Primary Osteoarthritis of the Hip: Etiology and Epidemiology

Franklin T. Hoaglund, MD, and Lynne S. Steinbach, MD

Abstract
Primary osteoarthritis (OA) of the hip has a distinct etiology and epidemiology compared with other types of arthropathy in the hip joint. Arthritis of the hip can be secondary to conditions such as osteonecrosis, trauma, sepsis, or rheumatoid arthritis. Certain conditions, such as congenital hip disease and slipped capital femoral epiphysis, involve predisposing anatomic abnormalities; in such cases, the term secondary OA is used. When either an anatomic abnormality cannot be determined or other specific causative entities are not identified, primary OA is the diagnosis of exclusion. The prevalence of hip OA is about 3% to 6% in the Caucasian population and has not changed in the past four decades. In contrast, studies in Asian, black, and East Indian populations indicate a very low prevalence of hip OA. Statistics on patients who underwent total hip replacement for primary OA in San Francisco and Hawaii demonstrate a virtual absence of the condition in Asians and low rates in the black and Hispanic populations. Family studies from Sweden, Britain, and the United States show increased rates of hip OA in first-degree relatives of the index patient when compared with the normal population. Occupations requiring heavy lifting, farming, and elite sports activity are associated with increased rates of hip OA. The low prevalence of hip OA in Asian and black populations in their native countries; the low incidence of total joint replacement for primary OA in Asian, black, and Hispanic populations in North America; and the familial association of hip OA in Caucasians all suggest that genetic factors may be involved in the occurrence of this disease. J Am Acad Orthop Surg 2001;9:320-327
diagnosis of primary OA rarely undergo total knee replacement, and vice versa.2 In two other studies, Japanese and Hong Kong Chinese populations had virtually no primary OA of the hip but a considerable incidence of knee OA.3,4

Epidemiology
The modern search for the causes of OA started with the work of British scientists Kellgren and Lawrence, who carried out epidemiologic studies encompassing several ethnic groups in a number of geographic areas, including western European and specifically British Caucasians, African and Jamaican blacks, and Native Americans.5-7 Responses to questionnaires and the clinical findings in randomly selected populations were evaluated, and radiographs of various joints were ex-

Osteoarthritis (OA) of the hip is manifested as degeneration of the tissues of the hip joint, including hyaline cartilage, fibrocartilage, bone, and synovium. Hip arthritis can result from several different patterns of joint failure. Underlying pathologic changes due to conditions such as osteonecrosis, trauma, sepsis, Pagets disease, and rheumatoid arthritis can produce degeneration of the joint. Conditions such as developmental dysplasia of the hip (DDH) and slipped capital femoral epiphysis (SCFE) leave the patient with predisposing anatomic abnor-

malities that can later result in osteoarthritic changes. When any of these conditions can be identified (Table 1), the degenerative process is termed secondary OA. When neither an anatomic abnormality nor any specific disease process can be identified, the condition is called primary OA, which is, therefore, a diagnosis made by exclusion. Clinical and epidemiologic studies indicate that OA of the hip is a distinct entity that behaves differently from OA in other synovial joints.1 Patients who have undergone total hip replacement (THR) because of a

Dr. Hoaglund is Professor (Emeritus) of Orthopaedic Surgery, University of California at San Francisco Medical Center, San Francisco. Dr. Steinbach is Professor of Radiology and Orthopaedic Surgery, University of California at San Francisco Medical Center. Reprint requests: Dr. Hoaglund, Department of Orthopaedic Surgery, UCSF Medical Center, 500 Parnassus Avenue (MU 320-W), San Francisco, CA 94143-0728. Copyright 2001 by the American Academy of Orthopaedic Surgeons.

