University of Southern California Dissertations and Theses

Pathomechanics of femoroacetabular impingement syndrome: utilizing subject-specific modeling approaches to investigate the influence of hip joint morphology and neuromuscular control

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Pathomechanics of femoroacetabular impingement syndrome: utilizing subject-specific modeling approaches to investigate the influence of hip joint morphology and neuromuscular control

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PATHOMECHANICS OF FEMOROACETABULAR IMPINGEMENT SYNDROME:
UTILIZING SUBJECT-SPECIFIC MODELING APPROACHES TO INVESTIGATE THE
INFLUENCE OF HIP JOINT MORPHOLOGY AND NEUROMUSCULAR CONTROL

by

Jordan Cannon

A Dissertation Presented to the
FACULTY OF THE USC GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
DOCTOR OF PHILOSOPHY
(BIOKINESIOLOGY)

May 2022

Copyright 2022 Jordan Cannon

ii

Dedication

This dissertation is dedicated to my family.

To my parents, Patricia and Michael Cannon, for their unending encouragement and support.
To my sister, Michela Cannon, for always being in my corner.
To my wife, Ali Courtemanche, for the kindness, love, and patience over the last 14 years.

Acknowledgements
This dissertation and the work throughout my PhD would not have been possible without
the support from many great people.
First and foremost, I would like to thank my advisor, Dr. Christopher Powers, for his
mentorship, guidance, and support throughout every stage of the PhD process. I have benefited
tremendously from his perspective, ability to simplify and clearly communicate ideas, and his
unique clinician-scientist approach. Very early in my research career I admired Dr. Powers’ work
and wanted to work with him. I am grateful he gave me that opportunity and for all the wisdom he
provided in my time working with him.
I was very fortunate to have a great guidance committee with expertise in a variety of areas
who helped improve my work. Each of my committee members challenged me in different ways
and asked questions that fostered a deeper understanding of concepts, mechanisms, and my data.
I am very grateful for the support, guidance, and advice of Dr. Kornelia Kulig. She was always
generous with her time, believed in me, looked out for me, and cared about my future. In every
meeting she is enthusiastic, curious, and excited to explore ideas. I left every meeting energized. I
will always appreciate the phrase “permission to speculate” – it is a gift that encourages students
to think deeply about data and is part of a great scientific philosophy. I am thankful to Dr. Kristi
Lewton for her perspective, critical questions, and approach to the scientific method. I gained a lot
from our long meetings discussing topics in detail. Each and every meeting with Dr. Jill McNitt-
Gray was fantastic. Her expertise in movement biomechanics and understanding of control
strategies are unparalleled. Her encouragement to explore individual strategies and
cause-effect relationships have undoubtedly improved my approach to data analysis.
Last, but certainly not least, I would like to thank Dr. Jeffery Rankin. His expertise in
modeling and simulation were particularly beneficial. Furthermore, he always provided
practical and pragmatic suggestions to keep projects moving forward.
I would like to acknowledge the financial support for this work provided by the University
of Southern California Provost Graduate School Fellowship, the International Society of
Biomechanics Matching Dissertation Grant, and the Division of Biokinesiology and
Physical Therapy. I would like to thank Dr. James Gordon for his support, wisdom, and helpful
conversations during my time in the PhD program. I would also like to thank Dr. Lori
Michener, Dr. George Salem, and Dr. Susan Sigward for their generous support, guidance, and
advice on my research and career.
I would like to thank Dr. Alexander Weber and Dr. Jia Liu for their efforts in recruiting
participants that were included in my dissertation. I would also like to thank Dr. Seol Park and the
DPT student volunteers, in particular Dr. Jessica Evaristo, for their help with data collection and
processing. I am also thankful for the support provided throughout my PhD from past and present
MBRL lab mates and staff within the division. Lastly, I would like to thank all the participants
who made this dissertation possible.
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iv

Table of Contents
Dedication ....................................................................................................................................... ii
Acknowledgements ........................................................................................................................ iii
List of Tables ................................................................................................................................. vi
List of Figures ............................................................................................................................... vii
Abstract .......................................................................................................................................... ix
Chapter 1 – Overview ..................................................................................................................... 1
Chapter 2 – Pathomechanics Underlying Femoroacetabular Impingement Syndrome: ..................
Theoretical Framework to Inform Clinical Practice ....................................................................... 3
1. Risk Factors Leading to Symptomatic Bony Impingement .................................................... 4
1a. Abnormal Bony Morphology (Pathway 1a, Figure 1-1) ................................................... 4
1b. Susceptible Populations and High Risk Activities (Pathway 1b, Figure 1-1) .................. 5
1c. Abnormal Hip/Pelvis Kinematics (Pathway 1c, Figure 1-1) ............................................ 6
Sagittal Plane ...................................................................................................................... 7
Frontal Plane ....................................................................................................................... 7
Transverse Plane ................................................................................................................. 8
Symptomatic Bony Impingement ........................................................................................... 9
2. Chondrolabral Damage Secondary to Impingement (Pathway 2, Figure 1-1) ...................... 11
3. Inflammation in Response to Intra-Articular Damage (Pathway 3, Figure 1-1) .................. 13
4. Neuromuscular and Capsular Responses to Inflammation (Pathway 4, Figure 1-1) ............ 14
Capsular Fibrosis .................................................................................................................. 14
Gluteal Muscle Inhibition ..................................................................................................... 16
5. Kinematic Consequences of Capsular Fibrosis and Gluteal Inhibition
(Pathway 5, Figure 1-1) ............................................................................................................ 18
Capsular Fibrosis Limits Protective Hip Joint Motion ......................................................... 18
Gluteal Inhibition Contributes to Altered Hip Kinematics. .................................................. 19
A Proposed Pathomechanical Model of FAIS (Figure 1-1) ...................................................... 20
Conclusion ................................................................................................................................ 21
Chapter 3 – Femoral and acetabular features explain acetabular contact pressure sensitivity
to hip internal rotation in persons with cam morphology: A finite element analysis ................... 22
Introduction ............................................................................................................................... 23
Methods..................................................................................................................................... 25

v

Participants ............................................................................................................................ 25
CT Scanning & Morphology Measurements ........................................................................ 26
Finite Element Model Development ..................................................................................... 29
Model Output and Post-Processing ....................................................................................... 31
Statistical Analysis ................................................................................................................ 31
Results ....................................................................................................................................... 32
Discussion ................................................................................................................................. 36
Conclusions ............................................................................................................................... 40
Chapter 4 – Gluteal Activation During Squatting Reduces Acetabular Contact Pressure in
Persons with Femoroacetabular Impingement Syndrome: A Patient-Specific Finite
Element Analysis .......................................................................................................................... 41
Introduction ............................................................................................................................... 42
Methods..................................................................................................................................... 44
Participants ............................................................................................................................ 44
Procedures ............................................................................................................................. 45
CT Imaging ....................................................................................................................... 45
Biomechanical Data Collection ........................................................................................ 46
Data Processing ..................................................................................................................... 47
EMG-Driven Hip Joint Model .......................................................................................... 48
Finite Element Model Development ................................................................................. 49
Statistical Analysis ................................................................................................................ 50
Results ....................................................................................................................................... 51
Discussion ................................................................................................................................. 53
Conclusions ............................................................................................................................... 56
Chapter 5 – Summary and Conclusions ........................................................................................ 57
Clinical Implications ................................................................................................................. 60
Directions for Future Research ................................................................................................. 61
Conclusions ............................................................................................................................... 64
References ..................................................................................................................................... 65
Appendix A ................................................................................................................................... 82

vi

List of Tables
Table 3-1: Participant demographics and morphological measurements (mean ± standard
deviation). ..................................................................................................................................... 26
Table 3-2: Stepwise multiple regression model results. Values represent coefficients
(confidence intervals). ................................................................................................................... 34
Table 3-3: Median and 95% CI from the bootstrapped regression for the adjusted R
2
and
individual coefficient estimates of the morphological variables included in the model. .............. 35
Table 4-1: Patient demographics. Alpha angle >50.5° on an axial oblique CT scan was
used to confirm a cam morphology. ............................................................................................. 44
Table 4-2: Comparison of outcome variables of interest between the non-cued and cued
gluteal activation squat conditions. ............................................................................................... 51

vii
List of Figures
Figure 1-1: Proposed theoretical framework which details the cascading events in FAIS.
Concomitant changes at the joint and neuromuscular level may be both a cause and
consequence of FAIS progression. ................................................................................................. 3
Figure 2-1: A) Normal femoral head-neck contour. B) Femur with a flattening of the
femoral head-neck junction demonstrating a cam morphology. Image modified with
permission from Meyer et al., 2006, Clin. Orth. Rel. Res. ............................................................. 4
Figure 2-2: Demonstration of a femur with a cam morphology. Image modified with
permission from Hellwig et al., 2015, Comput. Method. Biomech. Biomed. Eng. ........................ 4
Figure 2-3: During flexion and hip internal rotation, a femoral head without cam
morphology can rotate in the acetabulum unhindered. In FAIS, the cam morphology abuts
with the acetabulum, compressing the labrum and acetabular cartilage. Image modified
with permission from Byrd, 2010, Sports Health. .......................................................................... 9
Figure 2-4: Location of computed impingement zone and locations of cartilage and labral
damage. Images modified with permission from Tannast et al., 2008, Clin. Orth. Rel. Res. ....... 10
Figure 3-1: A) The alpha angle ( α) measuring the cam morphology on the axial oblique
plane; B) Femoral neck-shaft angle ( λ) of the proximal femur. ................................................... 28
Figure 3-2: A) Anterior Pelvic Plane and Acetabular Rim Plane; B) Transverse plane view
demonstrating the Acetabular Anteversion Angle ( Φ); C) Frontal plane view demonstrating
the Acetabular Inclination Angle (θ); D) Frontal plane view with the Acetabular Depth ( δ)
represented; E) Frontal plane view demonstrating the Lateral Center-Edge Angle (σ). .............. 29
Figure 3-3: Peak acetabular contact pressure at each hip internal rotation position with the
hip flexed to 90° for each participant. Linear goodness of fit across participants:
median R
2
= 0.97, mean R
2
= 0.87. ............................................................................................... 32
Figure 3-4: Simple linear regression plots of acetabular contact pressure sensitivity to hip
internal rotation (slope) versus each morphological variable of interest. ..................................... 33
Figure 3-5: Summary of adjusted R
2
values from bootstrap analysis.
Median value = 0.65 [0.37, 0.89]. ................................................................................................. 35
Figure 3-6: Pressure maps of two participants with low and high cam morphology
demonstrating high and low acetabular contact pressure sensitivity with increasing internal
rotation. Peak pressures are located on the anterior-superior acetabulum (anterior = right). ....... 38

viii

Figure 4-1: Overview of subject-specific modeling approach to calculate acetabular
contact pressure during squatting. ................................................................................................. 45
Figure 4-2: Peak acetabular contact pressure (GPa) of each participant for the non-cued
and cued gluteal activation squat conditions. Peak contact pressure is located on the
anterior-superior acetabulum (anterior = right) for all participants. ............................................. 52
Figure 4-3: Ensemble average time-series of gluteus maximus and medius muscle
activation and hip joint bone-on-bone contact forces for the two squat conditions.
Shaded region = standard error. .................................................................................................... 52
Figure 4-4: Ensemble average time-series hip angles for the two squat conditions.
Shaded region = standard error. .................................................................................................... 53

