The greater trochanter and peritrochanteric tissues can be viewed as being analogous to the greater tuberosity and rotator cuff tendons in the shoulder. Both the shoulder and the hip have powerful internal rotators — the subscapularis inserts onto the lesser tuberosity, while the iliopsoas inserts onto the lesser trochanter. The long head of the biceps brachii crosses the humeral head; the reflected head of the rectus femoris crosses in front of the femoral head. Each region features two abductor-external rotators prone to injury — in the shoulder, the supraspinatus and infraspinatus lie deep in the subacromial-subdeltoid bursae; in the hip, the gluteus medius and gluteus minimus lie deep in the trochanteric bursae. Overlying these, a more rigid structure — the acromion in the shoulder and the iliotibial tract in the hip — is implicated as a source for external impingement. In light of these parallels, some refer to the hip abductors — the gluteus medius, gluteus minimus, and to a lesser extent, the piriformis — as the “rotator cuff of the hip.”
Reports of the incidence of GTPS vary depending on the population studied. In one primary care study, the incidence was reported to be 1.8 patients per 1000 per year (24). Hip pain from GTPS occurs across many age demographics but peaks between the fourth and sixth decades (38). Most reports suggest a female predominance in GTPS, but other studies have shown an equal prevalence between men and women (36). Having low back pain may be a risk factor for GTPS. In one report, the prevalence of GTPS in adults with low back complaints ranged from 20% to 35% (42).
The incidence of gluteus medius and minimus tendinopathy is unclear, with relatively few studies reporting its occurrence in both the general and athletic populations. Bunker et al. (6) reported that incidental tears of the gluteus medius or minimus were encountered at their insertions in 22% of 50 consecutive patients who underwent operative management for femoral neck fractures. Howell et al. (18) reported degenerative changes in the hip abductors in 20% of 176 consecutive patients undergoing total hip arthroplasty for osteoarthrosis, and in 16% of these patients, the gluteus medius or minimus was the sole abductor involved.
Risk Factors, Etiology, and Pathophysiology
A number of risk factors have been implicated in the development of GTPS. These include age older than 40 years, female gender, osteoarthrosis, obesity, and low back pain (Table 3). Contact surface asymmetry — such as exclusively running on one side of a crowned road that is convex in the coronal plane — has traditionally been seen as a risk factor for GTPS in runners (41). In one study, 91.6% of patients with “trochanteric bursitis” had other conditions, including peripheral osteoarthrosis and lumbosacral pain (35). Female predisposition to GTPS may be attributed to biomechanical factors unique to women, including the size and shape of the gynecoid pelvis and its association with relative knee valgus and hip varus. This may result in higher tensile stresses to the iliotibial tract and hip abductors, predisposing them to injury.
Athletic risk factors include asymmetric shoe wear, particularly along the lateral aspect; iliotibial tract tightness; gluteus medius weakness or fatigability; running on a coronally convex surface; and typical overuse — doing too much, too fast, too soon. Other biomechanical faults include plantar arch abnormalities and leg-length discrepancy (LLD). Dynamic evaluations for limb length inequalities are likely to be more important than static observations on the examination table (37).
When discussing the pathophysiology of GTPS, it is important to appreciate the relatively wide differential diagnosis of conditions with symptoms that may radiate to the lateral hip (Table 2), as well as the relatively complex anatomy of the peritrochanteric structures. Direct macrotrauma to the lateral hip may result in myotendinous injury, as well as traumatic trochanteric bursitis. Eccentric hyperadduction may exceed tendon tensile elasticity, resulting in strains and tears of various degrees. Cumulative microtrauma — usually a result of overuse and faulty mechanics without adequate reparative recovery — may lead to injury. Iliotibial tract impingement may contribute to friction trauma upon the gluteus medius and minimus tendons, as well as the trochanteric bursae — not unlike subacromial impingement upon the subacromial bursa and rotator cuff tendons in the shoulder. Other potential causes of isolated trochanteric bursopathy include crystal deposition and infection (16). Finally, intrinsic degenerative tendinosis (also called angiofibroblastic tendinosis) also occurs in the hip abductors.
Calcifications about the greater trochanter have been reported in 13% to 40% of patients with chronic GTPS (25,35). A number of authors have found that peritrochanteric calcifications are typically located at the gluteus tendon insertions rather than in the bursae (25,35). The presence of calcific tendinoses in the hip abductors suggests that intrinsic degenerative tendinopathy occurs in chronic GTPS.
