– Written by Rintje Agricola, The Netherlands
Osteoarthritis (OA) of the hip is a common and disabling disease, especially among former athletes1. Historically, the cause of almost all cases of hip OA was unknown and therefore defined as ‘primary’ or ‘idiopathic’. Exceptions were some striking morphological problems as seen in sequelae of childhood hip diseases like Perthes’ disease, slipped capital femoral epiphysis and congenital hip dysplasia, which all pose a high risk for early development of hip OA2,3. OA as a result of these childhood hip diseases, is therefore also called ‘secondary OA’ i.e. OA with a known cause. Secondary OA was thought to account for a minority of all hip OA cases. However, half a century ago, it was suggested that many cases of ‘primary’ hip OA were actually a result of previously unrecognised, subtle shape deformities. For example, mild non-clinical forms of acetabular dysplasia were found to be associated with the development of OA and a non-spherical femoral head was also recognised as a potential risk factor for OA. A non-spherical femoral head, nowadays known as a cam deformity, was at that time described as a ‘tilt deformity’ by Murray and as a ‘pistol grip deformity’ by Stulberg et al4,5. It was not until a decade ago that a non-spherical femoral head became of great interest when the mechanism by which it may lead to hip OA was first hypothesised6.
FEMOROACETABULAR IMPINGEMENT
A pathophysiological explanation on how subtle shape deformities of the hip might lead to OA was provided by a Swiss group headed by Ganz. In 2001, they published a technique for a safe surgical dislocation of the hip, which allows an almost complete visualisation of the femoral head and described the observation that acetabular chondrolabral damage often co-existed with a non-spherical shaped femoral head7. In 2003 they proposed the mechanism of femoroacetabular impingement (FAI), in which a shape abnormality of the hip can cause motion-dependent soft-tissue damage6. Recently, a definition of FAI was provided:
“a clinical entity in which a pathologic mechanical process causes hip pain when morphologic abnormalities of the acetabulum and/or femur, combined with vigorous hip motion (especially at the extremes) lead to repetitive collisions that damage the soft-tissue structures within the joint itself”8.
FAI is usually subdivided based on whether the morphologic abnormality is located at the acetabulum (pincer) or at the proximal femoral head-neck junction (cam).
PINCER IMPINGEMENT
In contrast to cam impingement, only a few studies are available that investigate the association between a pincer deformity and OA. One of the reasons is that there is a lack of a proper definition of what a pincer deformity exactly is. A variety of morphological and orientation abnormalities can cause a global or focal overcoverage of the femoral head which may subsequently lead to pincer impingement. Examples are acetabular retroversion in which there is a prominent front of the acetabular socket, a femoral head that is positioned deep in the acetabulum (also referred to as protrusio or coxa profunda) or an isolated bony overgrowth of the acetabular rim. Due to the acetabular overcoverage, the femoral neck may impact upon the the labrum and acetabular rim, especially during hip flexion.
The pincer deformity is mostly quantified by the centre edge angle, which actually measures the amount of acetabular coverage relative to the femoral head. To obtain a good impression of the entire acetabular rim, the centre edge angle can be measured at two locations in one hip and therefore two radiographic views (anteroposterior and lateral) or 3D imaging techniques are desirable.
There are conflicting results regarding the relationship between a pincer deform-ity and hip OA. Some retrospective and cross-sectional studies show a moderate association with cartilage damage and/or OA, whereas other studies failed to identify an association or even suggested a possible protective effect of a pincer deformity. Gosvig et al found cross-sectionally a mild association between a deep acetabular socket and a joint space width <2 mm9. Moreover, Beck et al described the pattern of circumferential cartilage damage caused by excessive acetabular coverage, as observed during surgery in symptomatic patients10. However, it has also been suggested that acetabular overcoverage might be protective against cartilage delamination and labral lesions11. The only prospective study available quantified the presence of pincer deformity as a centre edge angle >40° on both anteroposterior radiographs and false-profile lateral radiographs of 1002 individuals without radiographic signs of hip OA at baseline. The presence of a pincer deformity on both the anteroposterior and lateral view in one hip (n=141) resulted in a significant protective effect for develop-ment of OA, with odds ratio of 0.34 (95% CI, 0.1 to 0.9) for incident OA (Kellgren-Lawrence score ≥2) at a 5 year follow-up and none of these hips developed end-stage OA (Kellgren-Lawrence 3,4 or total hip replacement)12.