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Abstract
Femoroacetabular impingement syndrome (FAIS) is a motion-related clinical disorder
characterized by abnormal hip joint morphology and subsequent premature contact between the
proximal femur and acetabulum. Osseous malformations on the femoral head-neck junction (cam)
and/or the acetabular rim (pincer) are responsible for early contact when the hip is in a flexed
position. Over the last decade there has been a marked increase in attention to, and interest in,
FAIS. Despite continued efforts by researchers and clinicians, the development, progression, and
appropriate treatment of FAIS remains unclear. While research across various disciplines has
provided informative work in various areas related to FAIS, the underlying pathomechanics, time
history, and interaction between known risk factors and symptoms remain poorly understood.
Given our limited understanding of the pathogenesis of FAIS, the purpose of this dissertation was
two-fold. The first aim was to develop a pathomechanical, multi-faceted, theoretical framework of
FAIS. Secondly, this dissertation sought to provide experimental evidence for two aspects of the
theoretical framework (structural and neuromuscular contributors to mechanical impingement)
utilizing subject-specific finite element modelling.
In Chapter 2, a synthesis of current literature on various aspects of FAIS was performed to
develop a hypothesis driven-theoretical framework of FAIS from a pathomechanical perspective.
The framework proposes a vicious cycle of FAIS in which concomitant changes at the joint and
neuromuscular level may act as both a cause and consequence of symptomatic impingement. The
review of existing literature that was used in the development of the theoretical framework
revealed two important gaps in our understanding of FAIS. First, what are the structural features
of the hip joint that may be contributory to mechanical impingement associated with FAIS?

x

Second, how does neuromuscular control influence mechanical impingement in persons with
FAIS?
To address the gap in the literature related to the structural features associated with FAIS,
Chapter 3 sought to determine which bony characteristics are most influential in contributing to
mechanical impingement in persons with a cam morphology. Twenty participants (10 female, 10
male) with a documented cam morphology participated in this study. Subject-specific finite
element models derived from computed tomography scans were used to determine which femoral
and/or acetabular morphologies accentuate acetabular contact pressure with increasing degrees of
hip internal rotation with the hip flexed to 90°. To determine the best predictor of acetabular
contact pressure sensitivity to internal rotation, all morphological variables were included in a
stepwise regression model. The predictors were then included in a bootstrapped multiple linear
regression analysis using 1000 iterations, resampling with replacement. Acetabular anteversion
angle (r = -0.56, p = 0.01), acetabular inclination angle (r = -0.50, p = 0.02), and femoral neck-
shaft angle (r = -0.60, p = 0.005) were found to be negatively correlated with pressure sensitivity
to internal rotation. Lateral center-edge angle was found to be positively correlated with pressure
sensitivity to internal rotation (r = 0.56, p = 0.01). Both the alpha angle (r = -0.25, p = 0.28) and
acetabular depth (r = -0.22, p = 0.36) were not associated with pressure sensitivity to internal
rotation. Results of the bootstrap analysis revealed that lower values of femoral neck-shaft angle,
acetabular anteversion, acetabular inclination, and a deeper acetabulum were able to explain 65%
[37%, 89%] of the variance in acetabular contact pressure sensitivity to hip internal rotation. The
findings of Chapter 3 suggest that mechanical impingement and the concomitant acetabular contact
pressure is modulated by multiple femoral and acetabular features in persons with a cam
morphology.

xi

To address the gap in the literature related to the neuromuscular influences underlying
mechanical impingement, Chapter 4 sought to assess the role of gluteal muscle recruitment on
acetabular contact pressure in persons with cam FAIS. Eight individuals (4 males and 4 females)
with a diagnosis of cam FAIS participated in this study. Participants underwent two data collection
sessions on separate days. The first session consisted of computed tomography imaging of the
pelvis and proximal femur while the second session consisted of a biomechanical assessment of
squatting (kinematics, kinetics, and electromyography). Two maximal depth bodyweight squat
conditions were evaluated: 1) non-cued squatting; and 2) cued gluteal activation squatting.
Utilizing subject-specific EMG-driven hip and finite element modelling approaches, hip muscle
activation, kinematics, bone-on-bone contact forces, and peak acetabular contact pressure were
compared between squat conditions using one-tailed paired t-tests. The results demonstrated that
modest increases in gluteus maximus (7% MVIC, p < 0.0001) and medius activation (6% MVIC,
p = 0.009) resulted in a significant reduction in hip internal rotation (5°, p = 0.024), and in doing
so reduced acetabular contact pressure by 32% (p = 0.023). Reductions in acetabular contact
pressure during the cued squat condition occurred despite no changes in hip abduction and
increased bone-on-bone contact forces.
Taken together, the experimental findings of this dissertation suggest that some individuals
with FAIS are more susceptible to mechanical impingement owing to their bony hip anatomy.
However, impingement may be minimized with adequate recruitment of the gluteal muscles.
Information gained from this work indicates that a more comprehensive assessment of an
individual’s bony hip joint morphology may improve characterization of FAIS. Additionally, this
dissertation highlights the importance of gluteal function in persons with FAIS and offers an
evidence-based foundation upon which specific training interventions can be designed.

1

Chapter 1 – Overview
Overview
Femoroacetabular impingement syndrome (FAIS) is a clinical syndrome resulting from
abnormal hip joint morphology and has become increasingly recognized as a common cause of
hip and groin pain in young, active adults (Griffin et al., 2016). The 2016 Warwick International
Agreement (Griffin et al., 2016) defines FAIS as “a motion-related clinical disorder of the hip with
a triad of symptoms, clinical signs and imaging findings”. This condition represents symptomatic
contact between the proximal femur and the acetabulum (Griffin et al., 2016). FAIS has been
posited as a precursor to hip osteoarthritis (Ganz et al., 2003); however, conflicting evidence exists
and the true progression of this condition currently is under investigation.
Despite increased interest in FAIS, its etiology is still largely unknown. It has been
suggested that abnormal hip kinematics combined with excessive loading during vigorous athletic
activity in adolescence is a major contributor to the development of FAIS (Kuhns et al., 2015;
Roels et al., 2014; Siebenrock et al., 2011). Although, a substantial portion of the symptomatic
FAIS population is comprised of former (or current) athletes in their second or third decade, many
patients remain asymptomatic in spite of the presence of osseous abnormalities associated with
FAIS (Allen et al., 2009; Byrd, 2010; Clohisy et al., 2013; Frank et al., 2015; Kang et al., 2010;
Kuhns et al., 2015).
Evidence-based interventions that address the various facets of FAIS remain elusive. This
is due, in part, to a limited understanding of the development and progression of FAIS. Although
recent reviews on the epidemiology, surgical treatment, imaging, joint tissue stress, and physical
impairments of FAIS have synthesized knowledge within respective subfields of interest, a
comprehensive view of FAIS from a pathomechanical perspective is lacking (Amanatullah et al.,

2

2015; Byrd, 2010; Clohisy et al., 2013; Diamond et al., 2015; Frank et al., 2015; Freke et al., 2016;
Ng et al., 2016; Pierannunzii, 2017; Pun et al., 2015).
The purpose of this dissertation was two-fold. First, the aim of Chapter 2 was to develop a
multi-faceted theoretical framework of FAIS. To accomplish this goal, a thorough literature review
was conducted to synthesize existing knowledge across subfields to provide a comprehensive
pathomechanical perspective on FAIS. Second, Chapters 3 and 4 sought to provide experimental
evidence for structural and neuromuscular components of the proposed framework using subject-
specific finite element modeling. Specifically, Chapter 3 addressed the question as to which bony
characteristics are most influential in contributing to mechanical hip impingement. In Chapter 4,
the influence of neuromuscular control in contributing to mechanical hip impingement was
examined. It is anticipated that information gained from this dissertation will provide important
empirical data to advance our understanding and treatment of this complicated clinical disorder.

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Chapter 2 – Pathomechanics Underlying Femoroacetabular Impingement
Syndrome: Theoretical Framework to Inform Clinical Practice

The purpose of this chapter is not to repeat recent reviews of FAIS, but rather to propose a
theoretical framework in which concomitant changes at the joint and neuromuscular level may be
both a cause and consequence of FAIS progression (Figure 1-1). In doing so, this chapter sought
to integrate relevant knowledge and understanding from the various subfields of FAIS and related
literature to provide a hypothesis-driven framework that can inform future research and the
treatment of the young, active patient with hip pain and FAIS. The chapter is structured such that
the following sections correspond to specific components/pathways of the theoretical framework
(Figure 1-1).

Figure 1-1: Proposed theoretical framework which details the cascading events in FAIS.
Concomitant changes at the joint and neuromuscular level may be both a cause and consequence
of FAIS progression.

4

1. Risk Factors Leading to Symptomatic Bony Impingement
1a. Abnormal Bony Morphology (Pathway 1a, Figure 1-1)
From an anatomical perspective, FAIS consists of osseous malformations that occur at the
femoral head-neck junction (cam-type) and/or acetabular rim (pincer-type). Cam and pincer
morphology may occur in isolation, or more commonly, in combination (Clohisy et al., 2013).
Cam-type morphology is a result of femoral head asphericity, which can be observed
radiographically as a flattening of the anterior-superior contour of the head/neck junction (Figure
2-1) or an osseous convexity leading to loss of normal offset at the femoral head-neck junction
(Figure 2-2) (Beck et al., 2005). This so-called ‘pistol grip’ morphology is often located on the
anterolateral or anterosuperior portion of the head-neck junction (Beck et al., 2005; Ganz et al.,
2003).

2
3

Pincer-type morphology is not associated with decreased femoral head-neck offset, but is
instead marked by acetabular over-coverage. This over-coverage can result from acetabular
retroversion, or may represent osseous abnormalities such as coxa profunda or protrusio acetabuli
Figure 2-1: A) Normal femoral head-neck
contour. B) Femur with a flattening of the
femoral head-neck junction demonstrating
a cam morphology. Image modified with
permission from Meyer et al., 2006, Clin.
Orth. Rel. Res.

Figure 2-2: Demonstration of a femur
with a cam morphology. Image modified
with permission from Hellwig et al., 2015,
Comput. Method. Biomech. Biomed. Eng.