While GTPS can develop from several processes, the most common cause of GTPS is likely hip abductor tendinopathy — principally of the gluteus medius and gluteus minimus. One study using magnetic resonance imaging (MRI) found that 14% of patients with lateral hip pain showed tendinosis or degenerative tears in the hip abductors, with the gluteus medius being involved most commonly (20). Only 5% had trochanteric bursal fluids accumulations, and none of these were in isolation. The remainder of the patients had unremarkable hip MRIs — presumably, the primary cause for their hip pain was radiating to the lateral hip from elsewhere (20). Of those with full-thickness tears to the gluteus medius — the so-called “bald trochanters” — 75% underwent surgery; biopsies showed degenerative changes consistent with advanced tendinosis (20). In another MRI study on patients diagnosed with “trochanteric bursitis,” 45.8% had gluteus medius tears, 62.5% had isolated gluteus medius tendinopathy, and none with trochanteric bursitis (3). Bunker et al. (6) reported that gluteus medius and minimus tears occurred most commonly in the anterior aspect near their insertions on the greater trochanter and were usually interstitial or deeper-surfaced tears having a circular or oval appearance with rolled, mature edges. The underlying bone showed reactive sclerotic changes, osteophytes, and cysts (6). The appearance of the pathology encountered in these studies was reminiscent of degenerative rotator cuff tears in the shoulder. In 2008, Silva et al. (39) reported on pathologic specimens from patients diagnosed with “trochanteric bursitis” after trochanteric bursectomy. Their bursal specimens revealed fibroadipose tissue with no signs of acute or chronic inflammation. In a more recent study, 24 participants with GTPS recalcitrant to conservative measures underwent open gluteal tendon reconstruction and trochanteric bursectomy (14). Gluteal tendon and trochanteric bursal specimens were examined histologically, revealing degenerative changes in all tendons and no acute inflammatory tendinitis. Degenerative changes were reported also in the bursae; no acute bursitis was seen (14). These findings strongly suggest that, at least in long-standing GTPS, bursal inflammation does not play a causative role in pain. Additionally the tendinosis encountered in GTPS is likely due to a process intrinsic to the tendon itself. Intrinsic tendinosis has been described in a number of other tendons — including the Achilles, lateral elbow, and rotator cuff (1,22,34). In the study by Bunker et al. (6), gluteus medius tears were reported to be interstitial or deep surface tears. If the primary pathology was external impingement against the iliotibial tract, the tendon lesions would be expected to be on the superficial surface instead.
In chronic cases of GTPS, the initial pathology is often gluteal tendinopathy, with trochanteric bursitis more likely being secondary and reactive — similar to subacromial bursitis occurring with shoulder rotator cuff tendinopathy (20). External impingement may occur, but this is often a secondary effect of myotendinous dysfunction and resulting mechanical derangements. In the shoulder, we have learned that rotator cuff tears may be caused by intrinsic tendon failure, traumatic avulsion, external impingement, or direct trauma, and this is likely to be true in the hip as well.
Clinical History and Physical Examination
GTPS classically presents with chronic, persistent, lateral hip pain in the region of the greater trochanter or peritrochanteric soft tissues. The onset of symptoms may be acute or insidious, and pain is often described as being related to physical activity. Pain may be dull, achy, sharp, or even lancing and may radiate distally along the lateral aspect of the thigh (16). In some cases, myofascial trigger points from gluteus dysfunction may cause referral pain patterns mimicking lumbar radiculopathy (2). This pain may radiate occasionally down to the calf. Exacerbatory factors include lying on the affected hip in a lateral decubitus position, repetitive hip flexion-extension activities (such as walking or running), prolonged standing, leg crossing, or single-legged activities. Repetitive hip internal or external rotation also may exacerbate symptoms.
On physical examination, there is typically direct tenderness to palpation over the greater trochanter, reproducing or accentuating the patient’s pain. Other authors have reported tenderness to areas just posterolateral or superior to the greater trochanter (3). If there was direct trauma to the area, abrasions or ecchymoses may be evident. Passive hip flexion with abduction, external rotation, and extension — the so-called Patrick or FABERE test — may reproduce symptoms. End-range adduction also may elicit lateral hip pain in GTPS. Pain typically is not exacerbated by passive internal rotation — pain with passive flexion and internal rotation suggests an intraarticular problem or perhaps femoroacetabular impingement (FAI). However lateral hip pain produced with active internal rotation, active external rotation, or resisted abduction, at 45° of hip flexion, suggests gluteus medius or gluteus minimus dysfunction. A positive 30-s single-leg stance test — in which pain was reproduced while standing on the affected limb for 30 s — was 100% sensitive and 97.3% specific for gluteal tendinopathy (27). The resisted external derotation test — in which the 90° flexed hip and knee is held with the hip in external rotation and then resisted as the patient attempts to return the limb to neutral rotation — was 88% sensitive and 97.3% specific for gluteal tendinopathy when lateral hip pain was reproduced (27). Additionally a positive Trendelenburg test — abnormal lateral pelvic tilt while assuming a single-legged stance on the symptomatic limb — can aid in detecting gluteus medius tears, with 73% sensitivity and 77% specificity (3). A positive Ober test indicates iliotibial tract contracture. Dynamic evaluation for lateral pelvic tilt and LLDs may reveal biomechanical risk factors that need to be addressed. An examination of the lumbosacral spine and musculoskeletal pelvis and lower extremity neurologic examination also are indicated to exclude potential mimickers in the differential diagnosis (Table 2).
