Does Running Cause Knee Osteoarthritis?

September 14, 2013


By Karin Katz, MD

Faculty Peer Reviewed

Post-summer is here. Despite the heat and what feels like 100% humidity, the East River Path is packed with runners. No amount of car fumes pouring onto the path could stop those in training. Others are circling the 6-mile-loop around Central Park. Or, if you are bored of running the typical routes, for a few Saturdays, Park Avenue will be shut down for automobile traffic. New Yorkers love to run (well, some do). And while unforeseen circumstances led to a cancellation of the NYC Marathon in 2012, in 2011, almost 47,000 people ran those well-known 26 miles. Given the epidemic of obesity, we should be celebrating this phenomenon! But, is there any reason to advise our patients to be cautious of such strenuous weight-bearing activity? Osteoarthritis is thought of as a disease of “wear and tear” on the joints. Is running a risk factor for developing osteoarthritis? If so, is the damage worse for marathon runners? Maybe we should be advising our patients to stick to water aerobics.

Approximately 19-28% of adults aged 45 or older have knee osteoarthritis (OA) [1]. OA is a degenerative joint disease characterized by articular cartilage failure, although all structures of the joint are involved in the pathologic process. Risks for developing osteoarthritis include systemic factors (age, female gender, genetic susceptibility), intrinsic joint vulnerabilities (previous damage such as meniscal tears, muscle weakness, increased bone density, malalignment), and joint stressors (such as obesity). Individuals who are overweight or obese may have three times the risk of incident knee arthritis [2]. While the risk that obesity confers on osteoarthritis is well established, the impact of exercise on weight-bearing joints is complex. Exercise in different forms has been shown to prevent, cause, accelerate, or treat osteoarthritis.

Let’s start slow with a study on the effects of walking on the development of knee osteoarthritis. Felson et al. published a longitudinal study of the Framinghmam Offspring cohort to evaluate the long-term effect of recreational exercise on the development of knee OA in older adults [3]. A total of 1,279 subjects were included with a mean age at baseline of 53 years. Most reported walking for exercise. Subjects were asked about their knee pain and anteroposterior and lateral knee radiographs were obtained. Nine years later, subjects were reexamined for osteoarthritis. The primary outcomes of the study included incident radiographic OA, symptomatic OA, and tibiofemoral joint space loss. Walking (categorized as less than 6 miles per week, or greater than or equal to 6 miles per week) was not associated with an increased or decreased risk of radiographic or symptomatic OA compared to subjects who did not walk for exercise. Joint space loss was also unaffected by this activity.

Moving on to running, a study in the American Journal of Preventative Medicine investigated differences in the progression of knee OA in middle- to older-aged runners compared to healthy non-runners over two decades [4]. This study included 45 long distance runners and matched controls with a mean age of 58 years. Most of these runners had been running for over a decade. The study examined radiographic knee OA (specifically tibiofemoral disease) by serial radiographs. At the start of this study, members of the runner’s club were running for an average of 214 minutes per week. By the completion of the trial, their running time decreased by 55%. A small proportion of the controls ran for exercise at baseline, but almost all had stopped running by the time the final radiograph was obtained. In the analysis, long-distance running was not associated with accelerated incidence or severity of radiographic OA over a mean observation time of 11.7 years. While this study has a number of limitations, perhaps the greatest one is that there was no analysis of subjects’ clinical symptoms. It is also important to note that the running group was slightly younger with a slightly lower BMI compared to the control group. These differences could have confounded the results. Finally, one must also wonder, why did the runners stop running? What if a runner acquired a knee injury and had to cut down their usual workout? In such cases, longer follow-up might be necessary to detect the development of OA in “retired” runners.

Another study in the American Journal of Sports Medicine showed that formerly competitive runners did not have higher rates of arthritis in their hips, knees or ankles when compared to nonrunners [5]. This retrospective study included Danish male runners who qualified for county teams from 1950 to 1955. The study was published in 1990. Only 30 subjects were included, and were assessed using pain scores, clinical examination and x-rays. There was no difference between runners and non-runners with regard to narrowing of the joint space or osteophytosis in the lower extremity joints. There was also no difference in range of motion of the joints. Some of the runners experienced pain, but clinical and radiographic findings in this particular group were considered normal. While this study is also not without limitations, it is small, retrospective, and much of the data is subjective- it is interesting to look at the effects of long-distance running on the joints over an extended period of time in this athletic population.