5

(Tannast et al., 2007). One large study of patients with symptomatic FAIS (n = 1076) reported that
47.6% of hips exhibited isolated cam morphology, 44.5% had combined cam/pincer morphology,
and 7.9% exhibited isolated pincer morphology (Clohisy et al., 2013). Similarly, Nepple et al.
(2014) reported on the radiographic findings of 100 patients with symptomatic FAIS (50 female,
50 male) and found that 45.5% had isolated cam morphology, 48.5% had combined cam/pincer
morphology, and that 6% had isolated pincer morphology. Others have reported a higher
prevalence of combined cam/pincer morphology in persons with a history of hip pain or injury
(61.8%), with isolated cam morphology (9.8%) and isolated pincer type morphology (22.8%)
being less common (Nepple et al., 2012). Another large study of 700 athletes with FAIS reported
radiographic evidence for cam and pincer type morphology with a prevalence of 72.1% and 97.8%,
respectively (Carton & Filan, 2019). However, this study did not report the prevalence of each of
these measures occurring in isolation or combination.
Regardless of the type of osseous deformity present (cam and/or pincer), the pathological
progression of FAIS as described in the sections below would be expected to be similar given the
mechanics required to create anterior impingement (described below). Indeed, a vast majority of
research in this area has focused on persons with cam FAIS, however the importance of pincer
FAIS should not be discounted.
1b. Susceptible Populations and High Risk Activities (Pathway 1b, Figure 1-1)
While the precise etiology of abnormal bony morphology associated with FAIS is
unknown, there is some association with pediatric hip conditions such as developmental dysplasia,
slipped capital femoral epiphysis, and Legg-Calve-Perthes disease (Chaudhry & Ayeni, 2014;
Nepple, Prather, et al., 2013). FAIS is primarily diagnosed in the young, active adult population
(55% female, 45% male) with an average reported age of 28.4 years (Clohisy et al., 2013). Pain

6

may be dismissed or misunderstood leading to a prolonged period before proper diagnosis and
intervention. In a multi-institutional epidemiological study of 1,076 patients, most had symptoms
for 12-36 months prior to surgery (Clohisy et al., 2013). Demographic data revealed that 87.8% of
patients were Caucasian and the average body mass index was 25.1 kg/m
2
(Clohisy et al., 2013).
Pincer-type FAIS typically presents in middle aged women, while cam-type impingement is more
common in younger men at a ratio of 3:1 (Byrd, 2014; Clohisy et al., 2013; Laborie et al., 2011).
Pain associated with FAIS typically is exacerbated with activities that involve repetitive
or sustained hip flexion such as squatting, stair climbing, and prolonged sitting (Ganz et al., 2003;
Hammond et al., 2017; Kennedy et al., 2009). Importantly, a link between high intensity athletic
participation in adolescence and onset of FAIS exists (Kuhns et al., 2015). Compared to their non-
athletic counterparts, athletes have a greater prevalence of FAIS, supporting the notion that high
and repetitive impact loading may contribute to the development of abnormal morphology
(Agricola et al., 2012; Ross, Bedi, et al., 2015; Siebenrock et al., 2011). However, the suggestion
that involvement in specific sports increases the risk of FAIS development appears to be limited
to the accessibility of athletic populations in the geographical regions in which the research was
conducted (Agricola et al., 2012; Lerebours et al., 2015; Philippon et al., 2007; Ross et al., 2015;
Siebenrock et al., 2011; Weber et al., 2016).
1c. Abnormal Hip/Pelvis Kinematics (Pathway 1c, Figure 1-1)
Anterior mechanical impingement is created with simultaneous hip flexion, adduction, and
internal rotation (Banerjee & McLean, 2011). As such, it has been postulated that greater
magnitudes of hip adduction and internal rotation motion during functional or athletic movements
that require substantial hip flexion may be contributory to FAIS development and progression. In
particular, kinematic studies of tasks requiring substantial hip flexion are most relevant for this

7

population (i.e. deep squats, drop jumps, and stair negotiation). While hip and pelvis kinematics
during gait have been studied with interest, this task only requires approximately 30% of the
available hip flexion range of motion, and likely would not expose an individual to mechanical
impingement (Alshameeri & Khanduja, 2014).
Sagittal Plane
In the sagittal plane, the most consistent finding across studies comparing persons with
FAIS to healthy controls is the tendency for persons with FAIS to display altered pelvis kinematics.
In particular, greater anterior pelvic tilt at maximum hip flexion (Bagwell, Snibbe, et al., 2016;
Lamontagne et al., 2009; Rylander et al., 2013), decreased posterior pelvic tilt motion (Bagwell,
Snibbe, et al., 2016; Lamontagne et al., 2009), and diminished sagittal plane pelvis excursion
(Lamontagne et al., 2009), has been described in persons with FAIS during dynamic tasks such as
a deep squat and stair climbing. Greater anterior pelvic tilt during tasks requiring substantial hip
flexion results in earlier mechanical abutment. In addition, decreased ability to posteriorly tilt the
pelvis during activities that involve deep hip flexion is important as this motion creates relative
hip extension and would serve to reduce bony abutment at a given hip flexion angle. In addition,
posterior pelvic tilt motion is kinematically coupled with femur external rotation (Bagwell,
Fukuda, et al., 2016; Duval et al., 2010), a motion that also protects against bony impingement
(see below).
Frontal Plane
Several studies have reported that persons with FAIS perform dynamic tasks with greater
degrees of hip adduction when compared to healthy controls (Diamond et al., 2017; Kennedy et
al., 2009; Kumar et al., 2014; Rylander et al., 2013). Regardless of whether hip adduction is the
result of movement of the femur-on-pelvis or pelvis-on-femur, this motion allows for

8

approximation of the cam morphology and acetabular rim (i.e. impingement) when the hip is in a
flexed position. Interestingly, when persons with FAIS perform constrained squats (i.e. narrow
stance width and neutral foot position, or restricted trunk lean) greater degrees of hip adduction
are evident compared to when unconstrained squats are performed (i.e. self-selected stance width
and foot position, or unrestricted trunk lean) (Diamond et al., 2017; Wilson et al., 2013). This
suggests that persons with FAIS have the capacity to limit hip adduction but may not be able to do
so under specific constraints.
Transverse Plane
In the transverse plane, several studies have reported that persons with FAIS exhibit
reduced hip internal rotation compared to healthy controls across a variety of dynamic tasks
(Bagwell, Snibbe, et al., 2016; M. A. Hunt et al., 2013; Kumar et al., 2014; Rylander et al., 2013).
This finding is consistent with studies that have reported that patients with FAIS have reduced
passive hip internal rotation range of motion based on clinical exam (Clohisy et al., 2009; Kapron
et al., 2015; Philippon et al., 2007; Zebala et al., 2007). It has been suggested that diminished hip
internal rotation observed in persons with FAIS during both dynamic and passive conditions may
be the result of bony abutment (Figure 2-3) as opposed to capsular tightness or other soft tissue
restrictions (Bagwell & Powers, 2017; Jorge et al., 2014; Kapron et al., 2015; Philippon et al.,
2007). As with the frontal plane, persons with FAIS also display less hip internal rotation during
unconstrained squatting tasks when compared to squatting tasks in which foot position is
constrained (Wilson et al., 2013), indicating that the ability of persons with FAIS to avoid bony
abutment may be compromised when an explicit movement pattern is required.

9

4

Figure 2-3: During hip flexion and internal rotation, a femoral head without cam morphology
can rotate in the acetabulum unhindered. In FAIS, the cam morphology abuts with the
acetabulum, compressing the labrum and acetabular cartilage. Image modified with permission
from Byrd, 2010, Sports Health.

As noted above, previous research has established that sagittal plane motion of the pelvis
and transverse plane motion of the femur are kinematically coupled during weight-bearing tasks
(Bagwell, Fukuda, et al., 2016; Duval et al., 2010). Specifically, posterior pelvic tilt is coupled
with femur external rotation and anterior pelvic tilt is coupled with femur internal rotation
(Bagwell, Fukuda, et al., 2016; Duval et al., 2010). Bony contact between the femoral head and
acetabulum is thought to drive the kinematic coupling between sagittal plane pelvis motion and
transverse plane femur motion (Duval et al., 2010). Therefore, the inability of persons with FAIS
to posteriorly tilt the pelvis (a protective motion in deep hip flexion) also may contribute to the
loss of protective hip external rotation motion.

Symptomatic Bony Impingement
Symptomatic bony impingement involves an interplay among abnormal bony morphology,
high risk activities, and abnormal hip & pelvis kinematics (Diamond et al., 2015; Ganz et al.,
2003). In particular, the loss of femoral head-neck concavity associated with cam morphology
leads to bony abutment (mechanical impingement) during tasks involving hip flexion, adduction,
and internal rotation (Amanatullah et al., 2015; Ganz et al., 2003; Ito et al., 2001). Mechanical

10

impingement occurs at the limit of hip range of motion when the femoral neck comes into contact
with the anterosuperior acetabulum (Banerjee & McLean, 2011; Kemp, Makdissi, et al., 2014;
Kubiak-Langer et al., 2007; Ng et al., 2015; Rylander et al., 2013). Several finite element studies
evaluating cam deformities have reported that peak shear stresses and contact pressures occur on
the anterosuperior acetabulum when the hip is flexed and internally rotated (Bagwell & Powers,
2017; Chegini et al., 2009; Hellwig et al., 2015; Jorge et al., 2014; Ng et al., 2012). The location
of peak stress magnitudes on the anterosuperior acetabulum corroborate with the locations of labral
and chondral damage observed intraoperatively (Figure 2-4) (Beck et al., 2005; Reichenbach et
al., 2011; Tannast et al., 2008).
5

Figure 2-4: Location of computed impingement zone and locations of cartilage and labral
damage. Images modified with permission from Tannast et al., 2008, Clin. Orth. Rel. Res.

The location of impingement, while most often at the anterosuperior acetabulum, is patient-
specific and not predictable from any single radiological measure (Asheesh Bedi et al., 2011).
Thus, the alpha angle, femoral head-neck offset angle, acetabular depth, acetabular anteversion,
and various morphological features likely will determine where in the arc of hip flexion motion

11

impingement occurs. While the degree of hip flexion required to create impingement is not
specifically known, approximately 90 degrees of hip flexion is required for bony abutment (Ganz
et al., 2003; Ito et al., 2001; Kapron et al., 2015; Myers et al., 1999; Notzli et al., 2002). Thus, the
precise magnitude of hip flexion required for impingement likely varies between individuals based
on the severity of osseous deformity. Additionally, hip kinematics in the frontal and transverse
planes also may influence the magnitude of hip flexion required to create impingement. For
example, the motions of hip adduction and internal rotation likely contribute to abutment earlier
in the arc of hip flexion motion.
It should be noted that the presence of abnormal osseous deformity (cam and/or pincer) is
not always associated with symptomatic FAIS. A systematic review of 26 studies (inclusive of
2,114 asymptomatic hips), reported that 37% of the general population and 55% of athletes had
asymptomatic cam deformities (Frank et al., 2015). It is possible that asymptomatic individuals
with abnormal morphology may not engage in at risk activities regularly (or vigorously) enough,
or display the abnormal hip/pelvis kinematics described above. Therefore, a combination of all 3
risk factor categories (1a-c) described above would likely be required to initiate symptomatic
FAIS.
2. Chondrolabral Damage Secondary to Impingement (Pathway 2, Figure 1-1)
Given that asymptomatic patients with confirmed radiographic osseous deformities exist,
it has been suggested that the initiation of anterior hip pain in persons with FAIS occurs only in
response to the degradation of intra-articular structures (Banerjee & McLean, 2011; Beck et al.,
2005; Byrd, 2010; Kuhns et al., 2015). In a large epidemiological study of 1076 patients (1130
hips) 93% of surgical persons with FAIS presented with labral damage, while 83% had associated
cartilage damage (Banerjee & McLean, 2011; Beck et al., 2005; Clohisy et al., 2013; Kuhns et al.,

12

2015). The most common form of labral abnormalities detected were detachment (56%) and
degeneration (25.2%), however labral ossification (7.5%) and full-thickness tears (4.2%) were also
reported (Clohisy et al., 2013). Articular damage presented most commonly as debonding (24.9%),
cleavage (24.8%), and chondromalacia (22%), occurring in the superolateral (76.3%) and anterior
(63.8%) quadrants (Clohisy et al., 2013). Thus, substantial joint damage occurs in a variety of
forms in response to impingement.
The cam morphology causes damage to the acetabular cartilage through compression and
shear stresses that occur during hip flexion when the cam lesion rotates through the anterosuperior
region of the acetabulum (Ganz et al., 2003; Kuhns et al., 2015). As noted above, chondrolabral
loading will increase with simultaneous hip adduction and internal rotation motions which can
result in cartilage delamination and secondary tearing of the labrum at the chondrolabral junction
(Beck et al., 2005). In comparison to cam-type impingement, pincer morphology primarily
damages the labrum as the hip flexes and compresses the anterior labrum against the femoral neck
(Kuhns et al., 2015). In either situation, labral microtrauma leads to gross tearing of the labrum
and separation from the articular cartilage. Later, acetabular cartilage damage occurs through a
“contrecoup” mechanism resulting from persistent pressure between the postero-inferior
acetabulum and the postero-medial aspect of the femoral head (Pfirrmann et al., 2006). Dwyer and
colleagues (2014) used cadaveric specimens to load the hip in various postures associated with
activities of daily living, and reported that the labral seal is compromised under certain postures
due to labral damage incurred secondary to FAIS. Therefore, additional joint changes may occur
in response to chondrolabral damage.

