Journal of Aging Research And Healthcare

Journal of Aging Research And Healthcare

Journal of Aging Research and Healthcare

Current Issue Volume No: 4 Issue No: 2

Review Article Open Access Available online freely Peer Reviewed Citation

Osteoarthritis and Neuromuscular Deficits: Can a Causative Role be Discounted- Key 2017-2022 Observations

Ray Marks 1  

1Department of Health and Behavior Studies, Teachers College, Columbia University, NY 10027, United States.

Abstract

Background

The origin of osteoarthritis, the most common disabling disorder of older adults remains uncertain.

Aim

This mini review examines the possible role played by various neuromuscular deficits in the osteoarthritis etiopathogenic process.

Methods and Procedures

Articles that haveaddressed the current topic of interest and were located in the PUBMED,Google Scholar, and Web of Science electronic data bases as of 2017-2022 were carefully sought and examined.

Results

Various neuromuscular mechanisms may have a bearing on the development and progression of osteoarthritis, but the data are largely unrelated and observational in nature.

Conclusion

More research to examine this issue is sorely needed and could have considerable merit in light of the growing populations of older adults at risk for disabling osteoarthritis in the face of few intervention options to help them to achieve an optimal functional level.

Author Contributions
Received 12 May 2022; Accepted 16 May 2022; Published 18 May 2022;

Copyright ©  2022 Ray Marks.

License
Creative Commons License     This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Competing interests

The authors have declared that no competing interests exist.

Citation:

Ray Marks (2022) Osteoarthritis and Neuromuscular Deficits: Can a Causative Role be Discounted- Key 2017-2022 Observations. Journal of Aging Research And Healthcare - 4(2):31-45. https://doi.org/10.14302/issn.2474-7785.jarh-22-4191

Download as RIS, BibTeX, Text (Include abstract )

DOI 10.14302/issn.2474-7785.jarh-22-4191

Introduction and background to the problem

Osteoarthritis, involving the destruction of one or more freely moving body joints such as the knee and hip is the among the oldest and most common disabling disorders affecting older adults, as well as many animal species, avians, non weight bearing mammals and marine reptiles 1, 2, 3. A chronic inflammatory disease frequently associated with some form of biomechanical derangement, wherein the articular cartilage lining of the joint is progressively destroyed, the disease is one where little progress has been made to date to mitigate, prevent, or reverse this condition successfully, and safely, despite decades of research 4, 5, 6, 7.

In this regard, although opinions differ, attention to the possible interaction of neuromuscular mechanisms and osteoarthritis, and a host of biochemical, molecular, functional, epigenetic, inflammatory, and structural changes that are commonly progressive and irreversible and that was documented almost 40 years ago, still remains open for examination. A potentially promising line of inquiry, wherein a variety of abnormal neuromuscular mechanisms may fail to protect one or more joints from damage, but may be challenging to detect, this mini review elected to examine some of the key current findings and their implications as published over the last five years, with a focus on the current year 2022. Since quality of life may be severely jeopardized by chronic osteoarthritis of one or more joints, and pain accompanying this disease is often intractable and causes unwarranted opioid related deaths, it was believed line of inquiry would prove highly fruitful to examine.

Indeed, this idea of a muscle-osteoarthritis linkage is not novel, and contrary to the ‘wear and tear’ theory so long propounded to explain osteoarthritis pathology, it has been proposed for some time. Thus, today one can find more than 5000 articles dedicated to this topic posted on PUBMED alone. These data have shown that it is quite feasible to believe that various manifestations of neuromuscular function if subnormal are sufficient possibly salient explanatory factors in this regard, and are hence of great interest to unravel as they may hold unique insights, plus multiple noteworthy clinical implications, for example fostering drug delivery efficiency and targeting, and cartilage chondrocyte genomics, while heightening protection against excessive mechanically derived inflammation 6, 8.

Aims

In light of the importance of achieving optimal health for all, and enhancing wellness opportunities for older populations, this mini review sought to establish if there is solid evidence to support further research to examine neuromuscular deficits as these may impact osteoarthritis risk among the elderly, and if so, whether this information can help to mitigate some of the excess health burden that is being evidenced among the elderly in all parts of the globe, regardless of locality.

A parallel aim was to establish whether any attributes in particular if strengthened or intervened upon through the application of one or more related therapeutic approaches would be more efficacious than not, regardless of the older adult’s physical health and socioeconomic status. Many current premature deaths due to opioid use by osteoarthritis sufferers might also be impacted favorably.

Rationale and Relevance

By 2030, the numbers of older adults in the United States and elsewhere will soar. However, not all will age successfully, even if they have no distinctive co-morbid health condition. On the other hand, this rapidly increasing number of older adults will probably have high rates of chronic diseases, such as osteoarthritis, which may be barriers to the achievement of a fully functional life, even if this is not evidenced by all sufferers or all older adults. However, without some more insightful approaches that can be applied universally or individually, at low cost, and with no side effects, the principle and vision of ‘successful aging’ for all is likely to fail. In this regard, muscle mechanical and metabolic factors that commonly interact with the static and/or dynamic features of a joint and that may be undermined in some way, can possibly be important to examine and mitigate or remediated in the context of osteoarthritis onset and progression.

