Determinants of MSK health and disability: Lifestyle determinants of symptomatic osteoarthritis




Abstract


It is frequently considered that, for many people, symptomatic osteoarthritis involving the lower limb joints is a largely preventable ‘lifestyle disease’. The purpose of this review is to evaluate the most recent scientific evidence examining the effect of various lifestyle factors, such as physical activity, obesity, diet, smoking, alcohol and injury, on the development of symptomatic knee or hip osteoarthritis. The strengths and weaknesses of various studies are discussed, the magnitude of any demonstrated risks presented and current overall conclusions drawn.


The societal burden of symptomatic hip and knee OA (osteoarthritis) is large and escalating worldwide with the ageing of the population Effective population-based strategies targeting evidence-based risk factors have the potential to reduce the incidence of symptomatic OA involving these large weight-bearing joints.


The aim of this review is to collate current evidence regarding modifiable lifestyle risk factors, such as physical activity, smoking, alcohol consumption, obesity, diet and injury that have been associated with an increased or decreased risk of developing painful OA involving the hips or knees. This review will be restricted to evidence provided by prospective longitudinal population-based studies as other forms of observational study design (case–control studies and retrospective studies) are vulnerable to bias and tend to inflate estimates of effect . We will also focus the review to studies evaluating the incidence of symptomatic disease, rather than those evaluating incident radiographic disease only. There are still several general limitations evident even in longitudinal cohort studies specific to this review. The measurement of lifestyle factors is difficult and often restricted to one baseline time point, so that changes over the follow-up period cannot then be accounted for. In addition, lengthy recall periods of lifestyle determinants are often requested, introducing considerable measurement error and only allowing for a crude estimation of actual exposure. For example, a frequently utilized physical activity questionnaire requires recall month by month over the past year. As with all self-report measures, over- or under-reporting of lifestyle determinants may occur depending on their social desirability. Importantly, many large population-based cohort studies have not been specifically set up to evaluate musculoskeletal disease risk and burden. Often, they are unable to provide a clinical assessment for symptomatic OA case ascertainment or measure important potential confounders affecting the relationship between lifestyle determinants and symptomatic OA such as a history of joint injury, exposure to heavy occupational work load, joint alignment, muscle strength or body composition (lean muscle mass vs. fat mass) .


Physical activity


Regular physical activity is recommended for people of all ages to reduce the risk of various age-related serious chronic diseases such as coronary heart disease, diabetes and dementia . However, concerns have been frequently raised by both health professionals and the general population that promoting or partaking in regular intensive leisure-time physical activity may lead to an increased risk of joint ‘wear and tear’ and thus development of painful OA in the hips or knees.


A variety of self-reported physical activity questionnaires have been developed, with little consensus regarding required content and scoring validity. Most of these physical activity questionnaires assess aerobic aspects (frequency/intensity) but not joint load, with little distinction or weighting for high-impact or high-loading activities such as running or weight lifting as compared with walking and swimming. Several recent population-based cohort studies have used the Minnesota Leisure Time Physical Activity questionnaire to determine physical activity . This interviewer-led questionnaire requires the assessment of frequency and amount of time spent on 63 non-occupational activities over the previous year on a month-by-month basis. A descriptive overview of the longitudinal cohort studies evaluating physical activity as a risk factor for symptomatic knee or hip OA (or joint replacement surgery) considered in this review is provided in Table 1 .



Table 1

Longitudinal studies evaluating the role of physical activity as a risk factor for incident knee or hip OA or joint replacement.




























































































































Study ID Location
Follow-up period
Baseline age (years)
Range
(mean)
N total/
N cases
Case definition Physical activity assessment Confounders considered
McAlindon
(1999)
USA
(Framingham)
4 years
63–94 1500/ Symptomatic radiographic knee OA
(clinic assessment)
Daily hours PA

  • 1.

    Light


  • 2.

    Moderate


  • 3.

    Heavy (>4 h)

Daily blocks walked, stairs climbed.
Age, sex, BMI, weight loss, knee injury, health status, total calorie intake, smoking
Felson
(2007)
USA
(Framingham Offspring) 9 years
26–81
(53)
1279/
173 knees
Symptomatic radiographic knee OA
(clinic assessment)
Walk for exercise

  • 1.

