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Training, Prevention, and Rehabilitation/Section Articles

Running Dose and Risk of Developing Lower-Extremity Osteoarthritis

Gessel, Trevor MD; Harrast, Mark A. MD

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Current Sports Medicine Reports: June 2019 - Volume 18 - Issue 6 - p 201-209
doi: 10.1249/JSR.0000000000000602
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Running is an increasingly popular sport and mode of physical activity. From 1990 to 2016, there was a 3.5-fold increase in U.S. mass running event participants with 17,000,000 finishers in 2016 (1). During that same period, there also was a notable increase in longer distance endurance events with a 6.3-fold increase in the number of half marathon finishers and a 2.3-fold increase in full marathon finishers. Additionally, marathon participants are older with 49% masters runners (age >40 years) in 2015 compared with 26% in 1980 (1).

With running being such a popular mode of exercise, patients frequently present to clinicians with running-related injuries (RRI). Common RRI include (with associated incidence) medial tibial stress syndrome (13.6% to 20%), patellar tendinopathy (5.5% to 22.7%), ankle sprains (10.9% to 15%), Achilles tendinopathy (9.1% to 10.9%), hamstring muscular injuries (10.9%), patellofemoral syndrome (5.5%) among other less frequent injuries (2,3). In addition to these RRI which are often discussed in large reviews on the subject, runners with knee and hip pain often are concerned about the risk of developing osteoarthritis (OA), and this can be a frequent topic of discussion in a clinician's office.

Lower-extremity OA is a growing health concern in our aging and increasingly overweight population, both of these being significant risk factors for the development of lower-extremity OA (4,5). According to the most recent data, approximately 10% to 12% of the adult population are currently experiencing symptomatic OA in any joint (6). Furthermore, the individual and economic burden of OA is only likely to increase in the future as half of all patients with symptomatic knee OA are currently younger than 65 years, and the number of patients in this group is increasing year to year (7). Given the substantial individual and societal impact of OA, it is vital to accurately understand risk factors for OA development so clinicians may effectively counsel patients on preventing individual secondary disability.

Up to this point, the exact interaction between running and the development of lower-extremity OA has remained unclear in the published literature. Proposed mechanisms for the development of OA include excessive loads on normal joint cartilage, or normal loads on abnormal joint cartilage (8,9). Given these proposed mechanisms, there has been concern that running could lead to the development of hip and knee OA, particularly in excessive amounts (10–13). Running also can possibly increase the risk of developing foot and ankle OA, but for the purposes of this article we will focus on knee and hip OA.

Despite the historic concern for a causal relationship between running and developing knee and hip OA, 78% of Canadian health care providers did not agree that running was detrimental for knee joint health (14), and in recent years, there is a growing body of research to support this viewpoint. The beneficial health effects of running, including lower body mass index (BMI) in runners (15) and potentially improved cartilage function secondary to joint remodeling in response to cyclical loading while running (16), likely contribute to running being protective against the development of knee and hip OA. Because there is a discrepancy between past and recent literature regarding the relationship of OA and running, we have reviewed the recent additions to the literature to help clinicians more effectively counsel their runner patients regarding individual risk of developing knee and hip OA.

Beneficial Effects of Running


The beneficial effects of exercise in general, and running specifically, include improved cardiovascular health (17–19), diabetic control (20), mental health, bone mineral density (BMD), decreased BMI (21–23), potential increases in pain threshold (24), balance (25), and potentially even improved joint cartilage function. These beneficial effects must be balanced with potential OA risk when counseling patients who would like to start or continue running.


There is a complex relationship between running and bone health. High-impact sports lead to gains in BMD (26–30); however, running does not seem to lead to as much improvement in BMD as compared with higher-impact sports, such as gymnastics, jumping sports, and ball sports, but is associated with higher BMD than nonimpact sports, such as cycling and swimming (30–32). There seems to be a direct dose-dependent relationship between running intensity and BMD with higher-intensity running leading to greater gains in BMD (33–35), and an inverse dose-dependent relationship between running distance and BMD with longer distance running potentially leading to a decrease in BMD (36). When counseling patients on the potential beneficial effects of running and bone health, caution must be used in patients with a low BMI (BMI < 18.5) and in premenopausal female patients with oligomenorrhea or amenorrhea because these patients may be at risk for reduced BMD with long-distance running (37).

Some have postulated that repetitive joint loading leads to cartilaginous edema and denatured collagens suggestive of early osteoarthritic changes (38). These findings were supported in a cohort of marathon runners who underwent MRI imaging before and after a marathon and were found to have ongoing MRI signal in articular cartilage, particularly in the medial and patellofemoral compartment of the knee, which persisted for up to 3 months after a single marathon (11). However, recent literature has described many potential beneficial effects on cartilage from joint loading including suppression of proinflammatory cytokines and actually a reduction in tissue degenerative changes, primarily through a modulatory effect on the expression and activity of the degradative enzyme MMP-3 (39). Research in the area of regenerative medicine has shed further light on this subject and suggests that there is a narrow range of loading and shear which induces greater tensile strength in ex vivo articular cartilage and that both excessive loads (load >10 MPa) and insufficient loads can have deleterious effects on such tissue (40). Furthermore, running can improve noncartilage aspects of the joint, such as soft tissue extensibility, blood flow, and synovial fluid mobility (41).

