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Factors, characteristics and influences of the changes of muscle activation patterns for patients with knee osteoarthritis: a review

Journal of Orthopaedic Surgery and Research volume 20, Article number: 112 (2025) Cite this article

Abstract

Background

Knee Osteoarthritis (KOA) is a prevalent condition worldwide, significantly diminishing quality of life and productivity. Except for the alignment change, muscle activation patterns (MAP) have garnered increasing attention as another crucial factor contributing to KOA.

Objective

This study explores the factors, characteristics, and effects of MAP changes caused by KOA, providing a neuromuscular-based causal analysis for the rehabilitation treatment of KOA.

Methods

Keywords including the association of MAP with KOA will be included. “Knee, Osteoarthritis, Electromyography(EMG), Muscle Activity patterns, activation amplitudes, activation time, Muscle Synergy, Co-contraction/activation” were used to search the databases of Science Direct, PubMed, Scopus, and Wiley. The criteria include studies from the past fifteen years that document changes in muscle contraction characteristics and causality analysis in patients with KOA. we compared MAP changes between individuals with and without KOA, such as the activation amplitudes, activation time, muscle synergy and co-contraction index(CCI). Additionally, we explored the potential relationship between muscle weakness, pain, and lower limb mechanical changes with the variations of MAP.

Results

A total of 832 articles were reviewed, and 44 articles that met the inclusion criteria were selected for analysis. The changes in biomechanical structure, pain, and muscle atrophy may contribute to the formation and progression of the changes in MAP in KOA patients. In moderate KOA patients, the vastus lateralis (VL) and biceps femoris (BF) exhibits larger activation amplitudes, with earlier and longer activation times. The vastus medialis (VM) shows a delayed activation time relative to VL. Gastrocnemius activation time is prolonged during mid-gait, while the soleus exhibits lower activation amplitudes during the late stance phase. There are fewer, merged synergies with prolonged activation coefficients, and a higher percentage of unclassifiable synergies. Additionally, the CCI is positively correlated with task difficulty and symptoms. It is higher in the medial and lateral than hamstrings and quadriceps, and CCI specifically respond to joint stabilisation and load.

Conclusion

In patients with moderate KOA, changes in MAP are mainly related to symptoms and the difficulty of tasks. MAP changes primarily result in variations in amplitude, contraction duration, muscle synergy, and CCI. The MAP changes can subsequently affect the intermuscular structure, pain, joint loading, and stiffness.

Clinical implications

These contribute to the progression of KOA and create a vicious cycle that accelerates disease advancement. Clinical rehabilitation treatments can target the MAP changes to break the cycle and help mitigate disease progression.

Introduction

Knee osteoarthritis (KOA) is a degenerative disease, which is common in middle-aged and elderly people [1]. The main symptoms are joint movement dysfunction and accompanying pain [2]. When exploring the causality of the disease, most studies focus primarily on changes in the lower limb alignment and knee joint structure, with less emphasis on the neuromuscular control [2,3,4,5,6,7,8]. Shinya Ogaya et al. demonstrated that individuals with KOA exhibited reduced knee extension acceleration by the vasti muscles during 15-25\(\%\) of the stance phase, alongside increased acceleration from the hip adductors compared to controls [9]. Most of the lower limb muscles contributed less to forward center of mass (COM) acceleration in KOA patients [10]. The altered knee control and flexed knee posture during movement in KOA patients subsequently affect knee mechanical loads [11, 12], making it difficult to walk at faster speeds [10]. Meanwhile, Derek Rutherford et al. found that the activation ratio of the lateral and medial hamstrings during treadmill walking was greater in the KOA group [13]. These findings highlight that alterations in neuromuscular control are strongly associated with KOA.

Currently, rehabilitation training of KOA primarily includes aerobic exercises, strength training, balance and proprioception exercises, neuromuscular control exercises, and other traditional therapies [14]. Most of these training processes involve neuromuscular control. The change of neuromuscular control in the patients is mainly manifested by the change of MAP [1, 9,10,11, 13, 15]. In early 1999, Maria GB et al. had reported evaluating the effectiveness of rehabilitation treatment in total knee arthroplasty (TKA) patients by assessing kinematic dynamics and MAP [16]. Booij, MJ et al. also found that modified gait via altering muscle activation patterns can reduce knee joint load [17]. These findings support that rehabilitation training, focused on appropriate MAP,has the potential to modify dynamic loading gait patterns associated with the clinical progression of KOA [18]. Therefore, understanding the changes of MAP in KOA patients is of high clinical value in the prevention and treatment of disease development in the patients. However, the current reviews focused on MAP in KOA are very few. They primarily described the alteration of muscle including strength and volume [19], ignoring the factors and influence of MAP in KOA [20], which is crucial in analyzing the origin and development of KOA. What’s more, increasing number of studies had explored the underlying causes of MAP changes and the associated alterations characteristics [9, 21, 22], Other studies [16,17,18] had also begun to focus on the related effects caused by MAP changes. Therefore, Analyzing the causes, characteristics, and impacts of MAP, along with understanding the interrelationships involved, is crucial for providing a comprehensive review of its role in the formation and development of KOA.

