On a pathologic basis, hip OA primarily affects the articular cartilage, subchondral bone, synovial fluid, and joint capsule.8,9,13,16 Figure 6-2 illustrates the expected changes in cartilage morphology associated with OA and the corresponding histologic grade as established by the Osteoarthritis Research Society International. Independent of the associated inflammation and underlying cause, the condition is essentially the result of a complex series of events.
The earliest change seen in OA is glycosaminoglycan depletion, which leads to a more permeable and hypertrophic matrix.15 In these early stages, swelling of the cartilage occurs, usually a result of increased (albeit aberrant) proteoglycan synthesis (e.g., increased water content), which may be an initial effort by chondrocytes to repair damaged articular cartilage. This stage is often characterized by hypertrophic repair of the articular cartilage. Although repair is hypertrophic, ensuing changes lead to reduced compressive stiffness and permeability changes.17 At this stage, changes are radiographically elusive.15 As the condition progresses, which may take years and may go unnoticed from a symptom perspective, the level of proteoglycans synthesized sharply declines, and the cartilage further loses elasticity. Although collagen content is still maintained in early stages, organization is haphazard and leads to decreased elasticity and strength.17 Further, owing to decreased strength and elasticity, the cartilage develops microscopic clefts (fissures) compromising the articular structure’s integrity and ability to absorb loads. Over time, a progressive loss of cartilage, referred to as chondropenia, occurs. It is at this stage that changes may be identified on radiographs. Chondropenia results in decreased joint space, often at areas of high load such as the superior joint space (Fig. 6-3). The changes (decreased joint space at areas of high load) seen with OA contrast with those of systemic inflammatory arthritides such as rheumatoid arthritis (RA) in which uniform joint space compromise is often seen. Erosion in the joint from a loss of cartilage and joint space occurs until subchondral bone is exposed and irregular (see Fig. 6-1, B). During this phase, denudation has occurred. The erosion leads to increased biomechanical stress to the subchondral bone, which responds with a process known as eburnation.15 Eburnation is a condition whereby exposed subchondral bone undergoes a sclerosing process and hardens, resembling an ivory-like appearance on radiographs. The traumatized subchondral bone often experiences synovial intrusion and undergoes cystic degeneration as well. Subchondral cysts may have a diameter up to 2 cm, although frequently less, and they may be seen at the acetabulum and femoral head (Fig. 6-4). Further, at areas of high stress along the articular margin, vascularization of the subchondral marrow, osseous metaplasia of connective tissue, and ossifying cartilage lead to the outgrowth of irregular new bone in a process referred to as osteophytosis (Fig. 6-5). Fragmentation of these osteophytes may occur, resulting in the presence of loose bodies. Moreover, as degeneration progresses the femoral head may lose normal sphericity (e.g., shape). At some point during the degenerative sequelae, the pathologic changes may lead to pain and adaptive shortening of the soft tissue structures surrounding the joint. Shortening of soft tissues such as the capsule, ligaments, and musculature invariably produces impairments that perpetuate the joint’s loss of function and play a vital role in the morbidity associated with hip OA.12,18,19
Pain experienced from OA is multifactorial and is presumed to arise from a combination of mechanisms.8 In particular, vascular congestion of the subchondral bone leads to increased intraosseous pressure and degenerative-type changes in the synovium, which may activate the synovial nociceptors. Additionally, osteophytosis may cause pain from the associated periosteal elevation. Moreover, joint effusion from edema may stretch an already shortened capsule and be a nociceptive source. Similar to other conditions, pain from OA may be chemically induced from injury to neighboring tissue (e.g., bursa or ligament) or coexisting problems such as muscle spasm, central sensitization, and psychological factors. From an impairment perspective, ensuing joint contractures lead to pain, decreased mobility, and stiffness of the joint. Collectively, the aforementioned degenerative changes and associated impairments serve a primary role in the disability burden associated with hip OA.
Epidemiology
Prevalence and Demographic Risk Factors
More than 27 million6,7 persons in the United States were reported to be clinically diagnosed with OA in 2005. It has been estimated that by 2030 the prevalence is expected to exceed 67 million.20 Internationally, OA is the most common articular disease, and as in the United States its reported prevalence is influenced by how the condition is defined, as well as by those seeking care. Prevalence studies have focused primarily on radiographic disease as inclusion criteria because it is easier to define than clinical presentation. On the basis of radiologic findings alone, 80% to 90% of persons older than 65 years of age have OA.20–22 The prevalence and incidence of OA are generally higher among women than men.23,24 The hip ranks second among large joints in the body affected by OA, trailing the knee, which has the highest prevalence.4,25 Box 6-1 presents an overview of prevalence and demographic risk factors associated with hip OA.
