Background
Osteoarthritis of the knee is a chronic degenerative articular disease that often affects the elderly [
1]. The pathological mechanism of knee osteoarthritis (KOA) involves destruction of the articular cartilage and the subchondral bone and gradual irritation of the joint synovium and ligaments with varying degrees of inflammatory changes and joint effusion [
2]. Pain is the main clinical manifestation in patients with KOA and is the main reason to seek medical attention. In severe cases, a considerable reduction in knee joint mobility, stiffness, and limited function markedly influences a patient’s quality of life [
3].
There are currently no disease-modifying therapies, and therefore, the goal of treatment is to treat KOA-related symptoms, including pain and stiffness, with the goal of minimizing dysfunction and improving the quality of life. Some solutions for treating this disease include lifestyle changes, medications, physical therapy, and finally surgical interventions [
4]. Among these methods, drug intervention is still the most commonly used prescription treatment for medical service providers and the most commonly used treatment for KOA patients, for example, oral non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac; however, the associated gastrointestinal, renal, and cardiovascular adverse effects of these agents can potentially limit their long-term use [
3]. Therefore, studies have shown an increased tendency of KOA patients to use complementary and alternative treatments [
5,
6], such as patient education, exercise, weight loss, and physical therapy, which can provide substantial benefits. However, the effect of exercise treatment decreases over time, and self-management education programs result in no or small benefits in people with KOA [
7].Currently, radiographs remain the usual means fortheassessment of osteoarthritic changes in the knee and their association with clinical features, mainly based on the Kellgren − Lawrence grade. However, many studies have shown a disagreement between common radiographic findings and clinical symptoms; it is estimated that up to 40% of patients with radiologic damage do not report pain [
8], even after total knee arthroplasty(TKA), and between 15 and 20% of patients are not satisfied with the results of the operation, with the main cause of dissatisfaction being pain [
9].
The pain of KOA may not be just arthrogenic; it may result from other factors. Myofascial trigger points (MTrPs) are considered hyperirritable spots in a taut band of skeletal muscle, which may produce pain, muscle weakness, and decreased ROM symptoms, depending on their relationship with symptoms [
10]. It is classified as active or latent according to its relationship to symptoms. The difference between active and latent MTrPs is that active MTrPs reproduce the pain symptoms experienced by an individual [
11], while latent MTrPs can be present without spontaneous symptoms, and when elicited, they do not reproduce the symptoms of an individual. However, latent MTrPs can induce motor dysfunctions, such as stiffness, restriction of range of motion, and muscle fatigue, supporting their clinical relevance.MTrPs have been shown to be related to various chronic skeletal muscle pains, such as neck and shoulder pain [
12], low back pain [
13], and chronic pelvic pain [
14], thatare also found to be associated with KOA. The prevalence of the MTrPs varied from 11 to 50% in different muscles of patients with mild to moderate painful KOA [
10] and a prevalence approaching 100% in patients in patients waitlisted for total knee arthroplasty, especially in the medial gastrocnemius and vastus medialis muscles [
15].The results of a few existing studies on the treatment of KOA by dry needling are very positive in terms of the improvementsin pain and function [
16,
17]. In contrast, a recent systematic review about the effects of dry needling on the MTrPs in patients with knee pain syndromes revealed that this approach was effective for decreasing pain in patellofemoral pain, but was not in knee OA [
18]. In fact, only two articles on dry needling for KOA were included in this study, and these studies had one thing in common: the targets of dry needling were all active MTrPs, and no latent MTrPs were involved. Indeed, the epidemiology of latent MTrPs shows a higher prevalence in KOA than active MTrPs [
10]. It remains unclear whether latent MTrPs play an important role in KOA, and whether treatment of latent and active MTrPs is effective in KOA.
This study aimed at determining the clinical effects of dry needling on latent and active MTrPs with stretching exercise for KOA and compared with the effect of oral diclofenac with stretching exercise over a 6-week treatment course. We hypothesized that dry needling on latent and active MTrPs combined with stretching can better improve the symptoms and functional abilities of patients with KOA.
Results
CONSORT flow diagram of the procedures
A flow chart of the procedures involving study participation and follow-up is illustrated in Fig.
