Adult Reconstruction, 1st Edition

Section 1 - HIP

Part B - Evaluation and Treatment of Hip Disorders

3

Osteoarthritis and Inflammatory Arthritis of the Hip

Mark J. Spangehl

Osteoarthritis and inflammatory arthritis are the most frequently encountered diseases in orthopaedics. They are the leading causes of joint disease in the hip, resulting in joint destruction, and often in the need for hip replacement. Symptomatic osteoarthritis of the hip is prevalent in 3% to 5% of the adult white population. Radiographic evidence of osteoarthritis is more common (9% to 10%), indicating that roughly half of the patients with some radiographic evidence of osteoarthritis are asymptomatic.

Degenerative joint disease (DJD) is a historic term, still often used, that implies degenerative changes owing to various causes. The term DJD can be confusing because it is often used synonymously for osteoarthritis, but can be applied to any condition that results in degenerative changes of the joint. A more correct use of terminology would be to avoid the use of DJD and use the correct underlying diagnosis instead.

Degenerative conditions of the hip can be broadly grouped into noninflammatory and inflammatory arthritis. Osteoarthritis is by far the most common condition of the noninflammatory group. Osteoarthritis results from a primary failure of the cartilage, whereas with inflammatory arthritis, the cartilage failure is secondary to the inflammatory response. Table 3-1 outlines the more common arthritides that can affect the hip joint.

Pathogenesis

Etiology

The development of osteoarthritis (OA) results from a multitude of conditions, with the end result being failure of the weight-bearing cartilage. Because of its various potential causes, OA can be thought of as a syndrome rather than a single entity. In the past, it was felt that most patients who developed osteoarthritis had primary OA without any identifiable cause, arising as a result of a yet unidentified weakness of the cartilage. Now, it is more evident that most patients with OA likely have an underlying mechanical cause that results in damage and subsequent degeneration of cartilage. However, still there are patients in whom no cause can be clearly identified, and these may represent a biologic condition that results in cartilage failure. These patients represent primary osteoarthritis, which can be considered a diagnosis of exclusion.

In recent years there has been a much clearer understanding of various mechanical problems, which may be termed prearthritic conditions, whose natural histories show progression to osteoarthritis. These conditions include mild hip dysplasia as well as femoroacetabular impingement (FAI). FAI has become recognized as a mechanical abnormality of the hip in which the anterior femoral neck impinges on the acetabulum, leading to shear damage of the articular cartilage. Two types of impingement have been described: cam type and pincer type. Originally felt to possibly represent an asymptomatic or subclinical slipped epiphysis, the cam type of impingement has been shown to be a developmental abnormality. During development the femoral head epiphysis and trochanteric apophysis share one physis, which separates into two distinct growth plates around 4 years of age. A delayed separation or abnormal, eccentric closure results in an abnormal morphology typically affecting the anterolateral femoral neck. The effect is a decreased head/neck offset, reducing the head/neck ratio in this region and resulting in impingement of the anterior femoral neck with the anterior rim of the acetabulum (Fig. 3-1). The pincer type of impingement is more a result of an acetabular abnormality. Approximately 16% of dysplastic acetabula are retroverted. This retroversion results in a relatively prominent anterior rim, also causing impingement in flexion. Additionally, a deep acetabulum (coxa profunda) may result in a prominent acetabular rim, causing impingement. Both cam and pincer types of impingement may coexist.

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TABLE 3-1 Arthritides Affecting the HIP

· Noninflammatory arthritis

· Osteoarthritis

· Primary (idiopathic)

· Secondary

· Dysplasia

· Femoroacetabular impingement

· Cam type

· Pincer type

· Slipped capital femoral epiphysis

· Legg-Perthes

· Traumatic

· Osteonecrosis of the femoral head

· Neuropathic

· Multiple epiphyseal dysplasia

· Paget disease

· Pigmented villonodular synovitis

· Chondrocalcinosis

· Hemophilic arthropathy

· Inflammatory

· Rheumatoid arthritis

· Systemic lupus erythematosus

· Spondyloarthropathies

· Psoriatic arthritis

· Ankylosing spondylitis

· Reactive arthritis (Reiter syndrome)