In regard to the hip, evidence suggests that the estimated lifetime prevalence of symptomatic OA is approximately 25%; thus, one in four persons will be affected by this condition.6 In terms of race, hip OA seems to have no consistently reported differences.26 As stated previously, gender differences exist, with women more likely than men to develop symptomatic hip OA.6,23 These differences are more evident after the fifth decade of life.23 Moreover, evidence suggests that the lifetime risk of receiving a total joint replacement for hip OA is approximately 7% for men and 12% for women.27 The economic burden of hip OA is difficult to capture because no current population-level estimates of both indirect and direct costs are available. Although reports on the total economic burden attributable to OA do not exist, reports do indicate that direct costs attributable to hospitalization for hip replacement in the United States for 2009 were approximately $13.7 billion.28 When combined, OA of the hip and OA of the knee rank as the eleventh highest contributors to global disability and the thirty-eighth highest in disability-adjusted life-years (measure expressed as number of years lost as a result of poor health, disability, or premature death).4
Unlike secondary hip OA, which has recognizable risk factors, the etiology of primary (idiopathic) OA may be elusive. Risk factors, particularly those that are modifiable, are of particular interest in reducing new incidence, in steering prevention efforts, and for attenuating disease progression. With advancing age, the incidence of hip OA rises, with most obvious increases occurring at 50 years of age and leveling off or declining by 80 years of age.23,29 Reports of pain related to hip OA also increase with age,26 an association that may be attributable to progression of the condition, as well as ensuing impairments and functional decline. Although age is associated with OA, age alone is not a sufficiently conclusive risk factor, nor is it a modifiable risk factor. Several genes have been directly associated with OA, thus leading to a genetic-hereditary association. Genes in bone morphogenic protein and wingless-type signaling cascades have been implicated in the etiology of OA. Moreover, genetic factors are also important in certain hereditable developmental defects and skeletal anomalies that can cause congenital joint misalignment. Trauma or surgical procedures involving the articular cartilage or supporting structures may lead to abnormal biomechanics and cytokine imbalance, which could incite or accelerate the degenerative process. Unlike direct trauma, occupational or lifestyle factors may expose the hip to degenerative changes through a microtraumatic effect.
Risk Associated With Previous Injury
Undue loading of a previously injured joint (intraarticular) may predispose the region to degeneration as excessive forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix. Previous injury to the hip is a clear risk factor for OA with an odds ratio of 5.0.30,31 Essentially, patients with a previous injury to the hip are five times more likely to develop OA when compared with persons without prior injury or trauma. In many cases, a previous injury creates changes to the articular surface, as well as biomechanical impairments that lead to an abnormal loading environment.
Modifiable Risk Factors
In regard to physical activity, evidence suggests a variable association with OA. Leisure time physical activities such as walking and cycling have been associated with a lower risk of hip replacement when compared with sedentary activity levels.32 Overall, recreational sport participation has a low risk.30 However, high exposure to competitive or elite sporting activity before the age of 50 years has been associated with a greater risk for hip OA.33 Unlike recreational participation, high-impact sports such as American football, track and field, and racket sports appear to increase the risk for hip OA.33,34 The risk among athletes is more evident among those participating at an elite level, with an odds ratio of 1.6 to 2.5.34
Activities such as recreational running may have a protective effect in part because of an association with reduced body mass. Most investigations have not identified an increased risk of OA in runners; however, mixed evidence exists as related to running pace and mileage.35–37 Some evidence suggests an increased risk of hip OA among runners, particularly as related to pace, mileage, or previous injury; whereas a large cohort study reported contrasting findings (e.g., running posed no risk for hip OA). In fact, one study found that those who ran at a higher energy expenditure had a decreased risk when compared with those who exercised at a metabolic equivalent (MET) of less than 1.8 hour/day. Recognizing that 1 MET is essentially the energy cost of sitting quietly, one may interpret the aforementioned MET of less than 1.8 hour/day as that of runners who were deconditioned and possessed other inherent risks. Nevertheless, in the same study, walking in lieu of running did not decrease OA risk.37 The investigators postulated that running has a protective effect, particularly because it attenuates weight gain, which is a known risk factor for hip OA. Given the association of running with a lower body mass index (BMI), it appears that recreational participation does not increase one’s risk for hip OA and may in fact reduce one’s risk profile.
