Findings

In terms of the topic specifically sought, it is safe to say most listed publications that initially appeared potentially relevant did not meet the desired criteria for this review that excluded invasive intervention discussions, diagnostic imagery studies, proposals for study or studies on other forms of shoulder dysfunction other than rotator cuff lesions. Moreover, among those deemed relevant, few were based on prospective or targeted studies of the older adult with forms of osteoarthritis other than the knee and hip and even then these were predominantly observational studies conducted with varied measurement tools, diverse imaging approaches, timing and samples. These were also generally non uniform in multiple design respects, exploratory or atheoretical, not necessarily commensurate with the human condition or only in the proposal rather than assessment stage. Bearing all the above limitations three categories of publication emerged as follows.

1. General observations: As outlined in increasing numbers of global reports the aging population and their common declines in wellbeing and challenges including those due to osteoarthritis remain a foremost public health issue seeking resolution. In this regard, past research shows that many aging adults who have a high risk of incurring sarcopenia and related muscle mass and strength declines often go on to manifest severe osteoarthritis, but this is not the only determinant. A disease with enormous disabling features in its own right, health conditions such as sarcopenic obesity, where lean muscle mass is replaced by fat mass, many with painful disabling osteoarthritis, as well as direct or chronic injuries are also potential factors. Others include obesity, chronic pain and often a reluctance to exercise even if advocated. The muscles around an osteoarthritic joint may undergo multiple degenerative features that also have a bearing on the emergent movement patterns, for example at the diseased shoulder joint pervasive mixotrauma incidents may induce intrinsic muscle fat impact alterations that perpetuate muscle dysfunction and pathology [11].
2. Muscle fat mass observations: Increasing numbers of studies confirm muscle fat deposition or infiltration may be a potent osteoarthritis disease muscle mediator [eg., 21-24]. Indeed, while neither well documented, nor universally applied to a degree commensurate with its possible diverse pathogenic disease ramifications, attributes and associations, shoulder muscle abnormalities potentially explain and may predict diverse aspects of the shoulder osteoarthritis progression phases. As distinct from obesity and its implications for both joint loading and inflammation, an independent role for muscle adipose tissue composition alterations including muscle fat deposition and possible changes in muscle mass or sarcopenia [a progressive muscle mass declining state] may not only impact mobility but may set the stage for inactivity and muscle fat fraction increases [12,25-27]. Others show a role for deforming contractures, varying degrees of muscle spasm and subnormal vector influences, plus functional changes in muscle biochemistry and muscle size [28] that have a unique or collective bearing on cartilage viability, and that may implicate or lead to muscle fat excesses and infiltration as well as deficits in lean muscle mass and muscle fibrosis [29,30].

In essence, this envisioned series of adverse interactions including heightened decrements in muscle force capacity and contractile responses and others may induce or be mediated by various degrees of muscle fat encroachment and/or enlargement plus progressively subnormal joint biodynamical, structural changes in muscle architecture, mobility and functional ability and largely irreversible osteoarthritis joint destruction processes [42]. As well, this idea is consistent with known age associated degrees of the gradual onset of subnormal muscle metabolic physiological states, losses of lean muscle mass, increasingly sedentary behaviors, those comorbid osteoarthritis associated health conditions such as diabetes and the loads needed for muscle regeneration that are increasingly excessive in the face of associated muscle volume declines [43]. In addition, there may be a reactive or causative array of intrinsic muscle cell mesenchymal alterations that prevent, inhibit or impair muscle repair [44].

Underlying local factors may also include possible painful muscle reactive adaptations due to persistent abnormal sensory inputs from one or more of the surrounding tissues in the presence of an increased muscle fat mass and that may impact the ability to attenuate joint loads significantly and effectively. Also known as myosteatosis, its presence in muscle exhibits a negative correlation with muscle mass, strength, mobility and a decrement in muscle quality, while serving as a biomarker for sarcopenia, cachexia and metabolic syndromes. It also induces pro-inflammatory changes that clearly contribute to declines in muscle function, compromise mitochondrial function and increase muscle inflammatory responses and possibly postural stability [35,46]. Worse effects occur in cases of higher muscle fat content and area presence [47].

