tion using dual X-ray absorptiometry and MRI at baseline

and 2 years. A strong positive association was found between

muscle mass in the lower limbs, muscle mass in all limbs,

and muscle mass in the total body and medial tibial cartilage

volume after adjustment for confounders such as age, sex,

BMI, medial tibial bone size and physical activity. Impor-

tantly, in the longitudinal analysis, increased muscle mass

was also associated with a reduction in the rate of loss of

both medial and lateral tibial cartilage volume. In contrast,

body fat was not associated with medial or lateral tibial

cartilage volumes or loss in adjusted analysis. This finding

was confirmed in a recent larger study suggesting that

apparent gender difference in articular cartilage volumes

(men demonstrating higher cartilage volume) may be largely

explained by fat-free muscle mass.35 However, another study

reported that increased muscle mass may predispose to

Table 1 Musculoskeletal conditions associated with obesity

Musculoskeletal conditions associated with obesity

OA (knee, hip, hand)

Low Back Pain

Diffuse idiopathic skeletal hyperostosis

Gait disturbance

Soft tissue conditions (for example, carpal tunnel syndrome, plantar fasciitis)

Osteoporosis

Gout

Fibromyalgia

Connective tissue disorders (rheumatoid arthritis)

Abbreviation: OA, osteoarthritis.

Obesity and musculoskeletal diseaseA Anandacoomarasamy et al

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International Journal of Obesity

lateral patello-femoral OA progression in women,36 whereas

in another, greater quadriceps strength was found to have no

effect on cartilage loss at the tibio-femoral joint, even in

malaligned knees.37

The association between knee structural alteration and BMI

was evaluated in a cross-sectional convenience sample of 372

largely healthy subjects.38 Apart from the lateral tibio-femoral

compartment, BMI was significantly associated with knee

cartilage defect scores such that obese subjects had higher

cartilage defect severity and prevalence. BMI was also

positively associated with tibial bone area but there was no

significant change in cartilage volume or thickness compared

to those with normal weight. This study shows that increasing

BMI may induce cartilage defects even in those with no

radiographic OA. The reasons for this remain to be elucidated.

There is some evidence suggesting that knee bone size may

be important in the development of knee OA. Knee bone size

is under strong genetic control and is higher in the offspring

of those with severe OA.38 The authors propose that a greater

BMI can induce larger knee subchondral bone size or that

knee subchondral bone may respond to higher loads by

expansion of the joint surface area. In this study, knee bone

size mediated, in part, the associations between BMI and

knee cartilage defects, because these associations were

attenuated after adjustment for bone size and vice versa.

Higher BMI is also associated with increased risk of

degenerative meniscal lesions.39 However, it is not certain

if degenerative meniscal lesions have an etiological role in

the development of knee OA.

Hip osteoarthritis

The First National Health and Nutrition Examination Survey

data show that obesity was more closely associated with

bilateral hip OA than with unilateral hip OA.40 A systematic

review found moderate evidence for a positive association

between obesity and the occurrence of hip OA (OR B2).41

The associations between obesity and hip OA were stronger

when the diagnosis included clinical as well as radiological

criteria.

Hand osteoarthritis

The association between obesity and hand OA is less certain

with some studies suggesting a link and others showing

conflicting results.16,42–47.In a large Finnish study, BMI was

found to be directly proportional to the prevalence of thumb

carpo-metacarpal OA in both sexes.48 The adjusted OR was

1.29 per 5 kg m�2 increment in BMI.

In the recent Rotterdam study, overweight showed a

significant association with hand OA independent of other

metabolic factors (OR 1.4).49 An association between over-

weight and hand OA infers other underlying mechanisms

apart from increased load across weight-bearing joints. In

this study, no intermediate effect of metabolic factors on the

association of overweight with hand OA was found. Leptin

may have an important role in the metabolic influence of

overweight on OA. Serum leptin, the product of the obese

(ob) gene, is involved in energy regulation at the level of the

hypothalamus and recent evidence suggests that leptin may

act locally in joint tissues.50 Leptin has been detected in

synovial fluid samples obtained from OA patients and levels

of leptin have been found to correlate with BMI.51 Leptin has

also been strongly overexpressed in human OA cartilage and

in osteophytes.

