Current and future advances in tendinopathies of the hip

Authors: Alison Grimaldi, Rebecca Mellor, Anthony Nasser, Bill Vicenzino, David J Hunter

Abstract

Tendinopathy describes persistent tendon pain and loss of function related to mechanical loading. Two common hip tendinopathies seen in practice are gluteal tendinopathy and proximal hamstring tendinopathy. Both conditions can be frustrating for patients and clinicians due to the delay in diagnosis, significant disability caused and lack of response to common treatments. Tendinopathy is a clinical diagnosis and can most often be made using findings from the patient interview and pain provocation tests, without the need for imaging. Specific education and progressive exercise offer a low-risk and effective option for gluteal tendinopathy and result in greater rates of treatment success than corticosteroid injection, both in the short term (8 weeks) and at 1 year. Proximal hamstring tendinopathy is a common, but less researched, and under-recognized cause of persistent ischial pain. As research on proximal hamstring tendinopathy is limited, this review summarizes the available evidence on diagnosis and treatment following similar principles to other well-researched tendinopathies.

Introduction

Tendinopathy is defined as persistent tendon pain and dysfunction related to mechanical loading [1]. Studies from the Netherlands and Denmark have found prevalence rates of lower limb tendinopathies average approximately two per 100 patient presentations [2, 3], and increase with age, and female sex [3]. Gluteal tendinopathy (GT) is the most common lower limb tendinopathy, affecting up to 23.5% of middle-aged women [4]. Often a cause of moderate to severe pain that interferes with sleep and physical function, levels of disability and quality-of-life in people with GT equate to that of end-stage hip osteoarthritis [5].

Gluteal tendinopathy is inconsistently identified/diagnosed—commonly diagnosed as ‘trochanteric bursitis’. This results in suboptimal management. ‘Bursitis’ implies underlying inflammation, which has traditionally been treated with passive strategies such as rest, electrotherapy, non-steroidal anti-inflammatory medications and corticosteroid injections (CSIs) [6]. Although it may co-exist with tendon pathology, isolated bursal pathology is uncommon, and inflammatory cells are rarely present [7, 8]. Structural change in the iliotibial band (ITB) also occurs in some individuals with trochanteric pain [9]. The primary pathology for GT is now understood to be a non-inflammatory insertional tendinopathy of the gluteus medius and/or gluteus minimus [7, 10, 11]. Despite this, many clinicians continue to target inflammation and deliver passive, ‘quick-fix’, low-value interventions [12].

The term Greater Trochanteric Pain Syndrome (GTPS) is commonly used as an umbrella term to encompass all soft tissue pathologies at the greater trochanter, but definitions in the literature are variable and treatment direction for a ‘syndrome’ is often unclear. Here, we use the term ‘gluteal tendinopathy’, a diagnosis that engenders more active treatment approaches, which will also benefit those with accompanying bursal or ITB change.

Proximal hamstring tendinopathy (PHT) is also common and, in the authors’ clinical experience, may occur concurrently with GT. It affects both less active individuals [13], usually perimenopausal women [14], as well as athletes involved in running sports (e.g. prevalence of 12% in distance runners [15]). The primary pathology is insertional tendinopathy of the proximal hamstring tendon(s), predominantly semimembranosus [16]. This pain reduces the ability to sit for prolonged periods [17], can impact athletic performance [18] and has significant occupational and social impacts. PHT is often misdiagnosed due to the complex anatomy of the buttock region, referred pain from other structures and limited awareness of the injury [19].

This review highlights recent advancements and future directions in assessing and managing these common hip tendinopathies and the important clinical implications for the Rheumatologist.

Pathoaetiological factors associated with the development of hip tendinopathy

Pathogenesis of tendinopathy is a multifactorial process, and several theories exist regarding contributing factors [20]. For a comprehensive review, see Millar et al. (2021). Rather than a neat alignment, in tendinopathy collagen fibres become disorganized, with an accumulation of glycosaminoglycans, dysregulated extracellular matrix homeostasis, greater micro-vascularity and neo-innervation [21], leading to loss of tendon integrity. Mechanical loading is an important stimulus for catabolic and anabolic tendon processes, with overload and underload affecting tendon integrity.