Based on the above premise, our review arm to: (1) elaborate on the factors of changes of MAP in the KOA patients; (2) introduce and feature the common changes of MAP in patients with KOA; and (3) highlight the effect with the alterations of MAP. In short, taking the MAP as the focal issue, this paper reviews the formation process of KOA extensively, focusing on the reasons, characteristics, and consequences with the changes of MAP. This paper also aims to provide a practical reference for rehabilitation therapists and engineers in carrying out the rehabilitation treatment for KOA patients based on the changing characteristics of MAP.

Methods

Literature retrieval methods

We used ScienceDirect, PubMed, Scopus, and Wiley for literature retrieval, and obtained articles related to the MAP of patients with KOA from 2010 to the present. The combined search keywords are: “Knee and osteoarthritis and neuromuscular”, “Knee and osteoarthritis and muscle contraction/activation patterns”, “Knee and osteoarthritis and muscle synergy”, “Knee and osteoarthritis and electromyography (EMG)”, and “Knee and osteoarthritis and co-contraction/activation”. Three researchers conducted the literature review. First, two of us independently screened articles that met the eligibility criteria. The final decision for inclusion was made by consensus between the two reviewers, and the third reviewer made the decisions as consensus was not reached. The search was conducted only for English literature research materials. The detail of Inclusion and exclusion criteria are described in Table 1.

Literature screening

A total of 832 articles were retrieved and 779 titles and abstracts were examined for relevance after deleting duplicate articles and overdue articles. In the end, there are 44 studies shortlisted for this research work as shown in Fig. 1.

Fig. 1
figure 1

The Flowchart of the article selection criteria for our research

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Table 1 Inclusion and exclusion criteria for articles
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Factors of change of MAP in the KOA

The factors of the changes in MAP in patients with KOA are complex. This review mainly analyzes the changes in MAP from the changes in lower limb biomechanical structure, pain, and neuromuscular system.

Changes of lower limbs biomechanical structure

Lower limb mechanics and movement patterns influenced the MAP across two primary dimensions:

  1. (1)

    The influence of knee cavity load caused by knee adduction moment (KAM) on MAP;

  2. (2)

    The influence of knee instability on MAP.

KOA patients tend to have higher KAM [23, 24]. Reduced quadriceps activation amplitudes and weakness can elevate knee adduction moment [21]. Long-term adduction torque can cause the wear of knee cavity cartilage and increase the load of the knee cavity [25]. Higher activation of the lateral hamstring(LH) and VL during gait has been shown to reduce medial compartment cartilage loss [26], while also being associated with changes in the moments of flexion, adduction, and lateral rotation within non-traumatic OA group [27]. Furthermore, Lim et al. demonstrated that joint effusion can alter intra-articular pressure, leading to an imbalance within the joint [28]. KOA patients often have knee instability [1, 29]. To maintain the stability of the knee, BF [30, 31] and hamstring [1] have to show a higher degree of activation amplitudes as shown in Fig. 2, as well as the hip adductor, in the early stage of gait, to complement the lateral stability [9]. In addition, there is a study show that the greater hamstring-to-quadriceps muscle thickness ratio and the muscle architecture and quality of medial quadriceps/hamstring play an important role in KAM [32], confirming the impact of these muscles on KOA through KAM.

In addition, based on the Kellgren-Lawrence (K-L) grading system, Andrea D et al. [33] found no significant difference in extensor strength across the different grades, which is consistent with other researches findings [34, 35]. After adjusting for gender, BMI, and age, a decrease in extensor torque appears to be more strongly associated with the development of knee malalignment in women. This suggests that weakness in the knee extensors may be a significant risk factor for the progression of K-L grading in women [33]. However, amplitude and temporal patterns of the medial gastrocnemius(MG), LH, and quadriceps varied significantly across the K-L grades [35].