Others show the presence of muscle fat derived inflammation that may not only evoke local muscle pain signals, but may elicit more widespread pain, bone attrition and sensory sympathetic inputs that contribute to the arthritis disease and disability cycle [48]. It also appears both externally or extrinsic as well as internally or intrinsic induced muscle fat infiltration and subsequent fibrosis may have a separate or combined cumulative and progressive effect on osteoarthritis structural pathology of the shoulder joint and others and regardless of whether this situation is causative or reactive [49]. Moreover, unless identified early on, it may be highly challenging to heighten the subject’s physical function or relieve longstanding pain, especially if there is progressive muscle atrophy plus a possible unwillingness or fear on the part of the affected adult to move their arm to counter increasing pain and stiffness, alongside muscle mass and sensory declines and joint stability deficits that may influence them to adopt abnormal and awkward movements to avoid pain and injury but that may place strain on the joints, further pain and possible diverse muscle associated adverse structural alterations that may vary depending on the degree of muscular fat infiltration [49].

Other muscle based determinants that may be related to the degree of muscle fat encroachment and presence involved in osteoarthritis include sarcopenic obesity [42]. As well, there is the possible development of a muscle nerve entrapment process by osteoarthritis bone spurs, muscle fibrosis, muscle inflammation, joint instability and an altered cartilage structure with the added risk of incurring more extensive joint pathology and pain than those generated in the presence of sufficient fat free lean muscle mass [50,56].

Adding to this subnormal cycle is a possible role for osteoarthritis associated muscle fat infiltration impacts on muscle metabolic alterations alongside widespread pain, atrophic muscle weaknesses, muscle volume deficits, inflammation and muscle architecture alterations [57,58]. At the shoulder joint, it appears muscle resident fibroadipogenic cells do serve as a key a contributor to rotator cuff tear pathological changes that cause immense pain and disability [13].

While mechanical injury is the most likely cause of osteoarthritis in most instances, emerging evidence showing functional ability declines in the presence of excess muscle fat could be causative or reactive or both. As well, those cases displaying atrophic muscle weakness are likely to also display disruptions in muscle genetics and muscular alterations such as declines in muscle force capacity and responsiveness that may further amplify the pain and dysfunction attributable to the local condition even after surgery where muscle fatty tissue infiltration and deposition may emerge or persist [59,60].

Discussion

As per a number of diverse current and past studies, it can be concluded shoulder osteoarthritis and impaired function can be significantly influenced by muscle atrophy, fatty muscle infiltration and fibrosis usually accompanying rotator cuff muscle degeneration [31]. In addition, MRI type scans and analyses, further reveal increased fatty infiltration in the infraspinatus muscle with age [41]. Moreover, in full-thickness rotator cuff tears in human samples tears of all sizes show significantly greater lipid content and smaller myofiber cross-sectional areas compared with partial-thickness tears and control muscles [61]. As well, a preclinical study of rabbit supraspinatus tenotomy outcomes showed this artificial injury to recapitulate key features of the pathophysiology of human rotator cuff tears, including muscle atrophy and degeneration, a lack of regenerative ability, fat accumulation and fibrosis [13]. Indeed, despite years of study and insights, what remains is a high re-tear rate after a successful repair of the rotator cuff that is a major clinical challenge attributed to muscle atrophy and fat accumulation of rotator cuff muscles over time [62]. Moreover, after successful arthroscopic repair, even if tendon tear-induced fatty infiltration can be almost negated and muscle atrophy slightly reversed in the case of a failed repair, these changes are further pronounced during the first 3 postoperative months [63].

Gerber, et al., note that it appears that muscle changes that occur after tendon release, may be exacerbated in the presence of denervation of the muscle due to an ensuing decrease in the pennation angle of lengthened muscle fibers, with a reduced mean cross-sectional area of pooled muscle fibers, a slow- to fast-type transformation and an increase in the area percentage of hybrid fibers, leading to overall significantly greater atrophy of the corresponding muscle [45].

Remarkably, the pattern of fat infiltration within the supraspinatus muscle of the shoulder joint changes from a laterally based location around the muscle-tendon junction to a more diffuse, global infiltration pattern when the whole muscle fat content exceeds 10% according to Wallenberg, et al., [58]. Hence, more translational research on diverse osteoarthritis samples of higher ages may prove promising in stressing a role for fat mass correlates that can foster extensive alterations in muscle force capacity and immense irreparable disabling outcomes if overlooked.