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Table 1 Causes of Secondary OA and Their Radiographic Appearance Condition Osteonecrosis Pagets disease Inflammatory arthropathy Traumatic remodeling Degenerative dysplasia of the hip Slipped capital femoral epiphysis Radiographic Features* Sclerosis, lucency, flattening of femoral head Osseous enlargement, trabecular coarsening, cortical thickening Joint-space narrowing, osteopenia, erosion Distortion of osseous contour with sclerosis and remodeling Shallow acetabulum with increased acetabular index, subluxation, or dislocation Medial and/or posterior displacement of femoral head, convexity at head-neck junction, short femoral head, coxa vara, short broad femoral neck

* In addition to joint-space narrowing and osteophytes.

amined with the use of standardized grading.5-7 Patients were considered to have generalized OA if three or more joint groups were involved. Evaluation of these data was the basis for an atlas that is still used today to characterize the various degrees of OA.5 These researchers found that the incidence of OA was not related to latitude or longitude. The highest prevalence of OA occurred in the Caucasians. It was noted that OA preferentially affected the distal interphalangeal joints and the first carpometacarpal joints of the hands, the knees, and the first metatarsophalangeal joints. Comparisons between ethnic groups were not particularly helpful in delineating the etiology of OA; however, the marked ethnic and racial differences in the incidence of hip OA were important observations.6

Population Studies Lawrence and Sebo6 studied the comparative incidence of radiographic OA of the hip by evaluating pelvic radiographs of European Caucasians, blacks, and Native

Americans from nine geographic areas. The term radiographic OA was used because there was no intent to distinguish primary or secondary OA from other specific causes of hip disease. Kellgrens grading system was used to characterize the degree of hip arthritis as absent (grade 0), doubtful (grade 1), minimal (grade 2), moderate (grade 3), or severe (grade 4). The incidences of grade 2-4 and grade 3-4 OA were higher in the Caucasian males than in the females (Table 2). The rate of moderate and severe OA in Caucasians was three to four times that in blacks and Native Americans. Hoaglund et al4 also evaluated conventional radiographs of the hands, knees, and hips of 500 Hong Kong Chinese subjects. An extremely low rate of OA of the hip (1%) was found, but the incidence of hand OA was similar to that in European Caucasians. A second study was done 20 years after the original study. Pelvic radiographs of 999 Hong Kong Chinese men obtained during intravenous pyelography demonstrated no change in the incidence of hip OA.8

In another study, a group of 51,777 East Indians who visited an orthopaedic clinic in India were examined.9 The incidence of OA was found to be less than 0.1%. Pelvic radiographs of American Caucasians demonstrated that the prevalence of hip OA in patients over 54 years of age was 2.7% to 3.5%,10 which is lower than the rate seen in European Caucasians. 6-11 In a Swedish study,12 pelvic radiographs obtained during doublecontrast colon examinations were evaluated. The overall incidence of hip OA was 3.4% in 1964. There has been no change in this rate over the past four decades, as demonstrated in follow-up studies performed in 1984 and 1993.13 In summary, population studies show that the rate of moderate to severe primary or secondary OA of the hip in Caucasians is 3% to 6%, compared with 1% or less in East Indians,9 blacks, Hong Kong Chinese, and Native Americans. The prevalence has not changed in four decades, suggesting that genetic and/or environmental factors remain constant.

Hip Disease in Hip Surgery Patients Specific causes of hip disease and OA in patients who underwent hip surgery in the 1940s and 1950s have been evaluated.14-16 The relative incidence of various hip diseases described in these series is quite different from the current incidence. During that era, 20% to 50% of surgical cases were due to Legg-Calv-Perthes disease, DDH, or SCFE. One might have expected a higher incidence of adults presenting with a painful hip due to arthritic changes from these causes, because there was no prophylactic treatment for these conditions or good early surgical reconstruction at that time. There has been an ongoing debate about whether the high rate of