Fig. 2
figure 2

Biceps femoris and hamstring have a higher degree of activation amplitudes (Sarah AR., 2021) [56]

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Pain

Pain can directly lead to changes in MAP. Studies showed that pain inhibited strength in hamstrings and quadriceps [2, 21, 36], Wilson, J.A.et al. [37] found that in patients with KOA, the activation patterns of lateral gastrocnemius(\(r^2\)=16.6\(\%\),P=0.009) and medial hamstrings (\(r^2\)=10.3\(\%\), P=0.04) during walking were significantly correlated with pain severity. This result could represent the body’s mechanism for compensating for high intra-articular joint loads during the gait cycle [37, 38]. In the comparison of symptomatic vs. asymptomatic knees and radiographic classifications among 3809 individuals, significant reductions in isometric extensor and flexor strength were observed in both men and women within the symptomatic groups. However, no significant differences in muscle strength were found across the K-L grades [34].

Pain can also aggravate the change of MAP by affecting the changes in lower limb mechanics. Studies showed that pain seemed to reduce thigh muscle strength, and individuals with more severe pain showed lower extensor and flexor strength [38]. The pain caused by walking in patients with KOA was related to KAM [23]. During the pain process, the two peak values of KAM decreased significantly with the maximum extensor torque and the peak flexor muscle decreased significantly as well [39, 40]. Furthermore, another study had found that central pain sensitization might exacerbate knee muscle co-contraction during fast walking in patients with KOA [41].

Motor sensory nerve change

Many studies showed that the neural pathway might be impaired in KOA patients [23, 42, 43]. One major reason for this factor is that pain affects neuromuscular control [42, 44]. Changes in motor unit recruitment and rate coding strategies in OA might be the primary reasons for altered MAP [45]. Recently, neurostimulation techniques such as transcranial direct current stimulation had been used in the treatment of pain in KOA patients [44, 46, 47], indicating that KOA patients may experience chronic pain or pain sensitization [44, 48]. Astephen Wilson et al. showed that pain severity is only reflected in gait speed and neuromuscular activation patterns in medial KOA [37]. This was due to the impairment of rapid neuromuscular activation and was considered to be an important cause of functional impairment in patients [42]. This impairment of neuromuscular activation might be due to changes in the neuromuscular junction (NMJ). In addition, many studies had shown that the proprioception of KOA patients was often impaired [21, 43, 49,50,51,52]. Chang et al. found that patients with knee motion control had insufficient afferent sensation [43], and harmed ankle joint and subtalar joint motion sensation in KOA patients [53]. This phenomenon of proprioception impairment might affect the patient’s perception of the motor parts, causing errors in the central nervous system.

Other factors

The data for inclusion should cover three main aspects. Al Khatib et al. highlighted that when comparing obese (OB) subjects with normal weight individuals, the strength of all muscle groups significantly increased in most postures, with much higher activation observed in the LHs and MG [54]. Regarding the effect of age, normal elderly individuals showed only increased activation amplitude in the VM and lateralis, as well as the medial and lateral hamstrings, compared to younger adults, with no other significant changes. Differences between muscles were primarily reflected in the principal component analysis (PCA) in PP1 and PP2 [55]. Sarah A. R. et al. similarly found that age alone did not lead to changes in the number of muscle activation modules, but patients with KOA exhibit alterations [56]. Between-group and muscle differences were mainly observed in the LH. In terms of gender differences, most studies indicated that women with knee osteoarthritis (KOA) exhibited more pronounced quadriceps weakness [57,58,59] and changes in body fat percentage [60]. Sisante JF et al. found that combined hamstring co-activation (HC) (P = 0.013) and lateral HC were inversely associated with quadriceps strength in women (P = 0.023), but not in men [61].

The characteristics of changes in MAP of KOA

Alterations in muscle synergy

Muscle atrophy is another major contributor to changes in MAP [62]. Non-negative matrix factorization (NMF) is a key technique to quantify muscle synergy patterns, which was used in many studies [63,64,65,66]. It can be noticed that the number of muscle synergy modules is significantly lower in mild and severe KOA compared with both the healthy subjects and the unaffected side [63, 64, 67], this phenomenon is also observed in elder groups [56, 63, 68]. The recruitment of low limb muscle modules and temporal variations increased with higher walking speeds in KOA patients [69]. These indicates that KOA patients tend to use more muscles to complete the gait cycle. Specifically, both the stance and swing stages observed this kind of muscle synergy module merge [63,64,65].