In addition, even though the source of muscle fat infiltration and why this may enlarge and become pathogenic is not well clarified and nutrition and physical activity behaviors may clearly be of high import, basic preclinical studies speak to a series of adaptive responses in the face of joint damage including those induced by neurological nerve damage as one factor, even if this does not apply in all cases [17,45]. As well, even if fatty tissue can be removed artificially the underlying muscle abnormalities, for example fibrosis may prevail [17]. The rotator cuff tendons can degenerate and/or tear from the greater tuberosity of the humerus, which is associated with several anatomical, physiological, biochemical and molecular changes in tendon and muscle. immunobiological responses following the rotator cuff lesion and the inherent repair mechanisms elicited by the body. The greatest difficulty in treating this pathology is that the muscle can undergo irreversible fatty infiltration in the setting of chronic tears that is associated with poor surgical outcomes. The article also investigates the key molecular pathways of the muscle homeostasis and energy metabolism to propose a possible mechanism for fatty infiltration [64]. The radiologic grading of muscle fat content was associated with the expression of various genes, including adipogenic, fibrotic, inflammatory and atrophy-related genes and these genes were closely correlated with each other in terms of expression [65].

Siso, et al., who studied patients with primary glenohumeral osteoarthritis awaiting total shoulder arthroplasty showed B3 glenoids had the greatest degree of fat presence of all rotator cuff muscles, implying a possible disabling correlation [14]. Although the cause effect association is unclear, high-grade rotator cuff muscle fatty infiltration is associated with B3 glenoids-subtype of arthritis, increased pathologic glenoid retroversion and increased joint-line medialization [25]. An additional thought is that posterior humeral head subluxation and glenoid retroversion, which are pathognomonic of the Walch type B shoulder, may lead to a disturbance in the length-tension relationship of the posterior rotator cuff, causing fatty infiltration [66].

Review of Key Points

What can be gleaned from the presently retrieved sources of peer reviewed information on osteoarthritis of the shoulder as well as osteoarthritis of other joints is as follows in our view:

1. i) How injury to a vital muscle group or its attachments to bone can independently as well as collectively induce joint attrition and immense immobilizing pain, as can the presence of excess muscle fat in its own right in cases of low muscle mass [42]
2. ii) The challenges in reversing the above interactions compound as time progresses. Moreover if this process is not halted or retarded in a timely manner reparative surgical interventions may fail

Indeed, failing to appreciate the complexity of what we do know about the triadic association of fatty tissue, sarcopenia and their osteoarthritis associations implies a lack of insightful analysis and intervention applications and/or especially a failure to appreciate the toxicity of muscle fat infiltration that may conceptually do much harm in multiple respects [42].

Fortunately, these clinical determinants of some forms of osteoarthritis do show this idea is not just theoretical but that fibro-adipogenic progenitors, a major population of resident muscle stem cells constitute the main source of intramuscular fibrosis and fatty infiltration that are key features of rotator cuff muscle degeneration and possible further joint tendon tears [23].

The implications here are that strategies to reduce injury exposure and others directed across adulthood towards enhancing or maintaining an optimally desired state of muscle mass, strength and endurance, plus efforts towards avoidance of repetitive or acute injurious joint loading activities appear highly indicated, as do routine body composition measures [42]. Muscle stress protection seems especially crucial as recent analyses reveal that in the presence of an injury, a hostile microenvironment characterized by heightened inflammation, fibrosis and muscle weakness may be forthcoming and is one shown to stimulate intramuscular adipose tissue expansion and impair its regeneration capacity and contractile functions especially in the face of a sedentary lifestyle [66].

In adults with rotator cuff tears and shoulder osteoarthritis, as well as instability, clinicians can track or look out for these features and work with the client to mitigate their impacts. Finally, rehabilitation programs targeting shoulder muscle function and pain should not neglect to examine shoulder proprioception that is showing promising initial results in restoring function and returning injured athletes to play.

At present, it appears safe to say that even though more solid uniform information on this topic is needed in multiple realms [25], most clinical researchers currently assume muscle problems of some sort underlie and impact osteoarthritis pain and if minimized will prove to have a bearing on osteoarthritis outcomes. However, distinctive efforts to study and address muscle fat deposition origins and impacts such as fears of movement, muscle deconditioning [68], muscle strength declines, pain and pain behaviours are desirable due to their possible cross talk effect between fat and body tissues and pain [68-74]. Developing effective osteoarthritis preventive as well as treatment strategies using more advanced technologies and analyses can also help to greatly advance the field as cited by most current researchers, including those who conduct joint replacement surgery, especially at the shoulder joint [25].