Modifiable Risk Factors Associated with the Development of OA

When counseling patients regarding OA risk, clinicians must consider all individual modifiable risk factors to potentially mitigate that risk. However, one must realize that these factors also are confounders that may have an impact on risk independent of running dose.


The relative risk of OA in obese patients (BMI >30 kg·m2), as measured by incidence rate ratios, is 4.20 in men and 1.96 in women. For those patients who are overweight (BMI, 25 kg·m2 to 30 kg·m2) the relative risk of developing OA is 2.76 in men and 1.80 in women (42). Also, Williams reported that the risk for OA increases by 5% for every 1 kg·m2 of BMI (15). Obesity is considered one of the primary drivers of developing OA, and the beneficial effects of running on reducing OA risk seems, in part, to be secondary to the weight controlling effects of running.

Joint Injury

After a joint injury it is difficult to modify the risk of developing OA, thus injury prevention is important in those without prior injury. In those with an injury, it is important to minimize further injury to the joint. The risk of developing OA secondary to joint injury is difficult to determine as there is variability in the relative risk based on the severity of the injury and involved structures.

Patellofemoral pain syndrome (PFPS) is often cited as a RRI (2,3). PFPS also has been correlated in the development of patellofemoral OA (43). It is unclear if PFPS directly leads to the development of patellofemoral OA but it is likely that these two conditions at least share similar biomechanical etiologies. Given this relationship, it is especially important that clinicians identify runners with patellofemoral syndrome and focus on helping these athletes improve any biomechanical deficits which may be contributing to the syndrome.

The strongest correlation between injury and the development of knee OA is with anterior cruciate ligament (ACL) and meniscal injuries. Twelve years after sustaining an ACL tear 51% of women and 41% of men demonstrate findings of at least Kellgren-Lawrence (KL) grade 2 knee OA on radiographs, even in patients <40 years old (44). Some suggest that OA can be found as early as 1 year after ACL injury in one of every four patients (45). Concurrent meniscal injury with an ACL injury further increases the risk of developing OA. Interestingly, the patellofemoral compartment seems to be at most risk for developing knee OA after ACL injuries (45,46), thus patellofemoral pain in a runner with a prior ACL injury may be more than just “runner's knee.”

Meniscal injuries also are strongly correlated with the development of knee OA, particularly tibiofemoral OA. Patients who have undergone meniscal repair are twice as likely as the general population to develop knee OA (47) and 43% to 60% of patients who undergo partial menisectomy develop knee OA by 15 years of follow-up, with at least half of these patients being symptomatic (43,48).

It is clear that certain prior joint injuries (meniscal and ACL injuries in particular) predispose subjects to knee OA, thus, it is important to screen for these past injuries when counseling a runner about risk of OA. However, it remains unclear how severe an injury must be to significantly increase the risk of developing OA.

In the hip, static morphologic abnormalities, such as femoroacetabular impingement and developmental dysplasia of the hip, are important and may be associated with the development of hip OA (49–53). Labral tears also have been correlated with chondropathy (52), and thus there has been a suggested relationship between labral tears and the development of hip OA.

Occupational Workload

Occupational workload and work environment can be contributing factors to the development of OA. Heavy physical work, such as farming and construction, has been consistently associated with an increased incidence of knee OA (16). Additionally, specific work activities, such as repetitive kneeling, are correlated with a higher incidence of knee OA (54).

Biomechanical Factors

There are many biomechanical factors suspected to contribute to the development of OA. These are all primarily associations and not definitively causative factors given the study limitations and confounding variables. A static varus, but not valgus, knee deformity is associated with tibiofemoral knee OA (55–57). Additionally, a varus thrust during gait also is associated with tibiofemoral knee OA (58). Knee extension moments and patellofemoral reaction forces when walking and running on inclines are associated with patellofemoral OA (43).

Sport Participation

Some studies suggest that there is a relative risk for increased incidence of OA with participation in any organized sport of 1.37 (95% confidence interval [CI], 1.14–1.64). Soccer seems to carry the greatest risk of OA and is likely secondary to the injury profile in soccer. Long-distance running seemed to have a slightly decreased risk compared with soccer, swimming, shooting sports, and weightlifting, and a similar level of risk as tennis (59). Like soccer, it seems that the risk of OA due to sport participation is more likely associated with the injuries incurred during sport participation rather than representing a novel risk factor.

Nonmodifiable Risk Factors Associated with the Development of OA

Identifying runners with nonmodifiable risk factors for OA is equally important as it allows us to accurately risk stratify patients (Table). Important nonmodifiable risk factors include sex, age, and genetics determining the cartilage molecular profile.

Risk factors for developing osteoarthritis.

