Abstract:Femoroacetabular impingement causes pain in the hip in young adults and may predispose to the development of osteoarthritis. Genetic factors are important in the aetiology of osteoarthritis of the hip and may have a role in that of femoroacetabular impingement. We compared 96 siblings of 64 patients treated for primary impingement with a spouse control group of 77 individuals. All the subjects were screened clinically and radiologically using a standardised protocol for the presence of cam and pincer deformiti… Show more
“…A hip with symptomatic FAI is likely to differ from a "normal" hip through a combination of its morphology, durability of its articular cartilage and labrum, and demands placed upon it, with regard to the range of movement and activity level of the patient. Recent evidence suggests a strong genetic component to FAI [3], which is in keeping with the known genetic predisposition to hip OA. Whether abnormal morphology is determined at conception, or is acquired during skeletal development, is not known.…”
Although Smith-Petersen described impingement of the native hip in 1936 [1], the success of replacement arthroplasty of the hip dominated the orthopaedic literature until the early contemporary reports of femoroacetabular impingement (FAI) at the turn of the millennium [2]. Subsequently, an exponential increase in interest in the subject has occurred, as demonstrated by the annual number of Pubmed hits for FAI, which reached 168 in 2010 alone. This interest is perhaps not surprising when one considers that FAI represents a new diagnosis for young adults with hip pain, an opportunity for advanced imaging and surgical techniques, and perhaps most tantalisingly, the possibility of altering the natural history of degenerative joint disease and limiting progression to endstage osteoarthritis (OA). With the explosion of recent interest in FAI, there are many controversies and unresolved issues that will be the targets for research over the next decade.
Aetiology of FAIFemoroacetabular impingement may occur secondary to paediatric hip disease or trauma, but the vast majority of cases have no underlying known cause and may be considered "primary FAI". A hip with symptomatic FAI is likely to differ from a "normal" hip through a combination of its morphology, durability of its articular cartilage and labrum, and demands placed upon it, with regard to the range of movement and activity level of the patient. Recent evidence suggests a strong genetic component to FAI [3], which is in keeping with the known genetic predisposition to hip OA. Whether abnormal morphology is determined at conception, or is acquired during skeletal development, is not known. It is conceivable that there is a genetic predisposition to subclinical slipped capital femoral epiphysis, for example. However, not all hips with abnormal joint morphology develop symptoms. A cam deformity is a common finding (approximately 20% incidence) in asymptomatic male subjects [4][5][6][7] and patients with FAI often have similar deformities in the contralateral asymptomatic hip [8]. This supports the notion that additional variables, such as the vulnerability of the labrum and articular cartilage to injury, and activity level, are important in modulating whether abnormal morphology results in symptoms. The importance of activity type and intensity needs further investigation. It stands to reason that an activity such as hurdling will potentially damage an at-risk hip by increasing the frequency and severity of impingement episodes. Better ways of grading activity are required in order to classify individuals. With regard to morphology, very little is known regarding the development of the nondysplastic hip through childhood and adolescence, and prospective studies during skeletal development may help to determine whether morphology is dependent on activity or other factors. Longitudinal studies of well-characterised cohorts will improve our understanding of how FAI develops.
Difficulties with imagingIt is crucial to appreciate that making a diagnosis of FAI relies on...
“…A hip with symptomatic FAI is likely to differ from a "normal" hip through a combination of its morphology, durability of its articular cartilage and labrum, and demands placed upon it, with regard to the range of movement and activity level of the patient. Recent evidence suggests a strong genetic component to FAI [3], which is in keeping with the known genetic predisposition to hip OA. Whether abnormal morphology is determined at conception, or is acquired during skeletal development, is not known.…”
Although Smith-Petersen described impingement of the native hip in 1936 [1], the success of replacement arthroplasty of the hip dominated the orthopaedic literature until the early contemporary reports of femoroacetabular impingement (FAI) at the turn of the millennium [2]. Subsequently, an exponential increase in interest in the subject has occurred, as demonstrated by the annual number of Pubmed hits for FAI, which reached 168 in 2010 alone. This interest is perhaps not surprising when one considers that FAI represents a new diagnosis for young adults with hip pain, an opportunity for advanced imaging and surgical techniques, and perhaps most tantalisingly, the possibility of altering the natural history of degenerative joint disease and limiting progression to endstage osteoarthritis (OA). With the explosion of recent interest in FAI, there are many controversies and unresolved issues that will be the targets for research over the next decade.
Aetiology of FAIFemoroacetabular impingement may occur secondary to paediatric hip disease or trauma, but the vast majority of cases have no underlying known cause and may be considered "primary FAI". A hip with symptomatic FAI is likely to differ from a "normal" hip through a combination of its morphology, durability of its articular cartilage and labrum, and demands placed upon it, with regard to the range of movement and activity level of the patient. Recent evidence suggests a strong genetic component to FAI [3], which is in keeping with the known genetic predisposition to hip OA. Whether abnormal morphology is determined at conception, or is acquired during skeletal development, is not known. It is conceivable that there is a genetic predisposition to subclinical slipped capital femoral epiphysis, for example. However, not all hips with abnormal joint morphology develop symptoms. A cam deformity is a common finding (approximately 20% incidence) in asymptomatic male subjects [4][5][6][7] and patients with FAI often have similar deformities in the contralateral asymptomatic hip [8]. This supports the notion that additional variables, such as the vulnerability of the labrum and articular cartilage to injury, and activity level, are important in modulating whether abnormal morphology results in symptoms. The importance of activity type and intensity needs further investigation. It stands to reason that an activity such as hurdling will potentially damage an at-risk hip by increasing the frequency and severity of impingement episodes. Better ways of grading activity are required in order to classify individuals. With regard to morphology, very little is known regarding the development of the nondysplastic hip through childhood and adolescence, and prospective studies during skeletal development may help to determine whether morphology is dependent on activity or other factors. Longitudinal studies of well-characterised cohorts will improve our understanding of how FAI develops.
