Commonly, the patient presents with a history of gradual onset of slowly worsening hip pain, localized primarily in the groin, aggravated by movement in the joint, and by weight bearing. This is accompanied by decreasing range of motion. The patient is limping and has difficulty to walk normally, particularly going up and down the stairs. Not infrequently, the patient may experience pain in the knee. This phenomenon occurs because branches of the obturator nerve innervate both the knee and the hip joints.

Some of the pathologic features of osteoarthritis were already outlined in Chapter 1. Generally, the disease is described as occurring in two stages: loss of articular cartilage, followed by reparative process in adjacent bone and cartilage in an attempt to remodel the joint. Gross specimens of resected osteoarthritic femoral head show alterations in the shape of the articular surface and damaged cartilage. In the weight-bearing areas, the cartilage may be entirely absent, and the subchondral bone has a dense, polished, marble-like appearance, termed eburnation (see Figs. 1.20A and 1.21). Cystic-like defects, known as geodes, may be found, filled either with thick fluid or with loose fibromyxoid tissue (see Fig. 1.25). In the non-weight-bearing areas and around its margins, osteophytes develop (Fig. 5.2, see also Fig. 1.20B). As the articular cartilage is progressively destroyed, the underlying subchondral bone is subjected to increasingly localized overload, leading to pressure necrosis (Fig. 5.3). This superficial necrosis is, however, different from primary avascular necrosis (osteonecrosis) that has distinct etiology and pathogenesis (see Chapter 11).

Histopathology shows hypertrophy and hyperplasia of the synoviocytes. Also present are areas of fibrillation, and increase in the ratio of water to the proteoglycan in the cartilage matrix leads to cartilage softening (chondromalacia) (see Fig. 1.22B), followed by formation of the fissures on the cartilaginous surface (see Fig. 1.23). Extension of the hyperplastic synovium (pannus) into the articular surface of the hip joint is a common finding (Fig. 5.4). In deeper sections, at the cartilage-subchondral bone junction, there is often present marked irregularity and duplication of the tidemark (see Fig. 1.24). In the more advanced stages, subchondral sclerosis predominates due to accelerated bone turnover and apposition of small strips of new bone through the process of increased endochondral ossification and osteoblastic deposition (see Fig. 1.25C).

There are four cardinal imaging features of degenerative joint disease in the hip:

These hallmarks of degenerative joint disease can be readily demonstrated on the standard radiographs of the hip (Fig. 5.5). Computed tomography (CT) (Figs. 5.6, 5.7, and 5.8B) and magnetic resonance imaging (MRI) (Figs. 5.8C and 5.9) may further delineate the characteristic features of osteoarthritis.

As articular cartilage is destroyed and reparative changes develop, evidence emerges of a change in the relation of the femoral head with respect to the acetabulum, known as migration. Generally, three patterns of femoral head migration can be observed: superior, which may be either superolateral or superomedial; medial; and axial (Fig. 5.10). The most common pattern is superolateral migration; the medial pattern is less common, whereas axial migration is only exceptionally seen. It should be kept in mind, however, that in inflammatory arthritis of the hip, such as rheumatoid arthritis, in which a previous axial migration of the femoral head is commonly associated with acetabular protrusio, degenerative changes might develop as a complication of the inflammatory process. Thus, one may see secondary osteoarthritis with axial migration (Fig. 5.11).

The osteoarthritis of the hip joint is typically characterized by the presence of osteophytes, which are commonly the most prominent imaging feature of the disease and represent the reparative response to joint destruction. Osteophytes are of two types: peripheral, which arise at the osseous-chondral junction of the femoral neck and head at the sites of capsular attachments, formed through the process of intramembranous ossification, and surface, central osteophytes, occasionally referred to as “surface bumps” because they produce a lumpy and irregular contour to the femoral head, which develop at low-pressure areas at the perimeter of the pressure zones, formed by the process of endochondral bone formation. Similar hypertrophic changes occur on the inferior-posterior wall of the acetabulum. Osteophytes do not develop in the weight-bearing areas because these segments are subjected to constant mechanical abrasions.

