Osteoarthritis and Running


Osteoarthritis (OA) is the most common joint disorder and a growing health concern in the United States. Approximately 10%–12% of the population, or 30.8 million adults, live with symptomatic OA in any joint. Aggregate annual medical care expenditures for OA are estimated at $185.5 billion ; and the economic burden of OA is projected to increase in the future as half of all patients with symptomatic OA are currently <65 years old. At the same time, there is significant growth in the popularity of running. A 3.5x increase in US mass running event participants was seen between 1990 and 2016 with 17,000,000 finishers in 2016, and there is a notable trend for increasing age among marathon participants with 49% master runners (age > 40) competing in 2015 in comparison with 26% of participants in 1980. Both primary care and sports medicine professionals are likely to encounter patients interested in beginning a running lifestyle, but with concern about the risk of developing OA. Runners with OA will also seek counseling and management of other running-related injuries. Therefore, the running medicine professional should be aware of the scientific literature at the intersection of running and OA in order to provide evidence-based, patient-centered, and goal-oriented care.

There is increasingly robust evidence for the benefits of general physical activity in the prevention and management of symptomatic OA at the hip and knee. An extensive review of recent literature by Kraus et al. found strong evidence for beneficial effects of physical activity on both pain and improved physical function, as well as significant evidence for improvements in health-related quality of life in those with hip or knee OA in comparison with less active adults with OA. Additionally, they found no evidence to suggest accelerated OA progression for physical activity below 10,000 steps per day. However, debate remains over the potential causal relationship between the development and progression of OA with higher-level physical activity such as running.

A recent survey of Canadian healthcare providers indicates that 78% do not agree that running is detrimental for knee joint health. In fact, there is increasing evidence that moderate dose running does not lead to OA of the knee and hip and may impart a protective benefit. The beneficial effects of running on general health are well established and include improved cardiovascular health, diabetic control, mental health, bone mineral density, decreased body mass index (BMI), potential increases in pain threshold, and balance. Additionally, proposed beneficial effects on joint function include improved cartilage structure secondary to joint remodeling in response to cyclical loading while running.

In order to effectively counsel patients on the relationship between running and OA, it is important to appreciate the interactions of individual factors influencing OA risk. The clinician must discuss with the patient concerns related to their running interests and goals ( Table 16.1 ). Success in the initiation, continuation, or modification of a running program will be closely tied to realistic goals and expectations. Informed and shared decision-making is essential in considering prevention, as well as the risks of development or symptomatic progression of OA.

Table 16.1
Examples of Patients who May Seek Counseling With Concerns for osteoarthritis (OA) and Running.
  • 1) Those interested in beginning a running program but concerned about long-term joint health

  • 2) Recreational runners with known OA desiring to continue running

  • 3) Obese patients initiating an exercise program regarding strategies for prevention of OA while optimizing the health benefits of running

  • 4) Older recreational athletes and those with hip or knee arthroplasties considering the risks and benefits of running on joint health

Proposed Mechanisms of Osteoarthritis in Running

Proposed mechanisms for the development of OA include (1) excessive loads on normal cartilage and (2) normal loads on abnormal cartilage. Given these proposed mechanisms, there has been concern that running could lead to the development of OA, specifically in weight-bearing joints such as the hip and knee. Some have postulated that repetitive joint loading leads to cartilaginous edema and denatured collagens suggestive of early osteoarthritic changes. These findings were supported in a cohort of marathon runners who underwent MRI imaging before and after a marathon. Runners in the cohort demonstrated ongoing MRI signal in articular cartilage persisting for up to 3 months after a single marathon, particularly in the medial and patellofemoral compartments of the knee. However, recent literature has described many potential beneficial effects on cartilage from joint loading including suppression of proinflammatory cytokines and a reduction in degenerative changes within tissue. Additionally, there appears to be a narrow range of loading and shear which induces greater tensile strength in ex vivo articular cartilage, which is consistent with the understanding that both excessive loads (>10 MPa), as well as insufficient loads, can have deleterious effects. This claim is supported by a series of patients from the Osteoarthritis Initiative observed over 4 years with MRI data of knee cartilage suggesting a similar “U” shaped relationship between the amount of physical activity suggesting more pronounced longitudinal changes in cartilage integrity in sedentary and vigorous activity groups in comparison with those primarily engaged in light to moderate intensity. Furthermore, running can improve noncartilage aspects of the joint such as soft tissue extensibility, blood flow, and synovial fluid mobility. Appropriately dosed running also improves joint proprioception and the strength of supportive hip and knee musculature imparting a protective effect on overall joint health by dispersing the contact forces throughout the kinetic chain.

Understanding Modifiable and Nonmodifiable Risk Factors for Development of Osteoarthritis

When counseling patients regarding OA risk, clinicians must consider all individual risk factors including modifiable and nonmodifiable entities in order to risk stratify and develop interventions to mitigate injury or risk of disease progression ( Table 16.2 ).

Table 16.2
Risk Factors for Developing Osteoarthritis
  • Obesity

  • Propensity toward musculoskeletal injuries

  • Heavy occupational load

  • Poor biomechanics

  • Sport participation

  • Age >50 years old

  • History of prior joint injury

  • Genetics, strong family history of OA

  • Female gender, postmenopausal

Nonmodifiable Risk Factors


The prevalence of OA rises with increasing age. Interestingly, there seems to be a nonlinear increase in OA risk between ages 50–75, but then a relative decrease in risk after the age of 75–80 years. 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 a joint. In contrast, there is evidence that any physical activity in these older age groups may lead to decreased symptoms of OA, including pain and joint stiffness.

Female biological sex

Female biological sex is associated with an increased risk of developing lower limb OA, particularly in the knees. According to one metaanalysis, females have an odds ratio of 1.68 (95% CI 1.37 to 2.07, I 2 = 72.5%) in comparison with males of developing knee OA. There seems to be less association, though still some, with gender and hip, as there is a slight increase in female-associated risk in the hip. Female:male hip OA incidence is 2.4:1.7 (99% CI 2.4–2.5:1.7–1.8), while in the knee it is 8.3:4.6 (99% CI 8.2–8.4:4.5–4.7). Furthermore, females are more likely to be symptomatic and have more severe radiographic OA.

Many have noted an increased incidence of OA at menopause, yet there are a few studies which have demonstrated that this increased incidence is not observed until even later in life. The increased OA incidence which seems to correlate with menopause has led many to theorize that estrogen has a protective effect, but there is no conclusive evidence to date to support this.

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, or reduced cartilage volume in females. There are also sex-specific biomechanical differences which may contribute to this risk. Kim et al. investigated women exclusively to determine if reproductive events were associated with the development of OA and found that a history of vaginal delivery compared with 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 unclear why there is such a profound difference in the incidence of OA between biological sexes. However there is strong evidence that females in the postmenopausal period have a higher incidence of OA, particularly at the knee, compared to other populations.


The influence of genetics in the pathogenesis and risk of developing OA has been a topic of interest among both research scientists and clinicians. Genetic factors are estimated to account for up to 60% of hip OA and 40% of knee OA. Many genes are implicated in the regulation of cartilage health, but this is beyond the scope of our current clinically oriented discussion. Suffice to say genetics, genomics, and epigenetics play a complex role in joint health and may represent targets for future medical innovation ; however, while these treatments remain on the horizon, it is valuable to obtain a thorough family history regarding OA and rheumatologic disease in order to risk stratify and appropriately counsel patients.

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