Occupational activity that involves heavy lifting, squatting, climbing stairs, and long-term exposure to standing have been associated with hip OA.31,38 Heavy versus light workloads, in particular, place persons at a three times higher risk for developing hip OA.39 Frequent or compulsory stair climbing has a reported odds ratio of 12.5.40 Moreover, a cross-sectional survey found that persons exposed to lifting, stooping, and vibration tools have an increased risk for hip OA.41 Evidence suggests that lifting burdens must be at least 10 kg (22 pounds), with performance for more than 10 years, to be related to hip OA.38 It seems logical that evidence-based recommendations for exercise among healthy persons should favor recreational running over squatting or stair climbing. Moreover, while occupational hazards could be recognized, one’s choice of occupation may itself be a risk factor.
Numerous studies have identified BMI and obesity as risk factors for hip OA, with odds ratios ranging from 1.6 to 15.4.31,42 Obesity (BMI ≥30 kg/m2) was associated with a higher prevalence of hip OA in a sample of 1157 Australians, with an adjusted odds ratio of 2.18.42 Of those patients with hip OA in the aforementioned study, obesity was associated with higher levels of pain, increased stiffness, decreased function, and reduced quality of life. A more recent metaanalysis reported that a 5-unit increase in BMI (e.g., 32 to 37 kg/m2) was associated with an 11% increase risk of hip OA.43 In addition to mechanical effects, obesity may be an inflammatory risk factor for OA because of its link with increased levels of adipokines, which may promote joint inflammation. Evidence does exist to support a relationship between obesity and risk of total hip replacement. In a study of 568 women who had reported receiving a hip replacement, those with a BMI of 35 kg/m2 or more had a relative risk of 2.6 compared with a reference population.44 Although it is clear that an association exists, patients with OA often adopt more sedentary lifestyles than reference populations, thus subsequently leading to increases in BMI and a perpetuation of risk.
Structural Morphology
Undue loading of a developmentally dysplastic joint may predispose the region to degeneration as excessive forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix. Developmental disorders such as dysplasia, congenital hip dislocation, Legg-Calvé-Perthes disease, and slipped capital femoral epiphysis have been associated with OA.45 Chapter 7 presents a detailed discussion of the aforementioned developmental disorders.
In regard to morphology, it has been suggested that femoral acetabular impingement and lower extremity length inequality may be associated with or may increase the risk of hip OA.46 Investigators have reported that patients with lower extremity length inequality are more likely to have hip OA, although the association is weak (adjusted odds ratio of 1.20), and it is not significantly associated with radiographic progression.47,48 With regard to the side of involvement, OA is more common when the contralateral leg is longer than when it is shorter (e.g., right hip OA would be more common when the left leg is longer).48 When considering the relevance of limb inequality, it should be recognized that hip OA itself may cause leg-length discrepancy, and a shortened leg may simply be the result of joint space narrowing or protrusio acetabuli (e.g., medial protrusion of the femoral head into the acetabulum), as opposed to structural length change. Independent of radiographic changes, patients with lower extremity length inequality are more likely to have hip pain, aching, and stiffness than those with symmetrical lower extremity length.49 Although the prevalence of radiographic hip OA and symptoms seems to be higher among patients with limb-length inequality, the association is weak. Moreover, having limb-length inequality is not predictive of radiographic or symptom progression.
Femoral acetabular impingement is an established risk factor for early hip OA and joint replacement.50–55 Mechanisms for impingement of the femoral head or neck on the acetabulum include the following: the cam variant (nonspherical femoral head); the pincer variant, which is essentially acetabular overcoverage; and a mixed cam-pincer variant. The cam-type morphology occurs more frequently in younger patients and is thought to cause a delaminating injury to the cartilage of the acetabulum (e.g., cartilage is sheared off bone). The pincer variant lends to labral impingement, which results in labral tears, degeneration, and ossification. Evidence suggests that patients undergoing hip arthroplasty have a high incidence of radiographic abnormalities consistent with impingement; however, early surgical intervention (see the later section on surgical treatment) is associated with good outcomes.51,53,54 Notably, in one investigation, 80% of patients who had undergone a surgical correction procedure were able to decelerate worsening of OA and did not progress to a joint replacement operation.53 Although outcomes are generally good, they depend on the degree of degeneration in patients with concurrent hip OA-impingement.56 Chapter 4 presents a detailed discussion of femoral acetabular impingement and labral tears.