Materials and Methods

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. 9, 10, 11, 12, 13, 14, 15, 16, 17

Figure 1.Schematic representation of some anticipated muscular abnormalities and their impacts and outcomes in the presence of muscle weakness and other forms of muscle dysfunction coupled with the absence of efforts to identify and mitigate these attributes specifically and in a targeted manner Adapted from references 9
Schematic representation of some anticipated muscular abnormalities and their impacts and outcomes in the presence of muscle weakness and other forms of muscle dysfunction coupled with the absence of efforts to identify and mitigate these attributes specifically and in a targeted manner Adapted from references 9

Osteoarthritis, now considered a disease of the whole joint 18, 19 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.

Search Results

As of April 30, 2022 there were 1993 articles listed in PUBMED and classified as representing the combined themes of muscle and osteoarthritis. Of these listings, 1156 tended to focus on knee osteoarthritis and muscle factors, 425 on hip osteoarthritis and muscle, and 144 on hand osteoarthritis and muscle as documented over the years of current interest of 2017-2022. Other joints studied sporadically in the past five years in this regard included those of the foot, ankle, mandible, and spine.Yet, in spite of these fairly robust publication numbers, as with prior analyses of this topic of muscle and osteoarthritis by previous authors, a topic studied since 1929, most currently cited citations failed to examine one or more muscle factors as a potential osteoarthritis determinant in the preclinical or early osteoarthritis realm, and the majority of the listed works tended to explore the execution of various exercise interventions, the examination of limited varieties of possible muscle deficits in isolation relative to established osteoarthritis and with no conclusion concerning any cause-effect association being reached. Data listed on GOOGLE SCHOLARand the WEB OF SCIENCE were largely duplicates and repetitive in this regard.

In examining the prevailing data in more detail, and despite a lack of any current emergent uniform set of conclusions, it appeared most authors who examined one or more neuromuscular attributes among various manifestations of osteoarthritic as well as healthy joints, do tend to agree that one or more neuromuscular abnormalities can be quite consistently observed in the realm of osteoarthritis pathology, and that muscle status may have a bearing on one or more osteoarthritis disease features such as cartilage and bone attrition, synovial inflammation, joint instability, pain, and functional deficits.

At the knee, the most well studied joint, multiple authors have indeed observed muscle strength deficits, problems in voluntary muscle activation, muscle mass or volume declines/deficits, deficits in muscle flexibility, excessive muscle tone, generalized muscle weakness of the affected limb, muscle endurance losses, muscle power and force control ability 21, 22, 23, 24, 25, 26, 27, 28. Along with associated alterations in neuromuscular communication processes one or more of these attributes may be instrumental in inducing various molecular and cellular adaptations within both muscle as well as cartilage tissues that further provoke pathological joint changes 29, while altering dynamic joint stability that appears to impact osteoarthritis progression 28.

Other data reveal that cases diagnosed as having symptomatic mid-foot osteoarthritis, a less well studied topic, are also found to exhibit weakness of the foot and leg muscles when compared to those of asymptomatic controls 30, while cases with hip osteoarthritis reportedly exhibited atrophic, bilateral hip and knee muscle weakness and volume deficits that were not evident in control subjects 13, 14, wherein the most seriously affected muscles may surprisingly be the knee extensor muscles 22. At the temporomandibular joint site, osteoarthritis is also possibly influenced by muscle imbalances among other factors, thus suggesting the role of muscle in joint attrition is a possible generalizable finding, rather than solely an isolated or spurious one 31.

Studies also show the presence of age-associated muscle mass losses may engender both the onset or degree of disability associated with knee osteoarthritis 32, including a decline in the rate of muscle force development 33, while knee muscle weakness may have a role to play in mediating radiographic osteoarthritic changes, especially in women who are obese 23, as well as pain 34 and falls injuries that may lead to joint damage 11. Carvalho et al. 35 show cases with patella femoral osteoarthritis exhibited impairments regarding muscle capacity of the hip and knee, higher level of pain and stiffness as well as compromised physical functioning in comparison with healthy controls, while Andrews et al. 36 concluded that measures of grip strength declines may incrementally induce osteoarthritic joint changes at the knee joint, as well as knee pain among men.

Other data indicate that muscle asymmetries from side to side as well as between muscle groups may also have a bearing on lower limb biomechanics and hence the degree of prevailing knee osteoarthritis 37, 38. The pathogenic role of muscle co contraction abnormalities and their impact on joint biomechanics as this pertains to osteoarthritis pathology has also been discussed 39 as has the fact that the presence of osteoarthritis may indeed affect muscle strength adversely and significantly, even if it is not a causative factor 40.

