Management of hip osteoarthritis

INTRODUCTION — Hip osteoarthritis (OA) is a prevalent disease that affects older adults and poses detrimental consequences on mobility and quality of life. Among those who will live until the age of 85 years, one in four will develop symptomatic hip OA [1]. Important risk factors for the disease, such as previous hip injury, occupations involving heavy physical activity, alterations in joint shape, and family history, may increase this risk substantially [2].

The management of hip OA is reviewed here. Separate pertinent topic reviews include the following:

●(See "Pathogenesis of osteoarthritis".)

●(See "Epidemiology and risk factors for osteoarthritis".)

●(See "Clinical manifestations and diagnosis of osteoarthritis".)

●(See "Overview of the management of osteoarthritis".)

●(See "Total hip arthroplasty".)

PRETREATMENT CONSIDERATIONS

General principles — Similar to the management of osteoarthritis (OA) in other joints, the management of hip OA involves a sequence of nonpharmacologic therapies followed by pharmacologic options aimed at relieving pain and improving function. When these interventions fail to alleviate symptoms and quality of life is compromised, eligible patients may be referred for total joint replacement. Other overall aspects of OA management, including patient education, self-management, and routine monitoring, are key treatment components that are discussed in detail separately. (See "Overview of the management of osteoarthritis".)

Despite its significant societal burden, research regarding both the etiopathogenesis and treatment of hip OA has lagged far behind that of knee OA. Treatment recommendations for hip OA are often extrapolated from the knee, despite specific features of hip joint morphology that may affect which treatment may be appropriate. Among specific features, particular biomechanics and joint shape alterations are probably the most important drivers of the disease. Detection of early disease stages, particularly among patients with alterations in hip joint morphology, may help identify those who will benefit from earlier intervention since they may progress more rapidly.

Our management approach is generally consistent with guidelines developed by professional organizations [3-5].

Assessment for alterations in hip joint morphology — It is important to identify patients in the early stages of hip OA whose disease may be attributed to alterations in hip joint morphology [6]. These patients are typically younger and have milder symptoms; they may benefit from earlier intervention with activity modification and physical therapy (particularly in the case of athletes) and/or referral to an orthopedic surgeon for a possible joint-preserving surgical intervention. (See "Overview of surgical therapy of knee and hip osteoarthritis", section on 'Hip osteotomy'.)

Femoroacetabular impingement (FAI) and acetabular dysplasia are two abnormalities in hip morphology that are associated with the development of early-onset hip OA [6] (see "Epidemiology and risk factors for osteoarthritis", section on 'Anatomic factors'). The more prevalent of these shape alterations is FAI (see "Approach to hip and groin pain in the athlete and active adult", section on 'Femoroacetabular impingement'). These abnormalities are typically detected on hip radiographs. However, radiographic changes related to FAI are common in asymptomatic individuals [7]; thus, routine screening with radiographs in the absence of suggestive symptoms is not indicated.

MANAGEMENT

Initial approach — Nonpharmacologic measures, including education and support for self-management, exercise, and weight control, should be part of the initial approach for all patients with symptomatic hip osteoarthritis (OA) regardless of the severity of symptoms.

Nonpharmacologic measures — Nonpharmacologic interventions for the management of patients with hip OA include exercise, walking aids, and, when pertinent, weight loss (algorithm 1).

Exercise — In all patients with hip OA, we suggest ongoing exercise for reduction of pain and improvement in physical function. No particular activity type has been shown to produce overwhelmingly superior results; thus, exercise programs should be personalized to reflect the unique needs and preferences of each patient [8]. Some of the exercise modalities typically used for hip OA include aerobic exercise, flexibility exercises to improve range of motion, strengthening exercises, and tai chi.