Degenerative “cysts” are one of the imaging hallmarks of osteoarthritis, although only some of these structures on histopathologic examination exhibit character of a true cystic lesion. More often, these are solid foci of fibrous or cartilaginous metaplasia; therefore, the term pseudocysts, cystlike lesions, or geodes is probably more accurate. They are usually small, circular, or piriform in shape and confined to subarticular area of sclerotic bone within the segment of high pressure. Larger lesion may also develop deeper in the femoral head and acetabulum. In some cases, a communication channel from the neck of the lesion into the joint cavity can be identified (see Fig. 1.25B).

Occasionally, the degenerative process in the hip may run a more rapid course. In a matter of weeks, a traditionally slowly progressive osteoarthritis of the hip is converted into the rapidly progressive, aggressively destructive disease that completely destroys the hip joint. In some of the patients, the major portion of the femoral head may completely disappear. The acetabulum became concentrically enlarged. The pain in the hip is typically disabling and unrelenting. This destructive arthrosis of the hip joint is known as Postel coxarthropathy, a condition characterized by rapid chondrolysis that may quickly lead to complete destruction of the hip joint. Originally described by Lequesne, and also by Postel and Kerboull in 1970, this unique hip disorder occurs predominantly in women, with age of onset at 60 to 70 years. In all cases, a rapid clinical course of hip pain is the consistent common symptom. The histologic findings are those of conventional osteoarthritis with severe degenerative changes in the articular cartilage. However, osteophyte formation is absent or minimal. Hypervascularity in the subchondral bone is a common finding. The bone trabeculae are either abnormally thickened or abnormally thinned. Occasionally, one can observe foci of fibrosis, interstitial edema and hemorrhage in the marrow spaces, focal marrow fat fibrosis, and focal areas of bone resorption. The precise pathogenesis of this condition remains unclear, although direct drug toxicity and the analgesic effects of nonsteroidal anti-inflammatory drugs have been implicated. Some investigators have suggested that intra-articular deposition of hydroxyapatite crystals might lead to joint destruction. Others have proposed subchondral bone ischemia, cell necrosis, and insufficiency fracture of the femoral head as a cause of this arthritis. Some investigators demonstrated elevated levels of interleukin-6 (IL-6) and interleukin-1 beta (IL-1β) in the joint fluid as well as elevated secretion of matrix metal-loproteinases by fibroblasts from the synovium and subchondral cysts. Because of the rapidity of the process, the radiographic presentation of this condition is marked by very little, if any, reparative changes, mimicking infectious or neuropathic arthritis (Charcot joint) (Figs. 5.12, 5.13, 5.14). More recently, Boutry and colleagues reported magnetic resonance imaging (MRI) findings of this form of osteoarthritis. These included joint effusion, a bone marrow edema-like pattern in the femoral head, neck, and acetabulum; femoral head flattening; and cystlike subchondral defects (Fig. 5.15).

Secondary OA is often seen in the hip joint in patients with predisposing conditions such as previous trauma (Figs. 5.16 and 5.17), slipped capital femoral epiphysis (Fig. 5.18), congenital hip dysplasia/dislocation (Fig. 5.19), osteonecrosis (Fig. 5.20), Paget disease (Fig. 5.21), infectious arthritis (Fig. 5.22), inflammatory arthritides (Figs. 5.23 and 5.24), and femoroacetabular impingement (FAI) syndrome (see text and figures in the next paragraph). The radiographic findings are the same as those described for primary osteoarthritis, but the features of the underlying process also can often be detected. Although the standard radiographic views are usually sufficient for demonstrating these changes, CT, arthrography, or MRI may at times be needed for a more accurate assessment of the status of the articular cartilage.