Summary of Risk Factors
Numerous risk factors have been associated with hip OA (see Box 6-1; Table 6-2 and Box 6-2). They include, but are not limited to, age, gender, obesity, trauma, genetics, occupational hazards, infection, congenital factors, and earlier surgical interventions. Early identification of modifiable risk factors may serve as the basis for preventive programs aimed at decelerating disease progression and associated symptoms. At a minimum, habitual physical conditioning,57 efforts to prevent obesity, and modification of occupational hazards are likely to have a positive effect on the presence of pain and physical function. Although age and developmental disorders such as dysplasia are not modifiable risk factors, improving the biomechanical environment by avoidance of aberrant loading while maintaining a reasonable level of physical activity may reduce the risk of developing OA. Furthermore, given the known risk association from earlier trauma or surgical procedures, it seems reasonable for future research to direct efforts toward surgical interventions that recreate the native joint anatomy and posttraumatic rehabilitation efforts to mitigate biomechanical abnormalities.
TABLE 6-2
Risk Factors Associated With Hip Osteoarthrosis
| Modifiable Risk Factors | Structural or Congenital Risk Factors |
| Compulsory occupational stooping and squatting | Hip dysplasia |
| Frequent stair climbing or vibration tool exposure | Legg-Calvé-Perthes disease |
| Long-term exposure to heavy lifting and standing | Slipped capital femoral epiphysis |
| Elite-level high-impact sport participation | Chondral defects |
| Obesity or high body mass index ≥30 | Femoral acetabular impingement |
Clinical Presentation
The diagnosis of hip OA can be made with a reasonable degree of certainty based on the physical examination alone, although radiographic findings constitute the visual reference standard. Patients with hip OA have a characteristic history (Box 6-3) and clinical examination findings that, combined with the presence of radiographic evidence, provide a definitive diagnosis. In the absence of diagnostic imaging, evidence-based clinical guidelines exist to help steer the diagnostic process.
History and Demographics
Patients with symptomatic hip OA are typically older than 50 years of age, although age alone is not a definitive diagnostic criteria.58 In a majority of cases, the onset is gradual, and progression is characteristically slow, with a noticeable decline in activity that coincides with advancing age. Patients with hip OA typically report ipsilateral pain in the groin (often described as a deep ache), lateral trochanteric, or buttock regions.59–62 Although pain location may vary as a result of different stages or periarticular adaptations, groin pain in particular possesses a degree of diagnostic utility for identifying hip OA, with a sensitivity of 0.84 and specificity of 0.70.60 Thus, one may interpret these results as indicating that only approximately 16% of patients with hip OA will not report groin pain.60 Pain patterns arising from hip OA are somatic, and pain may be referred to the anterior thigh and knee and in some cases below the knee (Table 6-3).59,60 Investigators have postulated that referred patterns are potentially derived from the femoral, obturator, and saphenous branch of the femoral nerve.60,63 Although evidence exists to suggest that patients with hip OA may have pain below the knee, it would seem logical that other conditions known for having similar pain referrals (e.g., advanced lumbar degeneration or diskogenic disorders) may coexist and thus should be included in the differential diagnosis. For example, shin (anterior leg) or calf pain, when present in patients with hip pain, has a specificity of 0.35 and 0.41, respectively, for a diagnosis of hip OA.60 Based on this information, one could surmise that in approximately 60% of cases, leg pain (e.g., shin or calf) when present, is not necessarily referred from hip OA. When a radicular pattern is present or pain is referred below the knee, concurrent lumbar disorders or alternate diagnoses should be considered (see Chapter 10 for the differential diagnosis of hip pain).
TABLE 6-3
Diagnostic Utility of Pain Patterns for Hip Osteoarthrosis
| Pain Location | Sensitivity (%) | Specificity (%) |
| Groin | 84.3 | 70.3 |
| Buttock | 76.4 | 61.1 |
| Anterior thigh | 58.8 | 25.9 |
| Posterior thigh | 43.7 | 59.9 |
| Anterior knee | 68.6 | 48.1 |
| Posterior knee | 50.9 | 44.4 |
| Anterior leg (shin) | 47.0 | 35.2 |
| Posterior leg (calf) | 29.4 | 40.7 |
Related posts:
Hip Disorders: Extraarticular
Influence of Lumbosacral Disorders on the Differential Diagnosis of Hip Pain
The Female Hip and Pelvis
Femoral Acetabular Impingement and Labral Tears
Musculoskeletal Sources of Abdominal and Groin Pain: Athletic Pubalgia, Hernias, and Abdominal Strains
The Pediatric and Adolescent Hip
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