Female Biological Sex

Female biological sex seems to carry an increased risk of developing lower-extremity OA, particularly in the knees (54,60–66). According to one meta-analysis, females have an odds ratio of 1.68 (95% CI, 1.37–2.07, I2 = 72.5%) greater risk than males of developing knee OA (54). There seems to be less association with sex and hip OA (60,63,66,67); however, there still seems to be a slight increase in female-associated risk in the hip as well (63,68). Female-male hip OA incidence is 2.4:1.7 (99% CI, 2.4–2.5:1.7–1.8), whereas in the knee, it is 8.3:4.6 (99% CI, 8.2–8.4:4.5–5.7) (63). Also, females are more likely to be symptomatic and have more severe radiographic OA (62,64,66,69).

Many studies have noted an increased incidence of OA at menopause (60,61,64,66), yet there are a few which have demonstrated that this increased incidence is not until even later in life (63). The increased OA incidence which seems to correlate with menopause has caused many to theorize that estrogen has a protective effect (60,61,64), but there is no conclusive evidence to support this (70).

Many other theories regarding the etiology of this difference between biological sexes in the incidence of OA have been proposed. Some think this risk may be secondary to a propensity toward baseline subchondral sclerosis (8) or reduced cartilage volume (61,66) in those of female biological sex. There are biological sex-specific biomechanical differences which also may contribute to this risk (60,64,71). Kim et al. (72) investigated women exclusively to determine whether reproductive events were associated with the development of OA and found that a history of vaginal delivery compared to a cesarean delivery may be protective for hip OA, and that parity >5 was associated with knee OA. With so many theories and no definitive studies, it is currently unclear why this biological sex difference in the incidence of OA exists, yet it seems conclusive that those in the postmenopausal period have a higher incidence of OA, particularly in the knee.


It is generally known that the risk of OA rises with increasing age (61–65). Interestingly, there seems to be a nonlinear increase in OA risk between the ages of 50 and 75, but then a relative decrease in risk after the age of 75 to 80 years (54,62). It is possible that age limits the healing ability of the joint leading to lower absolute forces overloading the repair mechanisms of joints. Age also affects proprioception and the function of the joint capsule, ligaments, and muscles and thus, may, through secondary mechanisms, affect the health of the joint (71). In contrast, there is evidence that any physical activity in these older age groups may lead to decreased symptoms of OA, including joint pain and stiffness (73).

The Relationship of Running Dose and the Development of OA

Running Dose

Running dose is a challenging concept to define. Multiple factors may affect what we consider a “dose” of running. Time spent running, mileage ran, pace, perceived effort when running, average heart rate, metabolic equivalents spent when running among other variables can all be used to partly define one's running dose. Running dose would ideally be measured to encapsulate the magnitude of exposure to running.

Recent studies investigating the relationship between running and the risk of developing OA often use similar control groups (8,15,16,34,59,68,71,73–76), usually defined as sedentary nonrunners, but vary widely in defining running dose and study groups. Some studies have used a combination of sports other than running alone (8,15,59,73,76), making it difficult to draw conclusions specifically about running. Studies examining running alone currently use various means to define running dose (16,34,68,71,74,75). Some simply divide the study group into somewhat equal subgroups based on activity levels, but do not always define these activity levels (34,74,75). Many studies compare recreational runners to elite runners, and define elite runners often as professional or those who have competed for their countries in international competitions (16,68). High-dose running groups being limited to professional runners limits the transferability of study findings to the general population. Ultimately, the lack of consistency among study group definitions makes drawing definitive conclusions on the risk of developing OA secondary to running dose nearly impossible. Despite this, the more recent studies do allow us to draw some inferences regarding running dose and the risk of developing OA.

For the purposes of our discussion, we will simply compare relatively low dose to relatively high-dose running loads. In future research, clear, consistent definitions of running dose will be important to provide more definitive conclusions. We recommend future investigations into the relationship between running and joint health include an account of mileage or time spent running, a measure of effort when running, and, depending on gait lab availability, an assessment of joint load for each study subject.

Lower running dose

Recent research demonstrates more convincing evidence that lower running dose is not associated with the development of OA. In fact, these current studies suggest that low-dose running may actually be protective against the development of OA. In a retrospective analysis from the Osteoarthritis Initiative, Lo et al., found that there was no increase in the odds of knee pain, radiographic OA, or symptomatic OA between runners and nonrunners (75). Unfortunately, Lo et al. did not clearly define low intensity (n = 261), medium intensity (n = 258), and high intensity (n = 259) running groups other than noting that the running group was split into tertiles and compared to nonrunners (n = 1,859) (75). Thus, without a clear definition of running dose and intensity it is difficult to translate the findings of this study to a broader population.

