Experimental evidence that physical activity inhibits osteoarthritis: Implications for inferring activity patterns from osteoarthritis in archeological human skeletons

Objectives Osteoarthritis (OA) is a common joint disease whose causes are not fully understood, but a longstanding hypothesis is that OA stems primarily from the cumulative effects of joint mechanical loading throughout life. Based on this wear and tear hypothesis, anthropologists have assumed that the presence of OA in archeological human skeletons can be interpreted as evidence of a highly physically active lifestyle. Here, we use guinea pigs to experimentally test the hypothesis that higher levels of routine physical activity result in greater OA degeneration. Materials and methods Guinea pigs are a useful model for OA research because they spontaneously develop the disease in a manner similar to humans. One group of growing animals was housed for 22 weeks in a large room that promoted voluntary physical activity (4.8 km of movement per day, on average), while animals in another group were housed in small cages that restricted their mobility (n = 15/group). After the experiment, histological and microcomputed tomographic analyses were conducted focusing on the knees. Results Rather than causing greater OA degeneration, elevated levels of routine physical activity resulted in significantly less knee cartilage deterioration, less synovial inflammation, smaller osteophytes, and maintenance of greater epiphyseal trabecular bone quantity. Discussion These results are inconsistent with the hypothesis that high levels of routine physical activity drive the pathogenesis of OA and call into question typical interpretations of OA in studies of archeological human skeletons.

Automated summary

In a study using guinea pigs as an experimental model for osteoarthritis (OA) research, it was found that higher levels of routine physical activity did not lead to greater OA degeneration, but instead resulted in less knee cartilage deterioration, reduced synovial inflammation, smaller osteophytes, and maintenance of greater epiphyseal trabecular bone quantity, challenging the long-standing hypothesis about the relationship between physical activity and OA progression.