1. A total of 166 patients were assessed for eligibility. A total of 68 patients were excluded (56 did not meet the inclusion criteria and 12 patients declined to participate in the study), thus resulting in a total of 98 patients who were included in the study. Furthermore, 49 patients were randomized to the DNG and 49 patients were randomized to the DG. During the 6-week treatment, four participants in the DNG and three participants of the DG discontinued treatment, two participants in the DNG and five of the DG withdrew due to lack of effect, three participants in the DG withdrew due to adverse event, and one participant in the DG withdrew for personal reasons. At the 6-month follow-up, three participants dropped out because of losing contact (1 in the DNG and 2 in the DG). Finally, the analyses were performed in 77 patients who completed the study (42 in the DNG and 35 in the DG).
Baseline characteristics
The baseline demographic data of the participants are presented in Table
1. There was no significant difference in gender, age, height,weight, body mass index (BMI), duration of pain, and the severity of knee involvement on the X-ray between the two groups. No statistically significant difference was observed in the baseline values of study outcomes.
Table 1
Baseline characteristics (mean ± SD)
gender (Male / Female) | 13/29 | 12/23 | |
Age (years) | 74.61 ± 6.43 | 75.39 ± 5.77 | 0.14 |
Height (cm) | 161.46 ± 7.56 | 163.46 ± 7.35 | 0.55 |
Weight (kg) | 68.41 ± 7.26 | 65.13 ± 8.95 | 0.31 |
Body Mass Index (kg/m2) | 26.10 ± 3.41 | 24.49 ± 3.29 | 0.76 |
Duration of pain (mo) | 59.41 ± 17.33 | 65.62 ± 15.05 | 0.37 |
Kellgren-Lawrence OA grade n (%) |
Grade 2 | 20 (47.6%) | 17 (48.6) | |
Grade 3 | 17 (40.5%) | 15 (42.9) | |
Grade 4 | 5 (11.9%) | 3 (9.6) | |
Prevalence of latent and active MTrPs
The prevalence of latent and active MTrPs are presented in Table
2. The prevalence of latent MTrPs in DNG was estimated to be 50.0%, 45%, 64%, 42.9%, 40.5%, 16.7%, 23.8%, 54.8%, 28.6%, 42.9%, 71.4%, and47.6%forrectus femoris, vastus medialis, vastus lateralis, tensor fasciae latae, hip adductors, gluteus maximus, gluteus medius, biceps femoris, semitendinosus-semimembranosus, popliteus, gastrocnemius, and soleus muscle, respectively. The prevalence of active MTrPs in DNG was estimated to be 38.1%,31%,54.8%,21.4%,23.8%, 7.1%, 16.7%,47.6%,11.9%,28.6%, 50%, and 33.3% forrectus femoris, vastus medialis, vastus lateralis, tensor fasciae latae, hip adductors, gluteus maximus, gluteus medius, biceps femoris, semitendinosus-semimembranosus, popliteus, gastrocnemius, and soleus muscle, respectively.