Weight reduction

Normal weight is associated with a decreased risk incidence

and progression of OA.15,52 Both the American College of

Rheumatology (ACR) and the European League Against

Rheumatism (EULAR) recommend weight loss and exercise

for obese patients with knee OA.53,54

In the Framingham study, evaluation of 800 women

showed a decrease in BMI of X2 kg m�2 in the preceding

10 years decreased the odds of developing symptomatic OA

by 450%.11 It has also been suggested that if all overweight

and obese people reduced their weight by 5 kg or until their

BMI was within the normal recommended range, 24% of the

surgical cases for knee OA might be avoided.55

Until recently, only a few nonrandomized clinical trials

have examined the effect of weight loss on pain and function

in knee OA, suggesting that the combination of dietary

weight loss plus exercise is effective.56–58 Recently, a large

clinical trial, the ADAPT study, randomized 316 overweight

or obese older subjects with knee OA to exercise only

(combined aerobic and strengthening), dietary weight loss

only, exercise plus dietary weight loss or a healthy lifestyle

control group. After 18 months, despite only modest

reductions in body weight, significant improvements in

pain and physical function were seen in the diet plus exercise

group compared to the healthy lifestyle group, but not for

the weight loss or exercise-only allocations.59

A subset of the ADAPT study cohort underwent biomecha-

nical analysis testing over an 18-month period.60 There was a

significant relationship between weight loss and reduction

in compressive knee-joint loads, with a four-pound reduc-

tion in knee-joint load per step for every 1 pound weight

loss. To date, there are no longitudinal studies evaluating if

weight loss slows the progression of knee OA but this effect

would appear to be clinically plausible. In the ADAPT study,

no changes in joint space narrowing were noted between the

different groups.61 However, the study was probably under-

powered to detect differences in joint space narrowing over

an 18-month period. MRI possibly allows a more sensitive

measure of joint space loss compared with radiography, but

thus far, no studies have looked at MRI outcomes in subjects

undergoing weight loss.

A second recent randomized clinical trial, evaluating a

rapid weight loss diet among 80 patients with knee OA,

found that a weight reduction of 10% improved function by


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28%. The authors found that less than four patients (95%

confidence interval 2–9 patients) would need to be treated

with a low-energy diet for one patient to achieve a X50%

improvement in the WOMAC score (a measure of joint pain,

stiffness and function) when compared to a control diet.62

The effects of weight loss and exercise interventions on

serum leptin were also assessed in the ADAPT cohort.63 In

the ADAPT cohort, serum leptin was significantly reduced by

a long-term diet (weight loss) intervention with modest

weight loss of 5–6%. Serum leptin was also related to self-

reported physical function with higher leptin concentrations

related to greater impairments in physical function. The

authors also found that initial baseline leptin levels were a

predictor for subsequent weight loss, with lower baseline

levels of leptin predicting greater weight loss.

Surgery

The need for joint replacement surgery has been escalating

with the increased burden of OA in the community. In

Australia, orthopedic surgery had the second longest median

waiting time in 2003–2004.64 With the increasing prevalence

of obesity, the proportion of joint replacements performed in

obese patients is likely to increase dramatically, with

estimates suggesting over a third of all total hip and knee

replacements are performed in the obese.65–68 A frequency-

matched case–control study found that very obese females

(BMI 440) were more likely to face joint surgery compared

with matched normal weight females in either the hips

(OR¼4) or knees (OR¼19).69 Similarly, obese males were

more likely to undergo joint replacement surgery compared

with non-obese males.

A recent review discussed the decision by three primary

care trusts in the United Kingdom to not entitle patients

with BMI 430 to hip and knee replacement surgery, and

evaluated the current evidence for outcomes in obese

patients for both total knee and hip replacement surgery.9

In the midterm, outcomes of knee replacement in the obese

(BMI 430) are probably comparable to the non-obese but

larger, prospective studies are needed to ascertain long-term

outcomes. However, there is some evidence that outcomes in

the morbidly obese (BMI 440) are consistently poor.9 Similar

data are not available for the effect of morbid obesity in hip

replacement.

