Epidemiology of osteoarthritis

Cyrus COOPER,a,bMA, DM,
Elaine DENNISON,b MB BChir,
aIHR Musculoskeletal Biomedical Research Unit
University of Oxford, UK
bMRC Lifecourse Epidemiology Unit, (University of Southampton)
Southampton General Hospital – Southampton, UK

Epidemiology of osteoarthritis

by C. Cooper, E. Denni son, M. Edwards ,
and A. Litwic,
United Kingdom

Osteoarthritis is a global degenerative joint disease involving the cartilage and many of its surrounding tissues. Prevalence and incidence estimates of osteoarthritis in different populations may vary considerably due to different diagnostic classifications; in general, radiographic case definition produces the highest estimates, with self-reported and symptomatic osteoarthritis definitions producing similar estimates. The World Health Organization’s Scientific Group on Rheumatic Diseases estimates that 10% of the world’s population aged 60 years or older have significant clinical problems that could be attributed to osteoarthritis. The highest osteoarthritis prevalence estimates are found in the hand joints, with women more commonly affected than men.

Medicographia. 2013;35:145-151 (see French abstract on page 151)

Definition and classification

Osteoarthritis (OA) is a degenerative joint disease involving the cartilage and many of its surrounding tissues. In addition to damage and loss of articular cartilage, there is remodeling of subarticular bone, osteophyte formation, ligamentous laxity, weakening of periarticular muscles, and, in some cases, synovial inflammation.1 These changes may occur as a result of an imbalance in the equilibrium between the breakdown and repair of joint tissue. Primary symptoms of OA include joint pain, stiffness, and limitation of movement. Disease progression is usually slow but can ultimately lead to joint failure with pain and disability.

There have been many attempts to accurately identify and grade radiographic disease in OA. Of these, the classification by Kellgren and Lawrence (K&L) is the most widely accepted and used. Overall, grades of severity are determined from 0 to 4 and are related to the presumed sequential appearance of osteophytes, joint space loss, sclerosis, and cysts.2 The World Health Organization (WHO) adopted these criteria as the standard for epidemiological studies on OA. Cross-sectional imaging methods, such as magnetic resonance imaging (MRI), can visualize joint structures in more detail and continue to undergo evaluation to determine if they will provide a means by which the definition of OA can be refined.

Many studies now report the prevalence of self-reported or symptomatic OA; these differing approaches may go some way toward explaining part of the heterogeneity in OA estimates.3 A recent systematic review3 attempted to understand the differences in prevalence and incidence of OA according to case definition in knee, hip, and hand joints and concluded that radiographic case definition afforded the highest estimates, while self-reported and symptomatic OA definitions presented similar estimates. The interrelationship between the different classifications used is shown in Figure 1.

Figure 1
Figure 1. Relationships between osteoarthritis (OA) classifications.

After reference 3: Pereira et al. 2011;19:1270-1285. © 2011, Elsevier Ltd.


OA may develop in any joint, but most commonly affects the knee, hip, hand, spine, and foot. In 2005, it was estimated that over 26 million people in the USA had some form of OA.4 Self-reported physician-diagnosed OA data from the 2004- 2005 Australian National Health Survey is shown in Figure 2.5 The incidence of hand, hip, and knee OA increases with age, and women have higher rates than men, especially after the age of 50 years. A leveling off or decline occurs at all joint sites around the age of 80 years. For example, the age- and sex- standardized incidence rate from the Fallon Community Health Plan in Massachusetts (USA) was highest for knee OA (240/ 100 000 person-years), with intermediate rates for hand OA (100/100 000 person-years), and lowest observed rates for hip OA (88/100 000 person-years) (Figure 3).6 The incidence rates found by the Dutch Institute for Public Health (RIVM) in 2000 were similar. For hip OA, the reported prevalence was 0.9 and 1.6 per 1000 per year in men and women, respectively, and for knee OA the corresponding figures were 1.18 and 2.8 per 1000 per year in men and women, respectively (Figure 4).7

Figure 2
Figure 2. Age-specific prevalence of osteoarthritis in Australia in 2004-2005 (Australian
Institute of Health and Welfare analysis of the Australian Bureau of Statistics’
2004-2005 National Health Survey).