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1988 using data from the 17 hospitals in or near the city (Table 4).22 Preoperative pelvic radiographs were evaluated for arthritis without the examiners knowledge of the gender or race of the patient. Total hip replacement statistics for Caucasians were compared with those for the sizable non-Caucasian populations (i.e., Asian, Hispanic, and black). Caucasians had a rate of THR of 75 per 100,000 persons, blacks had half the incidence, and Asians had only one tenth. There were markedly lower rates of THR performed because of primary OA in non-Caucasians; for example, the rate was 1.3 per 100,000 for the Chinese population, compared with 43 per 100,000 for Caucasians. The rates of THR for the other causes of hip disease, including secondary OA, were not significantly different among the various ethnic groups. This study was repeated in Hawaii, 23 with its large Asian and Pacific Islander population (750,000 persons). In the total Hawaiian population, medical insurance is available to more than 90% of the patients, thus minimizing the effect of access to care as a factor. The results of this study confirmed the markedly higher rates of THR in Caucasians, who predominantly had primary OA (Table 4). The rate of THR for secondary OA in the Caucasian population was not significantly different from the rates for the Chinese, Filipino, Hawaiian, and Japanese populations.

Table 2 Incidence of Hip OA in Male and Female Subjects in Population Studies6 Incidence (M/F), % Subjects (No.) Grades Grades 2-4 3-4

Caucasian (1,451) 20/12 6.5/5.75 Black (503) Native American (545) 2.3/3 9/8.0 1/1.6 2.7/1.6

secondary OA in that period continues today. Studies of THR patients in Europe and the United States have provided information about the frequency of all causes of hip arthritis in various populations. The prevalence data were comparable among Caucasian population groups in the United States, Scandinavia, and western Europe. The rate of THR varied from approximately 60 per 100,000 persons in the Mayo Clinic data to 140 per 100,000 in Norway 17 (Table 3). When other specific causes of hip disease were excluded, it was noted that primary OA was the underlying disorder in nearly 90% of osteoarthritic hips. Similar published statistics for Africa, South America, Hong Kong, or Japan are not available. The rate of THR for all residents of San Francisco has been measured for the years 1984 through

Incidence of Predisposing Anatomic Abnormalities In 1965, Murray24 suggested that secondary OA was more common than primary OA. In that study, radiographs were evaluated looking for evidence of DDH or femoral head tilt. Previous DDH was found in 37% of British women with OA, and a femoral-head tilt deformity was noted in 74% of British men with OA (Table 5). His conclusion that OA was in fact secondary 90% of the time has been supported by subsequent analysis of the data in uncontrolled series of hip surgery patients in the United States25,26 and South Africa.27 However, there is now considerable information from more recent surgical series that argues against such a high incidence of either DDH or SCFE as the cause of OA. Measurements of the center-edge (CE) angle in blacks (who are relatively unaffected by DDH and hip OA) are the same as those in Caucasians.28 (The CE angle is a measure of hip socket coverage. A low angle indicates a shallow socket, which can predispose to secondary OA). In one study, acetabular depth measurements and CE angles in British patients were the same in normal and osteoarthritic hips. 29 The incidence of DDH based on CE angle measurements in Hong Kong Chinese men was not different from that in British men, 8 yet osteoarthritic hips are much less frequent in the Chinese. Although Japanese persons have significantly smaller

Table 3 Relation Between THR and Primary OA in Various Nations17-21 Sweden Rate of THR per 100,000 persons Incidence of primary OA, %
*

Norway 140 68

Denmark 82 86

Finland 58 56

USA United Kingdom France Belgium 60 63 54 NA 108 NA 116 NA

130 NA

NA = data not available

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Table 4 Rates of THR for Secondary and Primary OA by Ethnic/Racial Background in Two Studies22,23* Chinese San Francisco study22 Women Men Hawaii study23 Women Men Japanese Filipino Caucasian Hispanic Black Hawaiian

1.8/1.4 0.4/1.1 0.31/0.84 0/0.52

2.9/2.9 0/0 0.17/0.24 0.06/0.08

0.9/3.1 0/0 0.06/0.25 0/0.25

6.7/52.6 1.8/33.9 0.29/2.35 0.11/2.32

0/6.2 0.8/6.3

1.1/19.2 0/10.1

0/0.30 0.06/0.16

* Adapted with permission from Hoaglund FT, Oishi CS, Gialamas GG: Extreme variations in racial rates of total hip arthroplasty for

primary coxarthrosis: A population-based study in San Francisco. Ann Rheum Dis 1995;54:107-110. Also adapted with permission from Oishi CS, Hoaglund FT, Gordon L, Ross PD: Total hip replacement rates are higher among Caucasians than Asians in Hawaii. Clin Orthop 1998;353:166-174. Values are expressed as rates for secondary OA/primary OA per 100,000 population/yr.