Obesity may not be a contraindication to simultaneous

bilateral total knee replacement surgery.70 However, a BMI

432 predicted failure in those undergoing minimally

invasive medial unicompartmental knee arthroplasty in a

retrospective series.71 Obesity is a risk factor for patients

undergoing high tibial osteotomy for the treatment of

unicompartmental knee OA in the presence of malalign-

ment.72 Outcomes relating to quality of life and satisfaction

following arthroscopic debridement of the knee were also

poorer in overweight women than the normal weight

group.73

Low back pain

Low back pain from degenerative disc disease of the lumbar

spine, spinal canal stenosis and zygo-apophyseal joint

disease is a very common problem in the community

resulting in significant morbidity.74 This has important

consequences in terms of productivity at work and utiliza-

tion of health services. The association between obesity and

lower back pain is conflicting.75–79 A recent review describes

the lack of a clear dose–response relationship between BMI

and low back pain.80

However, compared with non-obese patients, obese patients

were more likely to have radicular pain and neurologic

signs.81 Obesity was a significant, independent determinant

of chronicity in a prospective cohort study in workers

claiming compensation for lower back pain.82 In morbidly

obese subjects with lower back pain undergoing bariatric

surgery, weight loss significantly improved the degree of

functional disability,83 and resulted in less frequent lower

back pain and the use of reduced doses of medications.84

In a population-based study of 129 middle-aged working

men comprising machine drivers, construction carpenters

and office workers, persistent overweight was strongly

associated with decreased signal intensity of the nucleus

pulposus at follow-up MRI (adjusted OR 4.3).85 However, it is

not known whether these MRI findings correlate with

clinical symptoms. Spinal epidural lipomatosis is also

associated with obesity.86 Here, there is hypertrophy of the

epidural adipose tissue, causing a narrowing of the spinal

canal and compression of neural structures.

The relationship between ambulation and obesity in older

individuals with and without low back pain was assessed in a

retrospective study. BMI had a significant inverse relation-

ship with ambulatory measurements in terms of distance

walked, steps taken and walking velocity.87

A retrospective study assessing outcomes of sciatica found

that obesity was associated with adverse 6-month out-

comes.88 Being overweight and obese is also a risk factor

(OR 1.83) for postoperative meralgia paraesthetica after

posterior thoracolumbar surgery.89 However, outcome assess-

ment in elderly patients undergoing lumbar spinal surgery

did not find any difference in the obese group suggesting

that surgery in the elderly obese with appropriate symptoms

would be reasonable.90

Diffuse idiopathic skeletal hyperostosis

Diffuse idiopathic skeletal hyperostosis (DISH) or Forestier’s

disease, a chronic age-related condition, is characterized by

new bone growth especially at the entheses. DISH affects

many skeletal structures but typically affects the thoracic

spine. It is associated with obesity, diabetes mellitus,

hyperinsulinemia and hyperlipidemia.91,92 In an age- and

gender-matched case–control study, patients with DISH were

more likely to have elevated BMI than controls without


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DISH.93 A study examining the role of leptin in the

ossification of spinal ligaments found that serum leptin

levels were significantly elevated in subjects compared to

controls.94 The daughters of subjects who were severely

obese also had high serum leptin levels although they had

not developed the condition. Leptin may thus be genetically

and indirectly associated with the pathogenesis of the

ossification of spinal ligaments in female patients. The role

of obesity in the pathogenesis of DISH is yet to be clearly

defined and the effect of weight reduction in reversing/

slowing progression of disease has not been studied.

Gait disturbance

Obesity is also associated with structural and functional

limitations95 with impairment of normal gait,96 flattening of

the foot arches97–99 and pronation of the ankles. In a pilot

study, body composition was found to influence arch index

values in overweight and obese subjects.100 Obesity increases

rearfoot motion during walking and causes the forefoot

to abduct significantly more than in normal weight

individuals.101

Excess weight is associated with increases in the amount of

force across a weight-bearing joint.30,102 A study assessing

postural instability in extremely obese individuals found

these individuals had inadequate postural instability as

measured by time of balance maintenance and medial-

lateral sway of the trunk.103 After a 3-week body weight

reduction program and specific balance training, postural

stability could be improved which has the potential to

reduce the propensity of overweight individuals to fall while

performing everyday activities. In another study, obesity was

associated with attenuated dynamic balance performance.104

Poorer balance was found to be associated with higher pain

scores in t he presence of weaker knees.