Limitations

Although publication bias may prevail, these aforementioned observations are largely in agreement regarding a negative role for the presence of fatty tissue in muscles around a healthy as well as an osteoarthritis damaged joint. While not carefully explored to date, its enlargement in the face of poor management and non protective behaviors appears to have muscle as well as joint functional implications. At the shoulder, despite a lack of longitudinal study, it appears avoidance of an acute injury will favour the ability to resist muscle fat infiltration and/or its persistence and adverse signalling influences [75]. Hence although osteoarthritis is currently deemed a chronic progressively disabling condition with no known cure, research over the past 15 years or more has indicated that there is strong possibility that an array of muscle related factors that can contribute to the osteoarthritis pain and disease cycle and muscle fat infiltration perspectives appear to hold great promise, although not evident overall to date.

Moreover, while a diverse array of intervention approaches that focus on maximizing muscle structure and function appear advocated to potentially reduce the degree of disability in knee and hip osteoarthritis, that at the shoulder is rarely alluded to except for surgical research purposes. Muscle fat mass, a predictor of adverse joint events [68] alongside pain, regardless of its precise muscle site and disease severity is also not well articulated or even mentioned in the realm of shoulder exercise therapies.

This lack of attention to a topic of high explanatory and therapeutic potential with excellent preclinical model reports may inadvertently impact outcomes of life in general for many, especially those undergoing surgery to replace a diseased joint. Studies that combine both clinical as well as biopsy type analyses and those that foster well conceived sensorimotor, strength training and joint protection are likely to prove highly insightful and are urgently needed [10].

Additionally, symptomatic cases who do not receive careful instructions as to the considerable care they must take versus those who do should be studied. In this regard careful monitoring of the client and helping those with severe overweight to lose weight and avoid excessive muscle stretching and high frequency loading activities after periods of immobilization found to hasten cartilage destruction appear indicated and should be validated [75]. 

Conclusion

Although modern medicine has been quite successful in managing many acute health conditions and reducing infection and injury risk and magnitude in the older adult population, no similar simple solution prevails against osteoarthritis especially among those older adults who are possibly either over- or underweight. There may also be associated emergent signs of pain and need for surgery if nothing is done to avert preventable disease correlates. Meantime it appears:

1. High degrees of shoulder osteoarthritis impairment and suffering will persist among older adults if a role for muscle fat mass as both a precursor and progenitor remains fragmentary or unaccounted for
2. Dedicated efforts to assess and unravel the origins and profound impact of muscle fat mass deposition on shoulder joint health and how exercise may exacerbate this, rather than thwart this if poorly devised and implemented are indicated
3. Injuries involving macro or micro tears of the shoulder rotator cuff along with subsequent or pre-existing deconditioning and poor health and are poorly treated are likely to prove key contributors to shoulder osteoarthritis rather than age alone and warrant upstream and downstream prevention efforts
4. Research that examines the link between intramuscular fat and joint sensory functions and pain will prove insightful
5. A study of disease free older adults and how muscle fat affects joint loading and muscle regeneration and how this knowledge can be applied pre-emptively would also greatly advance the field

Current findings also strongly highlight the degree to which muscle fat infiltration and/or enlargement as well as muscle atrophy 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, at the shoulder it can be observed that although the temporal and causal relationships of these associations remain ambiguous, muscle atrophy and fat infiltration can be considered two discrete processes in the natural history of gleno humeral osteoarthritis and without due care and accurate assessments of fat extent, muscle joint stability, exercise may fail to achieve the desired outcome [41,69,79,80].

Indeed, it appears increasingly difficult to ignore a role for muscle fat mass deposition and/or its expansion as a potential pathogenic factor or co-factor in the cycle of progressive shoulder pathology and requiring attention even if surgery is contemplated [4]. Additionally, it appears that rotator cuff muscle volume is significantly decreased in those adults with definitive osteoarthritis and can thereby impact outcomes including muscle force capacity and joint protection [60].