    None


  • 2.

    <6 miles/week


  • 3.

    ≥6 miles/week

Intense exercise

  • 1.

    None


  • 2.

    <3 times/week


  • 3.

    ≥3 times/week

Age, sex, BMI, knee injury history
Fransen
(2014)
Australia
(CHAMP study)
2 years
Men only
70+
1587/
150
Self-report PASE score tertiles
Walked daily for exercise
Age, BMI, knee extensor torque, co-morbidity, back pain
Wang
(2011)
Australia
(Melbourne Collaborative Cohort)
5 years
40–69 39,023/
541 (knee)
468 (hip)
Knee or hip replacement Frequency exercise:


  • 1.vigorous


  • 2.

    moderate


  • 3.

    walking

Score 0–16 (total)
Age, gender, BMI, birth country, occupational physical activity, education.
Ageberg
(2012)
Sweden
(Malmo Diet and Cancer Cohort)
11 years
45–74
(58)
28,320/
467 (knee)
557 (hip)
Knee or hip replacement Minnesota LTPA
score quartiles
Age, gender, BMI, education, smoking, marital status
Martin
(2013)
UK
(British Birth
Cohort)
17 years
36 2957/
302
Knee OA
(clinic assessment)
Minnesota LTPA
score tertiles
Gender, BMI, family history OA, history of knee injury, occupational activity
Mork
(2012)
Norway
(HUNT study)
11 years
20+
(45)
30,000/
351 (knee)
322 (hip)
Self-report physician diagnosis hip/knee OA Physical exercise

  • 1.

    Inactive,


  • 2.

    0–0.9 h/week,


  • 3.

    ≥1 h/week

Age, gender, BMI, smoking, occupation
Barbour (2014) USA
(Johnston County OA Project) 7 years
45+ 1522/ Knee OA
(clinic assessment)
Minnesota LTPA
(minutes per week)

  • 1.

    Inactive (<10)


  • 2.

    low (10–150)


  • 3.

    medium (150–300)


  • 4.

    high (>300)

Age, gender, race, BMI, education, occupational activity, knee injury
Flugsrud (2002) Norway
(National Health Screening) 9 years
35–52 50,034/
672
Hip replacement Self-rated PA

  • 1.

    sedentary


  • 2.

    moderate


  • 3.

    intermediate


  • 4.

    intensive

Age, gender, BMI, physical activity at work, marital status, smoking.
Karlson (2003) USA
(Nurses’ Health study)
15 years
Women 30–55 121,701/568 Hip replacement Weekly hours of moderate/vigorous recreational activity Age, BMI, HRT, smoking, parity, alcohol use
Juhakoski (2009) Finland
(Mini Finland Health Examination Survey)
22 years
30+ 840/
44
Hip OA
(clinic assessment)
Physical exercise:

  • 1.

    inactive


  • 2.

    irregular


  • 3.

    regular

Age, gender, education, BMI, physical work load, smoking, alcohol, injury
Ratzlaff
(2011)
Canada
(Association of Retired Persons)
2 years
45–85 2918/
176
Self-report physician diagnosis hip OA Occupational, household, sport activity: CPFI quintiles Age, gender, previous hip injury
Cheng
(2000)
USA
(Cooper clinic)
11 years
76% men 20–87
(44)
16,961/
601
Self-report physician diagnosis hip and/or knee OA Walking or jogging, miles per week:

  • 1.

    <10


  • 2.

    10–20


  • 3.

    >20

Age, gender, BMI, smoking, alcohol, caffeine
Hootman (2003) USA
(Cooper clinic)
13 years
82% men
20–87
5284/
379
Self-report physician diagnosis hip and/or knee OA ‘Joint stress’ variable (9 sports).
Score quartiles
Age, gender, BMI, co-morbidity, smoking, joint injury, previous hip/knee injury or surgery

LTPA: Leisure-time physical activity.

HRT: Hormone replacement therapy.

CFPI: Cumulative peak force index.

PASE: Physical Activity Scale for the Elderly.