After reference 5: Australian Institute of Health and Welfare. 2007. Arthritis series no 5. Cat no. PHE
93. Canberra: AIHW. © 2007, Australian Institute of Health and Welfare.

_ Hand OA
The prevalence of radiographic hand OA varies greatly and has been reported to range from 27% to over 80%.8,9 In a study from the Netherlands, 75% of women aged between 60 and 70 years had evidence of OA in the distal interphalangeal (DIP) joints, and 10% to 20% of subjects aged below 40 years were reported to have OA radiological changes in their hands or feet.7 In a rural sample from the former Soviet Republic of Turkmenia,10 all males over the age of 65 years had at least one affected hand joint. Symptomatic hand OA, as defined by the American College of Rheumatology (ACR) criteria, is, however, far less common. Its prevalence was found to be 8% in the US National Health and Nutrition Examination Survey (NHANES III).11 Data from the Framingham cohort demonstrated a prevalence of 13.2% in men and 26.2% in women aged ≥70 years, with at least one hand joint with symptomatic OA.8 A study from Teheran showed that the prevalence of hand OA in people aged 40 to 50 years was 2.2%, rising with age to 22.5% in people aged >70 years.12 As with many studies, including the Framingham cohort, differentiation by sex in this population showed that women were more frequently affected than men.12 Interestingly, data from China based on thirteen surveys involving 29 621 adults demonstrated that symptomatic OA of the hand was rarely observed, irrespective of age or sex.13

Figure 3
Figure 3.
Incidence of clinical osteoarthritis of the hand, knee, and hip among participants in the Fallon Health Plan.

After reference 6: Oliveria SA et al. Arthritis Rheum. 1995; 38:1134-1141. © 1995, American College of Rheumatology.

Figure 4
Figure 4. Prevalence of clinical osteoarthritis of the hand, knee, and hip in a Dutch population.

Reproduced with permission from reference 7: van Saase JL et al. Ann Rheum Dis. 1989;48:271-280. © 1989, BMJ Publishing
Group Ltd.

_ Knee OA
Knee involvement occurs less frequently than hand OA, although, similarly, it is more common in women, with female- to-male ratios varying between 1.5:1 and 4:1. Prevalence rates for knee OA, based on population studies in the USA, are comparable to those in Europe. These studies report that severe radiographic changes affect 1% of people aged between 25 and 34 years and this figure increases to nearly 50% in those 75 years andabove.14 Few studies have reported secular trends in knee pain; a recent report from the Framingham Study found that the age- and BMI-adjusted prevalence of knee pain and symptomatic knee OA approximately doubled in women and tripled in men over 20 years (Figure 5, page 148); no such trend was observed in the prevalence of radiographic knee OA.15 Similarly, using questionnaire data enquiring about pain in and around the knee, the same researchers found that the age- and BMI-adjusted prevalence of knee pain increased by about 65%in NHANES from 1974 to 1994 among non-Hispanic white and Mexican American men and women and among African American women.15 These secular trends could not be fully explained by increasing obesity. According to data produced by the Dutch Institute for Public Health, the prevalence of knee OA in those aged 55 and above was 15.6% in men and 30.5% in women.7

