Degenerative Joint Diseases



Degenerative Joint Diseases





OSTEOARTHRITIS (OA)

Degenerative joint disease (osteoarthritis, osteoarthrosis) is the most common form of arthritis and represents a heterogeneous group of joint abnormalities with similar clinical, pathologic, and imaging features. Symptomatic OA is defined by the American College of Rheumatology as a group of conditions that lead to joint symptoms and signs, which are associated with the defective integrity of articular cartilage, in addition to related changes in the underlying bone at the joint margins. In 1994, at a meeting of the World Health Organization (WHO) and the American Academy of Orthopedic Surgery, a definition of osteoarthritis was proposed as follows: “OA is the result of both mechanical and biologic events that destabilize the normal coupling of degradation and synthesis of articular cartilage and subchondral bone. Although it may be initiated by multiple factors including genetic, developmental, metabolic, and traumatic, OA involves all of the tissues of the diarthrodial joint. Ultimately, OA is manifested by morphologic, biochemical, molecular, and biomechanical changes in both cells and matrix that leads to softening, fibrillation, ulceration and loss of articular cartilage, sclerosis and eburnation of subchondral bone, osteophytes, and subchondral cysts. When clinically evident, OA is characterized by joint pain, tenderness, limitation of movement, crepitus, occasional effusion, and variable degrees of local inflammation.” In its primary (idiopathic) form, OA affects individuals aged 50 years and older; in its secondary form, however, osteoarthritis may be seen in a much younger age group. Patients in the latter group have clearly defined underlying conditions leading to the development of degenerative joint disease (see Fig. 1.1).

Some authorities postulate that there are two types of primary degenerative joint disease. The first form is apparently closely related to the aging process (“wear and tear”) and represents not a true arthritis but a senescent process of the joint. It characteristically shows limited destruction of the cartilage, slow progression, lack of significant joint deformity, and no restriction of joint function. This process is not affected by gender or race. It is in reality a manifestation of aging and can be seen in virtually every species, from old fish to old people. The second type, a true osteoarthritis, is unrelated to the aging process, although it shows an increased prevalence with age. Genetic factors have been found to be strong determination of this form of osteoarthritis. The nature of the genetic influence, however, is partially speculative and may involve a structural defect (i.e., collagen), alterations in cartilage or bone metabolism, or alternatively a genetic influence on known environmental risk factors such as obesity, sports, and trauma. Several studies have implicated linkages to osteoarthritis on chromosomes 2q, 9q, 11q, and 16p, among others. Implicated genes include VDR, AGC1, IGF-1, ER alpha, TGF beta, cartilage matrix protein (CRTM), cartilage link protein (CRTL), and collagens II, IX, and XI. Most recent studies also suggested that mutations in the gene GDF5, also known as cartilage-derived morphogenetic protein 1, could be linked with etiology of osteoarthritis of the hip and knee. Some investigators suggested that osteoarthritis in some families might be caused by the mutations in the type II collagen gene COL2A1, which encodes a protein expressed almost exclusively in cartilage. This mutation weakens the matrix and leads to premature degeneration of the cartilage. Marked by progressive destruction of the articular cartilage and reparative processes such as osteophyte formation and subchondral sclerosis, true osteoarthritis progresses rapidly, leading to significant joint deformity. This form may be related to genetic factors, as well as to gender, race, and obesity. It has been shown that osteoarthritis tends to affect women more commonly than men, particularly in the proximal and distal interphalangeal joints and the first carpometacarpal joints. In the population older than 65 years, osteoarthritis affects Caucasians more commonly
than African Americans. Obesity is associated with a higher incidence of osteoarthritis in the knees, which may be related to an excessive weight-bearing load on these joints.