Usually the diagnosis of GTPS can be made on the basis of clinical history and physical examination. However diagnostic imaging may provide valuable clues should the diagnosis be unclear, to exclude other pathology or to evaluate cases recalcitrant to initial therapy.
Plain film radiography may show radio-opacities suggesting calcific tendinopathy or bursopathy. Trochanteric exostoses or osteophytes may be seen in long-standing cases of GTPS. Radiographs are often useful in assessing for osteoarthrosis, FAI, or bony avulsions as well.
MRI provides high-resolution imaging of the complex peritrochanteric anatomy. MRI may show degenerative changes to the gluteus medius and gluteus minimus tendons as abnormal T2 signal change with disturbed tendon architecture on T1-weighted imaging (Fig. 2) (7). Partial-thickness and full-thickness tears in the hip abductors — and in the older population, muscle atrophy, and fatty degeneration — can easily be seen on MRI (26). T2 signal change consistent with trochanteric bursopathy may be evident, but this is not usually seen in isolation.
Musculoskeletal ultrasonography is emerging as an accurate, cost-effective, readily available, and easily applied imaging modality in musculoskeletal medicine. Its most significant limitation, however, is that its diagnostic value is very operator dependent. In a recent study, Fearon et al. (14) showed that, in skilled hands, ultrasonography had a high positive predictive value for peritrochanteric abnormalities. Degenerative changes to the gluteus tendons can be visualized as tenohypertrophy, heteroechogenicity, neovascularity, and disturbed tendon architecture on ultrasonography (Fig. 3). Partial-thickness and full-thickness tendon tears are seen directly as hypoechoic or anechoic foci or indirectly as contour defects, through-transmission enhancement, or edge artifacts. Bursal effusions are seen as large anechoic collections.
Given the sensitivity of both MRI and ultrasonography, it is not surprising that peritrochanteric abnormalities can be seen in asymptomatic individuals (4). Although the absence of pathologic changes on MRI and ultrasonography makes GTPS unlikely, detection of these abnormalities alone is a poor predictor of GTPS and only as useful as the clinical correlation and diagnostic acumen of the physician.
GTPS has a wide differential diagnosis (Table 2). In a series of patients initially diagnosed with “trochanteric bursitis,” later failing conservative treatment, Traycoff (43) used the term “pseudotrochanteric bursitis” for disorders masquerading as GTPS. The most common mimickers were L2–L3 lumbar radiculopathy, lumbar facet syndrome, and subcostal and iliohypogastric entrapment neuropathies.
Given the similarities between the peritrochanteric hip and subacromial shoulder structures, parallels can be found in the management of GTPS and of shoulder rotator cuff (impingement) syndrome. Initial treatment includes relative rest and activity modification to avoid exacerbating activity, usually repetitive hip movements. The patient should be advised to avoid lying lateral decubitus on the side of the injured hip. If hyperadduction causes pain, consider the judicious use of hip abduction pillows. Ice and acetaminophen provide initial palliative relief. The use of nonsteroidal inflammatory drugs (NSAIDs) is controversial in GTPS. While effective as analgesics, long-term NSAID use has been shown to hamper tendon healing elsewhere in the body (8). Given the central role of gluteus dysfunction and tendinosis in GTPS, the potential detrimental effects of NSAIDs should not be overlooked. NSAIDs may be beneficial in acute cases but should be avoided in chronic cases of gluteal tendinopathy. Physical modalities — such as cryotherapy, therapeutic ultrasound, and electrical stimulation — have not been shown to dramatically affect long-term outcomes in GTPS but may play a palliative role when paired with a comprehensive therapeutic exercise program (39). Soft tissue mobilization and massage may be helpful for gluteal trigger points. In the rehabilitation of GTPS, stretching and maintaining normal hip range-of-motion are important — these include both passive and active stretching, including neuromuscular facilitation techniques. Iliotibial tract and tensor fascia lata contractures should be addressed with stretching as well. Painful eccentric strengthening — strengthening a muscle-tendon unit while lengthening the unit — has been shown to improve outcomes in degenerative tendinoses in other areas of the body, including hamstring, rotator cuff, elbow, patellar, and Achilles tendons (10, 19, 28, 32). It is likely that similar improvements in pain, function, and activity tolerance could be attained with eccentric rehabilitation of gluteal tendinosis. Given the importance of the hip abductors in core stabilization, a focus on flexibility, strength, and endurance of the other core and pelvic stabilizing muscles is appropriate. It is also reasonable to address potential biomechanical contributors to GTPS. Interestingly, LLDs have not been definitively established as a causative factor in GTPS by rigorous studies. In one study, measuring leg lengths in patients with and without GTPS, LLDs were not associated with GTPS (37). Nevertheless, a number of authors find it reasonable to look for LLDs and recommend that LLDs greater than 1 cm be corrected with orthoses or heel lifts (37). Pes planus and foot overpronation could be addressed with taping, strapping, or orthoses. Individuals with iliotibial tract contractures and engaged in running or other repetitive activities may find some relief with counterforce bracing, taping, or strapping.