Geographical variation in OA epidemiology also exists. Studies from China, which used similar methods and definitions to those used in the Framingham Study, found that the prevalence of bilateral knee OA and lateral compartment disease were two to three times higher in Chinese cohorts compared with estimates from the Framingham OA Study.16 Data on clinically diagnosed knee OA in the Community Oriented Program for the Control of Rheumatic Disorders studies (COPCORD) in Asia showed that the prevalence within this area ranged from 1.4%in urban Filipinos to 19.3%in rural communities in Iran.17 Part of the reason for this difference may be explained by the physical and socioeconomic environment. The COPCORD studies conducted in India, Bangladesh, and Pakistan looked specifically into differences between rural and urban populations. In India, it showed a significantly higher prevalence of knee pain in rural (13.0%) than in urban (8.1%) communities.17 Furthermore, in China, men aged 60 years and above from a rural community had approximately double the prevalence of symptomatic knee OA than their urban counterparts.16

Figure 5
Figure 5. Varying prevalence of radiographic
and symptomatic knee osteoarthritis over
a 20-year period among participants in the
Framingham Osteoarthritis Study.

Abbreviations: BMI, body mass index; OA, osteoarthritis.
Reproduced with permission from reference 15:
Nguyen US et al. Ann Intern Med. 2011;155:725-732.
© 2011, American College of Physicians.

_ Hip OA
Hip OA is less common than either hand or knee OA. The mean prevalence of primary radiographic hip OA in studies from Asia and Africa is 1.4% and 2.8%, respectively.17 These levels are much lower than those seen in Europe and North America. In the Study of Osteoporotic Fractures, the prevalence of radiographic hip OA was analyzed in women over the age of 65, using eleven different definitions. Excluding the definition of minimum joint space of less than 2.5 mm, the prevalence ranged from 1.0% to 6.2%, depending on the definition used.18

Risk factors

OA is referred to as “primary” in the absence of an extrinsic cause. The proportion of individuals with primary OA within a specific OA population varies greatly. As age increases, the likelihood of an individual having primary OA increases. There are also differences by sex; in the Queensland Aboriginal communities it was found that 88% of women had primary OA, whereas 82% of men had secondary OA.19

The risk of developing OA is determined by both systemic and local factors. Several systemic factors have been identified; these may act by increasing the susceptibility of the joints to injury, by direct damage to joint tissues, or by impairing the process of repair in damaged joint tissue. Local factors are most commonly biomechanical in nature and adversely affect the forces applied to the joint. Risk factors are discussed individually below; the varying prevalence of some, such as obesity and nutritional factors, may partly explain the differing rates of OA seen in different populations.

_ Age
The prevalence and incidence of radiographic and symptomatic OA considerably increase with age. The relationship between age and the risk of OA is likely multifactorial and is probably the consequence of numerous individual factors that may include oxidative damage, thinning of cartilage, muscle weakening, and a reduction in proprioception. Furthermore, the basic cellular mechanisms that maintain tissue homeostasis decline with age, leading to an inadequate response to stress or joint injury and resultant joint tissue destruction and loss.

_ Sex
The incidence of knee, hip, and hand OA is higher in women than men and in women it increases dramatically around the time of menopause. The latter finding has led investigators to hypothesize that hormonal factors may play a role in the development of OA, but the results of clinical and epidemiologic studies have not universally corroborated this.20-22 A recent systematic review of 17 studies found that there was no clear association between sex hormones and hand, knee, or hip OA in women, although single analysis of the studies was not possible due to study heterogeneity.23

_ Ethnicity and race
The prevalence of OA and patterns of joint involvement vary among different racial and ethnic groups. Both hip and hand OA were much less frequent among Chinese in the Beijing Osteoarthritis Study than in whites in the Framingham Study, but interestingly, Chinese women had a higher prevalence of knee OA, which may be explained by excessive knee loading from squatting.24 Indeed, prolonged squatting and kneeling has been associated with an increased risk of moderate to severe radiographic knee OA.24 Results fromthe Johnston County Osteoarthritis Project have shown that the prevalence of hip OA in African American women was similar to that in white women, but that the prevalence was slightly higher in African American men (21%) than in white men (17%).25

_ Genetics
Strong evidence from family clustering and twin studies indicates that the risk of OA has an inherited component. Classic twin studies have shown that the influence of genetic factors is between 39% and 65% in radiographic OA of the hand and knee in women, about 60% in OA of the hip, and about 70% in OA of the spine.26 Although specific genes have been identified, the individual effects are relatively small; for example, Kerkhof et al27 reported a genome-wide association study showing that the C allele of rs3815148 on chromosome 7q22 was associated with a 1.14-fold increased prevalence of knee and/or hand OA and also with a 30% increased risk of knee OA progression.