In conclusion, the currently available literature suggests that pincer impingement is a mechanism which might lead to pain and hip damage in studies of symptomatic patients, but on an epidemiological level acetabular overcoverage is not associated with hip OA and might even be protective.
CAM IMPINGEMENT
A cam deformity is an extra bone formation, most often found at the anterolateral head-neck junction. The cam deformity may be forced into the acetabulum during flexion and internal rotation of the hip, which we then call cam impingement (Figure 1). It may cause a specific type of cartilage damage, characterised by delamination of the acetabular cartilage from the subchondral bone.
A cam deformity is usually quantified by the alpha angle, which measures the extent to which the femoral head deviates from sphericity. Many alpha angle thresholds ranging from 50° to 83° have been used to quantify a cam deformity, but based on the bimodal distribution of the alpha angle, a recent epidemiological study proposed an optimal cut-off value of 60° to best define the presence of a cam deformity13.
There are more studies available on the presence of a cam deformity and development of OA than on the association between pincer impingement and OA, though properly designed pro-spective studies are also lacking for cam impingement. Prospective studies are of considerable importance when studying the relationship between a cam deformity and OA, because in an advanced stage of the OA process, the femoral head might flatten due to bone remodelling and mimic a cam deformity. This makes cross-sectional and retrospective studies difficult to interpret as it is unknown if a true cam deformity is measured or just a flattened femoral head due to OA itself. Still, there are several studies which strongly suggest that a cam deformity is a causative factor for development of OA14. Reichenbach et al showed in a cohort of 244 young males that a cam deformity might already cause a decreased cartilage thickness from the age of 20 years15. It can probably be assumed that the cam deformity measured at this young age is not a result of OA. These results were supported by the only prospective study available, which showed a strong relation between the presence of a cam deformity and development of osteoarthritis. In a nationwide study (the CHECK cohort) of 1002 males and females, not specifically focusing on athletes, without radiographic OA at baseline, it was shown that the strength of association between the presence of a cam deformity at baseline and development of end-stage OA after 5 years (Kellgren-Lawrence grade 3,4 or total hip replacement) resulted in an adjusted odds ratio of 3.7 (95% CI 1.7 to 8.0) for an alpha angle >60° and an adjusted odds ratio of 9.7 (96% CI 4.7 to 19.8) for an alpha angle >83°. Even more striking was what was observed when a radiographic cam deformity was present together with limited internal rotation of <20° at baseline – a clinical sign of cam impingement – the relationship became even stronger as reflected by an odds ratio of 25.2 (95% CI 7.9 to 80.6), for end-stage OA at a 5 year follow-up. Besides this study, another study with long-term follow-up is available (Chingford cohort). In a nested case control study of 1002 females, also not specifically focusing on athletes, alpha angle on baseline radiographs was analysed as a longitudinal measure instead of using a cut-off value to define a cam deformity. It was reported that every degree increase in alpha angle equated to a 5% increase in the risk for receiving total hip replacement at 19 years follow-up (adjusted odds ratio 1.052), independent of the presence of radiographic hip osteoarthritis at baseline. This means that a non-spherical femoral head increases the risk of developing OA, but also that major cam deformities confer a higher risk of OA. Almost all other cross-sectional and retrospective studies also show a relationship between the presence of cam deformities and OA.
The relationship between the presence of cam deformities and OA is probably modified by athletic activities. People with a cam deformity who do not perform repetitive vigorous hip motion (flexion and internal rotation) will probably not suffer from actual impingement, those who are active and often flex and internally rotate their hips are more likely to develop labral and cartilage damage. Although this might seem a logical hypothesis based on how we think that cam impingement biomechanically works, there are no studies showing any such interaction.
DEVELOPMENT OF A CAM DEFORMITY
Regarding the strong relationship between cam deformities and development of hip OA, it is important to understand their aetiology. The first question is whether a cam deformity is an irreversible developmental entity or a modifiable acquired entity:
· developmental would mean that genetics or other factors present before birth are likely to determine its presence and
· acquired would mean that interactions with the environment after birth influence its formation.