Mechanical factors

Occupational and sport-related factors such as overuse, sudden increase in intensity of activity, inadequate recovery, highly repetitive movement and poor ergonomics predispose to the development of tendinopathy [20]. This may also occur in less active/sedentary populations.

Specific types of load may adversely impact tendon health. A combination of high tensile and compressive load is most detrimental [22], particularly in repetitive situations. Conversely, the combination of low tensile loads and compression can compromise load capacity and predispose to pain—even at low activity levels [23].

Tendon loads are influenced by joint position and bony morphology. In GT, a more acute femoral neck-shaft angle may contribute to compressive forces by altering trochanteric offset [24, 25], also reflected in greater differences between iliac wing width and trochanteric width in this population [26] (Fig. 1). ITB compression over the trochanteric soft tissues can also be increased by joint positions such as hip adduction (e.g., sitting with legs crossed) [24].

Figure 1.: Bony features associated with gluteal tendinopathy

Loads imposed on the proximal hamstring tendons are influenced by sagittal plane hip joint position, as they are compressed against the ischium in positions of hip flexion, such as sitting and lunging [27]. The semimembranosus tendon is thought to be most vulnerable to compression due to its deep, lateral origin on the ischium [28].

Other factors

Age, sex and hormonal status are also risk factors [4], evidenced by a high prevalence in post-menopausal women. Advancing age is associated with slower tendon metabolism and poorer regenerative capacity. The ensuing poor collagen content impairs mechanical properties and healing. [29]. Reduced oestrogen levels are associated with reduced collagen synthesis and tensile strength, increasing the risk of tendon rupture [30].

Metabolic risk factors (e.g. obesity, hypercholesterolaemia and diabetes mellitus), have been associated with tendinopathy. Obesity may play a role both systemically and mechanically [31], and body mass index (BMI) is reportedly higher in people with GT than asymptomatic controls [32]. Genetic factors have also been associated with tendon injury; however, most studies have been performed in Achilles [33] and rotator cuff tendinopathies [20].

Various medications have been implicated. Fluoroquinolones can cause pathologic changes in tendon tissue, predisposing to tendinopathy and tendon rupture [34]. The Achilles tendon is the most affected site and is commonly affected bilaterally (44% of cases) [35]. Whilst incidence appears low (rates of 2.4 per 10 000 patient prescriptions for tendinitis and 1.2 per 10 000 for tendon rupture [34]), the risk may be higher in patients with certain comorbidities and magnify other known risk factors (chronic renal failure, diabetes, obesity and systemic corticosteroid use). Other drug types implicated in the development of tendinopathies include statins, glucocorticoids, aromatase inhibitors and anabolic steroids [35].

Assessment of gluteal tendinopathy

Assessment of patients with lateral hip pain involves making a diagnosis, negating other diagnoses, and an assessment of aetiological contributors and/or targets for intervention.

Differential diagnosis of lateral hip pain

The most common conditions associated with lateral hip pain are GT, hip osteoarthritis and lumbar radicular pain. The patient interview provides important clues for the differential diagnosis and directs the subsequent physical examination. Imaging may be required where the diagnosis is unclear, and the patient fails to progress.

Patient interview features

The features most useful in differentiating GT are the area of pain, behaviour of symptoms and absence of other features that are more indicative of hip osteoarthritis or lumbar-related pain (Fig. 2) [36]. Dermatomal pain distribution with paraesthesia is more likely to reflect radicular pain. Lumbar somatic referral may also occur in the lateral hip region (See Fig. 6 for features of somatic referral). GT is characterized by pain and tenderness over the greater trochanter, sometimes extending down the lateral thigh and upper leg, that impacts sleep and causes functional difficulties associated with pain on single-leg loading (stair-climbing, walking, dressing). It is important to note that patients may present with multiple sources of lateral hip pain, necessitating a comprehensive assessment to identify and address all contributing factors.

Figure 2.: Patient interview features of three key differential diagnoses for lateral hip pain

Diagnostic tests for gluteal tendinopathy

To diagnose GT, clinicians can perform palpation of the greater trochanter and various physical tests that load the gluteal tendons [37]. A recent meta-analysis of tests for GTPS [38] found that trochanteric tenderness alone is not adequate for diagnosis, but combining palpation with resisted hip abduction significantly increased the post-test probability of both a positive and negative diagnosis of GTPS. Adding the 30-second single leg stance test helps confirm a positive diagnosis (Fig. 3).