_ Nutrition (including vitamin D)
Dietary factors are the subject of considerable interest in OA.28,29 Protection against knee OA progression has been reported in older men and women with high dietary vitamin D intakes, and for those with high serum levels of vitamin D.28 The Rotterdam Study reported that low vitamin D intake increased the risk of progression of knee OA.30 The Osteoporotic Fractures in Men study found that men with vitamin D deficiency were twice as likely to have prevalent radiographic OA,31 but a recent longitudinal study of Finnish participants failed to find associations between low vitamin D status and risk of incident hip or knee OA.32 Although the results are inconsistent, a biologically plausible mechanism for the effect of vitamin D on OA could be postulated, through its important role in bone metabolism, which may modulate periarticular bone responses to excess loading and joint damage. The results of further studies are awaited.

Low vitamin C dietary intake has also been associated with an increased risk of OA progression among participants in the Framingham Study.33 A role for selenium has also been postulated. 34

_ Osteoporosis
Osteoporosis is, like OA, a common age-related skeletal disorder. While early results indicated that reduced bone mineral density might be protective against OA, further studies have been inconsistent with this finding. A systematic review and meta-analysis of the risk factors for the onset of knee OA in older adults has shown that there is a consistent strong association between increased bone mineral density and the onset of knee OA in the three studies that investigated this risk factor in women.35 Although a definite molecular basis and common pathophysiology have not been identified to explain the inverse relationship between OA and osteoporosis, a shared genetic component may explain why they seldom coexist.

_ Smoking
There have been conflicting reports on the role of smoking in OA. Some studies have reported a protective association between smoking and OA, but others in contrast, report that smoking may be associated with a greater risk of both cartilage loss and knee pain in OA. A recent meta-analysis of observational studies concluded that the observed protective effect of smoking in OA is likely to be false.35 It may be caused by selection bias, as many studies have been conducted in a hospital setting where control subjects have smoking-related conditions, and subjects were recruited as part of studies that were not primarily designed to investigate smoking.36

_ Obesity and metabolic disease
Obesity is one of the strongest and best-established risk factors of OA. The current literature suggests that, although both show significant associations, the relationship between obesity and hip OA is weaker than with knee OA.37 Recent data suggest that OA is associated with the metabolic syndrome, suggesting a possible common pathogenic mechanism involving metabolic abnormalities and systemic inflammation.38 Studies have specifically suggested significant associations between OA and cardiovascular risk factors, such as hypertension and hypercholesterolemia. However, clinical evidence of an association between diabetes and OA is inconsistent. Several studies did find an association between diabetes and OA39 and fascinating hypotheses explaining this association have been suggested, including that high glucose concentrations produce reactive oxygen species (ROS) and advanced glycation end products, which induce cartilage degeneration and degradation. Other studies have failed to confirm the association and further research is required.

_ Sarcopenia
Muscle weakness may be an important risk factor for knee OA. Men and women with pre-existing radiographic evidence of knee OA have been identified as having weaker quadriceps than those without OA, particularly when the joints are symptomatic.40 One consequence of quadriceps weakness is that the knee becomes less stable during physical activity. Quadriceps exercises may therefore offer some protective advantage to patients involved in activities that are known to be associated with a high risk of OA development. Greater muscle strength is not, however, always protective as it corresponds to higher forces and thus increased joint loading during activity. It has been shown that higher grip strength in men is associated with a greater risk of developing OA in the proximal interphalangeal, metacarpophalangeal, and first carpometacarpal joints—the joints subjected to the largest forces during grip.41