· Enteric spondyloarthropathy

Table 3-1 summarizes various types of inflammatory arthritides. Rheumatoid arthritis is the most common form of inflammatory arthritis. It has a prevalence of 0.3% to 1.5% in North America and is approximately 2.5 times more common in women. The cause is thought to be an autoimmune cell-mediated response. Further pathogenesis is discussed later. The inciting event that begins the inflammatory response has yet to be identified, but is likely an extrinsic factor (e.g., infectious, environmental) in a genetically susceptible host. A genetic predisposition (HLA-B27) has also been shown in seronegative (defined as rheumatoid factor–negative) arthropathies; however, an infectious cause has been more closely linked to certain types. Reactive and enteric spondyloarthropathies have been associated with various gastrointestinal and genitourinary infections.

Epidemiology

Although mechanical abnormalities may be the etiologic factor responsible for most osteoarthritis, there are epidemiologic factors as well. These epidemiologic factors may result in a predisposition of the joint to osteoarthritis as a result of altered mechanics or other yet to be defined biologic factors. Family and twin studies have shown an increased prevalence of osteoarthritis within families. Familial studies have documented an increased incidence in first degree relatives, with 8% to 13% requiring hip replacement or having symptoms of coxarthrosis. Twin studies further underscore the hereditary component of osteoarthritis. Monozygotic female twins older than 50 years of age have been shown to have an approximately 60% heritability or genetic factor for the development of hip osteoarthritis. Additional risk factors for the development of osteoarthritis include increased age (older), race (whites [3% to 5% prevalence] greater than in Asians), as well as gender. In those younger than 50 years of age, men have a higher risk of developing hip osteoarthritis; in those older than 50 years of age, women have a greater incidence of the disease.

Figure 3-1 Coronal oblique view of patient with cam type femoroacetabular impingement. Note the prominence of bone anteriorly (black arrow) resulting in poor head–neck offset and reduced head/neck ratio. Note also anterior labral tear (white arrow).

Although there is clear evidence that obesity is associated with osteoarthritis of the knee, the literature linking obesity to hip disease is less well defined. Nevertheless, a growing body of evidence now more strongly supports the relationship of obesity to hip osteoarthritis. This relationship seems to be important even at a younger age; increased body mass index (BMI) earlier in life (age 18) is a stronger predictor for the development of osteoarthritis than increases in BMI later in life and is associated with increased risk for requiring hip replacement. Increased BMI is also associated with changes in gait patterns. When comparing gait patterns of nonobese and obese persons, changes in gait symmetry, stride width, and hip abduction angles were noted,

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suggesting that a mechanical effect in obese patients could also result in the development of OA. Yet other studies suggest that patients who are obese suffer more hip complaints at the same radiographic stage than nonobese patients, therefore making them more likely to seek hip replacement at an earlier stage than nonobese patients. Possibly therefore, the incidence of radiographic OA is similar in obese and nonobese populations; however, obese populations are more symptomatic and seek treatment sooner for a given stage of osteoarthritis. In summary, studies have shown that obesity is a risk factor in the development of hip osteoarthritis. This association is stronger for women, in whom increased BMI early in life has been shown to be associated with an increased incidence of OA.

Figure 3-2 Etiologic factors associated with the development of osteoarthritis.

Similarly, occupational factors show less association with osteoarthritis of the hip than that of the knee. However, some population studies do suggest that occupation may have some influence on the development of hip osteoarthritis such as the higher prevalence of hip osteoarthritis in European farmers. Other studies have suggested that high-demand recreational activities (professional soccer, track and field, racket sports) may also contribute to hip arthritis. Figure 3-2 outlines various factors that contribute to the development of osteoarthritis.