Limited evidence suggests that exercise confers modest improvements in pain and function regardless of content, duration, intensity, or frequency [9,10]. In a Cochrane review including data from 9 trials with 549 patients with hip OA, land-based exercise (eg, functional training and aerobic fitness programs) resulted in reduced pain (standardized mean difference [SMD] -0.38, 95% CI -0.55 to -0.20) and improved physical function (SMD -0.38, 95% CI -0.54 to -0.05) immediately after treatment [10]. The reduction in pain and improvement in physical function translated to a reduction of 8 and 7 points, respectively, on a patient-reported visual analogue scale (0 to 100 points). Although generally favorable, there is less available evidence demonstrating the benefits of water-based exercise. A meta-analysis including 19 studies also reported short-term improvement in pain associated with hip OA for both land- and water-based exercises compared with a minimal intervention control [9]. Only four of the trials included water-based exercises, for which the pooled effect size was comparable to that of land-based exercise. The authors also point to additional theoretical benefits in which the buoyancy offered by the aquatic environment reduces weightbearing forces sustained by the lower limbs. This unloading of the hip joints may assist with pain relief. Water-based exercise in a heated pool has been anecdotally reported as providing additional pain relief. Although water-based exercise is potentially suitable for all individuals with hip OA, it may be especially preferable for those whose severe symptoms limit their ability to engage in land-based exercise.

We typically refer patients to physical therapy, particularly in circumstances where there is hip weakness, stiffness, or significant functional deficits [11]. Physical therapy for hip OA usually involves comprehensive assessment, an individualized exercise program, and adjunctive therapies such as walking aid prescription and manual therapies. The value of physical therapy for hip OA is controversial, with some evidence suggesting it offers little benefit beyond what could be expected from a self-guided exercise program [12]. One well-designed randomized trial compared 49 participants who received education and advice, manual therapy, a home exercise program, and walking aid (if appropriate) with 53 who received a sham treatment (inactive ultrasound and application of inert gel) [13]. The physical therapy group did not demonstrate statistically significant improvements in pain and function compared with the sham group. Two systematic reviews reported that the best available evidence does not support manual therapy for hip OA [9,14]; however, very few trials were available, and more are required to confirm these results. Despite the limited evidence available to support physical therapy treatments, in practice, people with hip OA may choose to consult with physical therapists for specific exercise prescription, advice on physical activity, and mobility problems.

Walking aids — Walking aids such as a cane (on the contralateral or unaffected side), a walker, or crutches may be used as needed for hip OA [15]. Situations in which walking aids may be appropriate may include the presence of severe lower limb joint pain or an increased risk of falling. While there are no data in support of the benefits of walking aids for hip OA, there is limited evidence that the use of a daily cane can reduce pain in patients with knee OA. (See "Management of moderate to severe knee osteoarthritis", section on 'Walking aids'.)

Weight loss — We generally advise that patients with hip OA who are overweight or obese lose weight. This suggestion is largely based on indirect evidence from knee OA, as there are no trials demonstrating the benefits of weight loss for hip OA [3,16]. Obesity is also a known risk factor for hip OA and is associated with more severe disease [17]. (See "Management of knee osteoarthritis", section on 'Weight loss' and "Epidemiology and risk factors for osteoarthritis", section on 'Obesity'.)

We encourage health care professionals to consult available local community programs or refer patients to a dietitian to ensure that patients with obesity or who are overweight are offered optimal support to lose weight. (See "Obesity in adults: Overview of management".)

Pharmacologic measures — Pharmacologic therapies can be used in concert with nonpharmacologic measures for patients with more constant and disabling pain, or after a trial of nonpharmacologic measures if no appropriate pain relief is achieved in around three months (algorithm 1). In our clinical practice, we recommend ongoing exercises even in patients with no or little clinical benefits after a three-month exercise trial led by a physical therapist.

Nonsteroidal anti-inflammatory drugs — For patients with hip OA who have had insufficient relief with nonpharmacologic measures, we suggest oral nonsteroidal anti-inflammatory drugs (NSAIDs), preferably on an as-needed basis. The efficacy of nonselective NSAIDs and cyclooxygenase (COX)-2 inhibitors (coxibs) compared with placebo has been demonstrated in the treatment of hip OA (mainly with respect to pain relief) in randomized trials of individual drugs and in meta-analyses of randomized trials [18,19]. A network meta-analysis of randomized trials comparing NSAIDs with acetaminophen or placebo for the treatment of pain for either hip or knee OA found that all of the NSAIDs included in the analysis improved point estimates of pain symptoms when compared with placebo or acetaminophen [18].