Additional research, albeit currently non-conclusive, also supports a role for muscle wasting 17, 29, 41, 42, neuromuscular deficits 43, and muscle activation abnormalities 44 that might tentatively be remediated through carefully construed intervention 12, 45. Other newer findings reveal a role for multiple muscular attributes in the osteoarthritis disability cycle including the possible combined influence of a related musculo-osteo-arthro-neuropathic syndrome that may underscore the discomfort and pain associated with the osteoarthritic condition, and that warrants a holistic treatment approach 46. Other data are portrayed in Table 1.

Table 1. Sample of key findings published in 2022 selected at random to depict the spectrum of findings in relationship to the interaction of muscle and osteoarthritis pathology.
ATTTRIBUTE ASSESSED KEY FINDINGS RESEARCH GROUP
Knee muscles There was a positive correlation between vastus lateralis stiffness measures and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores in patients with knee osteoarthritis compared with healthy, asymptomatic subjects Chang et al. 24
Skeletal muscle molecular attributes Muscle inflammatory and molecular catabolic gene expression attributes associated with end-stage osteoarthritis differ between the contralateral and surgical limbs as well as between the skeletal muscle surrounding the diseased hip versus knee joints Drummer et al. 47
Knee muscles Higher quadriceps and hamstring forces suggest that co-contraction with the gastrocnemius could lead to higher joint contact forces

Combined with the excessive loading due to a high external knee adduction moment this may exacerbate joint destruction		 Ghazwan et al. 39
Hamstring muscles The hamstring shear modulus measures were significantly higher in the knee osteoarthritis group than in the control group

The hamstring shear modulus in the osteoarthritis group was moderately positively correlated with pain, shear modulus, and physical function score		 Li et al. 25
Glenohumeral muscles Patients with eccentric glenoid wear in the setting of primary glenohumeral osteoarthritis and an intact rotator cuff appear to have both larger posterior rotator cuff musculature and higher rates of infraspinatus fatty infiltration

Although the temporal and causal relationships of these associations remain ambiguous, muscle atrophy and fatty infiltration should be considered 2 discrete processes in the natural history of glenohumeral osteoarthritis		 Moveman et al. 48
Knee extensor muscle strength There is low quality evidence that knee extensor muscle weakness is associated with incident symptomatic and radiographic knee osteoarthritis in women and men

Optimising knee extensor muscle strength may help to prevent knee osteoarthritis		 Oiestad et al. [ 16 ]
Knee muscles Altered neuro-muscular control around knee interferes with normal load distribution and facilitates osteoarthritis disease progression in knee joint Sharma et al. 49
Hand muscles In the early stages of hand osteoarthritis, there is a functional deficit associated with a reduced muscle activity of the wrist muscles during manual activities Tossini et al. 50
Vastus medialis muscle Muscle weakness is associated with non-contractile muscle tissue of the vastus medialis muscle in knee osteoarthritis Van den Noort et al. 51
Aged/damaged muscle cells Muscle cellular senescence may contribute to abnormal osteoarthritis signaling pathways, sarcopenia, excess mechanical exposure to trauma, osteoarthritis initiation and progression Wu et al. 41
Knee extensors Knee osteoarthritis patients have lower maximal knee extension strength, but intermuscle group differences prevail, but both are associated with cartilage thickness measures and perceived pain Yagi et al. 52

In addition to those studies depicted in Table 1, adding to the diversity of information retrieved is the fact that, as with prior research 53, almost all additional studies reviewed employed differing osteoarthritis samples, research questions, assessment approaches, and durations, and even if a similar variable or idea was examined, basically no two conclusions were alike. Indeed, some reported associations between reduced rates of torque development and osteoarthritis features, while others noted a propensity for fat cells in muscle to increase the risk for osteoarthritis [see Figure 1]. Yet, others noted the importance of abnormal dynamic muscular force adaptations, afferent sensory dysfunction, along with diminished strength capacity, co-ordination impairments, and problems with reduced muscle endurance.

Loureiro et al. 26 conclude, pre-existing deficits in hip muscle strength in individuals with mild-to-moderate hip osteoarthritis do appear to be accentuated over a 12-month period, despite a lack of any parallel changes in symptoms or joint structure measures. According to their synthesis of the literature, Tayfur et al. 27 found neuromuscular deficits to be consistently evident across different structural knee osteoarthritis severities including those of muscle strength, voluntary activation, muscle size, and force control ability, wherein women have tended to exhibit these alterations to a greater extent than men. Ghazwan et al. 39 note the possible role of an increased lateral muscle co-contraction in mediating hip joint osteoarthritis progression, whereas an increased medial muscle co-activation could potentially differentiate between whether osteoarthritis affects one- or more joint compartments in their view. As well, Lijema et al. 54 report that their recent findings of an increased medio-lateral trunk movement asymmetry in adults with knee osteoarthritis may be an indicator of impairment, rather than an adaptation. While requiring validation by future study, these authors argue that paying close attention to medio-lateral trunk movement asymmetry may be key to our understanding of osteoarthritis-related pain and disability. However, a longer follow-up period is clearly required to establish whether muscular factors do drive clinical and structural declines in these patients, as well as whether interventions to prevent or slow such abnormalities or declines may be relevant in the management of osteoarthritis.