_ Local mechanical risk factors
A traumatic knee injury is one of the strongest risk factors for the development of knee OA. Acute injuries, including meniscal and cruciate tears, fractures, and dislocations, can result in an increased risk of OA development and musculoskeletal symptoms. In addition to the direct trauma-induced damage to local tissues, disruption of normal biomechanics and altered load distribution within the joint also contribute to the subsequent increased OA risk. This risk is greater still if the subject has OA in another joint. The repetitive and excessive joint loading that accompanies specific physical activities increases the risk of developing OA in the involved joints. Workers whose jobs require repeated pincer grip have an increased risk of hand OA, particularly in the DIP joint.42 Similarly, prolonged squatting and kneeling stresses the larger joints and is consequently associated with increased risk of moderate to severe radiographic knee OA.

There have been conflicting results in studies examining the relationship between sporting activities and subsequent OA. There is some evidence that elite long-distance runners are at high risk of developing knee and hip OA.43 Other studies suggest that in the absence of joint injury, moderate recreational running and sports participation do not appear to increase the risk of hip or knee OA.44 The mechanical alignment of the knee influences load distribution across the articular surfaces. In a normally aligned knee, 60% to 70% of the weight-bearing load is transmitted through the medial compartment. Any shift in either a valgus or varus direction affects load distribution. Abnormal increases in compartmental loading are thought to increase stress on the articular cartilage—and other joint structures—subsequently leading to degenerative change. A systematic review has confirmed that knee malalignment is an independent risk factor for the progression of knee OA.45


OA is the commonest joint disease worldwide and mainly occurs in later life. It tends to be slowly progressive and can cause significant pain and disability. Symptoms and radiographic changes are poorly correlated and thus defining OA for research purposes is challenging. Established risk factors include obesity, local trauma, and occupation. These, in addition to genetic factors, may partly explain geographic variations in OA prevalence. There is conflicting evidence regarding the roles of nutrition, smoking, and sarcopenia, with the results of further studies awaited. _

