Article Text

Download PDFPDF

What causes cam deformity and femoroacetabular impingement: still too many questions to provide clear answers
  1. Rintje Agricola1,
  2. Harrie Weinans2,3
  1. 1 Department of Orthopaedics, Erasmus University Medical Center, Rotterdam, The Netherlands
  2. 2 Department of Orthopaedics and Department of Rheumatology, University Medical Center Utrecht, Utrecht, The Netherlands
  3. 3 Department of Biomechanical Engineering, Technical University Delft, Delft, The Netherlands
  1. Correspondence to Rintje Agricola, Department of Orthopaedics, Erasmus University Medical Center, Room EE16-14, P.O. Box 2040, Rotterdam 3000 CA, The Netherlands; r.agricola{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Cam deformities of the femoral head contribute to femoroacetabular impingement (FAI) and correlates strongly with development of osteoarthritis.1 Surgery on patients with FAI is performed with increasing frequency; it is unknown whether this prevents osteoarthritis in later life.2 As cam deformity is triggered during late puberty by impact loading of the hip, it is important to elucidate the aetiology of cam deformity.

Factors associated with the presence of a cam deformity

Sex, genetics and physical activity appear to influence whether or not a cam deformity develops. The prevalence of cam deformity is as high as 89% in athletes participating in activities that result in impact loading of the hip as compared to only 9% in non-athletic controls.3 What explains these differences? More than 40 years ago, Murray and Duncan4 recognised that by the loads applied to the hip during skeletal growth influenced, at least in part, development of a cam deformity. They postulated that cam deformity resulted from a mild undiagnosed slipped capital femoral epiphysis (SCFE) in young athletes but recent studies in adolescent athletes suggest SCFE is not involved.5 Hence, cam deformity result from bone adaptation in response to vigorous hip loading, which means that it should be preventable by adjusting the hip loads during a certain period of skeletal growth.

Type and frequency of athletic activity and development of cam deformity

The prevalence of cam deformity seems especially high in weight-bearing sports that require high flexion together with rotational movements of the hip (eg, soccer, basketball and ice hockey require these hip loading patterns). Ice hockey players were 4.5 times more at risk for having a cam deformity than skiers.6 Further, a dose–response relationship exists—elite soccer players who practiced more than three times a week before the age of 12 years were 2.6 times more likely to have a cam deformity than elite soccer players that practiced three times or less before the age of 12 years.7

Bone and growth plate are adaptive tissues

Bone and cartilage adapt to their mechanical environment and the cartilaginous growth plate is likely affected in its differentiation and ossification process by mechanical loads. Cam deformity on radiographs gradually develop from approximately 13 years until closure of the growth plate.5 Finite element (FE) models of the hip showed high mechanical stress on impact loading in the growth plate and surrounding bone, exactly where the cam deformity usually develops.8 This was particularly the case when the hip joint is in a position of flexion and external rotation. The high stresses were only present in hips with an open growth plate, while in models with closed growth plates the high stress patterns normalised.

Window of opportunity and dose–response: children should not stop playing sports

Why is the age of around 12–13 years in boys so important with respect to developing a cam deformity? During these years of the adolescent growth spurt, the skeleton is especially responsive to mechanical stimuli, when levels of growth hormone, testosterone and IGF-1 increase and when bone modelling is highly active.9 This might be a critical period since subtle mechanical triggers might interact with molecular stimuli and easily lead to bone formation. The growth spurt is therefore interesting for programmes to prevent the development of a cam deformity by changing the loads applied to the hip in a certain period of time.9

No prevention without understanding the aetiology: where do we need to go?

Although we have evidence now from various (small) cohort studies that cam deformities develop in adolescent athletes, there is still no clear aetiological basis. Finite element analysis revealed that the orientation of the growth plate combined with certain loading scenarios modulates bone formation. This means that a specific orientation of the growth plate with extension towards the femoral neck can result in a synergistic effect on bone formation in the anterolateral head-neck junction.8 Further, the orientation of the growth plate could even be a result of certain loading conditions (figure 1). Even though the FE models explain one of the earliest clinical observations concerning the onset of a cam deformity (see figure 1 for a hypothesis), such models require many assumptions and should be corroborated in future studies with athletes to guide future preventive measures.

Figure 1

A schematic representation (1) is provided for a hip that develops from the age of 2–12 years (1A–1C) and than either forms a normal hip (D1–D4) or a cam deformity (E1–E4) from the age of 12 to 18 years. Panel 2 shows corresponding X-ray examples. Before the growth spurt, the growth plate is relatively horizontal (A–C). During flexion and external rotation FE models show relatively large compressive stresses within the growth plate at the lateral side (E1–E2, red zone). 8 This results in more bone formation at the medial side as compared to the lateral side, which might lead to a growth plate that bends towards the neck (E2).8 This bended growth plate shape leads to shear stresses instead of compressive stresses and therefore now stimulates bone growth at the anterolateral portion of the head-neck junction (E3, green zone).8 This process probably continues until closure of the growth plate (E4). The growth plate extension towards the neck and its relation with cam deformity has also been shown in clinical studies (X-rays in 2). FE, finite element.

Prevention of potentially serious conditions such as cam deformity is a major sports medicine priority. That cannot be achieved until the following five questions are answered in large prospective cohorts of adolescent athletes and non-athletes: Does a cam deformity only develop when the growth plate is open? How does the development of a cam deformity relate to biological age and the growth spurt? Are there soft tissue structures such as cartilage that change even before a cam becomes radiographically visible? Is there a small window of opportunity to prevent the cam morphology and are flexion and external rotation important triggers? Do participants with cam deformity have other aberrant shape variations such as abnormal femoral retroversion?


View Abstract


  • Contributors Both authors contributed equally. The final version was approved by both authors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.