55: Hip Osteoarthritis

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Hip Osteoarthritis

Patrick M. Foye, MD; Todd P. Stitik, MD


Hip osteoarthritis

Hip degenerative joint disease

Degenerative hip joint


ICD-9 Codes

715.15   Primary (idiopathic) osteoarthritis of the hip

715.25   Secondary osteoarthritis of the hip

716.15   Traumatic osteoarthritis of the hip

ICD-10 Codes

M16.10   Unilateral primary osteoarthritis, unspecified hip

M16.11   Unilateral primary osteoarthritis, right hip

M16.12   Unilateral primary osteoarthritis, left hip

M16.7   Secondary unilateral osteoarthritis, hip

M16.50   Post-traumatic osteoarthritis, unspecified hip

M16.51   Post-traumatic osteoarthritis, right hip

M16.52   Post-traumatic osteoarthritis, left hip


Hip osteoarthritis (OA, also called degenerative joint disease) is the most prevalent pathologic condition at the hip joint. The hip joint (femoroacetabular joint) is a ball-and-socket joint, with the femoral head situated within the concavity formed by the acetabulum and labrum. This anatomic arrangement allows movements in multiple planes, including flexion, extension, adduction, abduction, internal rotation, and external rotation. Significant mechanical forces (three to eight times body weight) [1,2] are exerted on the hip joint during weight-bearing activities such as walking, running, jumping, and lifting. Additional stresses are created by recreational activities (e.g., impacts and falls during sports) and severe trauma (e.g., motor vehicle collisions). Hip trauma is significantly associated with unilateral but not bilateral hip OA, whereas obesity is associated with bilateral but not unilateral hip OA [3]. Occupational heavy lifting and frequent stair climbing seem to increase the risk of hip OA [4].

In a study of 2490 subjects aged 55 to 74 years, the prevalence of hip OA was 3.1%; 58% of hip OA cases were unilateral and 42% were bilateral [3]. The prevalence of hip OA is about 3% to 6% in the white population, but by contrast, it is far lower in Asian, black, and East Indian populations [5]. Total hip replacement in patients with hip OA is twice as common in women [6].

A central feature of hip OA is cartilage breakdown, thus compromising the femoroacetabular articulation. In addition to cartilage, other tissues affected by the disease process include subchondral bone, synovial fluid, ligaments, synovial membrane, joint capsule, and adjacent muscles. Eventually, the joint develops osteophytes (exostosis), joint space narrowing, bone sclerosis adjacent to the joint, and potentially even joint fusion (arthrosis). OA can be classified as either primary (idiopathic) or secondary [7]. The most common form of hip OA is primary [8], which represents the “wear and tear” degenerative changes that occur over time. Hip OA is considered secondary if a specific underlying cause can be identified, such as significant prior hip trauma, joint infection, or preexisting congenital or other deformities [7]. Among patients undergoing total hip replacement, the likelihood that the hip OA was primary (rather than secondary) is highest among white individuals (66%), followed by black subjects (54%), Hispanics (53%), and Asians (28%) [9]. Unlike rheumatoid arthritis, OA is relatively noninflammatory during most stages of the disease process. Symptomatic acetabular structural abnormalities can occur in patients with hip instability from classic developmental dysplasia or post-traumatic acetabular dysplasia as well as with retroversion of the acetabulum [10].


Groin pain is the classic manifesting symptom for hip OA. Other presenting symptoms of hip OA include hip pain, stiffness, and associated functional limitations. Many patients report “hip” pain when really they are referring to the superior lateral thigh region (e.g., greater trochanteric bursitis rather than hip joint disease). Hip joint pain typically presents as groin pain, perhaps with some referred pain down toward (and even beyond) the medial knee. Questioning the patient about lumbosacral, sacroiliac, or coccyx pain may reveal that the “hip” symptoms are actually referred from the spine. Hip OA pain usually has an insidious onset, is worse with activity (particularly weight bearing and rotational loading of the joint), and is somewhat relieved with rest [7]. Advanced OA may be painful even at rest [7]. The physician should specifically ask about any constitutional symptoms that might suggest infection or malignant disease and also about any history of hip trauma [11] (recent or remote).

Physical Examination

Antalgic gait is characterized by a limp with decreased single-limb stance time on the painful limb, a shortened stride length for the contralateral limb, and an increased double support time.

