**4. Pathogenesis**

The presence of a conflict between the acetabulum and the femoral head-neck junction was noted by several surgeons as being the cause of early hip osteoarthritis (**Figure 10**); however, it was Ganz [1] who was the first to describe details of FAI pathogenesis. He defined it as a condition of abnormal contact between femoral head-neck junction and the acetabulum due to abnormal morphological features and/or as a result of subjecting the hip to the excessive and supraphysiologic range of motion.

This repetitive contact causes a microtraumatic effect and subsequently irreversible chondral damage to the acetabular as well as femoral surfaces [18].

Based on a systematic review performed by Chaudhry and Ayeni, the etiology of FAI syndrome is likely multifactorial [4].

**33**

**Figure 10.**

*Femoroacetabular Impingement: Anatomy and Pathogenesis*

osteosynthesis of a neck or head fracture.

The main factors incriminated in the genesis of FAI belong to three groups:

• Factors related to the level and type of physical activity of the patient; indeed the FAI is particularly common among young athletes requiring extreme and repetitive movement of the hip in flexion and internal rotation such as hockey and basketball.

• Morphological abnormalities such as acetabular retroversion and coxa profunda or changes in hip morphology due to the history of childhood hip disease which may have altered the shape of the femoral head-neck junction such as slipped capital femoral epiphysis (SCFE) or Legg-Calvé -Perthes disease [4].

• Iatrogenic factors such as excessive correction of hip dysplasia or following an

*Pathogenesis of femoroacetabular impingement. (A) Normal morphology; (B) mechanism of impingement in* 

*pincer morphology; (C) mechanism of impingement in cam morphology.*

*DOI: http://dx.doi.org/10.5772/intechopen.90296*

*Essentials in Hip and Ankle*

was 3.2 cm [15].

**Figure 9.**

stood [14].

of motion.

**4. Pathogenesis**

*3.3.2.8 The sciatic nerve*

*3.3.2.9 The superior gluteal nerve*

these portal placements appear to be safe [15].

FAI syndrome is likely multifactorial [4].

The average minimum distance from the anterior portal to the femoral nerve

*A branch of the lateral femorocutaneous nerve accidentally cut in an anterior hip approach.*

The sciatic nerve averaged 2.9 cm from the poster lateral portal. From this study,

It averaged 4.4 cm superior to the anterolateral and posterolateral portals [15]. Relations of these structures with arthroscopic portals have to be assessed and topographic knowledge of the delicate anatomy surrounding the hip fully under-

The presence of a conflict between the acetabulum and the femoral head-neck junction was noted by several surgeons as being the cause of early hip osteoarthritis (**Figure 10**); however, it was Ganz [1] who was the first to describe details of FAI pathogenesis. He defined it as a condition of abnormal contact between femoral head-neck junction and the acetabulum due to abnormal morphological features and/or as a result of subjecting the hip to the excessive and supraphysiologic range

This repetitive contact causes a microtraumatic effect and subsequently irrevers-

Based on a systematic review performed by Chaudhry and Ayeni, the etiology of

ible chondral damage to the acetabular as well as femoral surfaces [18].

**32**

The main factors incriminated in the genesis of FAI belong to three groups:


#### **Figure 10.**

*Pathogenesis of femoroacetabular impingement. (A) Normal morphology; (B) mechanism of impingement in pincer morphology; (C) mechanism of impingement in cam morphology.*

Given that cam and pincer morphologies can be present in asymptomatic individuals, Casartelli [19] propose that other factors out with the bony structures may be involved with FAI syndrome. Weakness of deep hip muscles could not only compromise hip stability but also lead to overload of secondary movers of the hip, thus causing an anterior glide of the femoral head into the acetabulum and increased joint loading.