13

3. Inflammation in Response to Intra-Articular Damage (Pathway 3, Figure 1-1)
As noted above, chronic mechanical impingement can evolve from localized soft-tissue
damage to a degenerative cascade causing extensive, non-focal, intra-articular injury. Damage to
these intra-articular structures results in the release of tissue specific biological substrates and may
contribute to a rise in systemic markers of inflammation. Specifically, cartilage oligomeric matrix
protein (COMP), a glycoprotein found in articular cartilage that helps to stabilize and align type II
collagen, is released following cartilage destruction (Garvican et al., 2010). As a marker of
cartilage turnover, COMP blood levels are increased with joint inflammation and osteoarthritis
(Garvican et al., 2010; Posey & Hecht, 2008). Similarly, C-reactive protein (CRP), an acute phase
reactant that plays an integral role in initiating the systemic reaction to inflammation (Black et al.,
2004), is also elevated in patients with OA (Punzi et al., 2005). Elevated circulating levels of
COMP and CRP have been reported in athletes with FAIS when compared to pain-free controls
with normal hips (Bedi et al., 2013).
The presentation and progression of inflammation observed in FAIS may differ, at least
initially, from that of end-stage OA. Hashimoto et al (2013) attempted to characterize these
differences by examining the expression of inflammatory cytokine and chemokine, matrix-
degrading, and extracellular matrix genes in articular cartilage harvested from healthy hips, hips
with FAIS, and hips with end-stage OA. Articular cartilage at the impingement zone of hips with
FAIS were found to be more metabolically active and expressed higher levels of certain
inflammatory, anabolic, and catabolic genes. Similarly, Chinzei et al (2016) reported a different
molecular profile for FAIS versus OA in the gene expression of inflammatory cytokines and
metabolic (anabolic and catabolic) enzymes. In FAIS, the inflammatory response may extend
beyond the cartilage itself as significant infiltration of inflammatory cells, mainly mast cells and

14

macrophages, along with neovascularization has been demonstrated in harvested labral tissue
(Elias-Jones et al., 2015). Whether by direct effect, or as a consequence of disuse or maladaptation,
local inflammation and pain in the hip is seen in both OA and FAIS. The degradation of intra-
articular structures in response to impingement may lead to disruption of the labral seal and cause
synovitis with the ensuing inflammation acting to increase pressure within the joint capsule.
Furthermore, damage to the labrum and the proprioceptive nerve endings can alter the afferent
return of the joint and affect reflex control of surrounding musculature (Ralphs & Benjamin, 1994).
4. Neuromuscular and Capsular Responses to Inflammation (Pathway 4, Figure 1-1)
Systemic and tissue specific inflammation of hip joint structures may influence the
composition of the collagen tissue that comprises the joint capsule and affect the ability of
associated musculature to appropriately activate. Synovitis at the hip joint may cause secondary
capsular thickening, resulting in limited passive hip range of motion that may influence normal
joint kinematics. Additionally, inflammation mediates arthrogenic muscle inhibition by altering
afferent activity and diminishing efferent motor drive of affected muscles (Hopkins & Ingersoll,
2000). Both of these potential consequences of inflammation will be discussed below.
Capsular Fibrosis
Cellular changes induced by hip joint inflammation and mechanical damage, whether as a
result of FAIS or from generalized degeneration (such as OA), may extend beyond the intra-
articular structures. The hip joint capsule is an extra-articular ligamentous structure that stabilizes
the femoral head within the acetabulum and may thicken in response to tissue stress/strain and/or
joint inflammation. Increased compressive loading of the capsule (due to direct mechanical
abutment) can lead to acquired capsular thickening, likely as an adaptive mechanism, as it
previously has been demonstrated that a greater cross-sectional area of the hip capsular ligaments

15

is associated with higher absolute force to failure (Hewitt et al., 2001; Hewitt et al., 2002; Ralphs
& Benjamin, 1994). Furthermore, the hip joint synovium is attached to the deep capsular surface,
and therefore, synovial thickening (as seen in chronic synovitis and OA), may cause secondary
capsular thickening (Ralphs & Benjamin, 1994).
Adhesive capsulitis of the hip, is a known clinical entity characterized by synovial
inflammation leading to capsular fibrosis, and may occur with a spectrum of hip diseases,
including OA and FAIS (Looney et al., 2013). Using MRI imaging Rakhra et al. (2016) reported
that cam-FAIS and non-FAIS diseased hips had thicker hip capsules superiorly and anteriorly
compared to asympotmatic controls. Given that increased capsule thickness was not specific to
cam-FAIS, these authors postulated that increased compressive stress in the anterosuperior
quadrant of the capsule may occur even in the absence of direct mechanical abutment (Rakhra et
al., 2016). This suggests that physiological changes of the synovium (such as synovitis) could be
responsible for secondary capsular thickening. A study by Clohisy et al (2013) reported that 62.8%
of persons with FAIS presented with synovitis at the time of surgery. While it appears that capsular
thickening is not specific to FAIS, it likely occurs in conjunction with FAIS through both direct
and indirect mechanisms (Rakhra et al., 2016; Weidner et al., 2012).
While the exact mechanism of hip capsular thickening and fibrosis associated with FAIS
is not understood, analogous pathology found in the shoulder may be helpful in elucidating
potential causes of this finding. Adhesive capsulitis (AC), commonly called frozen shoulder, is an
inflammatory and fibrotic disorder primarily of the capsule and ligamentous structures of the
rotator interval (Hand et al., 2007; Pietrzak, 2016; Zuckerman & Rokito, 2011). Current
understanding of the AC disease process suggests that cytokine driven inflammation and
hyperplasia of the synovium progresses to capsular fibrosis with infiltration of chronic

16

inflammatory cells and cytokines (Hand et al., 2007; Pietrzak, 2016; Rodeo & Hannafin, 1997).
The onset of this cytokine driven signaling cascade appears to be both locally and systemically
driven. This is consistent with known risk factors for AC, including cardiovascular disease and
diabetes mellitus; disease processes that are strongly associated with chronic low-level systemic
inflammation (Monteiro & Azevedo, 2010). There appears to be some level of systemic
inflammation associated with FAIS (Bedi et al., 2013). While the underlying cause(s) of
inflammation may differ between AC and FAIS, there is the potential for the initiation of fibrotic
changes in the joint capsule, which in turn, will influence function.
Gluteal Muscle Inhibition
Arthrogenic muscle inhibition (AMI) is defined as reflex inhibition of musculature
surrounding a joint following injury or damage to joint structures (Hopkins & Ingersoll, 2000;
Hurley, 1997). Inflammation, pressure, pain, and atrophy have been implicated in mediating AMI
via altered afferent activity (Freeman et al., 2013; Hopkins & Ingersoll, 2000). Damaged joint
receptors (mechanoreceptors in particular) alter the afferent return and diminish efferent motor
drive, thus decreased motoneuron recruitment and force of contraction occurs (Hopkins &
Ingersoll, 2000). Consequently, muscle weakness and impaired proprioceptive function are
consequences of persistent AMI. AMI has been studied extensively at the knee, manifesting as
ipsilateral extensor (quadriceps) inhibition and flexor (hamstrings and soleus) facilitation (Hopkins
et al., 2001; Palmieri-Smith et al., 2007; Palmieri et al., 2003, 2005).
Existence of AMI at the hip joint has been suggested by Freeman et al. (2013) who reported
that increasing hip joint pressure via intra-articular injections of saline in healthy persons resulted
in diminished gluteus maximus activation (as determined through electromyography).
Interestingly, concurrent bilateral erector spinae facilitation also was observed following the intra-

17

articular injections. Although somewhat preliminary in nature, the findings of this study suggest
that diminished gluteal muscle activation could be mediated by pain and inflammation associated
with FAIS.
Although AMI has not been studied in persons with FAIS, evidence exists that persons
with FAIS exhibit diminished gluteus medius and deep lateral hip rotator activation during
functional tasks (Diamond et al., 2016). Additionally, tensiomyography analysis has revealed that
persons with FAIS display impairments in contraction time of gluteus maximus compared to
healthy controls (Seijas et al., 2016). Furthermore, biomechanical studies of persons with FAIS
have reported evidence of diminished use of the hip extensors during gait and squatting (Bagwell,
Snibbe, et al., 2016; Hunt et al., 2013).
Chronic disuse of the gluteal muscles, whether or not related to AMI, would likely reduce
available force capacity over time. In fact, Casartelli and colleagues (2011) measured hip muscle
strength in individuals with symptomatic FAIS and healthy aged-matched controls and found that
those with FAIS displayed significantly reduced strength in the hip flexors, abductors, adductors,
and external rotators. Additionally, Nepple et al. (2015) reported reductions in hip flexor and hip
abductor strength in the involved limb compared to the uninvolved limb in symptomatic persons
with FAIS. It has also been reported that persons with chronic hip pain have decreased hip external
rotation and internal rotation strength (at both 0
o
and 90
o
hip flexion) as well as decreased hip
abduction strength (at 15
o
abduction) of the involved limb compared to healthy controls (Harris-
Hayes et al., 2014). Interestingly, Harris-Hayes and colleagues (2014) also observed weakness in
external rotation (at 0
o
hip flexion) and abduction of the uninvolved limb of persons with unilateral
chronic hip pain, leading one to speculate on the nature of the cause and effect relationship between
hip pain and strength deficits. Although persons with FAIS appear to present with global hip