CE angles than British persons, they have much less hip OA.30 Lane et al31 found no difference in the incidence of an abnormal CE angle between American Caucasian women with OA of the hip and those without it (4% to 5% in each group). In this population, DDH did not account for more than a few osteoarthritic hips. If primary OA of the hip is due to a subtle dysplasia, it should be seen frequently in Japanese persons, with their extremely high rate of dysplasia; however, primary OA is rare in that population.3,32 The incidence of DDH in Caucasians is 0.5%. If OA developed in all children with DDH, this would account for only one eighth of the cases of OA in the Caucasian population. Hawaiian Japanese women have the same rate of THR for dysplastic OA as Caucasian women, but their rate of THR performed for primary OA is only one tenth of that for Caucasian women.23 In summary, when controlled studies of acetabular measurements are done and the rates of DDH and OA for each racial subgroup are considered, DDH accounts for only a small percentage (5% to 10%) of hip OA in Caucasians. Since the original publications of Harris, 26 Murray, 24 Stulberg and

Harris,25 and Solomon,27 which suggested that OA was often caused by SCFE (Table 5), there has been new information that SCFE or subclinical SCFE does not account for the high rate of primary OA. The tilt deformity seen in the adult with OA has been shown to be due to a remodeling process that causes progression of osteophytes, rather than to an old epiphyseal slip.33 Goodman et al34 identified a subtle or subclinical slip deformity in 8% of cadaver bone specimens from a large collection of disarticulated femora and pelves. There are some similarities of this subclinical SCFE to SCFE, such as a lower incidence in women,

increased left-side prevalence, and increased incidence in specimens from black subjects. However, clinical SCFE in the adolescent occurs in only 1 of every 800 boys (an incidence of only 0.125%). Whether subclinical SCFE is a forme fruste of SCFE remains to be proved. Even if it is, anatomically normal femora accounted for more than 80% of the OA in their series. Furthermore, although there is little primary OA in the black and Polynesian populations, as well as a low incidence of THR performed because of OA,22,23 these populations have two to four times the rate of SCFE in Caucasians.

Table 5 Incidence of OA Due to DDH and Femoral-Head Tilt in Men and Women in Four Studies24-27 Stulberg and Harris25

Murray24 Women DDH Tilt Men DDH Tilt

Solomon27

Harris26

37% 11% 11% 74%

69% 4.8% 8% 45%

68% 10% 15% 66%

65% 25%

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Etiology
Body Weight Bioengineering studies have shown that forces across the hip joint are multiplied by a leverage system involving muscles pulling against the weight of the body. For example, an individual standing on one foot has a force across the hip joint of three to four times his or her body weight. Therefore, obesity could be contributory in the etiology of primary OA of the hip. Although OA of the knee has been shown to be consistently related to obesity, there have been conflicting results regarding the relationship of body weight to the development of OA of the hip. Saville and Dickson35 found no difference in the average body weight of patients with primary or secondary OA of the hip compared with control subjects. Spector 36 and Tepper and Hochberg37 found no relationship between body weight or body-mass index and the occurrence of hip OA. However, other studies have shown an increased risk of OA of the hip in obese individuals.38,39 The conflicting findings concerning body weight and hip OA may be related in part to the fact that patients gain weight as a result of the immobility imposed by a painful hip. Occupational Factors The physical demands of work have been estimated to account for 40% of cases of hip OA,40 and carrying heavy loads has been associated with an increased rate of hip OA. Axmacher and Lindberg 41 found that farmers were at increased risk for hip OA in studies conducted in England, Sweden, and Franceall countries that are known to have high rates of hip OA. However, the researchers pointed out that farmers are usually members of families that have been involved in farming for many generations; therefore, hereditary factors cannot be ruled out.