However, physical therapies that address this pathogenic disease feature may greatly help to mitigate this disabling condition especially if they encourage efforts to safely increase lean muscle mass and balanced well modulated movements and stability, while reducing pain and the risk of further joint destruction [50]. 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 correlate and possible efficacious mitigation strategy.

Unfortunately, since this idea is by no means a universally accepted or practice based one, 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 may enable progress especially if conducted over extensive time periods utilizing a variety of possible patient specific interventions. As shown in Fig. 1 efforts to untangle these interactive reactionary states may prove especially revealing and help in the design of optimal osteoarthritis rehabilitation plans as well as reducing the need for surgery and its oftentimes less than optimal outcomes. Similarly conservative treatments of the shoulder and their scope and sequence may be enhanced such that: 1) older adults and those at risk for excess reactive or age associated muscle atrophy declines or both will suffer less in multiple respecrs; 2). It may be possible to elucidate how adverse joint impact generated internally or externally or both can induce of exacerbate osteoarthritis joint damage; 3). while not definitive, prevention appears highly promising as an adjunctive approach to avert and ameliorate the magnitude of muscle mass declines and attrition generated by injury both macro and micro and osteoarthritis disease severity even in cases that undergo joint replacement surgery; 4) securing an ample or desired level of motion as regards muscle health in a controlled progressive manner and avoiding excessive joint stretches may yet help to protect against excess movement generation, age related joint damage and injury, while speeding up recovery.

In this sense, regardless of the great benefits of current forms of rotator cuff diagnostics and repair, concerted parallel efforts to educate as to the role of excess weight and protect against cartilage damage and injury due to acute injuries and/or chronic loading, including repetitive joint loading impacts may be of the highest import in allaying the onset or progression of excess muscle fat infiltration at the shoulder joint and others [81,82]. Another point is that the presence of any subnormal muscle composition has previously been linked not only to poor function, but comorbidity and increased hospitalization and all cause mortality [76].

However, to advance this field successfully, well-powered and carefully conceived long term clinical, as well as epidemiological and basically oriented studies that employ advanced technologies, careful subgroup allocation and healthy as well as impaired subjects are sorely needed and strongly encouraged. Until more is known, we further assert shoulder osteoarthritis determinants that affect many older adults adversely are possibly compounded by modifiable muscle fat mass invasion processes and/or reactive infiltration and enlargement that can evoke a variety of increasingly subnormal bone-muscle interactions.

Moreover, since the presence of sarcopenic obesity may play a major role in diminishing the health of older adults, neglecting or overlooking the relevance of possible associated increases in disordered muscle and tendon composition, especially that attributable to age as well as injury risk and related fatty infiltration or expansion processes may duly hasten the onset of progressive muscle weakness, dysfunction, neuropathic pain, cartilage failure and its disabling life quality and functional implications quite markedly and significantly [83,84].

By contrast, possible long lasting adverse clinical implications can be offset by early detection, careful follow ups and record keeping and primary preventive [including robotic arm assistance and protective devices], rather than relying on late end stage interventions where possible surgery is often fraught with its own challenges, persistent pain, muscle strength decreases and long recovery periods [75]. Careful primary and secondary preventive measures against poor outcomes may also affect the need for reparative surgery or enable more practical solutions that reduce the spread of muscle fat to unaffected shoulder cuff muscles in the case of further muscle attrition and inflammation that heightens sarcopenic obesity risk [76,77,83,85]. It may help avoid or reduce the negative impact of excess body weight as well as frailty and poor proprioception on muscle fat mass, especially among those deemed at risk [78].

Final Comments            

Although seemingly an obscure topic in the realm of osteoarthritis mitigation- it is apparent much osteoarthritis suffering can be avoided or undone. In particular, a concerted desire to identify, track and examine muscle factors such as muscle fat mass in general in the realm of both osteoarthritis research and specific research at the shoulder joint-a common site of musculoskeletal pain, the design of optimal shoulder rehabilitation plans and their scope and sequence may well be vastly improved as well as far reaching at low cost and generate much success. However, as of 2025 with the exception of the knee joint, the predominant joint studied in this regard, its role, promise and life affirming potential remains speculative.

Conflict of Interests

The author declares no conflict of interest.

Funding/Sponsorship

This research did not receive any specific grant from funding agencies in the public, commercial or not-for-profit sectors.

Consent for Publication

Not applicable

Acknowledgments

None.

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