Hip osteoarthritis: What the radiologist wants to know
Introduction
Osteoarthritis (OA) is a non-inflammatory degenerative joint disorder associated with various degrees of cartilage degeneration and bony deformity. OA can result in altered joint mechanics with resultant alignment abnormalities and associated soft tissue contracture leading to limitations in motion. OA is the most common disease of the hip joint seen in adults [1], [2]. Most of the patients seen in the routine Orthopaedic practice with discomfort, pain, limping or stiffness of the hip joint, are most commonly suffering from OA.
Clinical and epidemiological data indicate that hip OA is a distinct entity that behaves differently from OA in other synovial joints [3]. Our understanding of hip OA comes from international population studies, joint replacement registries, and epidemiologic investigations. Understanding the etiology of hip OA depends on our ability to recognise and discriminate this entity from other causes of hip disease as well as to distinguish secondary from idiopathic OA. In the secondary type, the predisposing cause is well defined and the identification of the underlying pathology may have an impact on treatment. In the primary or idiopathic type, the underlying cause cannot be determined.
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Epidemiology
The reported incidence of hip OA in the general population varies considerably, depending on the different methods used for the selection of the sample, the diagnostic criteria applied, and the race and age of the subjects participating in different studies [3], [4], [5]. Population studies have shown that there are marked ethnic and racial differences. The rate of moderate to severe idiopathic or secondary OA of the hip in Caucasians is 3ā6%, compared with 1% or less in East Indians, Blacks,
Etiology of the idiopathic OA
It has been suggested [10], [11] that increased anteversion of the femoral neck may contribute to the development of hip OA, a statement which has been challenged by others [3], [12], [13]. Other etiological factors have also been discussed, not without criticism, in the literature such as farming, occupational heavy load, overweight and elite sport activity [3], [14], [15], [16], [17], [18], [19]. The strong relationship between race and OA of the hip and the relatively high incidence of the
Etiology of the secondary OA
Hip OA can be secondary to osteonecrosis, trauma, sepsis, Paget's disease or as a result of inflammatory arthropathy. Certain conditions such as congentital hip disease (CHD), Perthe's disease and slipped capital femoral epiphysis (SCFE), involve anatomical structures which lead to the development of OA in adulthood. Murray [14] stated that minimal anatomical variations exist in the majority of cases, which had been reported as idiopathic by previous authors, sometimes so slight that the
Classification of idiopathic hip OA
Different classification systems have been described using as criteria the direction of migration of the femoral head and the evolution of the destructive changes within the joint [15], [37], [38], [39], [40]. Most of them agree that there are two main types of head migration: superior and medial. The superior migration (or eccentric) may be superolateral or superomedial. The medial migration (concentric) is also referred to as axial or global.
The differential diagnosis of the superior
Pathogenesis of idiopathic OA
On cellular level, at the earliest changes of OA when the cartilage is morphologically still intact, an increase in water content and easier extractability of the proteoglycans is observed. A failure of the internal collagen network, which normally restrains the matrix gel, follows. At an intermediate stage, a loss of proteoglycans, which weakens the structure making it more susceptible to injury, is observed and cartilage defects appear. Later as the cartilage becomes less stiff, secondary
Clinical features
The symptoms in OA are usually unilateral and asymmetric at early stage. In late stages multiple joints may be involved. Patients usually present after middle age, although in some forms of secondary OA (e.g. CHD) symptoms start earlier. Pain is the usual presenting symptom. Initially pain is worsened by activity and relieved by rest, but eventually rest and night pain develop. Typically, the symptoms of hip OA follow an intermittent course, with periods of remission sometimes lasting for
Laboratory investigations
Lab evaluation will reveal a normal ESR, CRP and CBC, and synovial fluid analysis may show a normal or slightly elevated WBC count (10,000ā20,000) with normal differential. This pattern is found in most non-inflammatory arthropathies.
Plain radiographs
The radiographic evaluation has the following aims: (1) to confirm the clinical diagnosis of OA; (2) to establish the severity of OA; (3) to monitor disease activity and response to treatment and (4) to depict any complications of the disease or of its treatment. The conventional radiologic work-up of the hip, includes the anteroposterior and the āfrog-legā view. The latter needs a 45Ā° of abductions, which is not always achievable when patients suffer from pain or limitation of motion. Hip
Basic management strategies
Treatment of hip OA depends upon the stage of the disease, the patient's age and the functional impairment. The goals of treatment are pain relief, maintenance and restoration of function, and prevention of advanced changes.
At early stages the goals are: Maintenance of range of movement and muscle strength with physiotherapy and exercise, relieve pain with acetaminophen, paracetamol, classic NSAID's and modern anti-COX-2 NSAID's [79], [80], modification of daily activities and protection of the
Conclusion
To evaluate the symptoms of hip OA and come to a decision as to the proper surgical treatment, the clinical picture, activities of daily living as well as plain radiographs should be carefully studied. It is often though difficult to evaluate the disease based on clinical and radiographic grounds alone. If plain radiographs are inconclusive, MRI and/or MDCT, especially if combined with arthrography, may offer a direct demonstration of the cartilage, and illustrate erosions as well as bone
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