FAI results from incongruity of the femoral head and acetabulum and is one of the leading causes of precocious osteoarthritis of the hip joint. Two types of FAI have been described based on the predominance of anatomic abnormalities affecting either femoral head or acetabulum. In cam type, the nonspherical shape of the femoral head secondary to excessive bone formation at the junction of head and neck results in abutment against the acetabular rim. In pincer type, because of deep acetabulum (coxa profunda), acetabular protrusio, or acetabular retroversion, acetabular “over-coverage” of the femoral head limits the range of motion in the hip joint and leads to abnormal stresses on acetabular rim. In both types of FAI, the abnormal mechanism results in damage of the acetabular labrum, thus promoting secondary osteoarthritis. The diagnosis of FAI is based on (a) the patient’s clinical history of chronic pain; (b) physical examination revealing reduced range of motion in the hip joint, particularly flexion and internal rotation; and (c) imaging findings on conventional radiography, CT, and MRI. In cam type, conventional radiography demonstrates excessive bone formation at the femoral head/neck junction with loss of normal anatomic “waist” at this site (Fig. 5.25A), occasionally resembling the smooth hand grip of some pistols (“pistol grip deformity” or a “cam effect”) (Fig. 5.25B); an os acetabulum, which more likely represents an osseous metaplasia of the cartilaginous labrum or a fragment of damaged acetabular rim; and a radiolucent lesion at the head/neck junction, formerly called synovial herniation pit, and now designated as fibroosseous lesion. CT shows these abnormalities even better (Fig. 5.26). MR arthrography (MRa), particularly the radial reformatted images, in addition to the findings listed previously, clearly demonstrates abnormalities of the fibrocartilaginous labrum at the anterosuperior portion of the acetabulum (Fig. 5.27; see also Fig. 2.91). In pincer type, particularly in case of acetabular retroversion, conventional radiograph shows “crossover” sign, when more lateral projection of anterior acetabulum, which normally should project medially to the posterior acetabulum, “crosses” the posterior acetabular outline (Fig. 5.28). MRI demonstrates acetabular version and depth of the femoral head coverage (Fig. 5.29). To determine the sphericity of the femoral head and the prominence of the anterior femoral head/neck junction, the alpha angle is calculated on the oblique axial CT or oblique axial MR images (Fig. 5.30). Radial reformatted MR images are of particular value in this respect because they allow optimal visualization of the anterosuperior region of the femoral head/neck junction, where the most significant changes in the alpha angle occur (see Fig. 5.27). The normal alpha angle should not exceed 50 degrees. The larger the alpha angle, the more pronounced is nonspherical shape of the femoral head, and the greater is predisposition for anterior FAI.

In very early stages of FAI, open or arthroscopic trimming of acetabular rim and/or femoral head may be attempted. In younger patients, labral and acetabular repair and/or osteoplasty with reshaping of femoral head/neck junction contributed to satisfactory results. Occasionally, intertrochanteric flexion-valgus osteotomy may also relieve the clinical symptoms. Periacetabular osteotomy is an effective way to reorient the acetabulum in young adults with symptomatic FAI because of acetabular retroversion. Advanced osteoarthritis, whether primary or secondary, is usually treated surgically by total hip arthroplasty using, among the various types available, either a cemented or a noncemented hip prosthesis. The reader is referred to Chapter 4 for more detailed discussion of management. Nevertheless, we strongly recommend the orthopedic surgeon guidance related to expected outcome and possible complications of treatment.

The symptoms are similar to those experienced by the patients with hip osteoarthritis: swelling around the knee joint, crepitus and joint locking, restricted range of motion, short-lasting morning stiffness, and pain that increases with activity and is relieved by rest. Some patients may experience sleep-disrupting pain at night. As the arthritis is progressing, gross deformities of the knees are become obvious, such as valgus or varus configuration (Fig. 5.31).

The pathologic findings are very similar to those described for osteoarthritis of the hip. In the early stages, focal abnormalities are seen in the articular cartilage. Starting in the superficial layers, there is loss of proteoglycan, associated with flaking and surface cracking (Fig. 5.32), followed by formation of fissures (see Fig. 1.23) and focal necrosis (see Fig. 5.3). In the later stages, the exposed subchondral bone exhibits characteristic eburnation (Fig. 5.33). Separated fragments of intra-articular osteophytes and fragments of fibrocartilage and hyaline cartilage remain free in the joint cavity as loose intra-articular bodies. Proliferation of cartilaginous cells may occur on the surface of these loose bodies, and consequently, they grow larger (Fig. 5.34). Sometimes, these chondral bodies may reattach to the synovial membrane (Fig. 5.35A) in which case they are invaded by blood vessels, and through the process of endochondral ossification, they become osteochondral bodies (Figs. 5.35B and 5.36).