Generally, in osteoarthritis, the large diarthrodial joints such as the hip or knee and the small joints such as the interphalangeal joints of the hand are most often affected; the spine, however, is just as frequently involved in the degenerative process (Fig. 5.1). The shoulder, elbow, wrist, and ankle are unusual sites for primary osteoarthritis, and if degenerative changes are encountered in these locations, secondary arthritis should be considered. It should be kept in mind, however, that evidence exists for an association between degenerative arthritis in unusual sites and certain occupations. Even primary osteoarthritic changes may develop more rapidly, for example, in the lumbar spine, knees, and elbows of coal miners and in the wrists, elbows, and shoulders of pneumatic drill operators. Degenerative changes are also commonly seen in the ankles and feet of ballet dancers and in the femoropatellar joints of bicyclists.






Figure 5.1Highlights of the morphology and distribution of arthritic lesions in primary osteoarthritis.

Ordinarily, osteoarthritis manifests clinically by two cardinal symptoms: joint pain exacerbated by activity and usually short-lasting joints stiffness. Some other symptoms include focal swelling of the joints, cracking of the joints, locking of the joints, and difficulty with daily activities.

An overview of the clinical and imaging hallmarks of degenerative joint disease is presented in Table 5.1.









Table 5.1 CLINICAL AND IMAGING HALLMARKS OF DEGENERATIVE JOINT DISEASE
















































































































































Type of Arthritis


Site


Crucial Abnormalities


Techniquea/Projection


Primary osteoarthritis (F > M; >50 years)


Hand


Degenerative changes in:


Dorsovolar view




Proximal interphalangeal joints (Bouchard nodes)


Distal interphalangeal joints (Heberden nodes)


Hip


Narrowing of joint space


Subchondral sclerosis


Marginal osteophytes


Cysts and pseudocysts


Superolateral subluxation


Anteroposterior view


Knee


Same changes as in hip


Varus or valgus deformity


Degenerative changes in


Anteroposterior view


Weight-bearing anteroposterior view




Femoropatellar compartment


Patella (tooth sign)


Lateral view


Axial view of patella


Spine


Degenerative disk disease




Narrowing of disk space


Degenerative spondylolisthesis


Osteophytosis


Lateral view


Lateral flexion/extension views


Anteroposterior and lateral views



Spondylosis deformans


Degenerative changes in apophyseal joints


Foraminal stenosis


Spinal stenosis


Anteroposterior and lateral views


Oblique views (cervical, lumbar)


CT, myelogram, MRI


Secondary osteoarthritis


Hip


Similar changes to those in primary osteoarthritis


Standard views



Posttraumatic


Knee


History of previous trauma




Shoulder, elbow, wrist, ankle (unusual sites)


Younger age



FAI syndrome


Hips


Bone formation at the head/neck junction


Acetabular crossover sign


MRI/MRa



Slipped capital femoral epiphysis


Hips


Herndon hump


Narrowing of joint space


Osteophytosis


Anteroposterior and frog lateral views



Congenital hip dislocation (F > M)


Hips


Signs of acetabular hypoplasia


Anteroposterior and frog lateral views



Perthes disease (M > F)


Hip


Unilateral or bilateral


Osteonecrosis of femoral head


Coxa magna


Lateral subluxation


Anteroposterior and frog lateral views



Inflammatory arthritis


Hip


Medial and axial migration of femoral head


Standard views




Knee


Periarticular osteoporosis


Limited osteophytosis



Osteonecrosis


Hip


Increased bone density


Anteroposterior views (hip, shoulder)




Shoulder


Joint space usually preserved or only slightly narrowed


Grashey view (shoulder)





Crescent sign


Frog lateral view (hip)



Paget disease (>40 years)


Hips, knees, shoulders


Coarse trabeculations


Thickening of cortex


Standard views of affected joints


Radionuclide bone scan



Multiple epiphyseal dysplasia


Epiphyses of long bones


Dysplastic changes


Narrowing of joint space


Osteophytes


Standard views of affected joints



Hemochromatosis


Hands


Degenerative changes in second and third metacarpophalangeal joints with beaklike osteophytes


Chondrocalcinosis


Dorsovolar view



Acromegaly


Large joints


Joint spaces widened or only slightly narrowed


Standard views of affected joint




Hands


Enlargement of terminal tufts


Beaklike osteophytes in heads of metacarpals


Dorsovolar view


a Radionuclide bone scan is used to determine the distribution of arthritic lesions in the skeleton.