Table 2
Prevalence of active and latent MTrPs in patients with knee osteoarthritis (KOA)
rectus femoris | 21 | 50% | 16 | 38.1% | 19 | 54.3% | 14 | 40% |
vastus medialis | 19 | 45% | 13 | 31% | 18 | 51.4% | 12 | 34.2% |
vastus lateralis | 27 | 64% | 23 | 54.8% | 20 | 57.1% | 17 | 48.6% |
tensor fasciae latae | 15 | 42.9% | 9 | 21.4% | 12 | 34.3% | 7 | 20% |
hip adductors | 17 | 40.5% | 10 | 23.8% | 10 | 28.6% | 6 | 17.1% |
gluteus maximus | 7 | 16.7% | 3 | 7.1% | 4 | 11.4% | 2 | 5.7% |
gluteus medius | 10 | 23.8% | 7 | 16.7% | 11 | 31.4% | 6 | 17.1% |
biceps femoris | 23 | 54.8% | 20 | 47.6% | 18 | 51.4% | 14 | 40% |
Semitendinosus- semimembranosus | 12 | 28.6% | 5 | 11.9% | 7 | 20% | 3 | 8.6% |
popliteus | 18 | 42.9% | 12 | 28.6% | 12 | 34.3% | 8 | 22.6% |
gastrocnemius | 30 | 71.4% | 21 | 50% | 23 | 65.7% | 16 | 45.7% |
soleus muscle | 20 | 47.6% | 14 | 33.3% | 17 | 48.6% | 12 | 34.3% |
The prevalence of latent MTrPs in DG was estimated to be 54.3%, 51.4%, 57.1%, 34.3%, 28.6%, 11.4%, 31.4%, 51.4%, 20%, 34.3%, 65.7%,and 48.6%forrectus femoris, vastus medialis, vastus lateralis, tensor fasciae latae, hip adductors, gluteus maximus, gluteus medius, biceps femoris, semitendinosus-semimembranosus, popliteus, gastrocnemius, and soleus muscle, respectively. The prevalence of active MTrPs in DG was estimated to be 40%, 34.2%, 48.6%, 20%, 17.1%, 5.7%, 17.1%, 40%, 8.6%, 22.6%, 45.7%, and 34.3% forrectus femoris, vastus medialis, vastus lateralis, tensor fasciae latae, hip adductors, gluteus maximus, gluteus medius, biceps femoris, semitendinosus-semimembranosus, popliteus, gastrocnemius, and soleus muscle, respectively.
NPRS, WOMAC, and ROM
The results for treatment effects on symptom outcomes are shown in Table
3. In the DNG, the NPRS score was significantly decreased at the 6-week and 6-month follow-up compared to that at the pre-treatment timepoint (
P < 0.05). The NPRS score in the DG showed a significant decrease after the 3 week and the 6-month follow-ups compared with that at the pre-treatment timepoint (
p < 0.05). However, there was a significant increase in the NPRS score at the 6-month follow-up compared with that at the 6-week timepoint (
p > 0.05). Comparison between groups showed that there was no significant difference between the DNG and the DG before treatment (
p > 0.05), and the DNG showed significantly lower scores than the DG after 6 weeks and 6 months of follow-up (
p < 0.05).
Table 3
Treatment effects on symptom outcomes
NPRS | | | | 0.009 | 0.41 | 0.133 | 0.001 | 0.17 | < 0.001 | 0.136 |
| | | ( -0.42, 1.02) | (-1.496, -0.404) | (-1.835, -0.615) | 0.001 |
DNG(n = 42) | 6.15 ± 1.48 | 2.10 ± 1.28*△ | 2.45 ± 1.22*△ | | | | | | | |
DG(n = 35) | 5.85 ± 1.75 | 3.05 ± 1.18* | 3.68 ± 1.51*# | | | | | | | |
WOMAC-pain | | | | 0.042 | 0.068 | 0.081 | 0.01 | 0.165 | < 0.001 | 0.199 |
| | | (-0.068, 1.868) | (-1.626, -0.224) | (-2.035,-0.665) | < 0.001 |
DNG(n = 42) | 7.85 ± 2.18 | 2.6 ± 1.63*△ | 2.73 ± 1.38*△ | | | | | | | |
DG(n = 35) | 6.95 ± 2.17 | 3.53 ± 1.52* | 4.08 ± 1.69* | | | | | | | |
WOMAC-stiffness | | | | 0.003 | 0.640 | 0.097 | 0.005 | 0.175 | < 0.001 | 0.094 |
| | | (-0.486, 0.786) | (-1.096, -0.204) | (-1.415, -0.485) | 0.006 |
DNG(n = 42) | 3.53 ± 1.50 | 1.38 ± 1.13*△ | 1.63 ± 1.19*△ | | | | | | | |
DG(n = 35) | 3.38 ± 1.35 | 2.03 ± 0.86* | 2.58 ± 0.87* | | | | | | | |
WOMAC-function | | | | 0.006 | 0.49 | 0.254 | < 0.001 | 0.315 | < 0.001 | 0.174 |
| | | (-2.224, 4.644) | (-10.957, -4.725) | (-10.957, -5.493) | < 0.001 |
DNG(n = 42) | 28.05 ± 8.18 | 9.13 ± 5.82*△ | 11.45 ± 5.38*△ | | | | | | | |
DG(n = 35) | 26.85 ± 7.27 | 16.83 ± 7.45* | 19.68 ± 6.81* | | | | | | | |
WOMAC-total | | | | 0.018 | 0.242 | 0.296 | < 0.001 | 0.403 | < 0.001 | 0.251 |
| | | (-1.546, 6.046) | (-12.497, -6.053) | (-13.411, -7.639) | < 0.001 |
DNG(n = 42) | 39.43 ± 8.96 | 13.1 ± 6.53*△ | 15.80 ± 5.70*△ | | | | | | | |
DG(n = 35) | 37.18 ± 8.07 | 22.38 ± 7.88* | 26.33 ± 7.18*# | | | | | | | |
ROM | | | | 0.003 | 0.626 | 0.060 | 0.029 | | | 0.163 |
| | | (-8.245, 4.995) | (0.792, 14.458) | | | < 0.001 |
DNG(n = 42) | 96.63 ± 15 | 114.50 ± 15.31*△ | | | | | | | | |
DG(n = 35) | 98.25 ± 14.74 | 106.88 ± 15.39* | | | | | | | | |