Figure 3.: Diagnostic tests for gluteal tendinopathy

The role of imaging

Clinical examination is usually sufficient for diagnosing GT, with imaging reserved for cases of persistent symptoms. MRI is considered the gold standard for visualizing the gluteal tendons and adjacent soft tissues [7]. It can also provide information on abductor muscle size, quality and other potential pathologies. Ultrasound has also been shown to have good accuracy (US 72% vs MRI 65.2%) and sensitivity (US 89.5% vs MRI 64.7%), but poor specificity (US 16.7% vs MRI 66.7%) in detecting gluteus medius tendon pathology [39]. It is often user-dependent and focuses on an area of pain rather than a global assessment of the region of concern. It is important to note that imaging abnormalities are frequently present in individuals without symptoms [40], highlighting the need for matching imaging findings with the clinical findings.

Other clinical features

Recent work has highlighted impairments in muscle size, quality and function that may be targets for intervention, and psychological characteristics to be considered in the management plan. Patients with GT exhibit significant bilateral hip abductor muscle weakness, even in unilateral presentations [32, 41]. Abductor muscle weakness is accompanied by gluteal atrophy and fatty infiltration [42]. Fine-wire electromyography studies have reported alterations in abductor muscle behaviour during gait [41, 43] and biomechanical studies demonstrate altered gait characteristics that lead to substantially higher loads on the abductor tendons [44]. These impairments may be addressed through rehabilitative exercise.

Psychological factors may impact pain levels, disability, and treatment outcomes. Whilst isolated GT is not typically associated with high levels of psychological distress, patients with higher pain levels and poorer function are more likely to experience psychological distress [45]. Addressing pain, sleep disturbances and functional disability can help alleviate condition-related psychological distress, but some patients may require psychologically-informed rehabilitation or formal psychological intervention. Additionally, patients with multiple concurrent pain conditions may have greater distress [46] and a need for a multidisciplinary approach.

Management of gluteal tendinopathy

Early management of GT is important. Whilst passive interventions such as CSI can provide immediate pain relief, they may compromise tissue health, and the effectiveness of subsequent interventions, and alter patient expectations of care. Substantial advances in understanding and treatment approaches have recently culminated in the high-quality LEAP randomized clinical trial that showed education and exercise to be superior to CSI [47].

Education and exercise approaches

Educational content provided to those with GT aims to educate patients about their condition and implement specific load management strategies (Fig. 4) focusing on gradual progressive increases in load and reduced exposure to positions that compress the tendon. One specific target is reducing sustained or repetitive hip adduction in sitting, standing, sleeping, stretching, and dynamic function [48].

Figure 4.: Load management strategies for gluteal tendinopathy

Exercise therapy involves supervised exercise and/or a home programme, and commonly includes a combination of isometric hip abduction, exercises to improve frontal plane femoropelvic control, heavy slow abductor loading and lower kinetic chain conditioning [47, 49].

The LEAP trial compared the effects of education and exercises against CSI and wait-and-see [47]. The education and exercise group showed significantly higher success rates reflected in the Global Rating of Change measures, than the CSI and wait-and-see groups in both the short (8 weeks) and long term (52 weeks) (Fig. 5). CSI was superior to wait-and-see in the short term, but there was no difference in success rates at 52 weeks. Pain intensity was reduced most in the short term by education and exercise. In the longer-term, pain intensity was not different between exercise and CSI groups, but improvements in pain constancy, and quality-of-life were significantly better in the education and exercise group [47]. Economic analysis, using quality-adjusted life years and total economic costs, also supports education and exercise as a superior cost-effective intervention compared with CSI and wait-and-see groups [50].

Figure 5.: LEAP clinical trial outcomes for management of gluteal tendinopathy

Injection therapies

Despite the high-quality evidence supporting education and exercise as first-line management for GT, our pilot data and observations from the clinic suggest that CSI remains a common initial medical treatment for trochanteric pain in general medical practice. The rationale for CSI has traditionally been to address inflammatory processes underpinning ‘trochanteric bursitis’, although histological studies have shown an absence of typical cellular inflammation [8]. Corticosteroids appear to be potent short-term analgesics, but long-term benefits are usually no better than wait-and-see or other treatments [47, 51, 52]. One study compared CSI against placebo saline injection [53], with no significant between-group differences at 4 weeks or 6 months, concluding that CSI is of limited benefit, considering poor long-term outcomes and potential side effects.