CT, computed tomography; F, female; FAI, femoroacetabular impingement; M, male; MRa, magnetic resonance arthrography; MRI, magnetic resonance imaging.




OSTEOARTHRITIS OF THE LARGE JOINTS

The hip and knee joints are the most common sites of osteoarthritis. The severity of radiographic changes does not always correlate with the clinical symptoms, which may vary from stiffness and pain to severe deformities and limitation of joint function.


Osteoarthritis of the Hip


Clinical Features

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.


Pathology

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).






Figure 5.2Pathology of osteoarthritis of hip joint. Coronal section of the resected femoral head (A) and radiograph of the gross specimen (B) show a large flat osteophyte extending from the medial aspect to the region of fovea (arrows). (Modified from Bullough PG. Atlas of Orthopedic Pathology with Clinical and Radiologic Correlation. 2nd ed. New York, NY: Gower Medical Publishing; 1992, Figs. 10.11 and 10.12, p. 10.5.)

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).







Figure 5.3Pathology of osteoarthritis of hip joint. Coronal section of the osteoarthritic femoral head shows subchondral bone partially denuded of articular cartilage (arrow). Some articular cartilage remains intact (arrowhead). Observe in the exposed subchondral bone focal bone marrow necrosis (yellow area) because of localized overloading (curved arrow). (Modified from Bullough PG. Atlas of Orthopedic Pathology with Clinical and Radiologic Correlation. 2nd ed. New York, NY: Gower Medical Publishing; 1992, Fig. 9.31.)


Imaging Features

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



  • Narrowing of the joint space as a result of thinning of the articular cartilage.


  • Subchondral sclerosis (eburnation) caused by reparative processes (remodeling).


  • Osteophyte formation (osteophytosis) as a result of reparative processes in sites not subjected to stress (so-called low-stress areas), which are usually marginal (peripheral) in distribution.


  • Cyst or pseudocyst formation resulting from bone contusions that lead to microfractures and intrusion of synovial fluid into the altered spongy bone; in the acetabulum, these subchondral cystlike lesions are referred to as Eggers cysts.






Figure 5.4Histopathology of osteoarthritis of hip joint. Photomicrograph of a portion of the articular cartilage of a femoral head shows a fibrous pannus extending over the articular surface (H&E, original magnification ×4). (From Bullough PG. Atlas of Orthopedic Pathology with Clinical and Radiologic Correlation. 2nd ed. New York, NY: Gower Medical Publishing; 1992, Fig. 9.43, p. 9.17.)

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).


Postel Coxarthropathy

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).






Figure 5.5Osteoarthritis of the hip joint. A: A 51-year-old woman presented with a history of right hip pain for the past 10 years and no previous history suggesting predisposing factors for osteoarthritis. Anteroposterior radiograph of the hip demonstrates the radiographic hallmarks of osteoarthritis: narrowing of the joint space, particularly at the weight-bearing segment (arrow), formation of marginal osteophytes (open arrows), and subchondral sclerosis. Note the lack of osteoporosis. B: In another patient, a 65-year-old woman, observe in addition to joint space narrowing, subchondral sclerosis, and osteophytosis, formation of a typical Egger cyst in the acetabulum (arrow). C: Anteroposterior radiograph of the left hip of a 76-year-old man shows narrowing of the joint space mainly at the weigh-bearing segment, subchondral sclerosis, and geode within the femoral head (arrow). D: Conventional radiograph of the right hip joint of a 63-year-old woman with a long history of osteoarthritis demonstrates the classic features of this condition: joint space narrowing, subchondral sclerosis, and osteophytosis. E: Anteroposterior radiograph shows advanced osteoarthritis of both hip joints in this 70-year-old man.