In the past, corticosteroid injections were viewed as a principal treatment for GTPS, based on the assumption that an inflamed trochanteric bursa was to blame (5). These injections can be performed under ultrasound needle guidance or based on surface anatomic landmarks. Studies have shown good short-term relief of pain related to GTPS with corticosteroid injections (23). However longer-term studies have shown steroid injections alone to be inferior to both an exercise training program and extracorporeal shock wave therapy (ESWT) (33). This is likely because trochanteric bursitis is seldom present in isolation in chronic GTPS cases, and failure to address underlying gluteal tendinopathy and pelvic core dysfunction leads to symptom recurrence. Similar to rotator cuff injuries in the shoulder, corticosteroid injections are likely best used as an adjunct to a more comprehensive treatment program including rehabilitative eccentric training, core stabilization, and biomechanical fault correction.
The addition of low-energy ESWT has been shown to improve both pain and hip function in patients with GTPS failing an initial trial of nonoperative conservative treatment. These benefits were demonstrated by Furia et al. (15) in a group of patients with GTPS at 1, 3, and 12 months. Rompe et al. (33) have shown benefit up to 15 months. Presumably, ESWT works on the basis of stimulating a healing inflammatory response in degenerative tendinosis. Unfortunately equipment expenses and a paucity of musculoskeletal medicine specialists trained in the use of ESWT limits its availability in many areas of the United States.
Considered alternatives to more costly surgical procedures, other interventions for chronic degenerative tendinosis include regenerative and proliferative injection therapies. While studies on the effectiveness of these procedures have lacked consistency, their use in treating various tendinopathies is growing in popularity — including the Achilles tendon, patellar tendon, and lateral epicondyle of the elbow (11,12,21,29–31). To date, the use of these therapies in the treatment of GTPS, specifically, has not been well studied. As in ESWT, the aim of these treatments is to rekindle the healing inflammatory response, promote the influx of peripheral stem cells and reparative mediators, and encourage the collagen regenerative and remodeling processes. Prolotherapy involves the injection of nonorganic substances to elicit this response. Examples include 3% NaCl and 10% to 25% dextrose. Regenerative injection therapy involves the injection of biologic, usually autologous, tissue grafts. Examples include autologous whole blood, platelet-rich plasma concentrates, processed lipoaspirate concentrates, and bone marrow aspirate concentrates. Among physicians who perform regenerative and proliferative therapies, many frequently pair these injections with percutaneous needle tenotomy for the treatment of degenerative tendinosis (17). While these procedures can be done via surface anatomy landmarks, ultrasonographic needle guidance helps to ensure precision and higher effectiveness (17). Given the inconsistency in reported efficacy, more research on regenerative and proliferative therapies is needed.
For painful full-thickness and higher-grade partial-thickness tears of the hip rotator cuff tendons — recalcitrant to other treatments — surgery may be considered. Open procedures may involve debridement of devitalized or degenerative tissue, bursectomy, gluteal tendon repair, tendon reconstruction, exostosis and osteophyte excision, and bony fixation of avulsed tissues to the greater trochanter (26). Iliotibial tract lengthening may be performed also (9). Additionally surgeons experienced in hip arthroscopy are performing many of these procedures endoscopically with promising results (45).
GTPS is common and can be a challenge to manage. Trochanteric bursitis is implicated frequently in GTPS but is seldom the sole cause of pain in more chronic cases. It is important to address hip rotator cuff tendinopathy and pelvic core instability. By understanding the complex anatomy of the peritrochanteric structures and pathologic processes most likely responsible for symptomatology and dysfunction, the physician will be better able to provide effective long-term solutions for this common problem.
The authors declare no conflict of interest and do not have any financial disclosures.
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