Morbidly obese subjects also walk significantly slower than

their obese and lean counterparts.105 BMI was one of the

factors affecting the variance in walking distance. The effects

of obesity on gait need to be further understood as an

important part of management would include incorporating

an appropriate exercise program.

Soft tissue complaints

There is a high prevalence of pain in the neck (10–19%),

shoulder (18–26%), elbow (8–12%) and wrist/hand (9–17%) at

any given time in the community.106 Obesity is consistently a

significant risk factor associated with the occurrence of these

complaints. Obesity was also found to predict those who were

likely to develop upper extremity tendonitis associated with

work activity in a prospective cohort study over 5 years.107 In

another prospective survey of upper-limb work-related mus-

culoskeletal disorders in repetitive work, obesity again

increased the risk of ulnar entrapment at the elbow.108

A recent study assessed the point prevalence of painful

musculosketelal conditions in obese subjects before and after

weight loss following bariatric surgery.109 There was an

increased prevalence of these conditions at baseline com-

pared to the general population. There was a significant

decrease in pain at most sites following weight loss and

physical activity after 6–12 months, in particular the cervical

and lumbar spine, and foot.

Carpal tunnel syndrome is a common condition in the

community. In a large case–control study using the UK

General Practice Database, obesity was a significant risk factor

associated with carpal tunnel syndrome (OR¼2.06).110

Obesity has been shown to be an independent risk factor for

carpel tunnel syndrome in a number of studies.111,112 There is

also an association between obesity and shoulder repair

surgery for rotator cuff and other conditions, suggesting that

increasing BMI is a risk factor for rotator cuff tendonitis and

related conditions.113

Plantar fasciitis is a common soft-tissue disorder of the

foot. Obesity is a risk factor for developing unilateral plantar

fasciitis (OR 5.6 compared to normal BMI).114 Obesity is also

associated with chronic plantar heel pain.115 The link

between obesity and plantar heel pain is, however, not well

understood. Arch biomechanics are thought to play a role in

etiology but this has not been conclusive.116 Obesity is also a

risk factor for trochanteric bursitis, a frequent cause of lateral

hip pain in middle-aged and elderly individuals.117

Osteoporosis

A number of studies have demonstrated that body weight is

closely correlated with bone mineral density (BMD).118–120

In cross-sectional studies, a 10 kg increase in body weight is

associated with approximately a 1% increase in BMD. This

relationship has been demonstrated for both women and

men and across cultures but the effect of weight on BMD

appears to be stronger in women than in men,121–123 and

more in postmenopausal than premenopausal women.124,125

Several mechanisms have been proposed to explain the

effect of weight on bone density. Firstly, it could be due to

the amount of adipose tissue, which is the major site of

conversion of androgens to estrogen in both elderly men and

women. If estrogen has a greater role in preservation of bone

mass in women than men, this may explain why the effect of

weight is greater in women than men. This may also explain

why shortly after menopause, obese women do not lose bone

as rapidly as their non-obese counterparts.126,127 A second

mechanism relates to the increased mechanical load that

heavier individuals place on weight-bearing bones. This is

supported by some data suggesting that body size is a better

determinant in weight bearing rather than non-weight-

bearing sites.123 Although it is often considered that obese

subjects are at lower risk of osteoporosis, there is evidence

that changes in bone marrow fat with ageing may adversely

affect skeletal strength. Visceral fat may have a protective


215


effect on BMD128 through biochemical factors such as

adiponectin. The latter is an adipocyte-derived hormone

that regulates insulin sensitivity and energy homeostasis.