In the interim-as outlined above, consistent with the view that osteoarthritis may result from a number of different interrelated factors and is not merely a disease of a single tissue 55, muscular differences do appear to discriminate osteoarthritic muscle patterns from those of controls 44, 56, and to thereby possibly influence or explain the severity of the observed osteoarthritis manifestations 56. Moreover, while not necessarily comprehensive, those observations depicted in Table 1, and others further indicate a variety of muscle impairments may well differ among muscles of the same individual at both the early, as well as the later stages of osteoarthritis, as well as in muscles unrelated to the diseased joint, hence the possibility that some cases of osteoarthritis represent the outcome of a clinical neuromuscular set of subnormal mechanisms cannot be ignored. Lee et al. 57 who found leg muscle asymmetry patterns in men with knee osteoarthritis, regardless of obesity level, showed these patterns to be significantly associated with both knee pain as well as radiographic indicators of osteoarthritis severity. Lower limb strength asymmetry has been associated with increased odds of secondary osteoarthritic development, with a 1% increase in quadriceps symmetry resulting in a 4% lower odds of developing clinical osteoarthritis 58. Bird et al. 59 note hip abductor muscle quality and hip osteoarthritis to be related, while Drummer et al. 60 found evidence of differential inflammatory and catabolic gene expression between the contra lateral and surgical limbs along with differences between the skeletal muscles surrounding the diseased hip versus knee joints.

As such, these aforementioned muscle abnormalities clearly indicate that they may well have considerable independent as well as collective influence on joint status, including, but not limited to, multiple forms of strength loss and aberrant motor control attributes, pathological alterations in muscle molecular mechanisms and muscle structure, muscle temporal and contractile characteristics, muscle proprioception and fat content, plus muscle imbalances. However, even though it appears neuromuscular factors are being more accepted as possible osteoarthritis pathogenic determinants 61, which attributes are of specific clinical relevance, or of greatest import in the context of different phases of the disease process and a variety of joint sites remains impossible to discern with any clarity. Indeed, the lack of uniformity in cohorts studied, the unknown effects of age, weight, health and comorbid disease effects, differing research designs and questions, and small samples, along with confusion as to whether muscle strength or muscle balance or muscle power is a salient variable, and if so, in what way-precludes any meaningful synthesis of this research even though considerable recent research prevails. Moreover, even with prospective analyses, which are more supportive of a temporal relationship of the muscle and joint disturbances than not, attempts to isolate sub categories of muscle dysfunction for purposes of a systematic analysis persist in remaining extremely challenging at best to aggregate, because keywords selected to describe a specific topic, do not always comport with or yield the desired data. As well, which if any of the muscle function assays represent protective reactions, rather than pathological correlates or adaptations, is also impossible to discern with any clarity at the present time.

Discussion

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 15, 62, muscle relaxation associated deficits and their association with the extent of the prevailing pathology 23, 63, 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 61, 64. 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 65, 66, 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 12, 17, 41, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79. Box 1

Box 1. Selected approaches other than exercise that might be examined more specifically in diverse populations of adults of a broad spectrum of ages as regards their preventive, maintenance, and disability reducing capacity. Key Sources: (12, 17, 41, 67-79)
Electrical Muscle Stimulation
Exercise + Minimally Invasive Injection Therapy
Graded Motor Imagery and Muscle Relaxation
Kinesio Taping
Local Muscle Vibration
Minimize Sarcopenia
Modulation of Muscle Micro RNAs
Muscle Stretching and Low Level Laser
Neuromuscular Training
Strategies to Counter Muscle Cell Senescence
Pequi Oil Applications
Proprioceptive Training
Protein Supplements
Whole Body Vibration and Strengthening Exercises

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 53, 64, 74, 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.

Conclusion

While not conclusive, in light of many current innovative findings and years of collective and current research, we conclude a case for rejecting muscle as an important osteoarthritis determinant cannot be advanced.

We further conclude:

1. At least some osteoarthritis sufferers may well have underlying muscle related impairments that may be challenging to detect or unrecognized and diagnosed.

2. Varying muscular deficits do appear to prevail for some considerable duration in many osteoarthritis cases post surgery, despite pain relief and successful surgery, thus may have been present pre-clinically.

3. Muscle deficits may occur in both limbs even in the case of a unilateral disease diagnosis and in non traumatic cases.

4. Aging does not explain why some older adults with normal muscle function do not exhibit osteoarthritis degeneration and implies more attention to muscular factors and their specific remediation, versus generic based approaches, are indeed urgently indicated.

5. To establish how these facts interconnect at the development of osteoarthritis, as well as its progression and to apply this knowledge in a carefully and insightfully targeted manner consistent with chondrocyte physiology is a realm of great promise for many in our view and is strongly advocated.