Muscle contraction amplitudes and time

Quadriceps femoris

Weakness of quadriceps femoris is common in KOA patients [70]. The main manifestation is the weakness of vastus medialis (VM) and mid-gait EMG fibrillation [30]. Considering the underlying reasons, Ayumi Tsukada et al. found that muscle volume and strength were significantly lower on the affected side compared to the contralateral side in individuals with severe KOA [71]. However, Noehren B.et al. demonstrated that lower quadriceps function in moderate OA may not be attributed to impairments in fiber size [72]. Compared to healthy controls, individuals with KOA exhibited a reduction in type I fibers, an increase in type IIa/x fibers, greater extracellular matrix (ECM) content, lower satellite cell density, and elevated expression of profibrotic genes [72]. Some studies had also shown that patients have increased activation amplitudes of rectus femoris (RF) and VL in comparison with subjects without KOA [73]. The stronger activation amplitudes may be associated with a compensatory strategy in maintaining the stability of the knee. The changes in the activation time of quadriceps femoris are mainly characterized by the advanced or delayed activation start-time and the extension of the whole activation time. Specifically, in the process of walking, the onset time of VL activation time would be earlier [26], while significantly delayed when walking up or down the staircases [15]. The activation time of VL and RF was moderate and for severe patients, it was prolonged overall, and RF had a longer prolongation for severe patients [35].

Hamstring

Many studies showed that KOA patients exhibited stronger LH contractions [13, 74, 75]. Some studies showed that the amplitude of BF in patients tended to show a systematic and moderate increase compared with people without KOA, because of the lack of stability during standing in patients, and also during the 20\(\%\) to 60\(\%\) of the gait cycle [30]. Non-traumatic KOA group had also higher and prolonged LH EMG compared to healthy and post-traumatic OA groups [27]. Compared to non-pathological knees(NP), the peak force of hamstring muscle increased by 25\(\%\) in individuals listed for high tibial osteotomy surgery(pre-HTO) [76]. The prolonged contraction time of the LH primarily occurred during the mid-stance phase [27]. For moderate KOA patients, the prolonged activation time was observed in both the BF and semimembranosus [35].

Gastrocnemius

KOA patients showed a stronger tendency to activate the gastrocnemius, with more pronounced changes observed in severe individuals [73]. Compared to NP, the peak gastrocnemius muscle force reduced by 30\(\%\) in pre-HTO patients and by 18\(\%\) in those pre-undergoing total knee replacement [76]. When compared with severe patients, gastrocnemius activation amplitudes were higher in asymptomatic and moderate patients throughout the gait cycle [73], and some patients also showed tremor effect in gastrocnemius EMG, which might reflect the instability of knee joint [30]. The latest researchers have demonstrated that patients with KOA have increased gastrocnemius muscle stiffness, closely related to clinical symptoms [77].

The gastrocnemius muscle activation time of KOA patients was prolonged [74]. It was mainly manifested in the prolongation of mid gait [74], and the MG activation time of severe patients was longer than the lateral gastrocnemius [35]. In comparison with asymptomatic individuals, the MG activation time was delayed and remained longer, which was considered a key feature associated with the progression of KOA [35].

Other muscles

Other studies showed that the hip adductor activation amplitudes were enhanced in the early stage of gait [9]. In the middle and late stages of gait, the activation amplitudes of soleus in some patients were significantly lower than in subjects without KOA [10]. What’s more, the erector spinae and gluteus maximus have difficulty in performing maximum voluntary contraction and have decreased activation amplitude [22].

Muscle contraction duration and CCI

Data extracted from five studies. In terms of disease severity, Paul et al. had found that greater duration of medial muscle co-contraction and duration of medial relative to lateral co-contraction positively correlated with annual percent loss of medial tibial cartilage volume [78]. More severe KOA was associated with greater co-contraction of lower extremity muscles during the weight acceptance and swing phases [79]. Updated research also indicates that during the entire stance phase, the co-contraction of most lower extremity muscles is significantly higher in individuals with knee osteoarthritis compared to healthy controls [80]. Meanwhile, other research also found that the quadriceps, hamstring, and tibialis anterior muscles had longer muscle contraction duration in the KOA patients than control group during stance phase [81]. With varying task difficulty, as the knee flexion angle increased in a weight-bearing high-knee flexion position (\(>90^{\circ }\)), the level of muscle co-contraction also increased. Maximum activation occurred when knee flexion exceeded \(100^{\circ }\). Compared to gait, co-activation levels during high flexion transitions were approximately three times greater [82]. Within different OA [83], medial and lateral hamstrings muscle activation levels may serve as a useful gait biomarker for differentiating knee OA from both asymptomatic individuals and hip OA cohorts.