There is still controversy over the relative importance of

fat versus lean mass in the determination of BMD. Reid129

concluded that while both fat and lean mass are related to

bone measures, the effect of fat mass becomes more

important in postmenopausal women and that the relation-

ship between lean mass and bone density was substantially

accounted for by body size. Only a few studies have

investigated the association of bone mineral measures with

body composition components adjusted for body size or

their distribution (such as centrality indices).130

However, recent research suggests that obesity may

accelerate bone loss.131 Deng et al. showed, in two large

population samples, that the bone strengthening effects of a

heavy body were not due to fat but to elevated muscle mass,

which increases bone density.131 The authors report that

increased fat mass is associated with decreased bone mass,

when the mechanical loading effect of body weight on bone

mass is adjusted for. The risk of fracture in the obese is not

clear with conflicting associations being reported.132,133

There is also evidence from longitudinal studies that

weight loss is a risk factor for rapid bone loss in men and

women,134–136 although methodological differences between

machines in relation to measurement of BMD due to

changes in fat distribution may affect results. Another study

showed that overweight postmenopausal women may be

more susceptible to bone loss with weight reduction. Weight

loss correlated with BMD loss at the trochanter but not at the

femoral neck in the group receiving normal calcium intake

daily compared to high calcium intake.137 Weight loss due to

caloric restriction appears to induce rapid bone loss at

clinically important sites of fracture, unlike exercise-induced

weight loss.138 In addition, the rapid increase in obesity has

led to an escalation in the uptake of surgical techniques to

control weight. Procedures that involve duodenal bypassing

place individuals at risk for osteoporosis as this is the primary

site for calcium absorption.139 Obesity is also a risk factor for

vitamin D deficiency.140

Gout

Gout is the most common form of crystal-induced arthritis

and in the United States affects more than 1% of adults.141 It

results from the deposition of monosodium urate crystals.

Obesity is a well-known modifiable risk factor in the

pathogenesis of gout and serum uric acid is positively

associated with BMI.142 The size of the visceral fat area is

the strongest contributor to elevated serum uric acid

concentration, decreased uric acid clearance and increased

urinary uric acid/creatinine ratio.143 Weight loss is advocated

in the overall management of gout but no study has assessed

the effect of weight reduction on uric acid levels or attacks

of gout.

Fibromyalgia

Fibromyalgia is a complex disorder resulting in pain,

disturbed sleep and altered mood. A number of risk factors

are associated with this condition and obesity also plays a

role.144 In a pilot study of overweight and obese women with

fibromyalgia, the relationship between BMI and fibro-

myalgia symptoms were assessed after a 20-week behavioral

weight loss treatment.145 Participants lost, on average,

4.4% of their initial weight, and weight loss predicted a

reduction in fibromyalgia symptoms, pain interference,

body satisfaction and quality of life. In a study of obese

subjects undergoing bariatric surgery, there was a significant

reduction in fibromyalgia syndrome at follow-up 6–12

months later.109

Connective tissue disorders

Rheumatoid arthritis (RA) is the most common chronic

inflammatory joint disease. Obesity has been identified as a

risk factor for RA.146 Two population-based cohort studies

have shown an association between obesity and the devel-

opment of RA,147,148 whereas one149 did not. The association

appears to be a threshold effect with no relationship between

BMI and the risk for RA below a BMI of 30. Paradoxically, one

study in a cohort of 779 RA patients found that BMI was

inversely associated with mortality independent of metho-

trexate use. Corticosteroid use was not tabulated. Interest-

ingly, an interaction was found between BMI and

erythrocyte sedimentation rate and BMI was protective only

if the erythrocyte sedimentation rate was low.150 However,

obesity was also recently found to be independently

associated with impaired quality of life in patients with

RA.151 A marked increase in plasma levels of adipocytokines

(leptin, adiponectin and visfastin) have been noted in

patients with RA suggesting a role in the modulation of the

inflammatory environment in these patients.152

In systemic lupus erythematosus, obesity is a strong

predictor of preeclampsia.153 Obesity is common in the

lupus population, 36% prevalence in one urban university

clinic.154 However, obesity was not associated with hyper-

tension and diabetes in this cohort and contrary to

expectation, overweight systemic lupus erythematosus pa-

tients appeared to register the highest quality of life on

questioning.