Rheumatoid arthritis affects women more than men (2.5 times more common in women). A genetic predisposition is supported by studies that show familial clustering and a higher prevalence in monozygotic twins versus dizygotic twins, with monozygotes having a 3.5 greater chance of developing the disease. Further genetic predisposition is supported by the higher prevalence in Native American populations (5% to 6%). Seronegative arthropathies have a genetic predisposition that is dependent on the prevalence of HLA-B27 in a given population. Generally, the greater the prevalence of HLA-B27 in a given population, the higher the prevalence of spondyloarthropathies. HLA-B27 is common in certain Native American populations (up to 50% positive), relatively common in Europeans (7% to 20%), less prevalent in Asians and North American whites (7%), and uncommon in African Americans (1% to 2%). Spondyloarthropathies occur in approximately 5% to 14% of HLA-B27–positive individuals. Seronegative spondyloarthropathies can also occur, less commonly, in individuals who are HLA-B27–negative.

Pathophysiology

Osteoarthritis is a condition that begins as a result of overload of the cartilage. In rare situations there is a true genetic basis to joint destruction in which a generalized joint destruction occurs as a result of a mutation that codes for type II collagen. Much more commonly, the cartilage may be predisposed to damage because of various mechanical conditions in the joint that result in a gradual destruction of the cartilage. There is a failure of the chondrocytes to maintain or repair damaged cartilage. Although chondrocytes are metabolically more active in osteoarthritis, it is postulated that the increased response is inadequate against the increased degradation of products synthesized by the chondrocytes. Characteristic changes occur within the cartilage structure, including changes in water content (increased) and changes in proteoglycan concentrations (overall decrease with shorter chains and increased chondroitin/keratin sulfate ratio). Another characteristic change is collagen destruction: Interleukin 1 (IL-1) from various cells (chondrocytes, synovial cells, neutrophils)

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regulates the production of catabolic enzymes, e.g., metalloproteinases that degrade the core protein of proteoglycans and collagenase resulting in collagen destruction. IL-1 also influences the cartilage matrix by causing a decreased synthesis of types II and IX collagen and an increase in types I and III collagen.

In inflammatory arthritides, the cartilage degeneration is secondary to the inflammatory response, which begins in the synovium. In early rheumatoid arthritis (RA), a microvascular synovial injury appears to occur, resulting in edema and synovial cell proliferation. Lymphocytes and macrophages infiltrate the synovium early on, forming organized lymphoid tissue. Plasma cells are found in more advanced disease. With synovial hyperplasia, the pannus of synovium that extends to the edge of cartilage and bone begins to invade and destroy the bone and cartilage. Synovial macrophages produce cytokines (interleukin 1, tumor necrosis factor [TNF]-α and -β), which in turn regulate the production of various degradative enzymes (metalloproteinases, collagenase, stromelysin) by synovial fibroblasts and chondrocytes, resulting in cartilage destruction. Bony erosions result from multinucleated giant cells, which may originate from the pannus, which is rich in macrophages. Rheumatoid synovial T cells have been shown to produce osteoclast differentiation factor, which may be responsible for the transformation of synovial macrophages into multinucleated giant cells and the subsequent erosion of bone.

Diagnosis

Physical Examination and History

Clinical Features

Pain is the usual presenting feature of hip arthritis, regardless of the cause. Occasionally, there are symptoms that may differentiate osteoarthritis from inflammatory arthritis; however, both may present with similar symptoms of hip pathology.

Symptoms, at least initially, tend to be mostly mechanical with activity-related pain or pain with certain motions resulting from mechanical irritation or impingement. As the disease progresses and becomes more severe, symptoms may also become more constant and may include pain at rest.

Inflammatory arthritis most commonly has multijoint involvement, either polyarticular or oligoarticular. It is rarely monoarticular involving the hip. Although patients with inflammatory disease may have hip symptoms that are mechanical in nature, these patients tend to have a higher occurrence of constant hip pain or rest pain because of chronic synovitis and hip joint effusion.

Symptoms are typically localized to the groin and proximal anterior thigh (roughly 80% to 90% of patients). Pain often radiates down the anterior thigh toward the knee. Buttock and lateral thigh symptoms also occur in many patients, but these symptoms in isolation are less common. The lateral proximal thigh pain is usually felt more deeply and often more proximally (over the abductor muscles), than symptoms of trochanteric bursitis, which are typically over the posterolateral aspect of the greater trochanter and somewhat more superficial. Occasionally patients present with isolated knee pain; however, this pain tends to be more diffuse and slightly more proximal than pain that originates from the knee.