Knee OA


Longitudinal cohort studies evaluating risk factors for incident symptomatic OA can generally be crudely categorized as either a general population-based cohort (all adults) or an ‘at-risk’ cohort (cohort limited to older people). The Framingham cohort provides an ‘at-risk’ cohort. One of the first studies from the Framingham cohort specifically investigating physical activity as a risk factor for symptomatic knee OA among elderly people was published in 1999 . In multivariate analysis, this study found ‘heavy physical activity’ (>4 h per day) was associated with an increased risk of symptomatic knee OA. However, the number of cases was small, and no increased risk was found for moderate or light levels of physical activity or the daily number of blocks walked or stairs climbed. A later study conducted in the younger Framingham Offspring Cohort (mean age 58 years) evaluated walking >6 miles per week and heavy physical activity (working up a sweat >3 times a week) for incident symptomatic knee OA . The analysis was stratified for BMI (body mass index) (above and below median of sex-specific BMI). Even within the higher-BMI group (mean BMI >31), multivariate models indicated no significantly increased or decreased risk of incident symptomatic knee OA for either walking (OR (odds ratio) 0.8) or heavy physical activity (OR 1.0).


A longitudinal Australian study of knee pain among 1587 older men (aged ≥70 years) found that being in the two higher tertiles of physical activity, measured using the PASE (Physical Activity Scale for the Elderly) questionnaire, was a significant risk factor for incident knee pain over a 2-year follow-up period . However, the PASE questionnaire encompasses recreational sport and leisure activity, as well as home and work activities. Walking daily for exercise (67% of participants at baseline) was not a risk factor for incident knee pain in this elderly male cohort.


A recent systematic review evaluating risk factors for the onset of knee OA identified several studies that “generally suggested an increased risk of knee OA in those who exercise more regularly and frequently.” However, due to the limited number and variability of studies evaluating physical activity, pooling the results of the included studies was not considered to be valid or meaningful by the authors. Since this review (which included studies published until January 2008), the results of five large population-based longitudinal cohort studies evaluating physical activity as a risk factor for incident symptomatic knee OA or knee replacement surgery have been published.


The Melbourne Collaborative Cohort Study evaluated the risk of primary knee or hip replacement due to OA (linkage with the Australian National Joint Replacement Registry) over 5 years among 39,000 people mostly aged between 40 and 69 years at baseline. Physical activity over the last 6 months was reported as the frequency of vigorous activity (exercise ‘making you sweat or feel out of breath’), less vigorous activity and walking. This study found that those reporting a high level of physical activity had an increased risk of primary knee replacement during follow-up, compared to those reporting no physical activity. However, only 12% of people with incident knee replacement ( n = 541) reported vigorous physical activity and no clear dose–response relationship was found. No associations were found for moderate physical activity or walking. The lack of a dose–response relationship for vigorous physical activity was attributed to not being able to account for current knee OA or a history of knee joint injury. It is suggested that people with current knee OA or knee injury are more likely to be sedentary or only participate in moderate physical activity, attenuating the risk attributable to vigorous physical activity.


Another recent large population-based cohort conducted in Sweden also evaluated the effect of leisure-time physical activity on incident primary knee replacement or tibial osteotomy among 28,320 people aged 44–77 at baseline. Physical activity was measured using the Minnesota Leisure Time Physical Activity questionnaire and a summated score divided into quartiles of activity. There was a small non-significant trend for high risk demonstrated for increasing leisure-time activity levels. However, no adjustment could be made for a history of knee injury or current knee OA. For the four most commonly reported activities (walking, bicycling, using stairs and gardening), no association was found for incident knee replacement or osteotomy.


An evaluation of the effect of physical activity on incident knee OA (clinic assessment) was conducted within the 1946 British Birth Cohort at age 53 years, and then specifically for interactions between physical activity and BMI . Participation in any sports, vigorous leisure activities or exercises at ages 36, 43 and 53 years were evaluated using the Minnesota Leisure Time Physical Activity questionnaire, and participants were categorized as inactive, less active and most active (>5 times in previous 4 weeks). Among men, no association between leisure activity and incident knee OA was demonstrated. Among women, there was no association between leisure-time activity and incident knee OA; however, there was evidence of an interaction with BMI and leisure activity for knee OA risk (OR 1.8, 95% CI (confidence interval) 1.5–2.2), suggesting that women who are more active would benefit from reducing their BMI to avoid incident knee OA.