Hypoandrogenicity in males is common in obesity and in

chronic inflammatory conditions such as systemic lupus

erythematosus and RA.155 Leptin, as well reflecting adipose

tissue mass, is stimulated by tumor necrosis factor and is

associated with hypoandrogenicity in non-inflammatory

conditions. Leptin has been found to correlate negatively

with adrenal androgen concentrations in patients with

systemic lupus erythematosus and RA, suggesting that leptin

may be an important link between chronic inflammation

and the hypoandrogenic state.155


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Disability/quality of life

It is increasingly being recognized that obesity impacts on

health-related quality of life and disability. Obesity increases

the risk of disability among people who have arthritis.156–159

Obesity is also associated with disability in those without

self-reported arthritis.159,160 People who have disabilities are

2.5 times more likely to be obese than those who do not have

disabilities.161 In the ADAPT cohort, exercise and dietary

weight loss improved mobility-related self-efficacy and self-

reported pain.162 In cross-sectional data from the 1998

Quebec Health Survey, being overweight was significantly

associated with short- and long-term activity limitation

related to musculoskeletal disease.163

Obesity is also consistently associated with lower limb joint

pain (hip and knee)164–166 and back pain.167 Osteoarticular pain

(knee and hip pain) is a major predictor of poor health-related

quality of life in obese subjects168 and obesity is linked with

knee pain severity and disability among older knee pain

sufferers in the general population.169 Population-based surveys

have confirmed J-shaped associations between BMI and health-

related quality of life, with obese individuals significantly more

likely to report fair or poor general health status.170,171

Exercise capacity is decreased in obesity, both at submax-

imal and peak intensity, and during recovery.172

Importantly, weight reduction was found to have positive

short-term effects on musculoskeletal pain, perceived dis-

ability, and observed functional limitations.173 A recent

systematic review also provides category 1a evidence that

weight reduction reduces pain and disability in knee OA

patients.174

Obesity is also significantly associated with the frailty

syndrome. Frailty indicators include weakness, slowness and

low physical activity, and predisposes to loss of indepen-

dence. Physical frailty is common in community-dwelling

obese elderly men and women.175,176 In home-dwelling

elders, obesity was again one of the primary predictors of

decreased quality of life.177

Health costs

Clearly, obesity has an important impact on health-care costs

due to direct and indirect costs. Obesity cost Australians $21

billion in 2005, double the cost of Medicare in Australia. Lost

tax revenue, welfare and other government payouts incurred

by obesity sufferers was estimated at $358 million.178 In a

Dutch case–control study among self-employed insured

farmers, neck, shoulder, upper extremity and back disorders

accounted for 30% of claims for sick leave of less than 1 year.

Multivariate analysis assessing risk factors showed that

BMI427 was two times more likely to result in musculo-

skeletal disorders as a cause of sick leave.179 Obese subjects

were found to have more work-restricting musculoskeletal

pain than the general population in a Swedish study.180 In a

large cross-sectional study of patients with spinal disease,

obese patients had more comorbidities and were more likely

to be receiving worker’s compensation.81

Obesity also results in significantly higher primary care

drug prescribing in most drug categories including muscu-

loskeletal and joint disease as noted in a recent retrospective

review in the United Kingdom.181 There is also a positive

relationship between musculoskeletal disorders and the

consumption of disability products.182 Moreover, there is

an association between obesity and being on the disability

pension. A linear relationship was identified between BMI

and disabling knee OA.183 In Swedish 5 birth-year cohorts,

there was a J-shaped relationship between BMI and incidence

of disability pension (RR in obese subjects 2.8) and

musculoskeletal disorders were one of the primary rea-

sons.184 This is corroborated in a Finnish study.185

The increasing prevalence of obesity among patients and

caregivers can also lead to more frequent and serious

musculoskeletal injuries among caregivers.186 The ramifica-

tions include the need to utilize safe and appropriate

equipment to cope with obese individuals which inevitably

requires extra care and resources.

Conclusion

Obesity is associated with a number of musculoskeletal

conditions and is responsible for significant disability and

impaired quality of life. The global obesity epidemic has

significant consequences for both the individual and the

community in terms of direct and indirect health-care costs.

Further studies prospectively evaluating these conditions in

the obese population are imperative to define better the

mechanisms by which obesity mediates musculoskeletal

disorders, and to determine the effects of moderate to large

weight loss on these conditions. This has important

ramifications in both the prevention and development of

appropriate treatment strategies in the ongoing manage-

ment of these conditions.

Acknowledgements

Ananthila Anandacoomarasamy holds a National Health and

Medical Research Council Medical Postgraduate Research

Scholarship (ID number 402901).

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Obesity and Musculoskeletal System

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