Physical findings depend on the severity of disease. Loss of motion, typically internal rotation, is one of the initial findings. As the arthritis progresses, motion usually becomes more restricted and may eventually result in a nearly ankylosed hip. Adduction and flexion contractures typically occur. Patients may limp, with a decreased stance phase on the affected side, and may show a positive Duchenne sign because of pain and/or weakness. Patients with inflammatory disease usually have less restriction in range of motion unless the disease has caused severe erosion of the femoral head or a significant protrusio deformity of the acetabulum resulting in a captured femoral head.

Radiologic Features

Joint space narrowing as a result of articular cartilage loss is the general radiographic feature of arthritis. Specific radiographic characteristics help differentiate osteoarthritis from inflammatory arthritis. However, differentiation between these two conditions occasionally can be difficult, and both may be present radiographically.

The radiographic features of osteoarthritis of the hip are joint space narrowing, subchondral sclerosis, degenerative subchondral cysts, and peripheral osteophytes. Occasionally the joint space may still be well maintained, but the appearance is somewhat irregular and other features such as peripheral osteophytes or evidence of prearthritic conditions such as femoroacetabular impingement may be present. Initially, the joint space narrowing is often asymmetrical with either a superomedial or superolateral wear pattern. Eventually the entire joint space may disappear. Radiographic features are more hypertrophic than those seen with inflammatory arthritis (Fig. 3-3).

Inflammatory arthritis tends to show more diffuse symmetrical joint space narrowing with fewer hypertrophic changes. Peripheral osteophytes, although often visible, are usually small. Cystic changes are more evident than with osteoarthritis. Diffuse osteopenia is characteristic of inflammatory changes. The wear pattern is often symmetrical at onset, but may eventually lead to a more medial wear pattern with a protrusio deformity of the acetabulum and superomedial migration of the femoral head (Fig. 3-4).

Radiographic Grading of Osteoarthritis

Various grading systems of osteoarthritis have been described. It must be remembered that approximately 40% to 50% of patients with radiographic changes of osteoarthritis are asymptomatic. Joint space narrowing has been shown to correlate most strongly with clinical symptoms. A number of grading systems are presented in Table 3-2.

Diagnostic Workup Algorithm

The most important investigation for patients presenting with hip pain is to obtain good quality, properly exposed and oriented radiographs with the appropriate views. In a properly oriented anteroposterior pelvis radiograph, the

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obturator foramina appear symmetrical and the coccyx projects approximately 1 cm above the pubicsymphysis. A true lateral radiograph also should be obtained with attention focused on the contour of the anterior femoral head/neck junction and also the anterior acetabulum. Together with a thorough history, the large majority of conditions can be diagnosed with the use of plain radiographs.

Figure 3-3 Radiographic example of patient with osteoarthritis. Note the superolateral joint space narrowing, bony sclerosis, and large osteophytes. The changes are much more hypertrophic than that seen in inflammatory arthritis.

Figure 3-4 Radiographic example of patient with rheumatoid arthritis. Note the symmetrical joint space narrowing with an early protrusio deformity, and cystic changes. Large osteophytes are not present.

TABLE 3-2 Radiographic Grading of Osteoarthritis of the HIP

Grade

Tonnisa

Kellgren and Lawrenceb

Croftc

0

No signs

None

No features

No changes

1

Slight narrowing of joint space, slight lipping at joint margin, slight sclerosis of femoral head or acetabulum

Doubtful

Minute osteophytes, doubtful significance

Osteophytosis only

2

Small cysts, increased narrowing of joint space, moderate loss of femoral head sphericity

Minimal

Definite osteophytes, unimpaired joint space

Joint space narrowing only

3

Large cysts, severe narrowing or obliteration of joint space, severe deformity of femoral head,

Moderate

Moderate diminution of joint space

Two of: osteophytosis, joint space narrowing, subchondral sclerosis, and cyst formation