The recent Norwegian HUNT study evaluated the effect of BMI and physical exercise on incident self-reported physician-diagnosed knee OA over an 11-year follow-up among about 30,000 adults . Leisure-time physical exercise (walking, swimming, other sports, more than 1 h per week) was crudely categorized as inactive, low intensity (no sweat or heavy breathing) and high intensity (sweat and/or heavy breathing, nearly exhausted). While the study demonstrated the increased risk of knee OA associated with obesity, the results suggested that participation in exercise does not increase this risk. The study concluded that “exercise should be encouraged also among individuals with excessive body mass without concern for an increased risk of OA.”


Finally, the Johnston County Osteoarthritis Project study, uniquely a longitudinal cohort established to study hip and knee OA, recently specifically evaluated the effect of meeting physical activity guidelines (>150 min per week of moderate–vigorous activity) . Physical activity at baseline was calculated using the Minnesota Leisure Time Physical Activity questionnaire. This study found that meeting the physical activity guidelines was not significantly associated with developing symptomatic knee OA (HR (hazard ratio) 1.2, 95% CI 0.9–1.8).


Hip OA


Three of the above cohort studies also evaluated physical activity and incident hip replacement surgery or hip OA . Both studies evaluating hip replacement surgery incidence could not detect a significant association between high levels of physical activity and incident hip replacement surgery. In fact, one of these studies reported, specifically for women, a lower risk of hip replacement associated with the highest quartile of physical activity, compared with the lowest quartile. The results of the Norwegian HUNT study, similar to their findings for incident knee OA, could not find an association for either low or high physical activity, or any interaction with BMI, and incident hip OA .


Three large population-based cohort studies have specifically evaluated risk factors for hip replacement surgery due to OA or symptomatic hip OA incidence. The first was conducted in Norway among >50,000 people followed up for an average of 9 years . While intensive physical activity at work was a significant risk factor among men and women, no associations were found for moderate (some physical activity during at least 4 h per week), intermediate (regular activity) or intensive (several times per week of hard physical training for competition) leisure-time physical activity and incident hip replacement surgery. A second study conducted an analysis within the Nurses’ Health Study . No significant increased risk could be established for participation in moderate–vigorous recreational physical activity (>7 h per week). The third population-based study was conducted in Finland and had a 22-year follow-up . In contrast to heavy manual labour and a history of hip injury, regular leisure-time physical activity was not found to be a risk factor for symptomatic hip OA.


Recently, a Canadian study uniquely evaluated the effect of cumulative lifetime hip joint force on the risk of symptomatic hip OA among 2918 subjects aged 45–85 years . A ‘cumulative peak force index’ measure was calculated from lifetime exposure to occupational, household and sport physical activity using frequency, intensity and duration . This study found that sporting activity contributed only a small proportion of the overall hip joint forces, compared with occupational and household activity. While a non-significant effect for the highest quintile of occupational force was found, sport or household activity was not demonstrated to be associated with the development of hip OA during a 2-year follow-up period.


Hip and/or knee OA


Two large cohort studies have provided a risk factor analysis for self-reported physician-diagnosed hip and/or knee OA (undifferentiated). Both were conducted among people (mostly men) attending the Cooper Clinic . The first study ( n = 17,000) evaluated only the effect of walking and jogging . After a 10-year follow-up, walking or jogging >20 miles per week was associated with incident hip and/or knee OA, but only among men aged <50 years. However, a history of joint injury was not able to be included in the analysis. By contrast, a second Cooper Clinic study collected self-report data from a subset of 5280 adults (Aerobics Centre Longitudinal study) and evaluated a novel physical activity joint stress variable from a list of possible sports. For example, walking had a joint stress weighting of 9.5, while racquet sports a weighting of 21. This study found that, after adjustment for age, previous joint injury or surgery and BMI, an increased joint stress physical activity score was not associated with increased risk of hip and/or knee OA. The study concluded that “in the absence of significant joint injury, moderate types of physical activity (walking, cycling, swimming, etc.) do not increase the risk of hip and/or knee OA over a 12-year period.”