18

muscle weakness, it is important to consider how weakness of the gluteal muscles may impact the
functional capabilities of persons with FAIS, and the degree to which such deficits may be
responsible for the abnormal hip kinematics exhibited by this population.
5. Kinematic Consequences of Capsular Fibrosis and Gluteal Inhibition (Pathway 5, Figure
1-1)
The development of capsular fibrosis and gluteal inhibition/weakness in persons with FAIS
will have kinematic consequences at the hip joint. Fibrotic changes in the joint capsule may affect
ROM and kinematic coupling between the femur and pelvis. Inhibition of the gluteal musculature
can diminish the ability to generate the joint motions necessary to avoid the impingement position.
Each of these consequences will be discussed in detail below.
Capsular Fibrosis Limits Protective Hip Joint Motion
It has been reported that persons with FAIS exhibit diminished passive range of motion at
the hip compared to health controls (Clohisy et al., 2009; Guler et al., 2016; Kubiak-Langer et al.,
2007; Pun et al., 2015). In particular, a positive FABER test, which assesses combined passive
motions of abduction and external rotation in a flexed position, has been reported to discriminate
between persons with FAIS and healthy controls, as well as between the involved and uninvolved
limbs in patients with FAIS (Clohisy et al., 2009; Nepple et al., 2015; Philippon et al., 2009). Apart
from passive range of motion, Kennedy and colleagues (2009) compared active hip range of
motion at 90
o
of hip flexion between patients with FAIS and healthy controls and reported
decreased hip internal and external rotation in the FAIS group.
Thickening of the hip capsule likely is contributory to the reported limitations in passive
and active hip range of motion reported in persons with FAIS. In particular, the iliofemoral and
pubofemoral ligaments of the anterior capsule become taut at end ranges of hip abduction and

19

external rotation (Fuss & Bacher, 1991; Hewitt et al., 2002). As such, thickening of the anterior
capsule and associated capsule stiffness (Hewitt et al., 2002; Stewart et al., 2002) could limit hip
abduction and external rotation; motions that are thought to be protective against impingement
when the hip is in a flexed position (Rakhra et al., 2016; Weidner et al., 2012). Additionally,
capsular tightness may limit the normal coupling behavior between the pelvis and femur. As
described above, external rotation of the femur is kinematically coupled with posterior pelvic tilt.
The inability of persons with FAIS to posteriorly tilt the pelvis during tasks that require deep hip
flexion may be due in part to anterior capsular tightness or contracture (Alshameeri & Khanduja,
2014; Groh & Herrera, 2009; Turley et al., 2013). A kinematic consequence of the inability to
achieve a normal posterior pelvic tilt could be a loss of protective hip external rotation. It is also
possible that the loss of available hip external rotation may explain the inability to posteriorly tilt
the pelvis, as coupling behavior may be influenced in either direction.
Gluteal Inhibition Contributes to Altered Hip Kinematics.
As noted above, inhibition of the gluteal musculature could result in decrements in acute
force production and muscle weakness due to diminished motor unit recruitment over time
(Hopkins et al., 2001; Hopkins & Ingersoll, 2000; Hurley, 1997; Stokes & Young, 1984). This is
particularly problematic in the FAIS population since the reported motion impairments leading to
impingement are influenced by the gluteal musculature, particularly the gluteus maximus and
gluteus medius. Most important is the fact that the gluteus maximus primarily is responsible for
the motions of posterior pelvic tilt, hip external rotation, and contributes to hip abduction (Klein
Horsman et al., 2007; Neumann, 2010; Ward et al., 2010) Additionally, the gluteus medius is a
primary hip abductor and its function is necessary to control frontal plane pelvis motions,
especially during tasks that involve single limb support (Neumann, 2010).

20

The presence of AMI at the hip would be most problematic when the hip is in a flexed
position. With increasing magnitudes of hip flexion the gluteus maximus moment arms for external
rotation and extension decrease, as do the gluteus medius external rotation and abduction moment
arms (Klein Horsman et al., 2007; Neumann, 2010; Ward et al., 2010). Therefore, greater muscle
force production (via increased muscle activation) would be necessary when the hip is flexed to
produce muscle moments that would protect against impingement.
A Proposed Pathomechanical Model of FAIS (Figure 1-1)
The evidence presented in this review has outlined a series of events in which one cascades
into the next (Figure 1-1). Initially, the presence of the cam or pincer morphology combined with
abnormal hip kinematics during tasks involving deep hip flexion contribute to mechanical
impingement. This results in increased hip joint forces (anteriorly) and stress on the anterosuperior
acetabulum and associated soft tissues (Audenaert et al., 2011; Rakhra et al., 2016). In turn,
repetitive contact and higher localized loads promotes labral and chondral damage (Beck et al.,
2005; Kuhns et al., 2015).
The proposed theoretical framework presented here suggests that chronic pain and/or
inflammation resulting from chondrolabral damage may result in changes to the capsular tissue
and altered neuromuscular control of the hip. Capsular tightness combined with gluteal muscle
inhibition may limit the normal coupling behavior of the pelvis and femur, as well as the ability of
persons with FAIS to achieve positions or produce motions thought to be protective against
impingement (i.e. posterior pelvic tilt, hip abduction, and external rotation) in positions that require
substantial hip flexion. Therefore, a cyclical process may exist in which the consequences of FAIS
also act to contribute to the progression of the syndrome (Figure 1-1).

21

The review of literature related to the proposed framework suggests that certain aspects
related to the development and progression of FAIS may be modifiable. Targeted rehabilitation
aimed at correcting neuromuscular deficits of the gluteal musculature, improving hip joint
mobility, and correcting faulty movement strategies to reduce/avoid kinematics that promote
impingement (i.e. deep hip flexion, adduction, and internal rotation) may slow the progression of
FAIS, and possibly reduce the risk of future joint pathology following corrective surgery. Although
surgical procedures address the osseous deformities contributing to impingement, empirical
evidence shows that altered hip kinematics continue to persist despite improvements in self-
reported outcomes such as pain and function (Casartelli et al., 2015; Weber et al., 2016) This is
problematic considering the potential for future hip osteoarthritis in the FAIS population.

Conclusion
A theoretical framework is proposed that aims to understand the multifactorial and possibly
cyclical nature of FAIS development. While increased interest of FAIS as a relatively new clinical
syndrome continues, further research is necessary to test specific hypotheses related to the
development, progression, and treatment of FAIS. Additionally, components of this framework
(such as altered hip muscle performance, abnormal hip kinematics, and chondrolabral damage)
also may apply to persons with chronic hip joint pain (Harris-Hayes et al., 2014, 2018) or other
hip disorders not considered to be FAIS. While exploring the potential overlap between chronic
hip joint pain owing to mechanisms other than FAIS is beyond the scope of this chapter, it is hoped
that the proposed framework stimulates future research in this area.

22

Chapter 3 – Femoral and acetabular features explain acetabular contact
pressure sensitivity to hip internal rotation in persons with cam morphology:
A finite element analysis

A requisite component of the pathomechanical framework, and of FAIS itself, is
mechanical impingement between the proximal femur and acetabular rim (Pathway 1a, Figure 1-
1). Cam and pincer morphology are defining characteristics for the diagnosis of FAIS, yet cam
morphology has been documented in asymptomatic individuals. As noted in Chapter 2, many bony
structural characteristics have been associated with FAIS. However, it is not clear which of these
structural features are most contributory to mechanical impingement. Given that the cam
morphology is a three-dimensional bony prominence, any bony hip joint structural feature, or
combination of features, that reduce the impingement free range of motion likely influence
impingement when the hip is flexed. To address this gap in knowledge, the purpose of this chapter
was to determine which bony characteristics are most influential in contributing to mechanical
impingement in persons with a cam morphology. A comprehensive assessment of the
morphological contributions to mechanical impingement is necessary to improve characterization
of FAIS. Furthermore, an understanding of femoral and acetabular features that promote
impingement and elevate acetabular contact pressure may help explain who is most likely to incur
chondrolabral damage and develop symptoms.

23

Introduction
Femoroacetabular impingement (FAI) is a condition in which there is premature contact
between the proximal femur and acetabulum (Ganz et al., 2003; Griffin et al., 2016). When the hip
is flexed, this early contact is due to osseous malformations on the femoral head-neck junction
(cam morphology) and/or the acetabular rim (pincer morphology) (Ganz et al., 2003). Of the two
malformations, cam morphology has received greater attention in the literature because it is present
in >90% of symptomatic persons with FAI (Clohisy et al., 2013; Nepple et al., 2014; Ross,
Tannenbaum, et al., 2015) and has been linked with the development of hip osteoarthritis (Agricola
et al., 2013).
The motions of hip internal rotation and adduction accentuate mechanical impingement
(bony abutment) when the hip is flexed, with internal rotation at hip flexion angles of ≥90° the
most problematic (Bagwell & Powers, 2017; Beck et al., 2005; Chegini et al., 2009; Jorge et al.,
2014). Evidence suggests that internal rotation at high degrees of hip flexion in persons with a cam
morphology directly contributes to impingement and elevates acetabular contact pressure (Jorge
et al., 2014) and stress (Bagwell & Powers, 2017; Chegini et al., 2009), which in turn is thought
to increase the risk of chondrolabral damage and future hip pathology (Beck et al., 2005; Ganz et
al., 2003; Wagner et al., 2003).
The magnitude of cam morphology has been reported to contribute to greater acetabular
stress/contact pressure (Bagwell & Powers, 2017; Chegini et al., 2009; Hellwig et al., 2015; Ng et
al., 2012, 2019). However, previous literature suggests that elevated acetabular contact pressure
when the hip is flexed and internally rotated may be dependent on a number of morphological
characteristics beyond that of the cam or pincer morphology itself. For example, a lower femoral
neck-shaft angle (FNSA) has been reported in symptomatic cam FAI compared to control hips (Ng

24

et al., 2015), and has been found to increase acetabular stresses during squatting in persons with a
cam morphology (Ng et al., 2019). With respect to the acetabulum, morphological characteristics
such as acetabular depth (Anderson et al., 2012; Boone et al., 2012; Diesel et al., 2015; Fujii et al.,
2015; Nepple, Lehmann, et al., 2013), retroversion (Lerch et al., 2020; Siebenrock et al., 2003),
inclination (Nepple, Lehmann, et al., 2013), and superolateral extension (i.e. lateral center-edge
angle) (Kuhns et al., 2015; Lerch et al., 2020; Rhee et al., 2017) also have been implicated in FAI
and have been suggested to contribute to mechanical impingement.
Previous studies have evaluated the influence of bony morphology on acetabular stress,
however these investigations have focused only on one or two characteristics using simulated
changes in morphology or evaluated the extreme ranges of various morphological characteristics
(Bagwell & Powers, 2017; Chegini et al., 2009; Ng et al., 2019). For example, Ng and colleagues
(2019) utilized subject-specific geometry when investigating the influence of FNSA on acetabular
contact stress, but only compared persons with the highest and lowest FNSA values from a larger
cohort. Although such studies have been useful in identifying potential morphological contributors
to FAI, it is likely that multiple morphological characteristics in persons with cam morphology
interact to cause mechanical impingement. For example, an individual could have a large cam
morphology but when combined with a high FNSA and/or a high acetabular anteversion angle
may not be susceptible to high contact pressures. Conversely, an individual with a moderate cam
morphology may experience higher acetabular contact pressures when combined with a low FNSA
and a more retroverted acetabulum. Thus, the magnitude of acetabular contact pressure resulting
from a cam morphology may be modulated by various femoral and acetabular features, but the
interaction between these features remains unclear.