Figure 5.6CT of osteoarthritis of the hip joint. A: Coronal reformatted image shows diminution of the joint space, osteophytes, and subchondral cysts in the femoral head. B: In another patient, a 69-year-old man, 3D-reconstructed CT image of the pelvis shows advanced osteoarthritis of the right hip joint and moderate OA of the left hip joint.






Figure 5.7CT of osteoarthritis of the hip joint. A: Anteroposterior radiograph of the left hip of a 66-year-old woman shows narrowing of the joint space, subchondral sclerosis, and cystic-like lesion in the acetabulum, better demonstrated on the coronal reformatted CT image (B). In another patient, a 71-year-old woman, coronal reformatted CT image of the right hip joint (C) shows geodes in the femoral head and acetabulum. D: Coronal reformatted CT image of the left hip joint of a 55-year-old woman shows narrowing of the joint space, subchondral sclerosis, and osteophytosis.






Figure 5.8CT and MRI of osteoarthritis of the hip joint. A 57-year-old man presented with history of pain in the right groin and “locking” and “clicking” in the hip joint. A: Conventional radiograph shows advanced osteoarthritis of the hip joint. There is suggestion of an osteochondral body in the medial joint compartment, better demonstrated on the coronal reformatted CT image (B). C: Coronal T2-weighted fat-suppressed MR image shows in addition a large joint effusion.






Figure 5.9MRI of osteoarthritis of the hip. Coronal proton density-weighted fat-suppressed MR image of the right hip of a 68-year-old woman shows joint space narrowing, subchondral sclerosis and bone marrow edema, osteophytes arising from the femoral head and acetabulum, and joint effusion.






Figure 5.10Migration of the femoral head. A: Superolateral migration of the femoral head is present in this 59-year-old woman with advanced osteoarthritis of the right hip joint. B: Another example of superolateral migration of the femoral head in an 80-year-old man. C: Medial migration of the femoral head is apparent in this 48-year-old woman with osteoarthritis of the right hip. D: Another example of medial migration of the femoral head in a 70-year-old man. E: Axial migration of the femoral head is evident in this 57-year-old woman who was suspected of having inflammatory arthritis. Clinical and laboratory investigations, however, led to a diagnosis of idiopathic osteoarthritis, which was confirmed on histopathologic examination after total hip replacement.






Figure 5.11Rheumatoid arthritis with superimposed secondary osteoarthritis. Anteroposterior radiograph of the right hip of a 42-year-old woman with a known history of long-standing rheumatoid arthritis shows the typical changes of inflammatory arthritis, including axial migration of the femoral head and acetabular protrusio. Superimposition of secondary osteoarthritis is evident in subchondral sclerosis and formation of marginal osteophytes.


Secondary Osteoarthritis

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.


Femoroacetabular Impingement Syndrome

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.






Figure 5.12Postel coxarthropathy. A: Anteroposterior radiograph of the right hip of a 72-year-old man who had pain in the hip for 4 months shows the typical appearance of this arthrosis, which often mimics Charcot joint or infectious arthritis. Note the destruction of the articular portion of the femoral head, which is flattened and laterally subluxed. There is eccentric depression of the lateral articular surface. The same destructive process has led to widening of the acetabulum. B: Similar deformity of the right hip joint is seen in this 69-year-old woman. Note relative absence of osteophytes.






Figure 5.13Postel coxarthropathy. A: Osteoarthritis of the right hip joint in this 61-year-old woman markedly progressed in a very short time as seen on the radiograph obtained 5 months later (B).






Figure 5.14CT of Postel coxarthropathy. Coronal reformatted CT image of the right hip shows characteristic features of this destructive arthritis: marked deformity of the femoral head with flattening of the subchondral segment assuming hatchet-like appearance, widening of the acetabulum, and relatively only mild reactive changes.






Figure 5.15Arthrography and MRI of Postel coxarthropathy. A: Anteroposterior radiograph of the right hip of a 44-year-old man shows destructive changes of the femoral head and acetabulum. B: Aspiration arthrogram, which was performed to rule out infection, shows hypertrophic synovitis. C: Gradient echo T2*-weighted MRI shows joint effusion, hypertrophied synovium, and subchondral cysts in the acetabulum and femoral head.