Alentorn-Geli et al. (68) performed a recent meta-analysis of 25 articles (7 prospective cohort studies, 18 case-control or cross-sectional studies; pooled n = 125,810) which examined the relationship between running and the risk of developing OA and found that runners have an overall prevalence of lower-extremity OA of 3.66% (95% CI, 3.54% to 3.79%), whereas sedentary nonrunners have an overall prevalence of lower-extremity OA of 10.23% (95% CI, 9.89% to 10.58%) (68). The prevalence of lower-extremity OA found in this study is similar to most epidemiological studies which cite the prevalence in the general population at 10% to 12%. Some form of running dose measurement was cited in 13 of the 25 studies with common methods being min·wk−1 spent running (low dose, 95 to 224 min; high-dose, >250 min), and distance per week spent running (low dose, <10 to 28 miles; high dose, >20 to 52 miles). There was some overlap in the groups, but the recreational runners were mostly distinct and running usually <250 min·wk−1 and <25 miles·wk−1 (68). Despite trying to control for BMI, previous injury, and occupational workload when possible, there remains a large risk of bias as every study included in the meta-analysis individually had a high risk of bias in either selection, performance, detection, attrition, or reporting, and many of them a combination of these. There are certainly limitations of the Alentorn-Geli et al. study, including its applicability to patients who are sedentary, obese, or have other risk factors for OA who would like to begin running, but it was overall well designed and certainly suggests that low-dose running (running usually <250 min·wk−1 and <25 miles·wk−1) does not lead to the development of lower-extremity OA. Additionally, the Lo et al. and Alentorn-Gel et al. studies demonstrate growing evidence that low-dose running may be protective against the development of knee OA, but to definitively conclude this it would be important to have a controlled trial or prospective study specifically addressing this question and comparing low-dose runners to sedentary individuals.

There also is new evidence suggesting that low-dose running is not only protective against the development of OA, but also may be protective against the progression of OA. In a follow-up study from the Osteoarthritis Initiative, Lo et al., performed a nested cohort analysis of persons over the age of 50 who had radiographically diagnosed knee OA (n = 1203, 138 of these were runners). Baseline characteristics between the study group of runners and the control group of nonrunners were similar for age, BMI, and severity of baseline KL grade of OA, but there was a significantly higher proportion of men in the runner group (69.6%) compared to the nonrunner group (42.2%). Runners were identified as anyone who identified one of their top three physical activities as being running on their database surveys. The majority of these participants had run for six or more years over their life (74.6%), spent 5 to 12 months of the year running (92.7%), and ran more than four times per month (88.4%). Some had participated in competitive running (13%), and subjects in this subgroup tended to have a nonsignificant higher prevalence of KL grades 2 to 4. Lo et al., found that between runners and nonrunners there is an odds ratio for worsening KL grade of 0.9 (95% CI, 0.6 to 1.3), for new frequent knee pain of 0.9 (95% CI, 0.6 to 1.6) and for resolution of frequent knee pain of 1.7 (95% CI, 1.0 to 2.8). This suggests that running does not worsen structural knee OA in those previously diagnosed with knee OA, and may decrease the symptoms secondary to knee OA (74). This conclusion is limited by a risk of significant recall bias as both the participation in running and symptoms secondary to OA were reported retrospectively. Furthermore, running dose among this cohort was entirely self-selected, which in persons suffering from OA is likely at lower doses than in populations of runners without diagnosed OA. Thus, caution should be used when generalizing these findings.

The findings of this study are supported by another recent study that found runners, defined as subjects who had a membership in a running association or who had competed in running events, have a 50% reduced odds for undergoing surgery due to knee OA, when compared with nonrunners (8). This study also is limited by confounding variables as prior injury was not considered in the analysis, and it relied heavily on studies which investigated OA in relation to all sporting activities and not running alone.

Higher running dose

Although low-dose running may have a protective effect against the development of OA, there is considerable evidence suggesting that high-dose running is correlated with the development of lower-extremity OA. The Alentorn-Geli et al. subgroup analysis of professional and elite competitive runners found that the overall prevalence of lower-extremity OA is 13.3% (95% CI, 11.62% to 15.2%), compared to a prevalence in the recreational (lower dose) runner group of 3.5% (95% CI, 3.38% to 3.63%) and the 10.23% in the nonrunners (61). This finding is supported by other recent studies demonstrating elite athletes' higher incidence of lower-extremity OA across many sports (59,71,75,76). These recent findings are consistent with previous studies which generally demonstrated higher mileage, increased years of training, and higher pace during training as being associated with knee and hip OA (24,77–80).

Low-dose versus high-dose running

The mechanism of the association between running and OA is unclear, but when considering the dichotomous relationship of running with the development of lower-extremity OA, with low-dose running likely being protective and high-dose running likely being detrimental, this seems to support the proposed mechanism that OA develops as joint load exceeds the innate healing ability of a joint. Hence, low-dose running with low cumulative joint load may lead to optimized cartilage physiology as it likely induces a healthy amount of joint remodeling and response to stress leading to joint conditioning while not overwhelming repair capabilities (Fig. 1A) (16,38). However, once the load produces enough interval damage to the microenvironment of the joint to overwhelm repair capabilities, then the development of OA ensues, representing an inflection point in the relationship curve between running and OA (Fig. 1A). After this inflection point, it is unclear if there is a linear or nonlinear relationship between joint damage and marginal increases in joint load, but mechanistically it is more likely this proposed relationship is nonlinear with smaller marginal increases in load leading to greater amounts of joint damage.

Figure 1:
Possible relationship between running dose and the risk of developing osteoarthritis.