In light of their potential adverse effects, including gastrointestinal ulcers, cardiovascular disease, and renal damage, chronic NSAID use should generally be avoided. We administer oral NSAIDs in the lowest dose and duration possible in patients without contraindications who have substantial symptoms and inadequate response to nonpharmacologic measures. The use of oral NSAIDs as needed is preferred to fixed daily doses for patients with less severe symptoms. The different types of NSAIDs, doses, and adverse effects are discussed in detail separately. (See "Management of moderate to severe knee osteoarthritis", section on 'Oral NSAIDs'.)

Limited role of intraarticular glucocorticoids — We suggest against the routine use of intraarticular glucocorticoid injections for patients with hip OA. We limit the use of intraarticular glucocorticoid injection to patients with moderate to severe hip pain when short-term pain relief is desired and there are contraindications to, or failure of, other treatment alternatives. Image guidance (eg, with ultrasound or, less commonly, fluoroscopy) is usually required for intraarticular hip injections due to technical difficulties owing to the joint's depth and proximity to the femoral vessels.

There are fewer trials assessing the efficacy of intraarticular glucocorticoids for hip OA compared with knee OA. A systematic review including five relatively small trials found that an intraarticular glucocorticoid injection has moderate effects on pain up to eight weeks post injection compared with placebo [20]. In a larger trial including 199 patients with moderate pain from hip OA, patients were randomly assigned to receive advice and education, advice and education plus an ultrasound-guided injection of triamcinolone and lidocaine, or advice and education plus an ultrasound-guided injection of lidocaine alone [21]. Patients in the advice and education plus ultrasound-triamcinolone-lidocaine arm reported greater improvement on a 0 to 10 numeric rating scale of overall hip pain intensity over six months compared with advice and education alone (mean difference -1.43 [95% CI -2.15 to -0.72]). A greater mean improvement was detected at two weeks and two months, but not at four or six months. Hip pain intensity scores were similar in both of the ultrasound-guided injection groups; thus, a placebo response associated with the injections cannot be excluded. Otherwise, there is a paucity of long-term data, and the benefits of glucocorticoid injections appear to be limited after eight weeks. (See "Management of moderate to severe knee osteoarthritis", section on 'Limited role of intraarticular glucocorticoid injections'.)

A single trial investigated the effects of intramuscular injection of triamcinolone acetate compared with placebo for patients with persistent pain from hip OA despite the use of oral analgesics [22]. This trial was conducted to investigate a potential alternative method for glucocorticoid administration due to the inherent difficulties associated with intraarticular hip injections such as the need for imaging guidance. There were improvements in pain (difference -1.3, 95% CI -2.3 to -0.3, on a 0 to 10 numeric rating scale) and function up to 12 weeks in the group that received triamcinolone. It is important to note that systemic administration of glucocorticoids via the intramuscular route presents increased risks of systemic side effects such as hyperglycemia in patients with diabetes and is not routinely performed in most clinical practices for patients with hip OA. More data are needed before intramuscular glucocorticoid injections are offered as an alternative to intraarticular injections.

Limited data also suggest that intraarticular glucocorticoid injections in the hip may be associated with an increased risk of rapidly destructive hip disease (RDHD), characterized as rapidly progressive joint space narrowing, osteolysis, and collapse of the femoral head [23-27]. In a case-control study comparing 40 patients with RDHD with 717 controls who underwent total hip arthroplasty for OA, at least 1 intraarticular glucocorticoid injection was associated with a higher risk of RDHD (odds ratio 8.56, 95% CI 3.29-22.3) [23]. A dose-response effect was also observed, in which the risk of RDHD was higher with increasing the injection dose as well as the number of injections received. Post-injection RDHD was diagnosed radiographically at an average of 5.1 months after injection. RDHD and other complications associated with intraarticular joint injections are discussed in detail separately. (See "Joint aspiration or injection in adults: Complications".)