Figure 5.16Posttraumatic osteoarthritis. Anteroposterior radiograph of the pelvis of a 40-year-old man, who 7 years prior to this examination sustained a complex fracture of the right proximal femur and acetabulum, shows a deformity of the femoral head and neck associated with narrowing of the hip joint space, subchondral sclerosis, and osteophyte formation. Note the completely normal left hip joint.






Figure 5.17CT of posttraumatic osteoarthritis. A 64-year-old man, who in the past sustained complex right acetabular and femoral fractures, developed secondary osteoarthritis. A: Preliminary scout CT image shows posttraumatic deformity of the acetabulum and femoral head associated with acetabular protrusio. B: Axial CT section through both hips shows osteoarthritic changes of the right femoral head and ununited fracture of the anterior column (arrow). C: Coronal reformatted image demonstrates significant narrowing of the joint space, deformity of the femoral head, and periarticular sclerosis. All CT features are consistent with posttraumatic osteoarthritis.






Figure 5.18Secondary osteoarthritis because of slipped capital femoral epiphysis (SCFE). A: Anteroposterior radiograph of the pelvis of a 40-year-old man with history of SCFE shows osteoarthritic changes of the left hip joint. Note osseous remodeling at the junction of the femoral head and neck, a hallmark of this condition, known as a Herndon hump (arrow). B: In another patient, a 24-year-old woman with OA of the left hip joint, observe a characteristic Herndon hump (arrow) pointing to SCFE as the underlying cause of arthritis.






Figure 5.19Secondary osteoarthritis because of developmental dysplasia of the hips (DDH). Coronal reformatted (A) and 3D reconstructed with surface-rendering algorithm (B) CT images of the hips of a 30-year-old woman with history of bilateral congenital hip dislocation show dysplastic changes of both hip joints. There is evidence of secondary osteoarthritis manifested by narrowing of the joint spaces, subchondral sclerosis at the site of femoral heads and acetabula, and formation of small marginal osteophytes at the periphery of both acetabula.






Figure 5.20Secondary osteoarthritis because of osteonecrosis. A 48-year-old man, a chronic alcoholic, developed osteonecrosis of both femoral heads, marked by increased bone density and subchondral collapse. Secondary osteoarthritis is distinguished by narrowing of the joint space, marginal osteophytosis, and subchondral cyst formation.






Figure 5.21Secondary osteoarthritis because of Paget disease. A: Radiograph of the pelvis of an 80-year-old woman shows cool phase of Paget disease affecting pelvic bones and both femora. Note advanced osteoarthritis of both hip joints with almost complete obliteration of the joint spaces. B: In another patient, a 75-year-old woman with long-standing polyostotic Paget disease, anteroposterior radiograph of the right hip demonstrates advanced osteoarthritis associated with acetabular protrusio.






Figure 5.22Secondary osteoarthritis because of joint infection. Anteroposterior radiograph of the pelvis of a 49-year-old man with history of septic arthritis of the right hip joint and acetabular osteomyelitis shows deformity of the acetabulum, subchondral sclerosis, and significant narrowing of the joint space. Note unremarkable left hip joint.






Figure 5.23Secondary osteoarthritis because of inflammatory arthritis (RA). A: Radiograph of the right hip of a 60-year-old woman shows concentric narrowing of the joint space and acetabular protrusio, features of inflammatory arthritis. Superimposed are features of osteoarthritis comprising sclerotic changes of the femoral head and acetabulum and osteophytosis. B: In another patient, a 38-year-old woman with bilateral hip rheumatoid arthritis, observe typical features of inflammatory arthritis and secondary osteoarthritic changes manifesting mainly by formation of prominent osteophytes. C: Similar example of secondary osteoarthritis superimposed on rheumatoid arthritis affecting both hip joints is seen in an 81-year-old woman. D: Coronal reformatted CT image of the right hip of a 40-year-old woman with rheumatoid arthritis shows subchondral and osseous erosions of the femoral head and acetabulum and super-imposed secondary osteoarthritic changes in form of subchondral sclerosis of the acetabulum and osteophyte formation.