Indeed, despite a lack of consensus on the evolutionary impact of neuromuscular mechanisms on osteoarthritis, we conclude further insightful and carefully designed research may prove highly valuable in explicating those muscular mechanisms that may yet impact the immense disability associated with unrelieved osteoarthritis.

References

  1. 1.Gardner D L. (1983) The nature and causes of osteoarthrosis. , BMJ 286(6363), 418.
  1. 2.Rothschild B M, Xiaoting Z, Martin L D. (2012) Osteoarthritis in the early avian radiation: Earliest recognition of the disease in birds. , Cretaceous Res 35, 178-80.
  1. 3.Rothschild B M, Woods R J. (2012) Epidemiology and biomechanics of osteoarthritis. Principles of Osteoarthritis–Its Definition, Character, Derivation and Modality-Related Recognition. 22, 3-24.
  1. 4.O'Neill T W, McCabe P S, McBeth J. (2018) Update on the epidemiology, risk factors and disease outcomes of osteoarthritis. , Best Pract Res Clin Rheumatol 32(2), 312-326.
  1. 5.Sacitharan P K. (2019) Ageing and osteoarthritis. , Subcell Biochem 91, 123-159.
  1. 6.Reynard L N, Barter M J. (2020) Osteoarthritis year in review 2019: genetics, genomics and epigenetics. , Osteoarthritis Cartilage 28(3), 275-284.
  1. 7.Birrell F, Johnson A. (2022) The tear, flare, and repair model of osteoarthritis. , BMJ. Apr 26-377.
  1. 8.Wang Z, Wang S, Wang K, Wu X, Tu C et al. (2021) Stimuli-sensitive nanotherapies for the treatment of osteoarthritis. , Macromol Biosci 21(11), 2100280.
  1. 9.Al-Mahrouqi M M, MacDonald D A, Vicenzino B, Smith M D. (2018) Physical impairments in adults with ankle osteoarthritis: A systematic review and meta-analysis. , J Orthop Sports Phys Ther 48(6), 449-459.
  1. 10.Aydemir B, Huang C H, Foucher K C. (2022) Strength and physical activity in osteoarthritis: The mediating role of kinesiophobia. , J Orthop Res 40(5), 1135-1142.
  1. 11.Ikutomo H, Nagai K, Tagomori K, Miura N, Nakagawa N et al. (2019) Incidence and risk factors for falls in women with end-stage hip osteoarthritis. , J Geriatr Phys Ther 42(3), 161-166.
  1. 12.Hatfield G L, Costello K E, Astephen Wilson JL, Stanish W D, Hubley-Kozey C L. (2021) Association between knee joint muscle activation and knee joint moment patterns during walking in moderate medial compartment knee osteoarthritis: Implications for secondary prevention. Arch Phys Med Rehabil. 102(10), 1910-1917.
  1. 13.Krishnasamy P, Hall M, Robbins S R. (2018) The role of skeletal muscle in the pathophysiology and management of knee osteoarthritis. , Rheumatol (Oxford) 57(4), 22-33.
  1. 14.Loureiro A, Constantinou M, Diamond L E, Beck B, Barrett R. (2018) Individuals with mild-to-moderate hip osteoarthritis have lower limb muscle strength and volume deficits. , BMC Musculoskelet Disord 19(1), 303-10.
  1. 15.Suzuki Y, Iijima H, Nakamura M, Aoyama T. (2022) Rate of force development in the quadriceps of individuals with severe knee osteoarthritis: A preliminary cross-sectional study. , PloS One 17(1), 0262508.
  1. 16.Øiestad B E, Juhl C B, Culvenor A G, Berg B, Thorlund J B. (2022) Knee extensor muscle weakness is a risk factor for the development of knee osteoarthritis: An updated systematic review and meta-analysis including 46 819 men and women. , Br J Sports Med 56(6), 349-355.
  1. 17.Shorter E, Sannicandro A J, Poulet B, Goljanek-Whysall K. (2019) Skeletal muscle wasting and its relationship with osteoarthritis: A mini-review of mechanisms and current interventions. Curr Rheumatol Rep. 21(8), 40.
  1. 18.Chen D, Shen J, Zhao W, Wang T, Han L et al. (2017) Osteoarthritis: Toward a comprehensive understanding of pathological mechanism. , Bone Res 5, 16044.
  1. 19.Man G S, Mologhianu G. (2014) Osteoarthritis pathogenesis–a complex process that involves the entire joint. , J Med and Life 7(1), 37.
  1. 20.Allen K D, Thoma L M, Golightly Y M. (2022) Epidemiology of osteoarthritis. , Osteoarthritis and Cartilage 30(2), 184-195.
  1. 21.Burgess L C, Taylor P, Wainwright T W, Swain I D. (2021) Strength and endurance deficits in adults with moderate-to-severe hip osteoarthritis, compared to healthy, older adults. Disabil Rehabil. 22, 1-8.
  1. 22.Bieler T, Magnusson S P, Christensen H E, Kjaer M, Beyer N. (2017) Muscle power is an important measure to detect deficits in muscle function in hip osteoarthritis: A cross-sectional study. , Disabil Rehabil 39(14), 1414-1421.