25

To date, a comprehensive assessment of the primary contributors to mechanical
impingement in persons with cam morphology has not been undertaken. The purpose of the current
study was to determine which bony characteristics are most influential in contributing to
mechanical impingement in persons with a cam morphology. To accomplish this goal, we used
subject-specific models and finite element analyses (FEA) to determine which femoral and/or
acetabular morphologies accentuate acetabular contact pressure over increasing degrees of hip
internal rotation while the hip was flexed to 90°. Understanding how other morphological features
may predispose persons with a cam morphology to incur high acetabular contact pressures during
hip internal rotation may improve the identification of persons at risk of developing symptomatic
FAI.
Methods
Participants
Twenty participants (10 female, 10 male) with a documented cam morphology participated
in this study (Table 3-1). Ten of the participants were recruited from an orthopaedic surgeon and
ten were identified from an unrelated study in which computed tomography (CT) scans of the hip
joint were obtained (Liu et al., 2021). Cam morphology was confirmed if the alpha angle was
greater than 50.5° in the axial oblique plane (see below for details) (Ng et al., 2015; Notzli et al.,
2002; Rakhra et al., 2009). Prior to participation, informed consent was obtained from all
participants as approved by the institutional review board of the University of Southern
California’s Health Sciences campus.

26
Table 3-1: Participant demographics and morphological measurements (mean ± standard
deviation).
Female
(n = 10)
Male
(n = 10)
Total
(n = 20)
Age (years) 27.1 ± 5.6 28.4 ± 4.5 27.8 ± 5.0
Height (m) 1.69 ± 9.1 1.84 ± 4.4 1.76 ± 0.09
Mass (kg) 66.5 ± 10.0 77.6 ± 6.4 72.0 ± 9.0
Alpha Angle (°) 63.3 ± 8.2 68.7 ± 8.8 66.0 ± 7.8
Femoral Neck-Shaft Angle (°) 133.4 ± 2.8 134.4 ± 3.4 133.9 ± 3.1
Acetabular Anteversion Angle (°) 20.1 ± 6.2 19.3 ± 4.6 19.7 ± 5.3
Acetabular Inclination Angle (°) 45.3 ± 6.3 45.4 ± 7.4 45.4 ± 6.7
Acetabular Depth (mm) 19.4 ± 5.4 23.7 ± 4.1 21.6 ± 5.2
Lateral Center-Edge Angle (°) 33.1 ± 6.8 32.6 ± 5.9 32.8 ± 6.2
CT Scanning & Morphology Measurements
Each participant underwent CT scanning of the pelvis and bilateral proximal femora
(Toshiba Aquilion One 320 Slice CT scanner, Toshiba American Medical Systems, Tustin, CA).
Scans were performed with the participants supine and at a neutral hip alignment (0.5mm slice
thickness, zero tilt, 120 mA, 80 KVP). To reconstruct 3D models of the pelvis and proximal femur
bony geometry, CT images were segmented and smoothed using 3D Slicer (Fedorov et al., 2012;
https://www.slicer.org/). The same software was used to manually select fiducial points on the
most anterior aspects of the bilateral anterior superior iliac spines and pubic tubercles. A minimum
of 50 points were placed equidistant on the acetabular rim (excluding the notch) on the side of
27
interest. The 3D proximal femur was further segmented into separate head, neck, and shaft
components.
Following 3D reconstruction, models and fiducial points were imported to MATLAB
(MathWorks Inc., Natick, MA). Initially, a best fit sphere was fit to the femoral head, with the
centroid being used to identify the hip joint center (Bishop et al., 2021). Using the center of the
femoral head and radius of the best fit sphere, points on the femoral head surface directly anterior
and posterior to the center were created. In addition, a best fit ellipsoid to the femoral neck and
another to the femoral shaft were created to find the longitudinal vector running through the center
of these structures (Bishop et al., 2021).
The magnitude of the cam morphology was measured using the alpha angle on the axial
oblique plane. Determination of the axial oblique plane was established as the best fit plane of the
anterior and posterior femoral head points and the center of the best fit ellipsoid of the femoral
neck. The alpha angle was calculated as the angle between the line running from the center of the
femoral head through the center of the femoral neck and the line from the center of the femoral
head to the anterior point in which the femoral head exceeded the radius of the best fit sphere
(Figure 3-1A) (Ng et al., 2015; Notzli et al., 2002; Rakhra et al., 2009). The FNSA was calculated
as the frontal plane angle between the axial oblique plane and the femoral shaft vector (Figure 3-
1B) (Sangeux et al., 2015).
28
6
Figure 3-1: A) The alpha angle ( α) measuring the cam morphology on the axial oblique plane;
B) Femoral neck-shaft angle ( λ) of the proximal femur.
To obtain the acetabular morphology measurements of interest (anteversion angle,
inclination angle, depth, and lateral center-edge angle), a pelvis coordinate system and associated
planes were first defined in each model. The anterior pelvic plane (APP) was defined as the least
squares best fit plane of the points located on the anterior superior iliac spines and pubic tubercles
and comprised the frontal plane of the pelvis coordinate system (Figure 3-2A). The transverse
plane was defined as the plane perpendicular to the APP containing a vector passing through the
left and right ASIS. The sagittal plane was defined as the plane perpendicular to both the APP and
the transverse plane, containing a vector passing through the mid-ASIS and mid-PT points. The
acetabular rim plane (ARP) was defined as the least squares best fit plane of the (≥50) points on
the acetabular rim (Figure 3-2A). The normal (perpendicular vector) to the ARP (𝐴𝐴 𝐴𝐴𝐴𝐴𝐴𝐴 � � � � � � � � � � � ⃑
) was used
to represent the 3D orientation of the acetabulum.
The acetabular anteversion angle was calculated as the transverse plane angle between the
𝐴𝐴 𝐴𝐴𝐴𝐴𝐴𝐴 � � � � � � � � � � � ⃑
and the frontal plane of the pelvis (Figure 3-2B), with a higher angle representing a more
anteverted acetabulum. The acetabular inclination angle was calculated as the frontal plane angle
between the 𝐴𝐴 𝐴𝐴𝐴𝐴𝐴𝐴 � � � � � � � � � � � ⃑
and the sagittal plane of the pelvis (Figure 3-2C), with a higher angle
29
representing a more vertically oriented acetabulum. Acetabular depth was calculated as the
maximum perpendicular distance from the ARP to the lunate surface (Figure 3-2D). The lateral
center-edge angle (LCEA) was calculated in the frontal plane as the angle between two vectors
originating at the center of the hip joint, one directed superiorly and the other intersecting the most
lateral point on the acetabulum (Figure 3-2E).
7
Figure 3-2: A) Anterior Pelvic Plane and Acetabular Rim Plane; B) Transverse plane view
demonstrating the Acetabular Anteversion Angle ( Φ); C) Frontal plane view demonstrating the
Acetabular Inclination Angle (θ); D) Frontal plane view with the Acetabular Depth ( δ)
represented; E) Frontal plane view demonstrating the Lateral Center-Edge Angle (σ).
Finite Element Model Development
The portion of the hemipelvis of interest was extracted from the full 3D pelvis model to
limit the number of elements and associated model processing times. Surface geometry was
30
created for the hemipelvis and proximal femur and meshed using 1mm triangular elements
(Hypermesh, Altair Engineering Inc., Troy, MI). The meshed hemipelvis and proximal femur were
then imported into Abaqus (SIMULIA, Dassault Systems, Providence, RI) for finite element model
development and analysis.
The hemipelvis and proximal femur were modeled as 3D deformable shell bones (1.5 mm
thickness) with homogenous, isotropic, linear elastic materials having an elastic modulus of 17
GPa and a Poisson’s ratio of 0.30 (Anderson et al., 2005, 2008; Assassi & Magnenat-Thalmann,
2016; Bagwell & Powers, 2017; Chegini et al., 2009; Dalstra et al., 1995). A surface-to-surface,
finite sliding, hard contact algorithm was employed between the femoral head (primary surface)
and acetabulum (secondary surface) with a friction coefficient of 0.02 (representative of synovial
joints) (Bagwell & Powers, 2017; Chegini et al., 2009; Harris et al., 2012; Liu et al., 2016). The
hemipelvis was constrained in 6 degrees-of-freedom while the femur was constrained in 3
rotational degrees-of-freedom allowing for translation in all directions. The position of the
hemipelvis was held constant (in neutral) and the femur was rotated about the center of the femoral
head to 90° hip flexion.
The forces applied to the models were derived from the OrthoLoad HIP98 database
(Bergmann et al., 2001). The peak in-vivo joint loads from a stand-to-sit task were scaled to the
average mass of our participants (72 kg) and were applied at the center of the femoral head.
Specifically, the forces applied to each model consisted of 304 N medially, 69 N posteriorly, and
1061 N superiorly. Quasi-static loading simulations were performed at 90° of hip flexion and were
repeated over 3° increments of hip internal rotation (ranging from 0-15°), resulting in 6 simulations
for each participant. For each internal rotation simulation, the femur was internally rotated about
31
the center of the femoral head. Force application (magnitude, location, and global orientation) was
held constant across simulations.
Model Output and Post-Processing
The outcome variable of interest from each simulation was the peak contact pressure on
the acetabulum. Using the 6 peak contact pressures from each participant, the individual’s
“sensitivity” to internal rotation was quantified as the slope of the linear (least-squares regression)
fit to the observed values. R
2
values were used to assess goodness of fit and the slope of the
regression line was used for statistical analysis.
Statistical Analysis
Simple linear regression analyses were performed to determine the association between
each morphology variable of interest and sensitivity to internal rotation (i.e., acetabular contact
pressure sensitivity to hip internal rotation). To determine the best predictors of contact pressure
sensitivity to internal rotation, all morphological variables were then included in a stepwise
regression model (forward and backward).
Given the small sample size and high number of dependent variables examined, the best
predictors of pressure sensitivity to internal rotation based on the stepwise regression model were
subjected to a bootstrapping procedure. For these predictors, multiple linear regression was
performed using 1000 bootstrap iterations, resampling with replacement, to emulate the process of
obtaining new, distinct data sets to quantify variability and certainty of model parameters to small
changes in the data set (Bland & Altman, 2015; Ohtani, 2000). Median values and 95% confidence
intervals (CI) of the model coefficient of determination (adjusted R
2
) were the primary metrics of
interest from the bootstrap analysis. All statistical analyses were performed in R

(R Core Team,
2021) with statistical significance set to p < 0.05 for all tests.
32
Results
A wide range of sensitivity to internal rotation and morphology values were observed
among participants (Figure 3-3; Table 3-1). On average, peak acetabular contact pressure increased
linearly with increasing hip internal rotation (median R
2
= 0.97, mean R
2
= 0.87; Figure 3-3). In
all simulations, peak contact pressure occurred on the anterior-superior acetabulum.
8
Figure 3-3: Peak acetabular contact pressure at each degree of hip internal rotation with the hip
flexed to 90° for each participant. Linear goodness of fit across participants: median R
2
= 0.97,
mean R
2
= 0.87.
The results of the simple linear regression models are presented in Figure 3-4. The
acetabular anteversion angle (r = -0.56, p = 0.01), acetabular inclination angle (r = -0.50, p = 0.02),
and FNSA (r = -0.60, p = 0.005) were found to be negatively correlated with pressure sensitivity
to internal rotation. LCEA was found to be positively correlated with pressure sensitivity to
33
internal rotation (r = 0.56, p = 0.01). Both the alpha angle (r = -0.25, p = 0.28) and acetabular depth
(r = -0.22, p = 0.36) were not found to be associated with pressure sensitivity to internal rotation
(Figure 3-4).
9
Figure 3-4: Simple linear regression plots of acetabular contact pressure sensitivity to hip
internal rotation (slope) versus each morphological variable of interest.
r = -0.25
p = 0.28
r = -0.22
p = 0.36
r = -0.56
p = 0.01*
r = -0.50
p = 0.02*
r = -0.60
p = 0.005*
r = 0.56
p = 0.01*
34
The stepwise regression revealed that FNSA, acetabular anteversion angle, acetabular
inclination angle, and acetabular depth were the best combination of variables to predict contact
pressure sensitivity to internal rotation, explaining 55% of the variance (Table 3-2). Results of the
bootstrap analysis revealed that a median value of 65% [37%, 89%] variance in sensitivity could
be explained by these morphological variables (Figure 3-5, Table 3-3).
Table 3-2: Stepwise multiple regression model results. Values represent coefficients
(confidence intervals).
Dependent variable:
Pressure sensitivity to internal rotation
Femoral Neck-Shaft Angle -16.12
*
(-27.07, -5.16)
Acetabular Anteversion -7.35
*

