To clarify and examine the extent of support for the aforementioned premises, we attempted to locate salient data currently housed on PUBMED, GOOGLE SCHOLAR, and the WEB of SCIENCE repositories using the key terms, Osteoarthritis and Muscle/Neuromuscular Deficits. All modes of publication identified between the years 2017-2022 were deemed acceptable in this regard if they were published in English as full length reports and addressed the topic of interest from a pathogenic perspective rather than a reactive outcome perspective and regardless of methodological approaches. The most salient articles related to the current theme were duly downloaded and examined and those deemed somewhat new and noteworthy are highlighted here in narrative form. All modes of muscle dysfunction were accepted as valid, as were all definitions of osteoarthritis and their various manifestations. The article builds on previous works, thus was designed to serve as a general one to introduce the topic, as well as an update, rather than any systematic review. The goal was to present a descriptive snapshot of the prevailing trends in this realm and the potential of this construct for advancing osteoarthritis clinical understandings and preventive approaches. The article excluded post surgical observations and studies, as well as all intervention studies that have been reviewed elsewhere and studies in animal models of osteoarthritis.

The term neuromuscular deficit is used throughout to encompass or represent one or more muscle impairments including, but not limited to muscle imbalances, muscle activation deficits, poor muscle coordination, deficient muscle responsiveness, low muscle mass, muscle atrophy, muscle weakness and poor endurance, muscle spasm and inflammation, plus muscle fat cells and sarcopenia, as these may independently or interactively influence bone modeling, joint alignment and stability, especially impact loading. See Figure 1 below. 91011121314151617

Osteoarthritis, now considered a disease of the whole joint 1819 including muscle, is a topic of high interest among those seeking to better understand the etiology of the disease, plus potential remediable associations of its structural features with osteoarthritis risk or progression including malalignment, and lower muscle strength/quality 20.

To this end this narrative review examines some key findings regarding muscle and its inclusion as a potential osteoarthritis risk factor. The review draws on prior research and reviews, with a focus on new research and emerging topics reported since 2017, as well as seminal studies.

While aging is inevitable, increasing evidence suggests aging as a negative state does not have to be a foregone ordained experience of downward spiraling events and perceptions. This review explored the degree to which one or more muscle factors may be implicated in the pathology of osteoarthritis, a disabling disease, commonly believed to originate in the articular cartilage lining of one or more freely moving joints, and that affects the entire joint, including the associated muscles surrounding the joint. This brief highlights the research published in this respect since 2017, an area of research that is not well documented when compared to related studies of cell biology, tissue engineering, and molecular in vitro studies, among others. To this end, to update a prior analysis, PUBMED, GOOGLE SCHOLAR and the WEB of SCIENCEs indices were searched for information specifically regarding this topic using key words: Osteoarthritis and Muscle.

Among these studies, and bearing in mind, most were cross-sectional studies, based on knee osteoarthritis, these included a very broad array of thematic topics, rather than any uniform body of content. These topics included observations of how various forms of muscle dysfunction appear to interact with various forms of osteoarthritis pathology, various measures of pain, and various aspects of function, although very few tested any possible hypothesis that might prove revealing and most did not explore the underpinnings of the observed muscle alterations specifically. Others described the relationship between muscle power measures, the rates at which selected muscles contract 1562, muscle relaxation associated deficits and their association with the extent of the prevailing pathology 2363, and/or osteoarthritis disease progression 15, but not other overlapping factors, determinants of these impairments, or possible molecular or inflammatory joint associated influences.

However, since most results did not negate an important role for muscle in the osteoarthritic disease process, more carefully construed biomechanical, radiological, molecular, biochemical, and neuromuscular oriented prospective studies of adequate duration in the future may help to solidify the current observations, which at a minimum are supportive of a role for muscle strength as a salient remediable factor in the osteoarthritic disease process as outlined by others some time ago 6164. Newer research may also help to more clearly discern if muscle dysfunction may be a causative or pre existing, rather than a reactive disease factor 6566, as well as how several differing muscle factors are possibly associated with either the onset or progression of osteoarthritis at various joints.

In this regard, in addition to strength training, possible cited benefits that might accrue from other muscle oriented interventions, especially those cited below may prove revealing and should be examined in comparative studies to evaluate their possible impact on chondrogenic repair, muscle cell structures and mechanisms, and overall mobility, pain, and function 1217416667686970717273747576777879. Box 1

In short, contrary tothe enormous amount of available literature on osteoarthritis related topics of articular tissue biology, genetics, pharmacologic and surgical options for osteoarthritis, plus stem cell research and tissue bioengineering, where almost no singular approach has proven viable to date as either a preventive or treatment approach, a conceptual framework for guiding clinical practice remains elusive at best, but is one likely to fail if muscular factors are ignored.

Limitations to this review are its narrow focus, the sole use of three key data bases and not others and a lack of any systematic attempt to aggregate or critique the research approaches, that were deemed salient and their possible shortcomings. Moreover, not all articles may have been accessed or reported, and those that have may yet appear to support a muscle osteoarthritis association due to issues of publication bias, rather than the undoubted weight of the supportive evidence currently housed electronically in the world s leading data bases.

However, at the very least, and consistent with past reports 536474, the weight of the evidence and present results do appear to provide a reasonable body of current science based evidence that shows efforts to identify one or more possible attributes of muscle structure and/or function that may be subnormal in some way may well further our understanding of the etiology of some forms of osteoarthritis, as well as its tendency to flare or wax and wane, but ultimately to progress rather than undergo any disease reversal. Additionally, while not conclusive, a second feature is that a variety of alterations in muscle quality, function, metabolism, and/or estimates of muscle bulk or vibratory acuity, do appear to correlate temporally with selected features of the osteoarthritic pathological processes and extent of disability, regardless of age, even though long term studies and efforts to identify important muscle associated correlates are commonly lacking. Third, rather than exercise alone, multiple treatment approaches directed towards improving muscle structure and function in those with symptomatic osteoarthritis appear to hold promise for potentiating more favorable results than not. Conversely, a failure to identify what component of the muscle system may be specifically implicated in the osteoarthritis disease process may produce either null results or more negative clinical outcomes than not, for example if exercise induces fatigue.

Further research to examine the interaction of joint alignment, neurology, geometry, stability, and bone mass and the interplay of muscle metabolism, structure, mechanics and function on articular cartilage signaling mechanisms in a broad range of adults deemed at risk for osteoarthritis and that employ advanced biomechanical, electrophysiological, and imaging technologies is however strongly recommended in this regard. As well, as proposed by Becker et al. 65 in 2004, whether muscle dysfunction occurs not only at singular joint sites but represents a generalized presence of neuromuscular dysfunction is advocated as well. Examining the possible long term interactions of one or more neuromuscular attributes and the processes of joint attrition is also strongly warranted in this regard in our view, and could prove highly valuable in many spheres. In particular efforts to carefully explore the role of muscle mechanics and its mechanisms of control, and how one or more of these factors may interact with the multiple structural features of various joints affected by osteoarthritis is likely to prove insightful. Efforts to tease out the impacts of muscle on all joint structures affected by osteoarthritis, and particularly on cartilage content, genetics, molecular and structural organization features is also likely to prove of high clinical relevance and utility.

At the same time clinical efforts to examine the attributes of muscle strength, endurance, rate of force development, vibratory acuity, and possible inflammation and fat mass, along with muscle activation profiles, as well as sarcopenic indicators on the disease progression using advanced biological as well as biomechanical technologies is highly recommended in order to identify what interventions might be most helpful in retarding joint degenerative processes and why.