  1. 23.Culvenor A G, Felson D T, Niu J, Wirth W, Sattler M et al. (2017) Thigh muscle specific-strength and the risk of incident knee osteoarthritis: The influence of sex and greater body mass index. Arthritis Care Res (Hoboken). 69(8), 1266-1270.
  1. 24.Chang T T, Zhu Y C, Li Z, Li F, Li Y P et al. (2022) Modulation in the stiffness of specific muscles of the quadriceps in patients with knee osteoarthritis and their relationship with functional ability. , Front Bioeng Biotechnol 9, 781672.
  1. 25.Li F, Wang Z Y, Zhang Z J, Shen S H, Guo J Y et al. (2022) In hamstring muscles of patients with knee osteoarthritis an increased ultrasound shear modulus indicates a permanently elevated muscle tonus. Front Physiol. 202212, 752455.
  1. 26.Loureiro A, Constantinou M, Beck B, Barrett R S, Diamond L E. (2019) A 12-month prospective exploratory study of muscle and fat characteristics in individuals with mild-to-moderate hip osteoarthritis. , BMC Musculoskelet Disord 20(1), 283.
  1. 27.Tayfur B, Charuphongsa C, Morrissey D, Miller S C. (2022) Neuromuscular joint function in knee osteoarthritis: A systematic review and meta-analysis. Ann Phys Rehabil Med. 101662.
  1. 28.Xu C, Nie Y, Tan C, Zeng Y, Si H et al. (2022) Role of lower limb muscle strength in knee osteoarthritis progression for patients with mild and moderate knee osteoarthritis. , Am J Phys Med Rehabil 101(5), 433-438.
  1. 29.F De Ceuninck, Fradin A, Pastoureau P. (2014) Bearing arms against osteoarthritis and sarcopenia: When cartilage and skeletal muscle find common interest in talking together. Drug Discov Today. 19(3), 305-311.
  1. 30.Arnold J B, Halstead J, Grainger A J, Keenan A M, Hill C L et al. (2021) Foot and leg muscle weakness in people with midfoot osteoarthritis. , Arthritis Care Res (Hoboken) 73(6), 772-780.
  1. 31.Matsumoto R, Ioi H, Goto T K, Hara A, Nakata S et al. (2010) Relationship between the unilateral TMJ osteoarthritis/osteoarthrosis, mandibular asymmetry and the EMG activity of the masticatory muscles: A retrospective study. , J Oral Rehabil 37(2), 85-92.
  1. 32.Veronese N, Stefanac S, Koyanagi A, Al-Daghri N M, Sabico S et al. (2021) Lower limb muscle strength and muscle mass are associated with incident symptomatic knee osteoarthritis: A longitudinal cohort study. , Front Endocrinol (Lausanne) 12, 804560.
  1. 33.Ventura A, Muendle B, Friesenbichler B, Casartelli N C, Kramers I et al. (2019) Deficits in rate of torque development are accompanied by activation failure in patients with knee osteoarthritis. , J Electromyogr Kinesiol 44, 94-100.
  1. 34.Cheon Y H, Kim H O, Suh Y S, Kim M G, Yoo W H et al. (2017) Relationship between decreased lower extremity muscle mass and knee pain severity in both the general population and patients with knee osteoarthritis: Findings from the KNHANES V1-2. PLoS One. 12(3), 0173036.
  1. 35.Carvalho C, Serrão F V, Mancini L, PRMDS Serrão. (2021) Impaired muscle capacity of the hip and knee in individuals with isolated patellofemoral osteoarthritis: A cross-sectional study. Ther Adv Chronic Dis. 12, 20406223211028764.
  1. 36.Andrews J S, Gold L S, Nevitt M, Heagerty P J, Cawthon P M. (2021) Appendicular lean mass, grip strength, and the development of knee osteoarthritis and knee pain among older adults. , ACR Open Rheumatol 3(8), 566-572.
  1. 37.Chen Z, Ye X, Shen Z, Wang Y, Wu Z et al. (2021) Comparison of the asymmetries in foot posture and properties of gastrocnemius muscle and achilles tendon between patients with unilateral and bilateral knee osteoarthritis. , Front Bioeng Biotechnol 9, 636571.
  1. 38.Espinosa S E, Costello K E, Souza R B, Kumar D. (2020) Lower knee extensor and flexor strength is associated with varus thrust in people with knee osteoarthritis. , J Biomech 107, 109865.
  1. 39.Ghazwan A, Wilson C, Holt C A, Whatling G M. (2022) Knee osteoarthritis alters peri-articular knee muscle strategies during gait. PLoS One. 17(1), 0262798.
  1. 40.Hirschmüller A, Andres T, Schoch W, Baur H, Konstantinidis L et al. (2017) Quadriceps strength in patients with isolated cartilage defects of the knee: Results of isokinetic strength measurements and their correlation with clinical and functional results. , Orthop J Sports Med 5(5), 2325967117703726.