Corticosteroids have adverse biological effects on tendon health, reducing cell viability, collagen synthesis, and mechanical properties of the tendon [54], potentially impacting success of concurrent exercise-based interventions. Combining CSI with rehabilitation may delay and reduce long-term outcomes of physiotherapist-led interventions for tendinopathy [55]. Behavioural effects may also contribute to poorer outcomes. The immediate pain relief CSI provides appears to reduce mindful attention and priority patients place on implementing load management strategies, movement pattern modifications and their prescribed exercise programme. Furthermore, despite the effect waning after a few weeks, the rapid pain reduction imparted by CSI often results in the patient seeking repeat CSI over an active intervention. Although CSI is often provided as a ‘helpful adjunct’ to rehabilitation, it’s likely to be more of a hindrance.

Platelet-rich plasma (PRP) injection has emerged more recently as an alternative to CSI [57]. PRP is believed to induce tendon healing through the delivery of platelet-derived growth factors [56], although evidence of tendon healing in humans is lacking. PRP injections have shown positive effects on pain and disability in tendinopathy, but variable study methodologies make interpretation difficult [57]. Limited evidence, in the form of one trial, currently suggests that PRP for GT may be more effective than CSI in the medium to long term, when provided together with a home programme of advice and exercise [58]. No high-quality evidence exists for PRP against wait-and-see or education and exercise alone.

Shock wave therapy

Shockwave therapy (SWT) is another treatment for GT. This modality applies mechanical impulses to the trochanteric soft tissues to theoretically stimulate a healing response [59]. Low-level evidence exists for pain reduction in the medium-term, following SWT for GT [59]. However, associated pain and bruising often experienced with SWT and cost of multiple sessions should be considered. An education and exercise approach should be first-line management, with SWT reserved for refractory cases.

Hormone therapy

Hormone therapy aims to address the effect of waning oestrogen levels on tendon health in post-menopausal women. Only one study to date has explored the addition of transdermal hormone therapy, or a placebo cream, to an education and exercise intervention for GT [30]. Despite a lack of between-group effect, a responder analysis revealed that those with a BMI ≤ 25 who used the hormone cream had significantly better outcomes compared with the placebo cream group, suggesting that sublingual hormone therapy may be more effective due to higher levels of serum oestradiol and greater absorption of progesterone. Further investigation is needed, but this early evidence suggests that transdermal hormone therapy may benefit individuals with lower BMI when combined with an education and exercise programme.

Surgical interventions

Surgical interventions for GT are typically considered when non-surgical methods fail to provide satisfactory results. Whilst surgical studies show promising outcomes [60], the level of evidence is low due to research design limitations. Based on available evidence, both open and endoscopic gluteal tendon repair yield similar outcomes in terms of patient-reported scores, pain relief, and improvement in abduction strength [61, 62]. Open techniques have a higher reported complication rate [61].

Further high-quality studies are needed to clarify the effects of surgery and identify patients most likely to benefit. Studies investigating common pathways to surgery—i.e., previous treatments and effects—are also required. Multiple CSIs are common before surgery [63, 64]. Whilst it is appropriate to exhaust non-surgical interventions before surgery, the question arises whether multiple CSIs increase the likelihood of subsequent surgery due to the potential reduction in tissue quality and effects of education and exercise interventions. Higher numbers of previous CSIs are also a prognostic factor for poor clinical outcomes following endoscopic surgery for GTPS [65]. Thus, healthcare professionals should consider longer-term implications when advising patients on early treatment options.

Assessment of proximal hamstring tendinopathy

The patient interview and subsequent physical examination drive diagnosis of patients presenting with buttock pain. Imaging is helpful where the diagnosis is unclear, or the patient’s progress is stagnant.

Differential diagnosis of buttock pain

Common conditions associated with buttock pain include injuries to the proximal hamstring tendon-complex, somatic referral from the lumbar spine, hip joint or sacroiliac joint, radiculopathy, entrapment of the sciatic nerve and ischiofemoral impingement [66]. Stress fractures of the sacrum and pelvis, whilst rare, should also be considered, as PHT is common in runners and triathletes.