The influence of KOA movement pattern change

Intermuscular effects

Effect of quadriceps movement pattern changes on hamstring

When the muscle strength of quadriceps femoris in KOA patients decreased, hamstring activation amplitudes would increase muscle strength [1], which is reflected in the co-contraction of quadriceps femoris and hamstring [74]. Specifically, quadriceps femoris and hamstring had prolonged activation time in mid-stance [74] with BF and VL having an obvious co-contraction condition [84]. Also, BF and VM, have co-contraction in mid-stance [30]. To maintain the stability of the knee and unload the load on the medial knee joint, the body is forced to strengthen and change the activation amplitudes [13, 73, 74] and activation time [26, 74] of the lateral muscles. However, the co-contraction strategy of the lateral muscles of the knee joint can alleviate the load of the medial compartment to a certain extent, but it cannot fundamentally stop the development of the disease. This is mainly because VL may not be at the maximum strength when the maximum joint load occurs, which cannot fully reduce the load of the medial knee joint, thus causing medial chamber cartilage to still be in damaged condition [26]. The earlier onset of VL activation time may be related to the larger loss of medial ventricular cartilage volume.

Effect of quadriceps MAP on gastrocnemius

Bigham et al. showed that increased the activity of gastrocnemius could enhance the stability of knee joint by increasing compression force and joint stiffness, and Gastrocnemius also played an important role in stabilizing joint when quadriceps femoris was weak [73]. This effect was also reflected in the co-contraction of quadriceps femoris and gastrocnemius. This also naturally leads to gastrocnemius stiffness by itself [77]. A study found that the co-contraction rates of MG and VM, LG, and VL during walking were correlated negatively with the inversion thrust significantly [29]. This co-contraction pattern could change the gap of the inner compartment of the knee joint, causing a stiff knee joint and minimizing the varus thrust in maintaining the stability of the knee joint [29]. For moderate KOA patients, knee stability could be maintained by changing the hamstring movement pattern. However, the enhancement of co-contraction also increased the load of the knee joint and was significantly associated with cartilage loss [29]. In addition, the change of gastrocnemius activation pattern was one of the key mechanisms for maintaining knee stability in advanced KOA patients, however this strategy might negatively impact the knee joint cartilage [78], change the mechanical structure of the knee joint in the long term, and thus affecting the adjacent muscles, such as hamstring and iliotibial band lesions [85].

Effect on lower limb mechanics and pain

Muscular control strategies can vary depending on strength and coordination which in turn influences joint control and loading [76]. Higher quadriceps and hamstring forces suggest that co-contraction with the gastrocnemius could lead to higher knee joint contact forces. Meanwhile, increased medial muscle co-activation could potentially differentiate between uni- or multi-compartmental OA [76]. Although the changes of the MAP between muscles and adjacent muscles can alleviate pain and improve knee stability to a certain extent, it may eventually lead to further changes in the biomechanics of lower limbs and the occurrence of new pain. As mentioned earlier, KOA patients usually have higher KAM than people without KOA [15, 23, 49, 84]. By investigating the relationship between the maximum voluntary isometric contraction percentage of muscle EMG and joint torque, Selistre et al. showed that KAM was associated with quadriceps femoris [84]. KAM was often accompanied by increases in the medial compartment load of the knee. By using the principal component analysis method (PCA) to reduce the dimensionality of EMG and studying the relationship between EMG features and knee torque and angle, Robbins et al. showed that increased activation amplitudes of the LH, reduced the load on the medial compartment of the knee in patients with non-traumatic KOA [26, 27]. By studying the relationship between the quadriceps EMG and the participants’ gait, Hodges et al. showed that an increase medial muscle co-contraction duration by 1\(\%\), and annual loss of medial tibial cartilage volume would be greater than 0.14\(\%\) in KOA patients. Augmented medial knee muscle co-contraction accelerated progression of medial KOA [78]. By using the musculoskeletal model to analyze, Ogaya et al. showed decreased the soleus activation amplitudes in the middle and late stages of gait would directly produce a certain forward acceleration [10]. Ogaya et al. also showed that the increased activation amplitudes of the hip adductor in the early stage of gait were beneficial to the control of knee extension in patients with KOA [9]. The adductor of the hip was activated after heel contact with the ground in accelerating hip adduction and lateral movement of the center of gravity. Thus, activation of hip adductors after heel contact could transfer the position of the center of gravity to the stance limb, thus imparting stability to the body in the mediolateral direction [9].