4

Severe

Joint space greatly impaired with subchondral sclerosis

Same as grade 3 but requires three features

5

Same as grade 4, plus deformity of the femoral head

aBusse J, Gasteiger W, Tonnis D. Eine neue Methode zur röntgenologischen Beurteilung eines Hüftgelenkes—Der Hüftwert. Arch Orthop and Trauma Surg. 1972;72:1-9.

bKellgren JH, Lawrence JS. Radiological assessment of osteoarthrosis. Ann Rheum Dis. 1957;16:494-502.

cCroft P, Cooper C, Wickham C, Coggan D. Defining osteoarthritis of the hip for epidemiologic studies.Am J Epidemiol. 1990;132:514-522.

Figure 3-5 Diagnostic algorithm for patients presenting with hip pain.

Many patients who present with hip pain will have radiographic features of arthritis. If the clinical presentation correlates with the radiographs, then no further investigations are necessary. Patients who present with radiographic changes of arthritis but whose symptoms are atypical (isolated buttock, lateral hip or knee pain) may be further evaluated with an intra-articular local anesthetic injection placed under fluoroscopic guidance. If the symptoms are temporarily relieved by the injection, then hip pathology is highly likely. Patients who present with symptoms of hip pathology but whose radiographs appear normal, despite close scrutiny for conditions such as mild dysplasia, femoroacetabular impingement, or retroverted acetabulum, may require further investigation, usually with an MRI scan. If intra-articular pathology such as a labral tear is suspected, then a gadolinium arthrogram MRI is most valuable. Figure 3-5 outlines a diagnostic algorithm for patients presenting with hip pain.

Treatment

The most common surgical procedure for hip arthritis is total hip replacement. However, various other procedures are indicated for certain conditions. A more detailed discussion of specific management will be presented in subsequent chapters. For an overview, see Table 3-3.

Surgical Indications

Persistent hip pain, despite nonoperative management, is the usual indication for surgery. Occasionally patients complain more of restricted function and less of pain, but it is generally the pain that results in the restricted function and is the reason why patients seek hip replacement surgery. Prior to surgery, patients should receive an appropriate coarse of nonoperative management. For osteoarthritis, this includes activity modification, weight control if feasible, the use of walking aids, and medications (nonnarcotic analgesics and nonsteroidal anti-inflammatory medications). Presently, the routine use of corticosteroid or hyaluronate hip injections cannot be recommended. Patients with inflammatory arthritis are generally under the care of a rheumatologist or internist for nonoperative

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management. However, when considering surgery, certain considerations must be addressed; these are discussed below.

TABLE 3-3 Surgical Options for Patients with Osteoarthritis or Prearthritic Conditions

Procedure

Condition

Labral debridement

- Labral tear in isolation (likely a very rare situation—tears are usually associated with other boney conditions)

Anterior acetabular rim resection

- Acetabular torsion/version abnormality (pincer type FAI, coxa profunda, retroverted acetabulum)

Anterolateral femoral neck resection

- Poor femoral head/neck offset (cam type FAI)

Proximal femoral osteotomy

- Proximal femoral deformity (e.g., trauma, slipped epiphysis, Legg-Perthes)

Periacetabular osteotomy (PAO)

- Classic dysplasia (correct anterolateral deficiency)
- Retroverted acetabulum (reverse PAO for posterior deficiency)

Total hip replacement

- Moderate and advanced arthritis

FAI, femoral acetabular impingement; PAO, periacetabular osteotomy.

When total hip replacement is being considered, there is rarely a disadvantage in delaying surgery as long as the patient is able to maintain function. However, for conditions that may be considered prearthritic (e.g., femoroacetabular impingement, dysplasia without arthritic changes) there may be some merit in recommending joint-sparing surgery when symptoms initially begin or are relatively mild, rather than have the patient undergo a protracted coarse of nonoperative treatment. Symptoms should still be significant enough to justify the risks of surgery, but a long extensive coarse of nonoperative management may be counterproductive because further cartilage damage may occur during this time period. The goal of nonarthroplasty joint-preservation surgery is to relieve symptoms and if possible, also to alter the natural history and prevent or delay the onset of arthritic changes; hence there may be an optimum window of time in which such surgery is most successful. Unfortunately, definitive data on altering of the natural history by joint-preservation surgery is still lacking.