The WOMAC (pain, stiffness, function, total) scores in the DNG and DG were significantly decreased at the 6-week and 6-month follow-ups compared to those at the pre-treatment time point (P < 0.05). However, in the DG, there was a significant increase in the WOMAC (total) score at the 6-month follow-up compared with that at the 6-week timepoint (p > 0.05). Comparison between groups showed that there was no significant difference between the DNG and the DG before treatment (p > 0.05), and the DNG showed significantly lower scores than the DG after 6 weeks and 6 months of follow-up (p < 0.05).
With respect to active ROM of knee flexion, there was a significant increase in the DNG and DG at 6 weeks of treatment compared to that at the pre-treatment time point (P < 0.05). Comparison between groups showed that there was no significant difference between the DNG and the DG before treatment (p > 0.05), and the DNG showed a significantly increased ROM than the DG after 6 weeks of treatment (p < 0.05).
Adverse events
Common dry needling treatment-related adverse events include subcutaneous hematoma, continuous post-dry needling pain, and dizziness caused by hypoglycemia. Common adverse events related to oral diclofenac sodium are gastrointestinal adverse events, renal-function adverse events, and hepatic-function and cardiovascular adverse events. According to the previous literature, all of these adverse drug reactions are predictable. During the 6 weeks’ treatment period, two patients in the DNG dropped out of the trial because of continuous post-dry needling pain, three patients dropped out of the trial because of indigestion (n = 2) and abdominal pain (n = 1), and no serious adverse drug reactions were found in this clinical trial.
Discussion
The current study investigated the effect of treatment with dry needling latent and active MTrPs combined with knee muscle stretching, and it compared that effect with the effect of treatment with oral diclofenac and knee muscle stretching. After treatments, both the groups showed a good effect in knee pain, function, and ROM, However, the DNG showed significantly better results than the DG. Especially in the results ofthe 6-month follow-up, the results of the DNGweresuperior tothose of the DG.
Differentfrompreviousstudiesthat focused on dry needling active trigger points in the treatment of KOA, in this study, in addition to dry needling active trigger points, latent trigger points were also included, and there were several reasons why the latent trigger points dry needle were included. First, latent trigger points have a high prevalence in KOA. The research of Sánchez et al. [
10] showed that the prevalence of latent MTrPs varied from 11 to 50% in various muscles of patients with mild to moderate painful KOA.In contrast, the tensor fasciae latae showed the highest prevalence of latent MTrPs (50%). Our study showed a high prevalence of latent trigger points in rectus femoris, vastus lateralis, biceps femoris, and gastrocnemius, all of which wereover 50%, and gastrocnemius wasthe highest(68.8%). The prevalence of latent trigger points in other muscles was also higher than that in Sánchez et al. The reason may be that the participants of the two studies were different. Most of the participants in Sánchez's study were mild to moderate(Kellgren and Lawrence scale between 1–3). However, the subjects included in this study were mostly moderate to severe (Kellgren and Lawrence scale between 2–4). Therefore, it is possible that the more severe the symptoms of KOA patients, the higher the prevalence of latent trigger points.Second, compared with the activate trigger points, latent MTrPs do not produce spontaneous and recognizable pain under stimulation, however, latent MTrPs play a role in limiting the range of motion, reducing muscle strength, accelerating fatigability, and altering muscle contraction patterns [
30]. Restricted joint ROM is commonly observed in patients with latent MTPs. The number of latent MTPs has been reported to be negatively correlated with the baseline ROM [
31]. Baraja-Vegas [
32] observed an increased stiffness in individuals with latent MTPs,andthis increased muscle stiffness alters muscle contractile properties, restricts joint range of motion, provokes muscle weakness, and accelerates fatigability. In addition, Ge et al. [
33] found that this motor dysfunction may result in incoherent muscle activation of synergists inducing impaired motor control strategies.Third, in the past, latent trigger points were mostly included in the study of healthy subjects or asymptomatic subject [
34‐
36].