Refractory symptoms

Surgery — We refer patients for surgical evaluation when they have not improved after a trial of nonpharmacologic and pharmacologic options, have advanced structural hip OA, and have substantial symptoms impacting their quality of life (algorithm 1). Total hip arthroplasty, which is the most common surgical procedure for hip OA, is associated with excellent short- and long-term clinical outcomes when patient selection for surgery is appropriate [28]. (See "Total hip arthroplasty" and "Overview of surgical therapy of knee and hip osteoarthritis".)

THERAPIES LACKING EFFICACY OR OF UNCERTAIN BENEFIT — There are several approaches that have been used as adjunctive measures to treat patients with hip osteoarthritis (OA) that we do not routinely recommend due to the lack of data demonstrating efficacy. In addition, there are other therapies in which the benefit remains uncertain. We discuss a few of these alternative therapies along with the limited available evidence below:

●Duloxetine – Although duloxetine may be used as a therapeutic option for moderate to severe knee OA, there are limited data regarding the use of this agent in the context of hip OA. In an open-label randomized trial including patients with chronic hip or knee OA, 132 patients were administered either duloxetine plus usual care or duloxetine alone [29]. There were no statistically significant differences in Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain scores between the groups at 3 or 12 months. However, limitations to the trial include the high dropout rate, the fact that many participants in the intervention group stopped taking duloxetine, and that only 24 participants reported that their most affected joint was the hip. More data are needed regarding its effects on hip OA before routine use of this medication can be suggested for patients with moderate to severe hip OA. Nevertheless, due to the presumed similar pain mechanisms between patients with moderate to severe knee and hip OA, a trial of duloxetine may be reasonable when clinically appropriate. (See "Management of moderate to severe knee osteoarthritis", section on 'Duloxetine' and "Overview of the management of osteoarthritis", section on 'Mechanisms of pain'.)

●Glucosamine and chondroitin – There is insufficient evidence to support the regular use of glucosamine and chondroitin for hip OA. Only one trial investigated the effects of glucosamine on symptoms and radiographic progression in 222 patients with hip OA and found no benefits over placebo [30]. Many more trials have been performed to evaluate the effects on knee OA, the results of which are conflicting and are discussed in detail separately. (See "Management of knee osteoarthritis", section on 'Nutritional supplements'.)

●Acetaminophen – Due to safety concerns related to acetaminophen (paracetamol) use and emerging evidence of its limited effects on pain, we do not initiate treatment with acetaminophen for hip OA in our clinical practice [31]. A more detailed discussion of the limited efficacy of acetaminophen for knee OA can be found elsewhere. (See "Management of knee osteoarthritis", section on 'Acetaminophen'.)

●Hyaluronans – The use of any intraarticular hyaluronic acid (HA) formulation for hip OA is generally not recommended due to the lack of robust evidence demonstrating benefit. As with trials in knee OA, trials assessing the efficacy of intraarticular HAs for hip OA have found little to no benefit over placebo [32-35]. (See "Management of knee osteoarthritis", section on 'Hyaluronans'.)

●Acupuncture – Limited data suggest that acupuncture has limited to no effect on pain and function in patients with hip OA. A Cochrane meta-analysis found that acupuncture has little or no effect on pain and function in hip OA in the short term based on data from two trials with moderate-quality evidence [36]. There was a small number of participants included in the analysis (105 participants), and the estimates were not precise, suggesting that further research is needed. A single, unblinded trial found clinically significant improvements in clinical outcomes at 12 weeks in participants randomly assigned to acupuncture added to usual primary care compared with usual care alone [37]. Acupuncture is conditionally recommended for treatment of hip OA in the 2019 American College of Rheumatology guideline [4] but has not been included in the 2019 Osteoarthritis Research Society International (OARSI) guideline [5].

●Platelet-rich plasma injections – Due to the limited evidence supporting the efficacy of platelet-rich plasma (PRP) injections for hip OA, we do not recommend their use [38]. A meta-analysis of randomized trials comparing PRP injections with HA found that intraarticular injection with PRP was associated with a reduction in patient-reported pain scores at two months, which were not present at 6 and 12 months [39]. However, these findings are limited due to the small sample sizes, the variability between trials including the different preparations of the PRP, and the lack of placebo as a comparator.