(-13.13, -1.58)
Acetabular Inclination -4.82
(-9.80, 0.15)
Acetabular Depth 4.35
(-2.34, 11.04)
Constant 2,531.92
*

(1,145.71, 3,918.14)
Observations 20
R
2
0.65
Adjusted R
2
0.55
Residual Std. Error 65.03 (df = 15)
F Statistic 6.87
*
(df = 4; 15)
Note:
*
p < 0.05
35
10
Figure 3-5: Summary of adjusted R
2
values from bootstrap analysis. Median value = 0.65 [0.37,
0.89].
Table 3-3: Median and 95% CI from the bootstrapped regression for the adjusted R
2
and
individual coefficient estimates of the morphological variables included in the model.
Adjusted R
0.65
Variable Median [95% CI]
Adjusted R
2
0.65 [0.37, 0.89]
Femoral Neck-Shaft Angle -16.54 [-33.97, -6.11]
Acetabular Anteversion -7.34 [-13.13, -0.05]
Acetabular Inclination -4.45 [-9.57, 2.07]
Acetabular Depth 4.85 [-5.33, 12.83]
36
Discussion
Since the first proposed link between mechanical impingement and the development of hip
osteoarthritis, femoroacetabular impingement syndrome (FAIS) has emerged as a distinct clinical
condition garnering increased interest among clinicians and researchers (Griffin et al., 2016).
While FAI primarily is characterized by the presence of osseous malformations on the femoral
head-neck junction (cam morphology), the current investigation sought to determine how other
bony morphologies also may contribute to mechanical impingement and elevate acetabular contact
pressure during the motions of hip flexion and internal rotation. The primary finding of this study
revealed that lower values of FNSA, acetabular anteversion, acetabular inclination, and a deeper
acetabulum were able to explain 65% of the variance in contact pressure sensitivity. This finding
suggests that mechanical impingement and the concomitant acetabular contact pressure is
modulated by multiple femoral and acetabular features in persons with a cam morphology.
The most influential variable in terms of internal rotation contact pressure sensitivity was
FNSA. A lower FNSA would be expected to reduce the clearance between the femoral head-neck
junction and the acetabular rim, particularly with the hip in a flexed and internally rotated position.
This finding is consistent with studies that have reported persons with symptomatic FAI have a
lower FNSA than asymptomatic persons with a cam morphology or healthy persons with no cam
morphology (Ng et al., 2015). In addition, the finding that FNSA is a primary contributor to
internal rotation sensitivity is consistent with the work of Ng et al. (2019) who reported that
persons with a cam morphology and low FNSA incur higher acetabular stress during squatting
compared to those with a cam morphology and a higher FNSA.
Acetabular anteversion, acetabular inclination, and acetabular depth also were included as
predictors of internal rotation sensitivity, albeit to a lower degree than FNSA (Table 3-2 and 3-3).
37
A lower acetabular anteversion angle (i.e. more retroverted acetabulum) has been reported to
promote impingement during internal rotation (Lerch et al., 2020; Siebenrock et al., 2003) and is
thought to contribute to symptomatic FAI (Siebenrock et al., 2003). Although acetabular
inclination angle has not been studied in relation to FAI, a lower acetabular inclination (i.e., more
horizontal orientation) would be expected to increase lateral coverage of the femoral head
compared to higher acetabular inclination (i.e., more vertical orientation). Greater lateral coverage
of the femoral head would reduce clearance between a cam morphology and the acetabular rim,
particularly with the hip flexed to 90°. Acetabular depth primarily has been discussed in relation
to pincer morphology, measured dichotomously as coxa profunda, despite it being a poor indicator
of pincer FAI (Anderson et al., 2012; Boone et al., 2012; Diesel et al., 2015; Fujii et al., 2015;
Nepple, Lehmann, et al., 2013). Nonetheless, a deeper acetabulum would be expected to increase
coverage of the femoral head thereby reducing clearance.
Interestingly, the degree of cam morphology was not a significant predictor of acetabular
contact pressure with increasing degrees of internal rotation. This finding is consistent with
Chegini et al. (2009) who reported that an increase in the magnitude of cam morphology alone
(alpha angle increasing from 40 – 80°) did not increase peak contact pressure during a simulated
stand-to-sit task. Our results and that of Chegini et al. (2009) suggest that the magnitude of the
cam morphology should not be viewed in isolation as a cause of mechanical impingement. This
premise is best illustrated by two example participants (Figure 3-6). One had the fourth largest
cam morphology (alpha angle = 75°), yet acetabular contact pressure did not increase with hip
internal rotation motion. Conversely, another participant with the second lowest cam morphology
(alpha angle = 56°) exhibited a high degree of acetabular contact pressure sensitivity to hip internal
rotation. A more comprehensive evaluation of these two individuals revealed that the participant
38
with the large cam morphology had the second highest FNSA (138°) and a high acetabular
anteversion angle (24°). In contrast, the participant with the lower cam morphology had the joint
lowest FNSA (129°) and a low acetabular anteversion angle (14°). These examples highlight the
fact that mechanical impingement is a complex interaction of multiple morphological features.
11
Figure 3-6: Pressure maps of two participants with low and high cam morphology demonstrating
high and low acetabular contact pressure sensitivity with increasing internal rotation. Peak
pressures are located on the anterior-superior acetabulum (anterior = right).
Owing to the fact that the cam morphology is prevalent in asymptomatic individuals, some
researchers have argued that the alpha angle threshold that defines FAI should be increased
(Agricola et al., 2014; van Klij et al., 2020). Others have suggested that a more comprehensive
assessment of an individual’s bony structure (pelvis and femur) may improve characterization of
FAIS (Bouma et al., 2015). The results of the current study support the latter recommendation. A
complete understanding of an individual’s bony structure may help identify those most at risk of
developing symptomatic FAIS and future hip osteoarthritis. From a radiological perspective,
surgical decisions largely are made based on the degree of cam morphology (Peters et al., 2017),
which may help explain the high variability in surgical outcomes in this population (Bedi et al.,
39
2011; Dwyer et al., 2020; Emara et al., 2011; Griffin et al., 2018; Hunt et al., 2012; Kemp, 2020;
Mallets et al., 2019; Nwachukwu et al., 2017; Philippon et al., 2009; Thorborg et al., 2018). Future
research should work towards establishing a comprehensive morphological assessment of the
pelvis and femur to prospectively predict symptomatic FAI and guide appropriate treatment (i.e.,
operative vs. non-operative).
The results of the current study should be viewed in light of several limitations. First, the
finite element modeling approach quantified bone-to-bone interactions that did not include the
cartilage or labrum. Thus, absolute values for acetabular contact pressure are orders of magnitude
higher than acetabular contact pressures of acetabular cartilage and labrum reported in persons
with cam morphology due to the stiff contact between shell bones (Chegini et al., 2009; Jorge et
al., 2014). It could be argued that including cartilage and labrum in our models could have altered
the magnitude of acetabular contact pressure, but the overall trends in sensitivity to internal
rotation would likely remain the same. Second, we only evaluated internal rotation at 90° hip
flexion. Future studies should also consider the influence of hip adduction, either independently
or in combination with hip internal rotation. In addition, exploring other hip flexion magnitudes
would provide insight into impingement scenarios that occur while performing functional activities
(i.e., deep squatting). Third, the alpha angle used to define cam morphology was measured from
the axial oblique plane. The axial oblique plane may not capture the maximum degree of cam
morphology in persons where the cam is more superior on the femoral head-neck junction.
Previous authors have found that the location of maximum deviation differs among FAI
participants (Pfirrmann et al., 2006; Rakhra et al., 2009) but it is reported to occur most often in
the anterosuperior region (Mascarenhas et al., 2017; Pfirrmann et al., 2006; Rakhra et al., 2009).
Lastly, our sample size was relatively small for the evaluation of morphology-function
40
relationships. However, the results of the bootstrapping procedure provided evidence that the
stability of variance able to be explained by femoral and acetabular features was quite good.
Conclusions
Acetabular contact pressure sensitivity to hip internal rotation in persons with cam
morphology is multi-factorial and is influenced by hip joint structure beyond that of the degree of
cam morphology. Specifically, lower values of FNSA, acetabular anteversion, acetabular
inclination, and a deeper acetabulum explained 65% of the variance in acetabular contact pressure
sensitivity. Consideration of multiple measures of hip morphology may help identify persons with
cam morphology most at risk of developing symptomatic FAI and future hip osteoarthritis.
41
Chapter 4 – Gluteal Activation During Squatting Reduces Acetabular Contact
Pressure in Persons with Femoroacetabular Impingement Syndrome:
A Patient-Specific Finite Element Analysis
As proposed in Chapter 2, altered neuromuscular control has been implicated as being
contributory to FAIS. In particular, impaired function of the gluteal muscles owing to arthrogenic
muscle inhibition may be contributory to the cyclic nature of FAIS. Increasing gluteal muscle
recruitment to reduce abnormal hip kinematics (Pathway 5, Figure 1-1) and minimize impingement
(Pathway 1c, Figure 1-1) presents an opportunity to intervene and impede the cyclical progression
of this condition. The purpose of this chapter was to assess the influence of gluteal muscle
recruitment on acetabular contact pressure during squatting in persons with cam FAIS. With a
growing interest in non-surgical treatments for FAIS, establishing strategies that reduce acetabular
contact pressure is an important first step for informing interventions aimed at preventing
chondrolabral damage.
42
Introduction
Femoroacetabular impingement syndrome (FAIS) is a motion-related clinical disorder
characterized by abnormal hip joint morphology and subsequent symptomatic contact between the
proximal femur and acetabular rim (Griffin et al., 2016). FAIS is a common cause of hip and groin
pain in active young adults (Griffin et al., 2016; Siebenrock et al., 2011) and is a major etiological
factor in the pathogenesis of early hip osteoarthritis (Beck et al., 2005; Ganz et al., 2003, 2008;
Zebala et al., 2007). Persons with FAIS report high pain and low quality of life scores (Kemp,
2020), with the cost of treatment estimated at $23,120-$91,602 per patient depending on operative
vs. non-operative treatment approaches (Mather et al., 2018). Although surgical treatment of FAIS
is common, outcomes are mixed (Clement, MacDonald, & Gaston, 2014; Griffin et al., 2016;
Griffin et al., 2018; Kemp, 2020; Kemp et al., 2014; Mather et al., 2018; Wall et al., 2016; Zebala
et al., 2007). As such, there is a growing interest in the efficacy of non-operative treatment for
FAIS and the development of prevention strategies (Emara et al., 2011; Griffin et al., 2018; Hunt
et al., 2012; Mallets et al., 2019; Palmer et al., 2019).
Mechanical impingement associated with FAIS, occurs with simultaneous hip flexion,
internal rotation, and adduction (Banerjee & McLean, 2011; Leunig et al., 2005). High degrees of