Studies conducted in Sweden indicated an increased risk of OA in patients who had been involved in track, field, and racket sports as well as among soccer players (especially those who played professionally).42 The findings from these studies support the hypothesis that sports may exacerbate hereditary predisposition to OA of the hip.

Other Anatomic Considerations There is a known association between arthritis and previous DDH in patients with the mechanical factors that predispose to secondary OA, such as an acetabular abnormality or femoral anteversion. Therefore, investigations have also been done to determine the role of femoral anteversion alone in patients with primary OA of the hip. However, small studies involving cadaver specimens and patients with hip arthropathy have shown variable results. 43-46 In cadaver specimens without OA, there was no correlation between femoral anteversion and acetabular angles. A study of Hong Kong Chinese cadaver bones showed a high incidence of femoral anteversion compared with specimens obtained from Caucasian subjects. 47 Inasmuch as hip OA is rare in the Hong Kong Chinese population, this observation is inconsistent with anteversion being a factor in primary OA of the hip. Femoral anteversion in osteoarthritic and normal subjects has been measured with the use of biplanar and/or conventional (AP and cross-table lateral) radiographs; a mild increase in anteversion was found in some series but not in others. 43 This increase in femoral anteversion could be due to measurement error. Using accurate CT techniques, Reikers et al46 found no difference in femoral anteversion between control subjects and a series of Caucasian patients with OA.

Family Studies In 1984, Lindberg48 studied 289 siblings of 184 Swedish patients who had undergone THR for primary coxarthrosis. Coxarthrosis occurred in 8% of siblings. This represents a statistically significant (P<0.05) increase over the rate of 3.8% in control subjects. In an unpublished study, 72 patients with primary OA who underwent THR responded to a written family questionnaire. Analysis of the responses confirmed Lindbergs findings. Of the 238 firstdegree relatives over the age of 50, 13% reported a THR or symptoms of hip pain consistent with OA of the hip. This is significantly higher than the 3% to 6% prevalence of OA of the hip diagnosed radiographically. In black patients in San Francisco, the incidence of THR for primary OA was only 30% of that for Caucasian patients.22 This is the same as the incidence of Duffy or GM blood groups reported for black persons in the western part of the United States.49 (All Europeans have Duffy blood groups, but black Africans do not have them.) Therefore, the difference between the rates of THR for primary OA in Caucasians and in blacks is consistent with a genetic etiology. In a prospective cross-sectional survey of 264 British patients who underwent THR for idiopathic OA of the hip, the familial prevalence of THR was ascertained with a questionnaire distributed to their siblings.50 By using spouses as a control group, the researchers calculated the relative risk of THR in siblings as 1.86 (95% CI, 0.93 to 3.60). With the use of the threshold liability model, the heritability of endstage OA of the hip was estimated to be 27%. Twin studies in women have shown that the heritability rates of OA of the knee and hand are 49% and 65%, respectively.51 In more

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recent twin studies of OA of the hip, women showed a 50% heritability (95% CI, 20% to 74%).52 In summary, two different factors appear to be involved in the etiology of OA. First, the lower rates of primary OA in population studies of non-Caucasians and the difference in rates of THR for primary OA in patients with various racial backgrounds living in a common environment suggest that it is a disease primarily of Caucasians. Second, the relatively high incidence of the disease in siblings of Swedish and English patients who underwent THR because of primary OA suggests that genetic factors are operational as well.