Although there are other conflicting data, the medical literature generally does not support the idea that running contributes to the degeneration of articular cartilage [6]. Nonetheless, more advanced imaging techniques raise more questions about this potential association. A cohort study by Luke et al. used advanced MRI techniques to detect changes that could signify early osteoarthritis [7]. The loss of proteoglycan or glycosaminoglycan may be the initiating event in OA; this study used imaging markers to detect proteoglycan loss and collagen breakdown. In this investigation, the knee cartilage of 10 asymptomatic individuals was evaluated before and after a marathon (26.2 miles) using 3-T MRI techniques. A 3-T MRI is an MRI with a 3.0 tesla strength magnet, an advanced imaging technique that has been used assess the biochemical degradation of articular cartilage. Marathon runners were between the ages of 18 and 40 years and were matched to non-runners. The subjects had not participated in a marathon for at least 4 months. The inclusion criteria also included a BMI of less than 30. Runners had their first MRI within 2 weeks before the marathon, then had repeat imaging post-marathon (within 48 hours) and at 10 to 12 weeks after the race. One imaging technique used to describe the biochemical composition of cartilage is called a T1rho measurement. This measurement has been proposed for detecting damage to the proteoglycan-cartilage matrix. The study by Luke et al. demonstrated a significant increase in T1rho values on the post-marathon MRIs of runners. The T1rho values remained elevated 3 months later. Another MRI mapping technique for assessing biochemical changes in the joint is T2 MRI, which characterizes water content and collagen degradation. T2 signals were increased immediately after the marathon, but returned to baseline at 3 months. While this study shows that the biomechanics of knee joints change as a result of marathon running, these changes are not necessarily detrimental to the individual or their joints. The T1rho technique was previously validated in patients with OA, and the T2 relaxation time measurements has also been found to be a reliable means of detecting early degenerative changes of the cartilage. However, whether changes in T1rho and T2 after running lead to joint degeneration over time is not known. In addition, it is not clear how these changes correlate with patients’ symptoms [8,9].

Another interesting article assessing OA with advanced MRI techniques showed moderate exercise in subjects at high risk for OA was associated with joint composition changes that could have chondroprotective effects on the knee [10]. In this study, 45 subjects who underwent a partial medial meniscus resection (a group considered high risk for developing OA) were randomized to undergo a 4-month long supervised exercise regimen or to receive no intervention. The primary outcome was an estimate of cartilage glycosaminoglycan (GAG) content using delayed gadolinium-enhanced MRI techniques. The investigators found that the exercise group showed an improvement in cartilage quality. This suggests that the biochemical changes of exercise on the joint can be protective, rather than harmful.

At present, there is not enough long-term data to suggest that running is a risk factor for knee osteoarthritis. In addition, if patients are counseled that running is bad for their knees, this may deter them from physical exercise and deprive them of the benefits of staying active. An important consideration, however, is that in a patient with a prior knee injury, your advice may differ. Knee injury has been shown to confer a four-fold increased risk of developing knee osteoarthritis, and 50% of individuals with an ACL or meniscus tear may develop knee OA [2,11]. There is limited data to guide counseling patients on the prevention of OA after knee injury. The study by Roos et al. would suggest that some exercise is better than no exercise in such patients [10]. However, it is important to keep in mind that the exercise regimen in that study was supervised, and these patients were not running marathons. Athletes with a history of a knee injury who continue long-distance running may have a very different clinical course of disease.

Although there are more questions to be answered, this summer there’s no reason to tell your healthy runners to stick to the swimming pool and quit training for their next marathon.

Karin Katz, MD is a second-year internal medicine resident at NYU Langone Medical Center

Peer reviewed by Michael Pillinger, MD, Associate Professor, Department of Medicine, Rheumatology Divison, NYU Langone Medical Center

References

1. 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. Jan 2008;58(1):26-35.

2. 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. Jan 2010;18(1):24-33.

3. Felson DT, Niu J, Clancy M, Sack B, Aliabadi P, Zhang Y. Effect of recreational physical activities on the development of knee osteoarthritis in older adults of different weights: the Framingham Study. Arthritis Rheum. Feb 15 2007;57(1):6-12.

4. Chakravarty EF, Hubert HB, Lingala VB, Zatarain E, Fries JF. Long distance running and knee osteoarthritis. A prospective study. Am J Prev Med. Aug 2008;35(2):133-138.

5. Konradsen L, Hansen EM, Sondergaard L. Long distance running and osteoarthrosis. Am J Sports Med. Jul-Aug 1990;18(4):379-381.

6. Willick SE, Hansen PA. Running and osteoarthritis. Clin Sports Med. Jul 2010;29(3):417-428.

7. Luke AC, Stehling C, Stahl R, et al. 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. Nov 2010;38(11):2273-2280.

8. Li X, Benjamin Ma C, Link TM, et al. In vivo T(1rho) and T(2) mapping of articular cartilage in osteoarthritis of the knee using 3 T MRI. Osteoarthritis Cartilage. Jul 2007;15(7):789-797.

9. Nishii T, Kuroda K, Matsuoka Y, Sahara T, Yoshikawa H. Change in knee cartilage T2 in response to mechanical loading. J Magn Reson Imaging. Jul 2008;28(1):175-180.

10. Roos EM, Dahlberg L. Positive effects of moderate exercise on glycosaminoglycan content in knee cartilage: a four-month, randomized, controlled trial in patients at risk of osteoarthritis. Arthritis Rheum. Nov 2005;52(11):3507-3514.

11. Ratzlaff CR, Liang MH. New developments in osteoarthritis. Prevention of injury-related knee osteoarthritis: opportunities for the primary and secondary prevention of knee osteoarthritis. Arthritis Res Ther. 2010;12(4):215.

 

 

 

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