In conclusion, these longitudinal population-based cohort studies provide strong evidence that participation in moderate or high levels of leisure-time physical activity does not increase the risk of incident symptomatic knee OA or knee replacement surgery. The only caveat is the possibility of an increased risk among obese women reported in one study . The gender specificity of this finding may be related to the relatively poorer muscle strength evident for women and resultant reduced capacity to protect the knee from high impact loading . However, the optimal strategy for overall health benefits for these women is to lose weight rather than restrict leisure-time physical activity. These longitudinal studies also provide strong evidence that leisure-time physical activity itself does not increase the risk of symptomatic hip OA or hip replacement surgery for OA. However, it is suggested that people in occupations resulting in high-peak hip joint forces (heavy lifting, moving heavy objects and using heavy tools) may be specifically advised of their risk and the need to limit leisure time physical exercise to activities producing low hip joint loading (walking rather than jogging) and aim to keep their BMI within the normal range.




Smoking


The possibility of a reduced risk of OA provided by smoking has been attributed to a favourable effect of nicotine on chondrocyte metabolism . In fact, a recent meta-analysis of observational studies reported finding an overall significant negative association between smoking and incident OA when pooling the results of all identified observational studies . However, when a subgroup analysis was restricted to the eight longitudinal cohort studies identified by the review, the negative association was not significant (OR 0.9, 95% CI 0.8–1.1). The review concluded that the demonstrated overall protective effect of smoking is likely to be false and driven by selection bias from case–control studies, and particularly those conducted in a hospital setting. A prior systematic review evaluating many risk factors for incident OA reported a similar non-significant finding for smoking when meta-analysis was restricted to cohort studies only (OR 1.0, 95% CI 0.9–1.1).


Since these two reviews, the results of a large community-based study evaluating the association between smoking and incident total hip or knee replacement surgery have been published. This study was conducted among almost 55,000 elderly people (mean age 73 at baseline) participating in the Second Australian National Blood Pressure study with linkage to the Australian National Joint Replacement Registry from 1999 to 2010. A total of 3535 (8%) reported being a current smoker at baseline, with 1528 incident hip replacements and 2077 incident knee replacements over the follow-up period. After adjusting for age, gender, BMI, socio-economic status, co-morbidity score, exercising >30 min per week and competing risk of death, smoking demonstrated a significant protective effect for incident total hip replacement (0.7, 95% CI 0.6–0.9) and total knee replacement surgery (0.6, 95% CI 0.5–0.7). A significant protective effect remained when a sensitivity analysis was conducted for possible misclassification of smoking from 1% to 40%. However, this study was not able to account for a history of joint injury or heavy occupational activity. Further, the study population was quite old, limiting generalizability to younger people.


In conclusion, even if smoking confers some benefit in terms of reducing the risk of developing OA, it is hardly likely to be considered a valid population-based preventative strategy given the associated deleterious effects on overall health.




Smoking


The possibility of a reduced risk of OA provided by smoking has been attributed to a favourable effect of nicotine on chondrocyte metabolism . In fact, a recent meta-analysis of observational studies reported finding an overall significant negative association between smoking and incident OA when pooling the results of all identified observational studies . However, when a subgroup analysis was restricted to the eight longitudinal cohort studies identified by the review, the negative association was not significant (OR 0.9, 95% CI 0.8–1.1). The review concluded that the demonstrated overall protective effect of smoking is likely to be false and driven by selection bias from case–control studies, and particularly those conducted in a hospital setting. A prior systematic review evaluating many risk factors for incident OA reported a similar non-significant finding for smoking when meta-analysis was restricted to cohort studies only (OR 1.0, 95% CI 0.9–1.1).