Radiographic Criteria In the studies performed by Hoaglund and co-workers in San Francisco22 and Hawaii,23 the radiographs were read without knowledge of the race of the patient. The rate of secondary OA in the Caucasian population was not significantly different from the rates for Chinese, Filipino, Hawaiian, and Japanese subjects. The use of radiographic criteria has been criticized as being generally inadequate to establish that a case classified as primary OA is actually secondary OA. For example, DDH is thought to be underrepresented in women with primary OA, and SCFE or a variation of it is thought to be underrepresented in men. However, evaluation of the radiographs of equivalent large Japanese and Caucasian populations have demonstrated that these criteria can be used to distinguish between primary and secondary OA. The cumulative rates of THR for secondary OA (measured in cases per 100,000 person-years) are similar for Japanese women (0.17) and Caucasian women (0.29), but the rate for primary OA in Japanese women was only one tenth (0.24) of that for the Caucasian women (2.35).

If large numbers of cases of primary OA are in fact secondary OA, there should be sizable numbers in the Japanese women as well as in the Caucasian women. The statistics for men show the same disparity. The rate of secondary OA in Japanese men is 0.6, in contrast to the rate of 0.11 for Caucasian men. If no variant of SCFE were distinguished on the basis of radiographic criteria, comparable numbers of primary OA would be seen in both Caucasian and Japanese men. However, the rate of THR for Caucasians with primary OA is 29 times that for the Japanese men, but the rate of SCFE in Japanese men is only one half to one fifth of that in Caucasians. It seems clear, therefore, that use of radiographic criteria did not lead to underrepresentation of DDH in the female subjects. Similarly, use of those criteria did not lead to underrepresentation of SCFE or subclinical SCFE in male subjects.

Summary
Contributions to our understanding of the etiology of OA of the hip have come from international population studies, joint replacement registries, epidemiologic investigations, and, more recently, analysis of family pedigrees to investigate genetic factors in this disease. Attempts to elucidate the etiology of OA of the hip depend on our ability to recognize and separate this condition from other causes of hip disease, as well as our ability to distinguish secondary OA from primary OA. Secondary OA of the hip occurs when a condition such as DDH, SCFE, or Legg-Calv-Perthes disease results in a predisposing anatomic abnormality that leads to hip degeneration due to mechanical factors. A specific diagnosis of secondary OA is dependent on radiographic diagnosis and is more sensitive in the

early stages of degeneration, before it progresses and remodeling occurs. Radiographic studies of both Caucasian and Asian patients with and without OA suggest that a specific diagnosis can be made. Disagreement may arise in specific cases, but in a large series such cases should not affect the overall conclusions. It is noteworthy that studies of the Asian populations in San Francisco and Hawaii showed similar prevalences of all types of hip arthritis in those who underwent THR but virtually no underlying primary OA. As the same radiographic criteria were applied to all races, the high incidence in Caucasians indicates that the conditions are separable at least 90% of the time. The contribution of subclinical SCFE to the overall incidence of primary OA is small.34 In a study of cadaver femora and pelves, the underlying anatomy was normal in 83% of the specimens, and only 8% had subclinical SCFE. Interestingly, grade 2 OA developed in only 37% of the femora with subclinical SCFE; therefore, it appears that something other than the anatomic deformity is the main etiologic factor underlying OA. The results of comparison studies of Caucasian, black, Native American, and Hong Kong Chinese populations; the joint replacement statistics; and the comparative rates of THR in American non-Caucasian populations indicate that primary OA is a disease primarily of Caucasians of European ancestry. Incidence rates do not appear to have changed in the past four decades, suggesting that the etiologic factors have not changed. Although some studies suggest that factors such as obesity, high-performance athletics, strenuous occupations, and femoral neck anteversion may be contributory to OA, there is also evidence to the contrary. The minimal incidence of THR for primary OA in American Asians compared with

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Caucasians living in a similar environment suggests a genetic etiology. Apparently normal hip anatomy is present in more than 80% of patients in whom OA develops, and only a small percentage of patients with subclinical SCFE are subsequently found to have OA. Therefore, it is reasonable to postulate an underlying defect in articular cartilage or bone that leads to the eventual development of OA.

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