Figure 5.24Secondary osteoarthritis because of inflammatory arthritis (psoriasis). Radiograph of the pelvis of a 64-year-old man with clinically documented psoriasis shows characteristic for inflammatory arthritis concentric narrowing of the hip joints and axial migration of the femoral heads. In addition note the changes of super-imposed secondary osteoarthritis marked by subchondral sclerosis, osteophytosis, and cyst formation in the left acetabulum and in the right femoral head. The patient also developed left-sided sacroiliitis (arrow). The arrowhead points to unaffected right sacroiliac joint.






Figure 5.25Cam type of FAI. A: Anteroposterior radiograph of the right hip of a 39-year-old woman shows excessive bone buildup at the femoral head/neck junction (arrow). Note secondary osteoarthritis of the hip joint. B: In another patient, a 41-year-old man, tubular appearance of the proximal right femur and the osseous prominence at the femoral head/neck junction assumed a “pistol grip” deformity. Also evident is osteoarthritis of the hip joint.






Figure 5.26CT of cam type FAI. Coronal reformatted (A) and 3D-reconstructed (B) CT image in shaded surface display in a 34-year-old man show bone accretion at the femoral head/neck junction (arrows).







Figure 5.27MR arthrography of cam type FAI. Radial reconstructed MRa images of the hip joint show various characteristic features of this abnormality. A: In a 34-year-old woman—a decreased femoral head/neck offset associated with hypertrophic ossification (arrow). B: In a 32-year-old woman—a fibroosseous lesion at the anterosuperior aspect of the femoral head/neck junction (arrow). C: In a 38-year-old man—a tear of the superior anterior cartilaginous labrum (arrow). D: In a 30-year-old woman—a delamination injury to the acetabular labrum (arrow).


Treatment of FAI and OA of the Hip Joint

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.


Osteoarthritis of the Knee


Clinical Features

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).






Figure 5.28Pincer type FAI. A: Anteroposterior radiograph of the left hip in a 29-year-old woman shows a crossover sign. Note that the posterior acetabular rim outline (yellow line) projects medially (arrow) in relation to the anterior acetabular rim (red line), indicative of acetabular retroversion. B: In a normal hip joint, the posterior acetabular rim outline projects laterally to the anterior acetabular rim.






Figure 5.29MRI of pincer FAI. A: Axial oblique T1-weighted MR image shows deeply seated femoral head secondary to acetabular retroversion. Acetabular depth can be quantified by drawing a line (ab) connecting the posterior and anterior acetabular rims and a parallel line (cd) that passes through the center of the femoral head (red dot). The distance between these two lines defines the acetabular depth, with the value being positive (+) if the center of the femoral head projects lateral to the line connecting the acetabular rims. Negative values (-) indicate deep seating of the femoral head within the acetabulum. B: Axial oblique MR image of normal hip joint is shown for comparison.






Figure 5.30Femoroacetabular impingement—calculation of alpha angle. The alpha angle is formed by the intersection of two lines: line AB, drawn from the center of the femoral head (A) to the point where peripheral osseous contour of the anterior femoral head intersects the extrapolated circle of the femoral head (B), and the second line AC, drawn from the center of the femoral head (A) through the longitudinal axis of the femoral neck (C). Normal alpha angle should not exceed 50 degrees. A: Alpha angle calculated on the oblique axial CT image of the right hip in a patient with cam FAI. B: Alpha angle calculated on the oblique axial MR image of the left hip in a patient with cam FAI. The arrows point to excessive bone formation at the anterosuperior aspect of the femoral head/neck junction.






Figure 5.31Knee deformities. Patient with advanced osteoarthritis of the knee joints affecting predominantly the medial compartments developed varus deformities.


Pathology

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).

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Oct 1, 2018 | Posted by in GENERAL RADIOLOGY | Comments Off on Degenerative Joint Diseases

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