  1. 41.Wu C J, Liu R X, Huan S W, Tang W, Zeng Y K et al. (2022) Senescent skeletal cells cross-talk with synovial cells plays a key role in the pathogenesis of osteoarthritis. , Arthritis Research & Therapy 24(1), 1-7.
  1. 42.Jeon H, Lee S U, Lim J Y, Chung S G, Lee S J et al. (2019) Low skeletal muscle mass and radiographic osteoarthritis in knee, hip, and lumbar spine: A cross-sectional study. Aging Clin Exp Res. 31(11), 1557-1562.
  1. 43.Astephen J L, Deluzio K J, Caldwell G E, Dunbar M J, Hubley-Kozey C L. (2008) Gait and neuromuscular pattern changes are associated with differences in knee osteoarthritis severity levels. , J Biomechanics 41(4), 868-876.
  1. 44.Rutherford D, Baker M, Wong I, Stanish W. (2017) The effect of age and knee osteoarthritis on muscle activation patterns and knee joint biomechanics during dual belt treadmill gait. , J Electromyogr and Kinesiol 34, 58-64.
  1. 45.Marks R, Allegrante J P. (2005) Chronic osteoarthritis and adherence to exercise: a review of the literature. , J Aging and Phys Activity 13(4), 434-460.
  1. 46.Kalra S, Kumar V, Kapoor N. (2022) The MOAN (Musculo-Osteo-Arthro-Neuropathic) syndrome. , J Pak Med Assoc 72(2), 373-374.
  1. 47.Drummer D J, McAdam J S, Seay R, Aban I, Lavin K M et al. (2022) Perioperative assessment of muscle inflammation susceptibility in patients with end-stage osteoarthritis. , J Appl Physiol 132(4), 984-994.
  1. 48.Moverman M A, Puzzitiello R N, Menendez M E, Pagani N R, Hart P A et al. (2022) Rotator cuff fatty infiltration and muscle atrophy: relation to glenoid deformity in primary glenohumeral osteoarthritis. , J Shoulder and Elbow Surg 31(2), 286-93.
  1. 49.Sharma S K, Yadav S L, Singh U, Wadhwa S. (2017) Muscle activation profiles and co-activation of quadriceps and hamstring muscles around knee joint in Indian primary osteoarthritis knee patients. J Clin Diagn Res. 11(5), 09-14.
  1. 50.Tossini N B, Lessi G C, Simões Zacharias AL, GR Corrêa E Silva, ALS Seraphim et al. (2021) Impairment of electrical activation of wrist flexor and extensor muscles during gripping and functional activities in the early stage of hand osteoarthritis: A cross-sectional study. J Hand Ther. 34(1), 109-115.
  1. 51.JC van den Noort, Leeden M van der, Stapper G, Wirth W, Maas M et al. (2022) Muscle weakness is associated with non-contractile muscle tissue of the vastus medialis muscle in knee osteoarthritis. , BMC Musculoskeletal Disorders 23(1), 1-0.
  1. 52.Yagi M, Taniguchi M, Tateuchi H, Hirono T, Yamagata M et al. (2022) Relationship between individual forces of each quadriceps head during low-load knee extension and cartilage thickness and knee pain in women with knee osteoarthritis. , Clin Biomechan 91, 105546.
  1. 53.Marks R. (2017) Muscle and osteoarthritis joint status: Current research highlights and their implications. , SM J Orthop 3(1), 1050.
  1. 54.Iijima H, Eguchi R, Aoyama T, Takahashi M. (2019) Trunk movement asymmetry associated with pain, disability, and quadriceps strength asymmetry in individuals with knee osteoarthritis: a cross-sectional study. Osteoarthritis and Cartilage. 27(2), 248-256.
  1. 55.Brandt K D, Radin E L, Dieppe P A, Putte L Van De. (2006) Yet more evidence that osteoarthritis is not a cartilage disease. Ann Rheum Dis. 65(10), 1261-1264.
  1. 56.Zacharias A, Pizzari T, English D J, Kapakoulakis T, Green R A. (2016) Hip abductor muscle volume in hip osteoarthritis and matched controls. Osteoarthritis and Cartilage. 24(10), 1727-35.
  1. 57.Lee J Y, Han K, Park Y G, Park S H. (2019) Association of leg muscle symmetry with knee osteoarthritis. Clinical Rheumatology. 38(12), 3549-3556.
  1. 58.Halliwell C J, Moyer R. (2022) Association of lower limb strength asymmetries with stair ambulatory pain in individuals with or at risk for knee oa: data from the osteoarthritis initiative. Osteoarthritis and Cartilage. 30-133.
  1. 59.Bird A, Pedoia V, Majumdar S, Souza R B. (2022) Hip abductor muscle quality is associated with disease severity in individuals with hip osteoarthritis. , Osteoarthritis and Cartilage 30, 132-133.