1. Hutton CW. Osteoarthritis: the cause not result of joint failure? Ann Rheum Dis. 1989;48:958-961.
2. Kellgren J, Lawrence J. The epidemiology of chronic rheumatism: Atlas of standard radiographs of arthritis. Vol. 2. Oxford, UK: Blackwell Scientific Publications; 1963.
3. Pereira D, Peleteiro B, Araujo J, Branco J, Santos RA, Ramos E. The effect of osteoarthritis definition on prevalence and incidence estimates: a systematic review. Osteoarthr Cartilage. 2011;19:1270-1285.
4. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum. 2008;58:26-35.
5. AIHW (Australian Institute of Health and Welfare). A picture of osteoarthritis in Australia. 2007. Arthritis series no 5. Cat no. PHE 93. Canberra: AIHW.
6. Oliveria SA, Felson DT, Reed JI, et al. Incidence of symptomatic hand, hip, and knee osteoarthritis among patients in a health maintenance organization. Arthritis Rheum. 1995;38:1134-1141.
7. van Saase JL, van Romunde LK, Cats A, Vandenbroucke JP, Valkenburg HA. Epidemiology of osteoarthritis: Zoetermeer survey. Comparison of radiological osteoarthritis in a Dutch population with that in 10 other populations. Ann Rheum Dis. 1989;48:271-280.
8. Zhang Y, Niu J, Kelly-Hayes M, Chaisson CE, Aliabadi P, Felson DT. Prevalence of symptomatic hand osteoarthritis and its impact on functional status among the elderly: The Framingham Study. Am J Epidemiol. 2002;156:1021-1027.
9. Kloppenburg M, Kwok WY. Hand osteoarthritis—a heterogeneous disorder. Nat Rev Rheumatol. 2011;8:22-31.
10. Kalichman L, Ling L, Kobyliansky E. Prevalence, pattern and determinants of radiographic hand osteoarthritis in Turkmen community-based sample. Rheumatol Int. 2009;29:1143-1149.
11. Dillon CF, Hirsch R, Rasch EK, Gu Q. Symptomatic hand osteoarthritis in the United States: prevalence and functional impairment estimates from the third US National Health and Nutrition Examination Survey, 1991-1994. Am J Phys Med Rehabil. 2007;86:12-21.
12. Jamshidi AR, Tehrani-Banihashemi A, Dahaghin S, et al. Clinical hand osteoarthritis in Tehran: prevalence, signs, symptoms, and pattern—COPCORD Stage I, Iran Study. J Rheumatol. 2008;35:1467-1468.
13. Zeng QY, Chen R, Xiao JY, Chen SB, Wigley R, Chen SL, Zhang NZ. Rheumatic diseases in China. Arthritis Res Ther. 2008;10:R17.
14. Jordan JM, Helmick CG, Renner JB, et al. Prevalence of knee symptoms and radiographic and symptomatic knee osteoarthritis in African Americans and Caucasians: the Johnston County Osteoarthritis Project. J Rheumatol. 2007; 34:172-180.
15. Nguyen US, Zhang Y, Zhu Y, Niu J, Zhang B, Felson DT. Increasing prevalence of knee pain and symptomatic knee osteoarthritis: survey and cohort data. Ann Intern Med. 2011;155:725-732.
16. Fransen M, Bridgett L, March L, Hoy D, Penserga E, Brooks P. The epidemiology of osteoarthritis in Asia. Int J Rheum Dis. 2011;14:113-121.
17. Haq SA. Osteoarthritis of the knees in the COPCORD world. Int J Rheum Dis. 2011;14:122-129.
18. Arden NK, Lane NE, Parimi N, Javaid KM, Lui LY, Hochberg MC, Nevitt M. Defining incident radiographic hip osteoarthritis for epidemiologic studies in women. Arthritis Rheum. 2009;60:1052-1059.
19. Minaur N, Sawyers S, Parker J, Darmawan J. Rheumatic disease in an Australian Aboriginal community in North Queensland, Australia. A WHO-ILAR COPCORD survey. J Rheumatol. 2004;31:965-972.
20. de Klerk BM, Schiphof D, Groeneveld FP, et al. No clear association between female hormonal aspects and osteoarthritis of the hand, hip and knee: a systematic review. Rheumatology (Oxford). 2009;48:1160-1165.
21. Spector TD, Nandra D, Hart DJ, Doyle DV. Is hormone replacement therapy protective for hand and knee osteoarthritis in women? The Chingford Study. Ann Rheum Dis. 1997;56:432-434.
22. Cirillo DJ, Wallace RB, Wu L, Yood RA. Effect of hormone therapy on risk of hip and knee joint replacement in the Women’s Health Initiative. Arthritis Rheum. 2006;54:3194-3204.
23. Srikanth VK, Fryer JL, Zhai G, Winzenberg TM, Hosmer D, Jones G. A metaanalysis of sex differences prevalence, incidence and severity of osteoarthritis. Osteoarthritis Cartilage. 2005;13:769-781.