The point at which joint damage secondary to load equals the ability to repair the damage is highly individual and thus it is impossible to determine absolute load thresholds, or cutoffs of running dose, that can be applied to the general population. This relationship can be affected by the presence of cumulative modifiable and nonmodifiable risk factors for developing OA which will either directly influence the risk of developing OA, or reset the inflection point where joint injury from load equals healing ability to favoring lower running doses in those with higher cumulative risk. For example, obesity and prior meniscal injuries are all independent risk factors for developing OA and likely also contribute to higher loads through the knee and thus move this inflection point to the left (Fig. 1B). A patient with a favorable genetic profile leading to either resilient cartilage or increased healing ability would have their curve and inflection point shifted to the right compared to the general population (Fig. 1C). In the case of this latter example, it is conceivable that some may be able to withstand extremely high running doses and never experience detrimental effects at the joint level from running.

Preventing OA in Runners

For patients who would like to engage in running and are concerned about their risk of OA, discussions with their clinicians should entail a review of individualized preventive strategies such as conditioning and cross-training, modifications for obese individuals, and how to appropriately treat injuries when they occur (81). These recommendations are more empirical as they do not have robust evidence.


Important muscles groups that should be assessed for strength include the core, hip abductors, knee extensors, ankle stabilizers, and foot arch stabilizers (82). Often a preconditioning program before beginning a running program, with maintenance of conditioning can be helpful to ensure proper muscular support of the joints. Along with muscle strengthening, lower-extremity range of motion also must be considered with particular attention given to hip rotation, hamstring, and iliotibial band flexibility. In individuals who are at higher risk of developing knee and hip OA a formal gait evaluation and retraining program, preferably under the direction of the physical therapist, may be useful.


In obese individuals, it is often helpful to slowly increase activity when starting a running program. The initial phase of such a running program should focus on walking, and can still result in significant weight loss as obese individuals demonstrate increased caloric expenditure compared to nonobese individuals at comparable speeds (82). Progression to inclined walking, followed by an alternating run-walk transition period, and eventually to continuous running seems to be a reasonable overall approach. When undertaking this approach, it should be noted that continuous running may be too lofty a goal for some patients, in which case intermittent or alternating walk/jog/run training sessions may be a reasonable end goal.

Injury prevention and monitoring

At all times, there should be careful consideration given to preventing injury and appropriately addressing injuries when they occur. Methodical and careful increases in training volume can help prevent overuse injuries. In general, it is recommended to limit increasing training volume to 5% to 10% per week to prevent injury (75). It is important to monitor for pain and patients should be counseled that increasing pain during activity, pain which increases or persists at the same level by 24 h after cessation of activity, and night pain are all signs of possible injury (more serious tissue damage) and should be evaluated before resuming a running program (82). It also is often wise to space higher load workouts out by 2 to 3 d to provide for an appropriate amount of time to monitor for potential pain and injury due secondary to the higher load exposure.


Counseling patients about their risk for developing lower-extremity OA secondary to running can be a very difficult task for the clinician as it is impossible to provide the same recommendations to all patients. A clinician must carefully consider many factors including the many beneficial effects of running on cardiovascular and musculoskeletal/joint health, as well as the potential risk factors of the individual, both modifiable and nonmodifiable. The clinician also must consider the current evidence. Although not conclusive, it does suggest that low-dose running may be protective against the development of OA, but high-dose running may increase the risk of OA. It is important to realize that the evidence, though it is from numerous studies and fairly consistent, still only demonstrates this as an association and not causative. Finally, most studies are too heterogenous and not specific enough to be able to state an exact dose that is safe and one that is more risky for the development of OA in a generalizable manner.

When counseling patients who are interested in running for general health benefits, it seems reasonable for the clinician to preferentially recommend low-dose running as a good form of exercise due to the many beneficial effects of running on multiple body systems. However, there may be cases when the risk of developing OA is so great that a clinician is justified in recommending against running. Higher-dose running, which equates to higher intensity, longer distances, and over longer periods has more risk and thus the individual’s risk factor profile should be carefully balanced to consider appropriate recommendations. To assist with this assessment we have prepared a flow-diagram clinicians may use to help assess individual risk (Fig. 2) and determine how to approach counseling their patients. However, these recommendations are limited to those patients who do not have diagnosed OA and counseling patients with known OA about running is more challenging. There is recent evidence to suggest patients with radiographically evident OA still may benefit from self-selected running doses, particularly in pain reduction, but there remains a lack of sufficient evidence to provide definitive recommendations for this population.

Figure 2:
Reasonable flow diagram to assess potential risk of developing osteoarthritis secondary to running.

The authors declare no conflict of interest and do not have any financial disclosures.