  1. 60.Drummer D J, McAdam J S, Seay R, Aban I, Lavin K M et al. (2022) Perioperative assessment of muscle inflammation susceptibility in patients with end-stage osteoarthritis. J Appl Physiol.
  1. 61.Jackson B D, Wluka A E, Teichtahl A J, Morris M E, Cicuttini F M. (2004) Reviewing knee osteoarthritis—a biomechanical perspective. , J Sci Med Sport 7(3), 347-357.
  1. 62.Callahan D M, Tourville T W, Slauterbeck J R, Ades P A, Stevens-Lapsley J et al. (2015) Reduced rate of knee extensor torque development in older adults with knee osteoarthritis is associated with intrinsic muscle contractile deficits. , Exp Gerontol 72, 16-21.
  1. 63.arabon N, Čeh T, Kozinc Ž, Smajla D. (2020) Adapted protocol of rate of force development and relaxation scaling factor for neuromuscular assessment in patients with knee osteoarthritis. , The Knee 27(6), 1697-707.
  1. 64.Herzog W, Longino D. (2007) The role of muscles in joint degeneration and osteoarthritis. , J Biomech. 40 Suppl 1-54.
  1. 65.Becker R, Berth A, Nehring M, Awiszus F. (2004) Neuromuscular quadriceps dysfunction prior to osteoarthritis of the knee. , J Orthop Res 22(4), 768-773.
  1. 66.Noehren B, Kosmac K, Walton R G, Murach K A, Lyles M F et al. (2018) Alterations in quadriceps muscle cellular and molecular properties in adults with moderate knee osteoarthritis. , Osteoarthritis Cartilage 26(10), 1359-1368.
  1. 67.Barati K, Esfandiari E, Kamyab M, Ebrahimi Takamjani I, Atlasi R et al. (2021) The effect of local muscle vibration on clinical and biomechanical parameters in people with knee osteoarthritis: A systematic review. , Med J Islam Repub Iran 35, 124.
  1. 68.Cantero-Téllez R, Pérez-Cruzado D, Villafañe J H, García-Orza S, Naughton N et al. (2022) The effect of proprioception training on pain intensity in thumb basal joint osteoarthritis: A randomized controlled trial. , Int J Environment Res Publ Hlth 19(6), 3592.
  1. 69.Chen Guang QI, Chun Sing CH, Simon. (2022) Kwoon Ho CH, Wing-Hoi Cheung Rm. , J Rehabil Med 54.
  1. 70.Dharmakulsakti P, Roopsawang I, Aree-Ue S. (2022) Sarcopenia among older adults with knee osteoarthritis: A cross-sectional study of prevalence and its associated factors. , Pacific Rim Int J Nurs Res 26(1), 125-138.
  1. 71.R de Faro Silva, Barreto A S, Trindade G D, Lima C M, AA de Souza Araújo et al. (2022) Enhancement of the functionality of women with knee osteoarthritis by a gel formulation with Caryocar coriaceum Wittm (“Pequi”) nanoencapsulated pulp fixed oil. , Biomed & Pharmacother 150, 112938.
  1. 72.Gurudut P, Jaiswal R. (2022) Comparative effect of graded motor imagery and progressive muscle relaxation on mobility and function in patients with knee osteoarthritis: A pilot study. Altern Ther Health Med. 28(3), 42-47.
  1. 73.Klika A K, Yakubek G, Piuzzi N, Calabrese G, Barsoum W K et al. (2022) Neuromuscular electrical stimulation use after total knee arthroplasty improves early return to function: a randomized trial. , J Knee Surg 35(01), 104-111.
  1. 74.Noh H M, Choi Y H, Lee S K, Song H J, Park Y S et al. (2022) Association between dietary protein intake, regular exercise, and low back pain among middle-aged and older korean adults without osteoarthritis of the lumbar spine. , J Clin Med 11(5), 1220.
  1. 75.Robbins S R, Alfredo P P, Junior W S, Marques A P. (2022) Low-level laser therapy and static stretching exercises for patients with knee osteoarthritis: A randomised controlled trial. Clin Rehabil. 36(2), 204-213.
  1. 76.Sims K. (1999) The development of hip osteoarthritis: implications for conservative management. , Manual Therapy 4(3), 127-135.
  1. 77.Mao H Y, Hu M T, Yen Y Y, Lan S J, Lee S D. (2021) Kinesio taping relieves pain and improves isokinetic not isometric muscle strength in patients with knee osteoarthritis-a systematic review and meta-analysis. , Int J Environ Res Public Health 18(19), 10440.
  1. 78.Tognolo L, Maccarone M C, S De Trane, Scanu A, Masiero S et al. (2022) Therapeutic exercise and conservative injection treatment for early knee osteoarthritis in athletes: a scoping review. , Medicina 58(1), 69.
  1. 79.Zeng C Y, Zhang Z R, Tang Z M, Hua F Z. (2021) Benefits and mechanisms of exercise training for knee osteoarthritis. , Front Physiol 12, 794062.

Cited by (1)

  1. 1.Cloninger C. Robert, Cloninger Kevin M., 2016, , , (), 247, 10.1007/978-3-319-39724-5_19