Since these two reviews, the results of a large community-based study evaluating the association between smoking and incident total hip or knee replacement surgery have been published. This study was conducted among almost 55,000 elderly people (mean age 73 at baseline) participating in the Second Australian National Blood Pressure study with linkage to the Australian National Joint Replacement Registry from 1999 to 2010. A total of 3535 (8%) reported being a current smoker at baseline, with 1528 incident hip replacements and 2077 incident knee replacements over the follow-up period. After adjusting for age, gender, BMI, socio-economic status, co-morbidity score, exercising >30 min per week and competing risk of death, smoking demonstrated a significant protective effect for incident total hip replacement (0.7, 95% CI 0.6–0.9) and total knee replacement surgery (0.6, 95% CI 0.5–0.7). A significant protective effect remained when a sensitivity analysis was conducted for possible misclassification of smoking from 1% to 40%. However, this study was not able to account for a history of joint injury or heavy occupational activity. Further, the study population was quite old, limiting generalizability to younger people.


In conclusion, even if smoking confers some benefit in terms of reducing the risk of developing OA, it is hardly likely to be considered a valid population-based preventative strategy given the associated deleterious effects on overall health.




Alcohol


There is an absolute scarcity of longitudinal cohort studies evaluating alcohol consumption as a risk factor for incident OA. The longitudinal cohort study of Cooper Clinic attendees categorized alcohol consumption in quartiles (0, 0.01–50, 50–150 and 150+ g per week) and only found an increased risk of knee and/or hip OA for the highest quartile among men aged <50 years . However, this study was unable to account for a history of joint injury or heavy occupational load, both risk factors likely to be more prevalent among younger men, compared with older men or with women. The Nurses’ Health study evaluated alcohol use (categorized as 0, <5, 5–9, 10–14 and ≥15 g per day) every 4 years in their cohort and could not detect an association with incident hip replacement surgery in multivariate analyses .


In conclusion, there is little evidence that regular alcohol consumption either increases or decreases the risk of developing symptomatic OA.




Obesity


Obesity imposes both biomechanical and biochemical stresses on knee and hip joints. Biomechanical stresses are reasonably well documented and comprise increased joint loading . Biochemical stress, consequent to adipose tissue expansion and dysfunction in obesity, is increasingly receiving attention.


Adipose tissue is a major endocrine and immunological organ that actively secretes adipokines – proteins that may act locally in a paracrine/autocrine fashion or more remotely as endocrines – a number of which are pro-inflammatory. In obesity, the expansion of adipose tissue (especially visceral) and adipocyte hypertrophy result in cellular dysfunction or ‘adiposopathy’ . Outcomes of adiposopathy include ectopic lipid deposition in other tissues (consequent to fatty acid overflow from adipose tissue) and upregulation of adipocyte adipokine expression . The enhanced release of adipokines into the bloodstream and fatty acid overflow result in a state of low-grade systemic inflammation (or meta-inflammation) and insulin resistance . Obesity-linked low-grade systemic inflammation is implicated in the aetiology of cardiometabolic diseases and also of OA . OA has been nominated as a component of the metabolic syndrome and ‘metabolic osteoarthritis’ is recognized as an OA phenotype . Metabolic OA is the next most frequent phenotype (after age-related OA) that affects patients enrolled in clinical studies .


The elevated risk of OA conferred by the presence of obesity is likely confounded (dampened) because many overweight and obese patients within cohort studies will be using a prescribed statin. Statins competitively inhibit the rate-limiting step in cholesterol biosynthesis and hence they lower LDL (low-density lipoprotein) cholesterol and reduce/prevent cardiovascular events . Statins may also alter the risk of OA by virtue of their lipid-lowering and anti-inflammatory properties. The incidence of clinical OA at the 10-year follow-up among a cohort of 16,609 patients with cardiovascular disease drawn from the UK General Practice Research Database was about 60% lower (Cox regression rate ratio 0.4, 95% CI 0.3–0.5) for those in the highest statin dose quartile (>18.5 mg/day for at least 2 years; other statins standardized to equivalent simvastatin dosage) compared with non-users, adjusted for covariates such as age, gender, BMI and pain-modifying drugs . An earlier longitudinal study in which incidence and progression of knee or hip OA was evaluated among statin users and non-users in a subgroup of the large Rotterdam Study demonstrated a more than halved risk reduction (OR 0.4, 95% CI 0.3–0.8) of knee OA incidence/progression for statin users, but no effect on risk of hip OA.