1. Running USA Web site [Internet]. Annual reports [cited 2019 Jan 29]. Available from:
2. Lopes AD, Hespanhol Júnior LC, Yeung SS, et al. What are the main running-related musculoskeletal injuries? A systematic review. Sports Med. 2012; 42:891–905.
3. Arnold MJ, Moody AL. Common running injuries: evaluation and management. Am. Fam. Physician. 2018; 97:510–6.
4. Vina ER, Kwoh CK. Epidemiology of osteoarthritis: literature update. Curr. Opin. Rheumatol. 2018; 30:160–7.
5. Zhang Y, Jordan JM. Epidemiology of osteoarthritis. Clin. Geriatr. Med. 2010; 26:355–69.
6. Hunter DJ, Schofield D, Callander E. The individual and socioeconomic impact of osteoarthritis. Nat. Rev. Rheumatol. 2014; 10:437–41.
7. Desphpande BR, Katz JN, Solomon DH. Number of persons with symptomatic knee osteoarthritis in the US: impact of race and ethnicity, age, sex, and obesity. Arthritis Care Res (Hoboken). 2016; 68:1743–50.
8. Timmins KA, Leech RD, Batt ME, et al. Running and knee osteoarthritis: a systematic review and meta-analysis. Am. J. Sports Med. 2017; 45:1447–57.
9. Goldring MB, Goldring SR. Osteoarthritis. J. Cell. Physiol. 2007; 213:626–34.
10. Franciozi CE, Tarini VA, Reginato RD, et al. Gradual strenuous running regimen predisposes to osteoarthritis due to cartilage cell death and altered levels of glycosaminoglycans. Osteoarthr. Cartil. 2013; 21:965–72.
11. Luke AC, Stehling C, Stahl R. High-field magnetic resonance imaging assessment of articular cartilage before and after marathon running: does long-distance running lead to cartilage damage? Am. J. Sports Med. 2010; 38:2273–80.
12. Lucchinetti E, Adams CS, Horton WE, et al. Cartilage viability after repetitive loading: a preliminary report. Osteoarthr. Cartil. 2002; 10:71–81.
13. McDermott M, Freyne P. Osteoarthritis in runner with knee pain. Br. J. Sports Med. 1983; 17:84–7.
14. Esculier JF, Krowchuk NM, Li LC, et al. What are the perceptions about running and knee joint health among the public and healthcare practitioners in Canada? PLoS One. 2018; 13:e0204872. Available from: doi: 10.1371/journal.pone.0204872.
15. Williams PT. Effects of running and walking on osteoarthritis and hip replacement risk. Med. Sci. Sports Exerc. 2013; 45:1292–7.
16. Miller RH. Joint loading in runners does not initiate knee osteoarthritis. Exerc. Sport Sci. Rev. 2017; 45:87–95.
17. McMullen CW, Harrast MA, Baggish AL. Optimal running dose and cardiovascular risk. Curr. Sports Med. Rep. 2018; 17:192–8.
18. Nystoriak MW, Bhatnagar A. Cardiovascular effects and benefits of exercise. Front Cardiovasc Med. 2018; 5:135. Available from: doi: 10.3389/fcvm.2018.00135.
19. Kodama S, Tanaka S, Saito K, et al. Effect of aerobic exercise training on serum levels of high-density lipoprotein cholesterol: a meta-analysis. Arch. Intern. Med. 2007; 167:999–1008.
20. Dubé JJ, Fleishman K, Rousson V, et al. Exercise dose and insulin sensitivity: relevance for diabetes prevention. Med. Sci. Sports Exerc. 2012; 44:793–9.
21. Stevinson D, Hickson M. Changes in physical activity, weight and wellbeing outcomes among attendees of a weekly mass participation event: a prospective 12-month study. J. Public Health (Oxf.). 2018. Available from: 10.1093/pubmed/fdy178.
22. Williams PT. Asymmetric weight gain and loss from increasing and decreasing exercise. Med. Sci. Sports Exerc. 2008; 40:296–302.
23. Williams PT. Maintaining vigorous activity attenuates 7-yr weight gain in 8340 runner. Med. Sci. Sports Exerc. 2007; 39:801–9.
24. Spector TD, Harris PA, Hart DJ, et al. Risk of osteoarthritis associated with long-term weight bearing sports: a radiologic survey of the hips and knees in female ex-athletes and population controls. Arthritis Rheum. 1996; 39:988–95.
25. Oja P, Titze S, Kokko S, et al. Health benefits of different sport disciplines for adults: systematic review of observational and intervention studies with meta-analysis. Br. J. Sports Med. 2015; 49:434–40.
26. Rector RS, Rogers R, Ruebel M, et al. Lean body mass and weight-bearing activity in the prediction of bone mineral density in physically active men. J. Strength Cond. Res. 2009; 23:427–35.
27. Fehling PC, Alekel L, Clasey L. A comparison of bone mineral densities among female athletes in impact loading and active loading sports. Bone. 1995; 17:205–10.
28. Heinonen A, Oja P, Kannus P, et al. Bone mineral density in female athletes representing sports with different loading characteristics of the skeleton. Bone. 1995; 17:197–203.
29. Mosekilde L. Osteoporosis and exercise. Bone. 1995; 17:193–5.
30. Grimston SK, Willows ND, Hanley DA. Mechanical loading regime and its relationship to bone mineral density in children. Med. Sci. Sports Exerc. 1993; 25:1203–10.