24. Zhang Y, Hunter DJ, Nevitt MC, et al. Association of squatting with increased prevalence of radiographic tibiofemoral knee osteoarthritis: The Beijing Osteoarthritis Study. Arthritis Rheum. 2004;50:1187-1192.
25. Nelson E, Braga L, Benner J, et al. Characterization of individual radiographic features of hip osteoarthritis in African American and White women and men: the Johnston County Osteoarthritis Project. Arthritis Care Res. 2010;62:190-197.
26. Spector TD, MacGregor AJ Risk factors for osteoarthritis: genetics. Osteoarthritis Cartilage. 2004;12:S39-S44.
27. Kerkhof HJ, Lories RJ, Meulenbelt I, et al. A genome-wide association study identifies an osteoarthritis susceptibility locus on chromosome 7q22. Arthritis Rheum. 2010;62:499-510.
28. McAlindon TE, Felson DT, Zhang Y, et al. Relation of dietary intake and serum levels of vitamin D to progression of osteoarthritis of the knee among participants in the Framingham Study. Ann Intern Med. 1996;125:353-359.
29. Felson DT, Niu J, Clancy M, et al. Low levels of vitamin D and worsening of knee osteoarthritis: results of two longitudinal studies. Arthritis Rheum. 2007;56: 129-136.
30. Bergink AP, Uitterlinden AG, Van Leeuwen JP, et al. Vitamin D status, bone mineral density, and the development of radiographic osteoarthritis of the knee: the Rotterdam Study. J Clin Rheumatol. 2009;15:230-237.
31. Chganti RK, Parimi N, Cawthon P, Dam TL, Nevitt MC, Lane NE. Association of 25-hydroxyvitamin D with prevalent osteoarthritis of the hip in elderly men: theosteoporotic fractures in men study. Arthritis Rheum. 2010;62:511-514.
32. Konstari S, Paananen M, Heliovaara M, et al. Association of 25-hydroxyvitamin D with the incidence of knee and hip osteoarthritis: a 22-year follow-up study. Scand J Rheumatol. 2012;41:124-131.
33. McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum. 1996;39:648-656.
34. Jordan JM, Fang F, Arab L, et al. Low selenium levels are associated with increased risk for osteoarthritis of the knee. Arthritis Rheum. 2005;52:s455.
35. Blagojevic M, Jinks C, Jeffery A, Jordan KP. Risk factors for onset of osteoarthritis of the knee in older adults: a systematic review and meta-analysis. Osteoarthritis Cartilage. 2010;18:24-33.
36. Hui M, Doherty M, Zhang W. Does smoking protect against osteoarthritis? Meta-analysis of observational studies Ann Rheum Dis. 2011;70:1231-1237.
37. Grotle M, Hagen KB, Natvig B, et al. Obesity and osteoarthritis in knee, hip and/ or hand: An epidemiological study in the general population with 10 years follow- up. BMC Musculoskelet Disord. 2008;9:132.
38. Puenpatom RA, Victor TW. Increased prevalence of metabolic syndrome in individuals with osteoarthritis: an analysis of NHANES III data. Postgrad Med. 2009;121:9-20.
39. Frey MI, Barrett-Conner E, Sledge PA, et al. The effect of noninsulin dependent diabetes on the prevalence of clinical osteoarthritis. A population based study. J Rheumatol. 1996;23:716-722.
40. Slemenda C, Brandt KD, Heilman DK, et al. Quadriceps weakness and osteoarthritis of the knee. Ann Intern Med. 1997;127:97-104.
41. Chaisson CE, Zhang Y, Sharma L, Kannel W, Felson DT. Grip strength and the risk of developing radiographic hand osteoarthritis: results from the Framingham Study. Arthritis Rheum. 1999;42:33-38.
42. Hadler NM, Gillings DB, Imbus HR, et al. Hand structure and function in an industrial setting. Arthritis Rheum. 1978;21:210-220.
43. Buckwalter JA, Lane NE. Athletics and osteoarthritis. Am J Sports Med. 1997; 25:873-881.
44. Spector TD, Harris PA, Hart DJ, et al. Risk of osteoarthritis associated with longterm weight-bearing sports: a radiologic survey of the hips and knees in female ex-athletes and population controls. Arthritis Rheum. 1996;39:988-995.
45. Tanamas S, Hanna FS, Cicuttini FM, Wluka AE, Berry P, Urquhart DM. Does knee malalignment increase the risk of development and progression of knee osteoarthritis? A systematic review. Arthritis Rheum. 2009;61:459-467.

Keywords: burden; epidemiology; osteoarthritis; risk factor