However, in recent years, latent trigger points have received attention and have been included in the treatment of various skeletal muscle pain. Calvo Lobo's research showed that dry needling intervention of the latent MTrPwasassociated with the key active MTrP of the infraspinatus reduces pain intensity in the short term in older adults with nonspecific shoulder pain [
37]. The results of Sánchez-Infante's study showed that the application of one session of DN over LTrP decreased the pressure pain, dynamic stiffness, and muscle stiffness values at 72 h after treatment [
38].Another study by Sánchez-Infante showed that one session of DN intervention in latent trigger points of the upper trapezius muscle reduced muscle stiffness and the pressure pain threshold for the dry needling group compared to the sham dry needling group [
30]. Latent trigger points have alsobeenincluded in studies of nonspecific chronic low back pain [
39]. However, in the trigger point treatment of KOA, no latent trigger point has been involved.
Currently, for the treatment of KOA, the active trigger point is primarily involved, and the active trigger point of quadriceps femoris is primarily included because the referred pain of the quadriceps femoris is near the patellofemoral joint. When activated, there is pain in the patellofemoral joint. Patellofemoral Pain Syndrome(PFPS), as the early lesion of OA, often achieves positive effects by needling the active trigger point of the quadriceps femoris [
40,
41]. However, only the active trigger point was included in the treatment of KOA, which cannot achieve a positive effect [
18,
42]. Therefore,latent trigger points may also need to be included in the treatment of KOA, and the reason may be because active and latent MTrPs, as a bundle spasm of muscle fibers, can cause muscle force imbalance, which generates an uneven stress to a certain location in the joint and accelerates cartilage destruction [
43]. If it is not treated in time, eventually, this can result in articular dysfunction from synovial stagnation, hypoxia, synovial hyperplasia, biochemical derangements, angiogenesis, effusion, bone remodeling, and inflammation [
44].In this study, the muscles involved included the quadriceps, the tensor fasciae latae, the hip adductors, the hip abductors, the hamstrings, and the triceps calf and popliteus muscles. These muscles affect the function and biomechanics of the knee joint. Once the trigger points (latent or active) appears, it may lead to abnormal cartilage load through muscle weakness or tightness, and this may further exacerbate the degenerative process of the knee joint [
45,
46].
The effects of the included muscles on joint mechanics are as follows:
-
(1). Quadriceps tightness can lead to an increased compression force of the patellofemoral joint [
47,
48], or because themedial and lateral components of the quadriceps exert different mediolateral forces at the patella, their unbalancemay alter the pressure distribution across the patellofemoral joint and patellar kinematics [
40,
49].
-
(2). The tensor the fascia lata is connected to the patellofemoral through the iliotibial band (ITB) and the sateral patellar retinaculum. The increased tension of the tensor fascia lata increases thepatellar lateral translation and tilt and increases thelateral cartilage pressure [
50,
51].
-
(3). The hamstrings, apart frombeing the primary mechanism of knee flexion, also protect the knee from eccentric contraction during the support phase. These both function to cushion the joint and to generate limb deceleration during gait [
52]. In addition, as an antagonist of the quadriceps, tightness of the hamstrings may require higher quadriceps force production or cause slight knee flexion, resulting in increased patellofemoral joint reaction forces [
53,
54].