Knee OA


There is extensive strong and conclusive evidence that the presence of obesity is a risk factor for the development of symptomatic knee OA or knee joint replacement surgery. Prospective longitudinal studies that have categorized obesity according to the World Health Organization BMI definition (≥30 kg/m 2 ) demonstrate that the presence of obesity confers up to a nearly sevenfold higher risk for incident symptomatic and/or radiographic knee OA and a three- to tenfold higher risk of knee replacement compared with the reference category ( Table 2a ). The few studies that have provided other assessments of obesity (e.g., waist circumference or percent body fat) demonstrate a three- to sevenfold higher risk of developing symptomatic knee OA and/or knee replacement ( Table 2a ). Studies that examined BMI as a continuous variable arrived at estimates of risk per specified increment of BMI and ranged from a 10% increase in risk of knee OA for every 1 kg/m 2 increment in BMI to 80% increase in risk for every 5 kg/m 2 increase in BMI ( Table 2a ).



Table 2a

Longitudinal studies evaluating the role of obesity as a risk factor for incident knee OA or knee joint replacement .












































































































































































Study ID Location
Follow-up period
Gender Baseline age (years, mean) and/or Range N total/
N cases
Case definition Obesity assessment Risk estimate Confounders considered
Felson
(1997)
USA
(Framingham OA study)
∼8 years
Men & women ∼62 598/
93 knees
Symptomatic radiographic knee OA (clinic assessment) BMI
continuous
OR per 5 kg/m 2 increase
F 1.8,
(95% CI 1.2–2.6)
M 1.0
Age, gender, knee injury, physical activity, smoking status
Gelber (1999) USA
(Johns Hopkins Precursors Study)
36 years
Men only
23
1180/84 Self-report, verified, arthritis knee or hip BMI
continuous
RR per 2.7 kg/m 2 increase (one SD)
Knee 1.7,
(95% CI 1.3–2.1)
Age, physical activity in medical school, injury
Hootman (2003) USA
(Aerobics Center Longitudinal Study)
13 years
82% men
20–87
5284/
379
Self-report physician diagnosis hip and/or knee OA BMI
continuous
OR per 1 kg/m 2 increase
F 1.1,
(95% CI 1.1–1.2)
M 1.1,
(95% CI 1.0–1.1)
Age, joint stress score, co-morbidity, smoking, joint injury, previous hip/knee injury or surgery
Hochberg (2004) USA
(Baltimore Longitudinal Study of Ageing)
4–14 years
Men & women 19–93 562 knees/53 knees Radiographic knee OA BMI
continuous
OR per 5 kg/m 2 increase
1.5,
(95% CI 1.2–2.3)
Age, gender, smoking, contralateral knee OA, time between radiographs
Järvholm (2005) Sweden
(National health control program)
11 years
Men only, construction workers 15–67 320,192/502 (knee) Knee replacement BMI
Obese 30–35 kg/m 2
Ref 20–24 kg/m 2
RR
Knee 4.8,
(95% CI 3.7–6.4)
Age, smoking status
Jinks (2006) UK
(3 general practices, North Staffordshire)
3 years
Men & women >50 1996/483 Self-report, chronic knee pain BMI
Obese ≥30 kg/m 2
Ref 20–24.9 kg/m 2
RR
Knee pain 1.3,
(95% CI 1.0–1.7)
Severe knee pain 2.8, (95% CI 1.8–4.5)
Age, gender, deprivation, previous knee injury, widespread pain
Liu (2007) UK
(Million Women Study)
3 years
Women only
50–69