31. Tenforde AS, Frederiscon M. Influence of sports participation on bone health in the young athlete: a review of the literature. PM R. 2011; 3:861–70.
32. Hegle EW, Aagaard P, Jakobsen MD, et al. Recreational football training decreases risk factor for bone factors in untrained premenopausal women. Scand. J. Med. Sci. Sports. 2010; 20(Suppl. 1):31–9.
33. Piasecki J, McPhee JS, Hannam K. Hip and spine bone mineral density are greater in master sprinters, but not endurance runners compared with non-athletic controls. Arch. Osteoporos. 2018; 13:72.
34. Li Z, Liu SY, Xu L, et al. Effects of treadmill running with different intensity on rat subchondral bone. Sci. Rep. 2017; 7:1977.
35. Ni GX, Liu SY, Lei L, et al. Intensity-dependent effect of treadmill running on knee articular cartilage in a rat model. Biomed. Res. Int. 2013; 2013:172392. Available from: doi: 10.1155/2013/172392.
36. Burrows M, Nevill AM, Bird S, et al. Physiological factors associated with low bone mineral density in female endurance runners. Br. J. Sports Med. 2003; 37:67–71.
37. Tenforde AS, Carlson JL, Sainani KL, et al. Sport and triad risk factors influence bone mineral density in collegiate athletes. Med. Sci. Sports Exerc. 2018; 50:2536–43.
38. Chen CT, Burton-Wurster N, Lust G, et al. Compositional and metabolic changes in damaged cartilage are peak-stress, stress-rate and loading-duration dependent. J. Orthop. Res. 1999; 17:870–9.
39. Sun HB, Cardoso L, Yokota H. Mechanical intervention for maintenance of cartilage and bone. Clin. Med Insights Arthritis Musculoskelet Disord. 2011; 4:65–70.
40. Salinas EY, Hu JC, Athanasiou K. A guide for using mechanical stimulation to enhance tissue-engineered articular cartilage properties. Tissue Eng. Part B Rev. 2018; 24:345–58.
41. Hamann N, Zaucke F, Heilig J, et al. Effect of different running modes on the morphological, biochemical, and mechanical properties of articular cartilage. Scand. J. Med. Sci. Sports. 2014; 24:179–88.
42. Guh DP, Zhang W, Bansback N, et al. The incidence of co-morbidities related to obesity and overweight: a systematic review and meta-analysis. BMC Public Health. 2009; 25:88.
43. Crossley KM, Stefanik JJ, Selfe J, et al. 2016 Patellofemoral pain consensus statement from the 4th International Patellofemoral Pain Research Retreat, Manchester. Part 1: terminology, definitions, clinical examination, natural history, patellofemoral osteoarthritis and patient-reported outcome measures. Br. J. Sports Med. 2016; 50:839–43.
44. Roos EM. Joint injury causes knee osteoarthritis in young adults. Curr. Opin. Rheumatol. 2005; 17:195–200.
45. Culvenor AG, Collins NJ, Guermazi A, et al. Early knee osteoarthritis is evident one year following anterior cruciate ligament reconstruction. Arthritis Rheumatol. 2015; 67:945–55.
46. Harris K, Driban JB, Sitler MR. Five-year clinical outcomes of a randomized trial of anterior cruciate ligament treatment strategies: an evidence-based practice paper. J. Athl. Train. 2015; 50:110–2.
47. Persson F, Turkiewicz A, Bergkvist D, et al. The risk of symptomatic knee osteoarthritis after arthroscopic meniscus repair vs partial meniscectomy vs the general population. Osteoarthr. Cartil. 2018; 26:195–201.
48. Roemer FW, Kwoh CK, Hannon MJ, et al. Partial meniscectomy is associated with increased risk of incident radiographic osteoarthritis and worsening cartilage damage in the following year. Eur. Radiol. 2017; 27:404–13.
49. Wagner S, Hofstetter W, Chiquet M, et al. Early osteoarthritic changes of human femoral head cartilage subsequent to femoro-acetabular impingement. Osteoarthr. Cartil. 2003; 11:508–18.
50. Ganz R, Leunig M, Leunig-Ganz K, et al. The etiology of osteoarthritis of the hip: an integrated mechanical concept. Clin. Orthop. Relat. Res. 2008; 466:264–72.
51. Hapa O, Yüksel HY, Muratli HH, et al. Axial plane coverage and torsion measurements in primary osteoarthritis of the hip with good frontal plane coverage and spherical femoral head. Arch. Orthop. Trauma Surg. 2010; 130:1305–10.
52. Kemp JL, Makdissi M, Schache AG, et al. Femoroacetabular impingement and patient-reported outcomes. Br. J. Sports Med. 2014; 48:1102–7.
53. Zhang C, Li L, Esdaile JM. Femoroacetabular impingement and osteoarthritis of the hip. Can. Fam. Physician. 2015; 61:1055–60.
54. Silverwood V, Blagojevic-Bucknall M, Jinks C, et al. Current evidence on risk factors for knee osteoarthritis in older adults. Osteoarthr. Cartil. 2015; 23:507–15.
55. Sharma L, Song J, Dunlop D, et al. Varus and valgus alignment and incident and progressive knee osteoarthritis. Ann. Rheum. Dis. 2010; 69:1940–5.
56. Matsumoto T, Hashimura M, Takayama K, et al. A radiographic analysis of alignment of the lower extremities—initiation and progression of varus-type osteoarthritis. Osteoarthr. Cartil. 2015; 23:217–23.