Range of motion should be evaluated not only at both hip joints (in multiple planes) but also at the lumbosacral spine, knees, and ankles to more thoroughly evaluate the kinetic chain. The earliest sign of hip OA is loss of hip internal rotation [12,13]. Limping, groin pain, or limited hip internal rotation supports a diagnosis of a hip (rather than spine) disorder [14], but it still remains prudent also to perform a lumbosacral physical examination when lumbosacral pain generators are being considered. Whereas no one physical examination maneuver is diagnostic of hip OA or other form of intra-articular hip disease, assessment for painful range of motion about the hip, palpation, manual muscle testing, screening for radiculopathy and neuropathy, observation for systemic signs of OA, and performance of a provocative maneuver known as the Patrick test represent a reasonable evaluation. The Patrick test is performed by having the patient supine with the ipsilateral heel on the contralateral knee, thus forming the figure four position, also referred to by the acronym FABER (hip flexed, abducted, and externally rotated) maneuver (Fig. 55.1). The physician pushes the raised leg toward the table, producing groin pain that suggests intra-articular hip disease or back or buttock pain that suggests sacroiliac joint disease.

FIGURE 55.1 FABER maneuver (Patrick test). Pain produced in the groin suggests intra-articular disease, such as hip OA; pain produced in the back or buttock suggests sacroiliac disease.

Palpation of the tissues about the greater trochanteric region, proximal iliotibial bands, sacroiliac joints, gluteal muscles, underlying piriformis and obturator internus muscles, and ischial bursae may reveal pain generators other than the hip joint itself.

Weak hip girdle muscles may be due to pain or disuse, but radiculopathy and neuropathy can also be considered. Hip abductor weakness may be manifested with a Trendelenburg gait [13]. With hip OA, the remainder of the neurologic examination in the lower limbs is normal (e.g., muscle stretch reflexes and sensory testing).

On inspection of the fingers, hypertrophic degenerative changes (exostoses), such as Heberden nodes at the distal interphalangeal joints [12], are independent risk factors for hip OA [11]. Their presence thus increases the likelihood of similar findings at the hip joint.

Functional Limitations

Patients with hip OA often report functional limitations in weight-bearing activities such as walking, running, and climbing stairs. The hip range of motion restrictions may cause difficulties with activities such as donning or doffing socks and shoes, picking up clothing from the floor [15], and getting in and out of cars. Hip pain and weakness may necessitate use of the upper limbs to arise from a chair [15]. A careful history can elicit details of occupational, recreational, and other functional activities that the patient has decreased or ceased because of the hip OA.

Diagnostic Studies

Plain radiography is the primary diagnostic study for hip OA [16] (Fig. 55.2). The severity of radiographic hip OA findings can be categorized on the basis of the minimal joint space (MJS), defined as the shortest distance on the radiograph between the femoral head margin and the acetabular edge [15]. MJS is determined by four joint space measurements (medial, lateral, superior, and axial). Croft’s MJS grades are 0 (MJS > 2.5 mm), 1 (MJS > 1.5 mm and ≤ 2.5 mm), and 2 (MJS ≤ 1.5 mm) [15]. MJS is predictive of hip pain, is strongly associated with other radiographic features of hip OA, and has a high inter-rater reliability [17]. Alternatively, the Kellgren-Lawrence grading system of hip OA is a scale of 0 to 5 that considers not only joint space narrowing but also three additional factors: presence of osteophytes, subchondral sclerosis, and subchondral cysts [15]. Both MJS and Kellgren-Lawrence grade are associated with clinical symptoms of hip OA [15].

FIGURE 55.2 Radiograph demonstrating hip OA, including joint space narrowing, superior migration of the femur within the acetabulum, and subchondral sclerosis.

Magnetic resonance imaging is generally not needed to diagnose hip OA, but it is superior to radiography or bone scan when the differential diagnosis includes avascular necrosis or hip labral tear [18]. Hip joint arthrography is also generally unnecessary for the diagnosis of hip OA but may help define labral tears. Diagnostic musculoskeletal ultrasound can assist in early detection of hip OA, can sometimes demonstrate gross evidence of bone and cartilage damage, can detect associated synovitis [19], and can detect concomitant iliopsoas bursitis [20]. Hip pain that is relieved through intra-articular diagnostic injection of local anesthetic (e.g., with ultrasound [21] or fluoroscopic guidance) can help confirm that the patient’s symptoms are arising from the hip joint and predicts a good surgical outcome with joint replacement [21]. Patients who fail to obtain adequate relief with image-guided anesthetic injection tend to have alternative pathologic processes at the spine (61%) or knee (16%) [21].

Electrodiagnostic studies should be considered when the differential diagnosis includes lumbosacral radiculopathy or peripheral nerve disease.

Differential Diagnosis


Avascular necrosis

Protrusio acetabuli

Hip labral (cartilage) tear

Hip joint infection

Acetabular fracture

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