For non-traumatic KOA patients, the earlier activation time of the VL leaded to the increase of medial ventricular cartilage loss, due to the peak of muscle activation being earlier than the peak of joint load [26]. Therefore, although the increase of VL activation amplitudes is beneficial in reducing the loss of medial compartment cartilage, the joint activation time is advanced, which cannot match the joint load sufficiently, resulting in the loss of medial cartilage [26].

The change in MAP may also be related to new pain. The effects of changes with lower limb MAP on mechanics and pain could be divided into two categories. The first type delayed the increase of the load in the knee cavity, then reduced the impact and wear, reducing the occurrence of pain. The second type increased the stability of the knee. However, these two kinds of effects have certain hysteresis effects, which cannot completely offset the increase of knee cavity load and the decrease of knee stability, or even cause the occurrence of pain in other parts.

Table 2 Muscle patterns change
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Overall conclusion and future perspectives

In this paper, the factors, characteristics, and influences of the changes of MAP for patients with KOA were discussed from the aspects of biomechanical changes and neuromuscular control. The changes of MAP are primarily characterized as: larger activation amplitudes and earlier, longer activation times in both VL and BF. VM exhibits a delayed activation time relative to the VL in moderate KOA patients. The activation time of the gastrocnemius is prolonged during mid-gait, while the soleus shows lower activation amplitudes during the late stance phase. Fewer muscle modules with prolonged activation coefficients are observed in KOA patients, and a higher percentage of unclassifiable synergies is noted. Additionally, the CCI is positively correlated with task difficulty and symptoms. It is higher in the medial-lateral muscles than in the quadriceps-hamstrings, and specifically responds to joint stabilization and load. Specific literature had been shown in Table 2.

We identified a vicious cycle related to the change of MAP, as shown in Fig. 3, which appears to be crucial in the formation and progression of KOA. In short, the changes in lower limb mechanics can cause pain and long-term pain leading to nerve pathway damage, which will result in changes in the MAP, which leads to a change in the lower limb biomechanical structure and pain, creating a vicious cycle. According to the vicious circle, clinically, the impact of MAP changes can be reduced and the progression of KOA can be slowed by strengthening the quadriceps, modifying co-contraction patterns, and alleviating pain. In addition, the damage to muscle fibers cause by changes in MAP can also lead to muscle weakness. And obesity, gender, task difficulty, and the severity of K-L grade may also partly contribute to the alternation of MAP.

Meanwhile, this study also has some limitations that should be continuously analyzed in the future study. Initially this study has a quite small number of studies that are included in the literature review, mainly caused of the narrow of this study. Although related research has begun to focus on the MAP in individuals with KOA, much of it centers on the impact of lower limb alignment and its changes on joint loading. Therefore, the description of MAP in patients with KOA is still partial. In addition, while this study considers factors such as gender, age, and task difficulty in relation to changes in MAP, it lacks sufficient detailed analysis. In this study, there was a higher proportion of females, which, while more representative of real-world situations, may introduce some bias and reduce the applicability of the findings to males. Furthermore, this study did not consider the muscles of the lower back, which may also be factors affecting the lower limbs in KOA. Future research should take these muscles into consideration.

Fig. 3
figure 3

The vicious cycle related to the change of MAP (MAP: muscle activation patterns)

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  1. Shizhong Liu and Zuyu Du contributed equally to this work.

Authors and Affiliations

  1. Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, 300072, China

    Shizhong Liu & Yuan Liu

  2. Department of Rehabilitation, Tianjin Medical University General Hospital, Tianjin, 300072, China

    Shizhong Liu

  3. State Key Laboratory of Precision Measurement Technology and Instruments, Tianjin University, Tianjin, 300072, China

    Zuyu Du, Le Song, Haoyue Liu & Huanyu Liu

  4. Department of Electrical and Information Engineering, Zhejiang Normal University, Hangzhou, 321004, China

    Clarence Augustine T. H. Tee

  5. Department of Electrical Engineering, Faculty of Engineering, University of Malaya, Kuala Lumpur, 50603, Malaysia

    Clarence Augustine T. H. Tee

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Liu, S., Du, Z., Song, L. et al. Factors, characteristics and influences of the changes of muscle activation patterns for patients with knee osteoarthritis: a review. J Orthop Surg Res 20, 112 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s13018-025-05484-x

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Journal of Orthopaedic Surgery and Research

ISSN: 1749-799X