There are no studies investigating the relationship between specific genes and cam deformities but there are a few studies available which at least suggest some genetic involvement. For example, the prevalence of cam deformities is substantially lower in Chinese people than in Caucasian people. It has also been shown that the siblings of patients with a cam deformity have an almost three-fold increased risk of having a cam deformity compared with the patients’ spouses16. Thus, there is some indirect evidence that genetics might be involved.
A cam deformity might also be an acquired phenomenon as it is already known by means of bone density that the internal bone structure is influenced by athletic activities. This is illustrated by studies showing that the dominant arm of professional tennis players has a much higher bone mass than the contralateral arm17. In addition, many studies showed a higher bone mass at specific locations in the proximal femur of athletes who participated in high impact sports such as football, basketball and jumping sports18-21. Thus, by increasing external loading of the hip, internal bone formation occurs as an adaptive process23. Conversely, when the loads applied to bone decrease, an increase in bone resorption and a subsequent decrease in bone formation takes place, just like in astronauts during space flight or during prolonged bed rest22.
If a cam deformity were to be regarded as an acquired phenomenon, the actual bone shape or orientation should also be affected by external factors. This phenomenon has already been demonstrated in other joints: in shoulders of elite baseball players there is more proximal humeral retrotorsion and glenoid retroversion in their throwing arm than in their non-throwing arm24. Doing load-bearing sports during childhood and adolescence is associated with development of genu varum (bowlegs) in the knees25.
CASE CONTROL STUDIES
For the hip, there are currently two studies available which compare the shape of the hip between athletes and non-athletes. In these studies, a significantly higher prevalence of cam deformities was found in basketball players and football players, when compared with non-athletic peers26,27. The prevalence of a cam deformity in young skeletally mature basketball players was as high as 89% compared with only 9% in non-athletic controls27. Moreover, other studies without a control group showed a higher prevalence of cam deformities amongst ice hockey players and American football players than can be expected in the general population.
Another indication that a cam deformity is acquired during growth is that a radiological cam deformity is not present before the age of 13 years26. Furthermore, unpublished results from a prospective study of adolescent football players which I presented at the 3rd Aspetar Sports Groin Pain Centre Conference, indicate that a cam deformity develops gradually over time, but only during skeletal maturation of the hip (Figure 2). After closure of the growth plate, there is no further change in hip morphology. These results are supported by epidemiological studies of adults with long-term follow-up, which do not show an increase in the prevalence of cam deformities over time. A considerable proportion of cam deformities are therefore likely to be a result of an adaptive process in response to high impact loading during skeletal maturation.
Interestingly, these findings also suggest that these cam deformities could be prevented by elucidating the biomechanical trigger during skeletal maturation. One could think of a training schedule in which certain high impact activities are replaced by low impact activities, such as swimming and cycling. However, it is unknown which exact movement patterns lead to the development of a cam deformity and whether there is a dose response interaction between high impact athletic activities and development of a cam deformity. These uncertainties make preventive strategies impossible at this time and further research in this area is needed.
FUTURE RESEARCH
With regard to the future, preliminary data on finite element models presented at the 3rd Aspetar Sports Groin Pain Centre Conference showed that movements involving flexion and external rotation while weight-bearing in particular might lead to the formation of a cam deformity in hips with an open growth plate.
CONCLUSION
In summary, FAI is a recently recognised condition which has gained increasing attention over the past decade. Epidemiological studies do not show an association between pincer impingement and development of osteoarthritis, whereas cam impingement is strongly associated with osteoarthritis of the hip. This relationship is probably even stronger in athletes such as football players, basketball players and ice hockey players, as they experience repetitive vigorous hip motion. Cam impingement might therefore be the main explanation for the high prevalence of hip osteoarthritis in athletes. A cam deformity develops only during skeletal maturation of the hip and is a result of high impact athletic activities during growth. Interestingly, this implies that the development of a cam deformity can be prevented. If the prevalence of cam deformities in football players can be decreased, osteoarthritis will not always be the price to be paid for an active football career.
Rintje Agricola M.Sc.
Ph.D. student
Erasmus University Medical centre
Rotterdam, The Netherlands
Contact: r.agricola@erasmusmc.nl
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Image via voetbal foto