Difficulties with imagingIt is crucial to appreciate that making a diagnosis of FAI relies on...
“…Third, clinicians familiar with the radiographic evaluation of FAI and dysplasia understand the classification of acetabular depth is highly dependent on the radiographic criteria of choice. Reported upper limits of cutoff values for normal LCE angle range from 35°to 45° [12,30]. In our study, overcoverage was diagnosed by a LCE angle of greater than 40°, the midrange of reported LCE angles.…”
Section: Discussionmentioning
confidence: 59%
“…While coxa profunda has been defined most commonly by the acetabular fossa projecting medial to the ilioischial line [3,21,36], some studies have used anterior center edge (ACE) and LCE angles to classify hips as having coxa profunda, although there is no standard cutoff value [13,14,17,22,30] (Table 4). For example, while Pollard et al [30] suspected global overcoverage in hips with coxa profunda (fossa medial to ilioischial line), they also indicated other measurements of acetabular coverage were relevant (based on 95% CI of normal hips without osteoarthritis), such as an LCE angle of greater than 38°and/or an acetabular index of less than À3.7°(men) or less than À4.9°(women) or protrusio acetabuli. Using an LCE angle of greater than 45°, 15.2% of the 1332 men and 19.4% of the 2288 women from the Copenhagen Osteoarthritis Substudy had a deep acetabulum [12].…”
Background Coxa profunda, or a deep acetabular socket, is often used to diagnose pincer femoroacetabular impingement (FAI). Radiographically, coxa profunda is the finding of an acetabular fossa medial to the ilioischial line. However, the relative position of the acetabular fossa to the pelvis may not be indicative of acetabular coverage. Questions/purposes We therefore determined the incidence of coxa profunda and evaluated associations between coxa profunda and other radiographic parameters of acetabular coverage commonly used to diagnose pincer FAI and acetabular dysplasia.Methods We evaluated the radiographs of three cohorts for coxa profunda, lateral center edge (LCE) angle, acetabular index, posterior wall sign, and crossover sign. Data from 67 collegiate football players were collected prospectively (Cohort 1). We identified two patient cohorts Results In all three cohorts, we detected no difference in the LCE angle or acetabular index between hips with and without coxa profunda. Coxa profunda existed in hips representing the spectrum of acetabular coverage measured by LCE angle (À18°to 60°) and acetabular orientation determined by the crossover sign. Conclusions Coxa profunda was a common radiographic finding in both symptomatic patients and asymptomatic football players. Coxa profunda existed in hips representing the spectrum of acetabular coverage and was not associated with an overcovered acetabulum. We conclude coxa profunda is unrelated to overcoverage and suggest its use in diagnosis of pincer FAI be abandoned in favor of other determinants of focal or general overcoverage. Level of Evidence Level III, diagnostic study. See Instructions for Authors for a complete description of levels of evidence.
“…This has led to increased interest in the early diagnosis of FAI via potential screening, especially in patients who are considered to be at high risk, such as elite athletes [10], athletes who participate in sports that have higher risks for changes in morphologic features of the hip [16,24], and siblings of patients with impingement [30]. Abnormalities of morphologic features that can lead to FAI include cam abnormality on the femoral side and/or pincer overcoverage on the acetabular side [15,33].…”
Background Femoral rotation on AP radiographs affects several parameters used to assess morphologic features of the proximal femur but its effect on femoroacetabular impingement parameters remains unknown. Question/purposes We therefore evaluated and characterized the potential effect of femoral rotation on (1) AP alpha angle, (2) lateral-center edge angle (LCEA), and (3) medial proximal femoral angle (MPFA) on AP hip radiographs. Methods We took seven AP hip radiographs at intervals of successive femoral rotation on a single dry, cadaveric specimen: 60°, 40°, and 20°internal rotation; 0°neutral/ anatomic rotation; and 20°, 40°, and 50°external rotation. The AP alpha angle, LCEA, and MPFA were measured on all radiographs by two independent evaluators.Results Within the range of femoral rotation studied, the AP alpha angle ranged from 39°to 62°, the LCEA from 25°to 35°, and the MPFA from 70°to 115°. MPFA and AP alpha angle showed a linear relationship with femoral rotation. Each additional degree of internal rotation produced a reciprocal reduction of the MPFA by 0.36°and the AP alpha angle by 0.18°and vice versa in external rotation. The LCEA, especially within the internal rotation range, showed minimal variation. Conclusions These changes in radiographic parameters emphasize the importance of femoral rotation and patient positioning. We recommend radiographs be evaluated for excessive femoral rotation or nonstandardized positioning before interpretation for diagnostic and treatment implications. It may be prudent to repeat radiographs in these circumstances or, when standardized positioning is not feasible, proceed toward advance imaging.
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