●Opioids – Given the relatively high incidence of adverse effects associated with opioid analgesics, we avoid the use of opioids whenever possible. In addition to safety concerns, there is also evidence that opioids lack clinically meaningful benefits for knee and hip OA patients [40-42]. A randomized trial that included 240 patients with severe chronic back pain or hip or knee OA found that the effects on pain-related function over 12 months was similar between the opioid and nonopioid group, with more adverse medication-related effects in the opioid group [42]. (See "Management of knee osteoarthritis", section on 'Opioids'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Osteoarthritis".)

SUMMARY AND RECOMMENDATIONS

●Similar to the management of osteoarthritis (OA) in other joints, the management of hip OA involves a sequence of nonpharmacologic therapies followed by pharmacologic options aimed at relieving pain and improving function (algorithm 1). Despite its significant societal burden, research regarding hip OA has lagged far behind that of knee OA. Treatment recommendations for hip OA are often extrapolated from the knee, despite specific features of hip joint morphology that may affect which treatment may be appropriate. (See 'General principles' above.)

●It is important to identify patients in the early stages of hip OA whose disease may be attributed to alterations in hip joint morphology, as they may benefit from earlier intervention with activity modification and physical therapy and/or referral to an orthopedic surgeon for a possible joint-preserving surgical intervention. Femoroacetabular impingement (FAI) and acetabular dysplasia are two abnormalities in hip morphology that are associated with the development of early-onset hip OA. (See 'Assessment for alterations in hip joint morphology' above.)

●For all patients with hip OA, we suggest ongoing exercise for reduction of pain and improvement in physical function (Grade 2C). No particular type of activity has been shown to produce overwhelmingly superior results; thus, exercise programs should be personalized to reflect the unique needs and preferences of each patient. (See 'Exercise' above.)

●Walking aids such as a cane (in the contralateral or unaffected side), walker, or crutches may be used as needed for hip OA. While there are no data in support of the benefits of walking aids for hip OA, there is limited evidence from patients with knee OA that the use of a daily cane can reduce pain. (See 'Walking aids' above.)

●We generally advise that patients with hip OA who are overweight or obese lose weight. This suggestion is largely based on indirect evidence from knee OA as no trials have evaluated the effects of weight loss on hip OA. Obesity is also a known risk factor for hip OA and is associated with more severe disease. (See 'Weight loss' above.)

●For patients with hip OA who have had insufficient relief with nonpharmacologic measures, we suggest oral nonsteroidal anti-inflammatory drugs (NSAIDs) rather than acetaminophen, preferably on an as-needed basis (Grade 2B). The choice of NSAID is based on a variety of factors including adverse effect profile, patient comorbidities, cost to patient, and patient preference regarding frequency of administration. (See 'Nonsteroidal anti-inflammatory drugs' above.)

●We suggest against the routine use of intraarticular glucocorticoid injections for patients with hip OA (Grade 2C). We limit the use of injections to patients with moderate to severe hip pain when short-term pain relief is desired and there are contraindications to, or failure of, other treatment alternatives. Image guidance (eg, with ultrasound or, less commonly, fluoroscopy) is usually required for intraarticular hip injections due to technical difficulties owing to the joint's depth and proximity to the femoral vessels. (See 'Limited role of intraarticular glucocorticoids' above.)

●We refer patients for surgical evaluation when they have not improved after a trial of nonpharmacologic and pharmacologic options, have advanced structural OA, and have substantial symptoms impacting their quality of life. (See 'Surgery' above.)

●There are several approaches that have been used to treat patients with hip OA that we do not routinely recommend due to the lack of data demonstrating efficacy. In addition, there are other therapies in which the benefit remains uncertain. Examples of such therapies include duloxetine, glucosamine and chondroitin, acetaminophen, hyaluronans, acupuncture, platelet-rich plasma (PRP) injections, and opioids. (See 'Therapies lacking efficacy or of uncertain benefit' above.)