Surgical Considerations

Prior to surgery, patients with both noninflammatory and inflammatory arthritis should be counseled as to the risks, possible complications, and usual recovery related to the procedure. Patients should be medically stable, and any chronic medical conditions should be assessed preoperatively and optimized prior to surgery. This includes maintaining proper nutrition and also eliminating potential sources of infection by specifically asking about their dental history or any urinary problems. A careful skin evaluation is also necessary.

Patients with inflammatory arthritis have unique concerns that require consideration before surgery. These concerns include polyarticular disease, medication used for management of inflammatory disease, as well as unique reconstructive challenges because of bone deformity or loss. Patients with inflammatory arthritis, particularly rheumatoid disease, generally have polyarticular involvement. Prior to surgery, C-spine lateral flexion and extension views are necessary to exclude C1-C2 instability. Additionally, in most circumstances, lower extremity surgery should be planned prior to upper extremity surgery and hip replacement prior to knee replacement when both are needed. It is more difficult for the patient to regain knee motion if there is significant hip disease. Patients with inflammatory disease are often on immunosuppressive agents (corticosteroids, disease-modifying antirheumatic drugs—e.g., methotrexate, TNF-α antagonists). The use of these before surgery should be reduced if possible or temporarily discontinued. This is particularly true for TNF-α antagonists, which are potent immune suppressors; continued use during the perioperative period may increase the risk of infection. Last, patients with rheumatoid arthritis often have osteopenic bone, which is at increased risk of intraoperative fracture. These patients may also have acetabular bone loss related to a protrusio deformity, which may require bone grafting or the use of special implants (e.g., deep profile cup or in severe cases an acetabular reconstruction cage). As in all reconstructive cases, appropriate surgical planning is necessary to anticipate and have available any special implants, instruments, or bone graft that may be required.

Suggested Readings

Felson DT. Obesity and vocational and avocational overload of the joint as risk factors for osteoarthritis. J Rheumatol. 2004;31 (suppl 70):2–5.

Ganz R, Parvizi J, Beck M, et al. Femoroacetabular impingement. A cause for osteoarthritis of the hip. Clin Orthop. 2003;417:112–120.

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Gelber AC. Obesity and hip osteoarthritis: the weight of the evidence is increasing. Am J Med. 2003;114:158–159.

Giori NJ, Trousdale RT. Acetabular retroversion is associated with osteoarthritis of the hip. Clin Orthop. 2003;417:263–269.

Harris WH, Bourne RB, Oh I. Intra-articular acetabular labrum: a possible etiological factor in certain cases of osteoarthritis of the hip. J Bone Joint Surg. 1979;61A:510–514.

Karlson EW, Mandl LA, Aweh GN, et al. Total hip replacement due to osteoarthritis: the importance of age, obesity and other modifiable risk factors. Am J Med. 2003;114:93–98.

Klippel JH, ed. Primer on the Rheumatic Diseases. 12th ed. The Arthritis Foundation, Altanta, Georgia; 2001.

Li PLS, Ganz R. Morphologic features of congenital acetabular dysplasia. One in six is retroverted. Clin Orthop. 2003;416:245–253.

MacGregor AJ, Antoniades L, Matson M, et al. The genetic contribution to radiographic hip osteoarthritis in women. Arthritis Rheum. 2000;43:2410–2416.

Radin EL. Who gets osteoarthritis and why? J Rheumatol. 2004;31(suppl 70):10–15.

Reynolds D, Lucas J, Klaue K. Retroversion of the acetabulum: a cause of hip pain. J Bone Joint Surg. 1999;81B:281–288.

Siebenrock KA, Wahab KHA, Werlen S, et al. Abnormal extension of the femoral head epiphysis as a cause of cam impingement. Clin Orthop. 2004;418:54–60.



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