Although osteoarthritis is currently deemed a chronic progressively disabling condition with no known cure, research over the past 10 years or more has indicated that there is strong possibility that an array of muscle related factors as well as obesity can contribute to the osteoarthritis pain and disease cycle.

Conversely, a diverse array of intervention approaches that focus on maximizing muscle structure and function appear advocated to potentially reduce the degree of excess muscle fat mass often noted in this population alongside pain, so as to foster desirable outcomes, regardless of joint site and disease severity.

Excess muscle fat may also impact outcomes of surgery to replace a diseased joint, stressing its importance. Applying what we do know towards primary prevention of injuries, and the adoption of active living rather than sedentary behaviors by many will however likely foster overall joint as well as general health, while helping to reduce enormous public health resource demands from depletion, even in the face of surgical solutions and especially among those in advanced disease stages. Key supportive approaches such as enabling sound dietary practices, electrical muscle stimulation, sensory motor and strength training, and Tai Chi, are likely to prove efficacious as well as safe for many in this regard.

To achieve optimal results, however, a role for cognitions cannot be ignored, given the fact that pain is widespread and fear and depression are readily provoked among those with osteoarthritis and severe pain. Additionally, cases need to be carefully educated as to the considerable care they must take however, to avoid overexertion, muscle fatigue, and repetitive movements, which can heighten muscle pain inputs and accelerate cartilage destruction, as well, as excess sedentary practices. Additional care and careful monitoring to avoid overstretching the joint, and helping those with severe overweight to lose weight is advocated as well. As well, avoiding high frequency loading activities after periods of immobilization found to hasten cartilage destruction is clearly of additional import.

At this point, and despite limitations of this review as well as the state of the research, it appears that while osteoarthritis continues to be described as both inevitable as well as incurable, this immensely painful disabling condition can be mediated or moderated by factors other than age or wear and tear. As such, based on cumulative and emergent evidence, it seems plausible to suggest that the osteoarthritis sufferer s wellbeing can be effectively mitigated if not reversed if efforts to minimize muscle fat invasion of vulnerable joints is forthcoming, especially if tailored to the overall health status and needs and abilities of the individual and supported by objective measures of muscle composition, force capacity, pain, cognitions, plus weight. In particular, to avert rapid or excess disease progression and disability, and its association with immense social and mobility-related losses, there appears to be an increasing body of research that supports the view that efforts to reduce muscle fat encroachment is a highly salient osteoarthritis disease mitigation strategy. Hence, even if not the key pathogenic cause of osteoarthritis, its prevention must be seen of paramount importance in minimizing osteoarthritic joint pain and dysfunction.

However, since this is by no means a universally accepted idea or practice, more studies that tease out the possible relationship between muscle factors and osteoarthritic pain along with central factors that affect pain and muscle fat encroachment are warranted. Carefully controlled intervention studies with larger samples with similar muscular and disease related characteristics conducted over extensive time periods utilizing a variety of possible interventions could prove insightful as well.

Presently, as per earlier studies, a recent study 66 that strove to characterize lower limb muscle quality in cases with knee osteoarthritis revealed an unanticipated associated of a higher degree of fat infiltration and lower normal-density in the hip muscles rather than the knee extensors (commonly targeted in isolation and thought to predominate the condition). It appears therefore that knee osteoarthritis cases may suffer in part due to associated altered levels of hip abductor and external rotator muscle metabolism alterations, including muscle fat deposition associations, rather than the knee extensors 70. Another that assessed muscle cross-sectional areas, echo intensity, and shear modulus in the knee muscles of 24 knee osteoarthritis cases and 24 controls indicated osteoarthritis muscle and strength losses, poor flexibility and increased passive tension, and possibly reductions in its contractile components and muscle force generating capacity that may accompany knee osteoarthritis 68. Another revealed high levels of intramuscular fat and poorer function than controls 41 with possible significant implications including pathological disease mechanisms, muscle strength, impaired muscle regeneration, and life quality outcomes 7172737475.

In short, although limited, current findings strongly highlight the degree to which muscle fat infiltration and/or enlargement may play a disabling role in the osteoarthritis disease cycle, as well fostering multiple levels of focal and systemic dysfunction, severe pain, and biomechanical and metabolic challenges. Moreover, a failure to appreciate and understand the importance of identifying, tracking, and examining muscle factors such as muscle fat mass in general in the realm of both osteoarthritis research and the design of optimal osteoarthritis rehabilitation plans and their scope and sequence may be shortsighted at best and warrants more careful study and one supported by possible AI diagnostics 31.