-
(4). Inanopen-chain, the gastrocnemius muscle can bend the knee joint and ankle plantar flexion, and the soleus muscle can also bend the ankle plantar flexion. However, inaclosed-chain, the gastrocnemius muscle and soleus muscle pull the lower end of the femur and the lower leg backward to straighten the knee joint [
55]. In fact,thegastrocnemius and quadriceps femoris have a co-activation effect when squatting up. However, when the soleus muscle is insufficient, the quadriceps femoris has to use more force to stabilize the knee joint, resulting in strain ofthequadriceps femoris [
56].The primary role of the popliteus muscle is to internally rotate the tibia in relation to the femur in open-chain and stabilization of the external rotation of the femur in relation to the tibia in closed chain situations, and the popliteus muscle tightness will cause difficulty in stretching the knee joint [
57,
58].
-
(5). The gluteus medius is theprimary abductor of the hip. During walking, weak hip abductors of the stance limb produce a pelvic drop on the swing limb and stance knee varus angulation that shifts the line of gravity (LOG) away from the stance knee. This LOG shift increases the knee adduction moment and the medial joint compressive forces, leading to progressive degeneration. The hip adductor muscles may eccentrically counteract the varus angulation of the knee and consequently might unload the medial tibiofemoral joint [
59]. A systematic review identified moderate quality evidence that suggested substantial hip abductor and adductor muscle weakness in people with knee OA [
60].
-
(6). Hip external rotation (the posterior fibers of the gluteus medius and maximus muscles) act eccentrically to control the movements of hip medial rotation during activities with body weight support.The weakness of hip external rotation leads to the internal rotation of the femur, and this contributes to increased lateral forces acting on the patella and greater stress on the lateral patellofemoral joint [
61,
62].
Previous studies have reported that ROM of the knee joint is decreased gradually in individuals with KOA [
63]. It is essential to restore normal length and flexibility to the muscles. Thus, stretching exercises are an effective complementary therapy and play an important role in the treatment of patients with KOA [
16,
64]. The stretching technique for muscles improved pain ratings, joint stiffness, function, and ROM, and specifically, stretching therapy for the surrounding muscles of the knee can improve muscle flexibility and correct muscle imbalance so as to decrease the stress concentration in the knee. However, one should be careful of achieving this by direct stretching exercises when a muscle is still in pain and spasm. Direct stretching may cause more pain and more spasm in the painful muscle [
65]. Therefore, stretching is appropriate after pain relief. In this study, dry needling and oral drugs in the DNG and DG groups significantly reduced pain, and the ROM of both groups significantly improved through treatment combined with stretching. However, the ROM of the DNG group was significantly better than that of the DG group. Similar to this study, previous research has reported improved joint ROM follwing dry needling trigger points [
66,
67]. The observed changes in joint ROM could be associated with a relaxation of the MTrPs [
68]. The reason might be that TrPS can change the structure of the muscle by increasing the stiffness in muscle cells and tissues, and the dry needling can release the contracture nodule of the trigger points, thus decreasing resistance when stretching the muscle [
69,
70].
Traditionally, clinicians have relied heavily on the use of NSAIDs, including diclofenac sodium to treat the symptoms of KOA, such as inflammatory pain and joint stiffness. Diclofenac is a proven, commonly prescribed nonsteroidal anti-inflammatory drug (NSAID) that has analgesic, anti-inflammatory, and antipyretic properties and has been shown to be effective in treating a variety of acute and chronic pain and inflammatory conditions.Despite its side effects, diclofenac sodium still remains the drug of choice [
71]. Clinical studies have repeatedly shown that NSAIDs can alleviate pain and improve function in KOA patients [
72]. In terms of the NPRS and WOMAC function, DNG and DG improved significantly in 6-week and 6-month follow-ups compared with pre-treatment. However, the DNG showed advantages in the NPRS and WOMAC function whether in the 6-week or 6-month follow-up. Moreover, DG showed significant regression at the 6-month follow-up compared with the 6-week in NPRs and WOMAC- total. However, DNG showed no significant difference between 6-months follow-up and 6-week. The advantages of dry needling trigger points may be that compared with oral diclofenac, dry acupuncture trigger point can not only alleviate pain, but also restore the mechanical imbalance of the skeletal muscle around the knee joint caused by the trigger point, thus improving the clinical symptoms of knee osteoarthritis.
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