490,532/974 (knee) Knee replacement BMI
Obese ≥30 kg/m 2
Ref <22.5 kg/m 2
RR
Knee 10.5,
(95% CI 9.5–11.6)
Age, residential region, deprivation
Grotle (2008) Norway (musculoskeletal pain study)
10 years
Men & women 42
24–66
1675/197 Self-report OA of knee or hip BMI
Obese ≥30 kg/m 2
Ref <25 kg/m 2
OR
Knee 2.8,
(95% CI 1.3–6.0)
Age, gender, work status, leisure physical activity
Lohmander (2009) Sweden
(Malmö Diet and Cancer Study Cohort)
11 years
Men & women 45–73 27,960/471 (knee) Symptomatic knee OA and knee replacement/HTO Medians for quartiles
BMI
Obese Q4 30.1 kg/m 2
Ref Q1 <∼22 kg/m 2
RR
Knee 8.1,
(95% CI 5.3–12.4)
Age, gender, smoking, physical activity
WC
Obese Q4 90  cm F, 105 cm M
Ref Q1 67 cm F, 82 cm M
Knee 6.7,
(95% CI 6.5–9.9)
% fat
Obese Q4 37% F, 26% M
Ref Q1 25% F, 15% M
Knee 3.6,
(95% CI 2.6–5.0)
Niu (2009) USA
(Mulitcenter Osteoarthritis Study)
2.5 years
Men & women High-risk cohort, ∼80% obese
62
2623/163 Radiographic knee OA BMI
Obese 30–34.9 kg/m 2
Very obese ≥35 kg/m 2
Ref <25 kg/m 2
RR
2.4,
(95% CI 1.3–4.3)
3.2,
(95% CI 1.7–5.9)
Age, gender, race, BMD, history of knee injury
Wang
(2009)
Australia
(Melbourne Collaborative Cohort)
5 years
Men & women 40–69 39,023/
541 (knee), 468 (hip)
Knee or hip replacement BMI
Q4 >29.3 kg/m 2
Ref Q1 <23.2 F , <24.7 M
HR
3.4,
(95% CI 2.8–4.2)
Age, gender, birth country, occupational physical activity, education.
WC
Q4 >87 F, >99 M
Ref Q1 <71 F, <87 M
2.8,
(95% CI 2.3–3.4)
% Fat
Q4 >44.6 F, >32.6 M
RefQ1 <35.3 F, <25 M
3.0,
(95% CI 2.5–3.6)
Toivanen
(2010)
Finland
(Mini-Finland Health Survey and Health 2000 Survey)
22 years
Men & women ≥ 30 823/94 Symptomatic physician diagnosed knee OA BMI
Obese ≥30 kg/m 2
Ref <25 kg/m 2
OR
6.8,
(95% CI 3.4–13.7)
Age, gender, work effort, leisure physical activity, smoking, injury
Mork
(2012)
Norway
(HUNT study)
11 years
Men & women ≥20 29,957/
351 (knee)
Self-report physician diagnosis knee OA, chronic pain BMI
Obese ≥ 30 kg/m 2
Ref 18.5–24.9 kg/m 2
RR
F 4.4,
(95% CI 3.0–6.3)
M 2.8,
(95% CI 1.6–4.8)
Age, frequency of physical activity, smoking, occupation
Wang (2013) Australia
(Melbourne Collaborative Cohort Study)
8.4 years
Men & women 40–69 28,046/1180 (knee) Knee replacement BMI
Obese ≥30 kg/m 2
Ref <25 kg/m 2
HR
F 4.8,
(95% CI 3.9–5.9)
M 4.0,
(95% CI 3.0–5.4)
Age, country of birth, education; stratified by gender
Fransen
(2014)
Australia
(CHAMP study)
2 years
Men only
>70
1587/
150
Self-report, chronic knee pain BMI
Obese ≥30 kg/m 2
Ref <25 kg/m 2
OR
2.6,
(95% CI 1.3–5.1)
Age, knee extensor torque, co-morbidity, back pain
Monira Hussain (2014) Australia
(Melbourne Collaborative Cohort Study, subset)
7 years
Men & women ∼65 20,430/660 (knee) Knee replacement Central obesity (WC > 80 cm F, >94  cm M)
Ref no central obesity
HR
Knee 1.6,
(95% CI 1.3–2.0)
Age, gender, physical activity, country of birth, education, BMI
Metabolic syndrome: central obesity plus any two of MetSx components
Ref no MetSx
Knee 1.2,
(95% CI 1.0–1.5)

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Nov 10, 2017 | Posted by in RHEUMATOLOGY | Comments Off on Determinants of MSK health and disability: Lifestyle determinants of symptomatic osteoarthritis

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