57. Long MJ, Papi E, Duffell LD, et al. Predicting knee osteoarthritis risk in injured populations. Clin. Biomech. (Bristol, Avon). 2017; 47:87–95. Available from: doi: 10.1016/j.clinbiomech.2017.06.001.
58. Sharma L, Chang AH, Jackson RD, et al. Varus thrust and incident and progressive knee osteoarthritis. Arthritis Rheumatol. 2017; 69:2136–43.
59. Tran G, Smith TO, Grice A, et al. Does sports participation (including level of performance and previous injury) increase risk of osteoarthritis? A systematic review and meta-analysis. Br. J. Sports Med. 2016; 50:1459–66.
60. Park JH, Hong JY, Han K, et al. Prevalence of symptomatic hip, knee, and spine osteoarthritis nationwide health survey analysis of an elderly Korean population. Medicine. 2017; 96:e6372.
61. Palazzo C, Nguyen C, Lefèvre-Colau MM, et al. Risk factors and burden of osteoarthritis. Ann. Phys. Rehabil. Med. 2016; 59:134–8.
62. Plotnikoff R, Karunamuni N, Lytvyak E, et al. Osteoarthritis prevalence and modifiable factors: a population study. BMC Public Health. 2015; 15:1195.
63. Prieto-Alhambra D, Judge A, Javaid MK, et al. Incidence and risk factors for clinically diagnosed knee, hip and hand osteoarthritis: influences of age, gender and osteoarthritis affecting other joints. Ann. Rheum. Dis. 2014; 73:1659–64.
64. Johnson VL, Hunter GJ. The epidemiology of osteoarthritis. Best Pract. Res. Clin. Rheumatol. 2014; 28:5–15.
65. Neogi T, Zhang Y. Epidemiology of osteoarthritis. Rheum. Dis. Clin. North Am. 2013; 39:1–19.
66. Srikanth VK, Fryer JL, Zhai G, et al. A meta-analysis of sex differences prevalence, incidence and severity of osteoarthritis. Osteoarthr. Cartil. 2005; 13:769–81.
67. Cooper DJ, Scammell BE, Batt ME, et al. Factors associated with pain and osteoarthritis at the hip and knee in Great Britain's Olympians: a cross-sectional study. Br. J. Sports Med. 2018; 52:1101–8.
68. Alentorn-Geli E, Samuelsson K, Musahl V, et al. The association of recreational and competitive running with hip and knee osteoarthritis: a systematic review and meta-analysis. J. Orthop. Sports Phys. Ther. 2017; 47:373–90.
69. Paterson KL, Kasza J, Hunter DJ, et al. The relationship between foot and ankle symptoms and risk of developing knee osteoarthritis: data from the osteoarthritis initiative. Osteoarthr. Cartil. 2017; 25:639–46.
70. Roman-Blas JA, Castaneda S, Largo R, et al. Osteoarthritis associated with estrogen deficiency. Arthritis Res. Ther. 2009; 11:241.
71. Ni GX. Development and prevention of running-related osteoarthritis. Curr. Sports Med. Rep. 2016; 15:342–9.
72. Kim SM, Cheon JY, Park YF, et al. The associations between parity, other reproductive factors, and osteoarthritis in women aged over 50 years; data from the Korean National Health and nutrition examination survey V (2010–2012). Taiwan. J. Obstet. Gynecol. 2017; 56:153–8.
73. Peeters GM, Pisters MF, Mishra GD, et al. The influence of long-term exposure and timing of physical activity on new joint pain and stiffness in mid-age women. Osteoarthr. Cartil. 2015; 23:34–40.
74. Lo GH, Musa SM, Driban JB, et al. Running does not increase symptoms or structural progression in people with knee osteoarthritis: data from the osteoarthritis initiative. Clin. Rheumatol. 2018; 37:2497–504.
75. Lo GH, Driban JB, Kriska AM, et al. Is there an association between a history of running and symptomatic knee osteoarthritis? A cross-sectional study from the osteoarthritis initiative. Arthritis Care Res. 2017; 69:183–91.
76. Lefèvre-Colau MM, Nguyen C, Haddad R, et al. Is physical activity, practiced as recommended for health benefit, a risk factor for osteoarthritis? Ann. Phys. Rehabil. Med. 2016; 59:196–206.
77. Puranen J, Ala-Ketola L, Peltokallio P, et al. Running and primary osteoarthritis of the hip. Br. Med. J. 1975; 2:424–5.
78. Marti B, Knobloch M, Tschopp A, et al. Is excessive running predictive of degenerative hip disease? Controlled study of former elite athletes. BMJ. 1989; 299:91–3.
79. Kujala UM, Kaprio J, Sarna S. Osteoarthritis of weight bearing joints of lower limbs in former elite male athletes. BMJ. 1994; 308:231–4.
80. Cheng Y, Macera CA, Davis DR, et al. Physical activity and self-reported, physician-diagnosed osteoarthritis: is physical activity a risk factor? J. Clin. Epidemiol. 2000; 53:315–22.
81. Bennell K, Hunter DJ, Vicenzino B. Long-term effects of sport: preventing and managing OA in the athlete. Nat. Rev. Rheumatol. 2012; 8:747–52.
82. Vincent HK, Vincent KR. Considerations for initiating and progressing running programs in obese individuals. PM R. 2013; 5:513–9.
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