hip flexion (≥ 90°) in combination with internal rotation is particularly problematic (Ganz et al.,
2008; Ito et al., 2001) as these motions produces the highest articular contact pressures on the
anterior-superior acetabulum (Bagwell & Powers, 2017; Chegini et al., 2009; Jorge et al., 2014).
Furthermore, the area of impingement on the anterior-superior acetabulum corresponds with the
location of intra-articular joint damage (Beck et al., 2005; Reichenbach et al., 2011; Tannast et al.,
2008). Repetitive impingement and concentrated loading on the acetabulum results in
43
chondrolabral damage and is thought to be contributory to symptomatic progression of FAIS (Beck
et al., 2005; Byrd, 2014; Cannon et al., 2020; Kuhns et al., 2015).
Previous studies have reported that persons with FAIS perform squat tasks with altered
pelvis and hip kinematics and kinetics (Bagwell, Snibbe, et al., 2016; Diamond et al., 2017; Kumar
et al., 2014; Malloy, Neumann, et al., 2019) and altered hip muscle activation (Catelli et al., 2019;
Diamond et al., 2019). Impaired hip muscle performance, particularly of the gluteal muscles, has
been identified in persons with FAIS (Malloy, Stone, et al., 2019; Seijas et al., 2016) and is
recognized as a potential contributor to mechanical impingement during tasks that require high
degrees of hip flexion (Cannon et al., 2020). Gluteus maximus and gluteus medius are of particular
interest given their potential to avoid impingement during squatting by producing the motions of
hip external rotation and abduction.
Although the importance of gluteal muscle function in persons with FAIS has been
recognized, the role of these muscles in protecting against mechanical impingement has not been
established. Using a patient-specific finite element analysis approach, the purpose of this study
was to assess the influence of gluteal muscle recruitment on acetabular contact pressure during
squatting in persons with cam FAIS. We hypothesized that increasing gluteus maximus and medius
activation via cueing would reduce hip internal rotation and adduction motion during squatting,
thereby decreasing acetabular contact pressure in the anterior-superior acetabulum. Establishing
strategies that reduce acetabular loading in persons with FAIS is an important first step for
informing interventions aimed at preventing chondrolabral damage and symptoms.
44
Methods
Participants
Eight individuals (4 males and 4 females) between 21-35 years of age were recruited for
this study (Table 4-1). Each was diagnosed with cam FAIS and scheduled for surgery. The
diagnosis of cam FAIS was determined using the following criteria: 1) alpha angle >50.5° on an
axial oblique computed tomography (CT) scan; 2) pain reproduced with hip flexion, adduction,
and internal rotation; 3) limited internal and external rotation with the hip flexed to 90°, and 4) a
positive FABER test. Exclusion criteria included pregnancy, previous surgery of the lower
extremity or back, traumatic injury, or chronic lower extremity or low back pain (not related to
FAIS). Prior to the beginning of the study, informed consent was obtained from all participants as
approved by the institutional review board of the University of Southern California’s Health
Sciences campus.
Table 4-1: Patient demographics. Alpha angle >50.5° on an axial oblique CT scan was used to
confirm a cam morphology.
Age (years) Height (m) Mass (kg) Alpha Angle (°) Sex
P01 21 1.63 63.3 69 F
P02 23 1.68 71.4 64 F
P03 27 1.76 71.7 78 M
P04 32 1.79 71.0 57 M
P05 35 1.88 89.1 81 M
P06 38 1.65 76.5 56 F
P07 27 1.89 81.2 62 M
P08 34 1.66 76.2 56 F
Mean ± SD 29.6 ± 6.0 1.74 ± 10.4 77.5 ± 6.4 65 ± 10 -
45
Procedures
Participants underwent two data collection sessions on separate days. The first session
consisted of CT imaging of the pelvis and proximal femur while the second session consisted of a
biomechanical assessment of squatting (kinematics, kinetics, and EMG). Data obtained from both
data collection sessions were used as input variables for the development of subject-specific
models (Figure 4-1). For all participants, data were obtained from the symptomatic side. In the
case of bilateral symptoms, the most painful limb was tested.
12
Figure 4-1: Overview of subject-specific modeling approach to calculate acetabular contact
pressure during squatting.
CT Imaging
Each participant underwent computed tomography (CT) scans of the pelvis and bilateral
proximal femora (Toshiba Aquilion One 320 Slice CT scanner, Toshiba American Medical
Systems, Tustin, CA). Scans were performed with the participants laying supine and at a neutral
hip alignment (0.5 mm slice thickness, zero tilt, 120 mA, 80 KVP).
46
Biomechanical Data Collection
Patients were first instrumented for surface electromyography (EMG). EMG data were
used as input for an EMG-driven hip model to estimate hip muscle and bone-on-bone contact
forces (see below for details). Rectangular disposable electrodes (Myotronics, INC., Kent, WA,
USA) consisting of two 9-mm Ag/AgCl discs with an inter-electrode distance of 20 mm were
secured to the skin over the muscle bellies of the gluteus maximus, gluteus medius,
semitendinosus, biceps femoris, adductor longus, and rectus femoris of the limb being tested.
Electrode placement was consistent with recommended guidelines (www.seniam.org). Following
placement of EMG electrodes, participants performed maximum voluntary isometric contractions
(MVIC) for each muscle for the purpose of normalization. EMG data were collected at 1500 Hz
using a wireless telemetered transmitter EMG system (Noraxon TeleMyo DTS, Noraxon USA
inc., Scottsdale, AZ, USA).
Following the MVIC testing, patients were instrumented for motion capture. Three-
dimensional kinematics of the lower extremity and trunk were collected using an 11-camera
motion capture system (Qualisys, Göteberg, Sweden), sampled at a rate of 250 Hz. Reflective
markers were adhered to the skin over the following bony landmarks of both limbs and the trunk:
distal foot, 1
st
and 5
th
metatarsal heads, medial and lateral malleoli, medial and lateral femoral
condyles, greater trochanters, iliac crests, anterior superior iliac spine, and acromion, as well as
the suprasternal notch and spinous process of C7. Rigid body plates containing a minimum of 3
reflective markers were adhered over the feet, shank, thigh, sacrum, and at the level of T12. Ground
reaction forces were recorded from two in-ground force plates (AMTI, Watertown, Mass, USA)
sampled at a rate of 1500 Hz.
47
Following a static calibration trial, two bodyweight squat conditions were evaluated in the
following order: 1) non-cued squatting; and 2) cued gluteal activation squatting. For the non-cued
squat condition, participants adopted a self-selected stance position in which the hips were slightly
abducted (wider than pelvis width) and externally rotated approximately 15° from neutral.
Participants then performed 5 repetitions of the non-cued squat to maximal depth. Squat descent
and ascent speed was controlled with the use of a metronome at 60 beats per minute, with 3 seconds
for descent and 3 seconds for ascent. The arms were flexed to 90°, parallel to the ground,
throughout the squat motion.
Following the non-cued squat trials, the cued gluteal activation squats were performed. In
the same stance position as described above, participants were instructed to grip the floor with
their feet, squeeze glutes/buttocks together, and isometrically push the feet against the floor
laterally and into external rotation (McGill, 2009). Participants were encouraged to aim for
approximately 20% of their maximum effort and maintain this level of activation throughout the
entire duration of the squat. Participants were given time to practice the cued squats prior to data
collection. Once comfortable with the cueing procedure, five squat trials were obtained using the
same movement speed and arm position described above.
Data Processing
Raw EMG data had the direct current bias removed and were digitally bandpass filtered
between 30 and 500 Hz using a second-order dual-pass Butterworth filter. EMG signals were then
full wave rectified and low-pass filtered using a second-order single-pass Butterworth filter (2.5
Hz cut-off frequency) to produce a linear envelope. EMG signals were normalized to the maximum
muscle activation elicited during the MVIC for a given muscle.
48
Marker coordinate and analog force plate data were low-pass second order Butterworth
filtered (dual-pass) to produce a final cut-off frequency of 6 Hz and 12 Hz, respectively. Visual
3D software (C-Motion, Rockville, MD, USA) was used to compute three-dimensional joint
kinematics for the ankle, knee, and hip using Cardan rotation sequences of X-Y-Z, corresponding
to sagittal-frontal-transverse planes at the joint. Force plate data were down sampled to 250 Hz for
time synchronization with kinematic and EMG data. Net joint moments (internal) were calculated
at the ankle, knee, and hip using inverse dynamics equations on the linked segment model
developed from the standing calibration trial.
EMG-Driven Hip Joint Model
An EMG-driven hip joint model was used to calculate hip joint bone-on-bone contact
forces in the superior-inferior, anterior-posterior, and medial-lateral directions acting on the
acetabulum in the pelvis coordinate system (Cambridge, 2019; Cannon et al., 2019, 2021). Hip
joint angles were input to an anatomically detailed 3D hip joint model to calculate individual
muscle parameters (i.e., length, velocity, moment arms) throughout the squat tasks. Instantaneous
muscle forces were calculated using a Hill-type muscle model taking into consideration the
normalized EMG signals, muscle length and contraction velocity, physiological cross-sectional
area, and passive force contributions (Hof & Van den Berg, 1981a, 1981b, 1981c, 1981d). In total,
96 muscle elements representing 22 muscles were included in the model. Activation profiles of
deep muscles unable to be measured from surface EMG were estimated from appropriately
matched superficial muscles. The method of pooling muscles and implying deep muscle activation
amplitude using surface muscles has been reported to provide a reasonable estimate of hip muscle
forces for biomechanical analyses (Brown & Potvin, 2007; Heller et al., 2005; McGill et al., 1996).
49
EMG-assisted optimization was utilized to match the EMG-driven estimates of hip net joint
moments in three planes to the calculated net joint moments using the inverse dynamics equations.
The objective function was to match the moments with minimal adjustment to the EMG-driven
estimates of muscle force (Cholewicki et al., 1995; Cholewicki & McGill, 1994). The quadratic
optimization routine assigned a gain to each muscle for each frame of the squat task, ensuring that
all muscles were adjusted.
Finite Element Model Development
To reconstruct 3D models of the pelvis and proximal femur bony geometry, CT images
were segmented and smoothed using 3D Slicer (Fedorov et al., 2012; https://www.slicer.org/). 3D
models were then imported to Matlab (MathWorks Inc., Natick, MA). Initially, a best fit sphere
was fit to the femoral head, with the centroid being used to identify the hip joint center (Bishop et
al., 2021). The alpha angle – used to confirm cam morphology – was calculated as the angle
between the line running from the center of the femoral head through the center of the femoral
neck and the line from the center of the femoral head to the anterior point in which the femoral
head exceeded the radius of the best fit sphere.
To limit the number of elements and model processing times, the 3D model of the pelvis
was cropped to a smaller portion of the hemipelvis of interest. Surface geometry was created for
the hemipelvis and proximal femur and meshed using 1mm triangular elements (Hypermesh, Altair
Engineering Inc., Troy, MI). The meshed hemipelvis and proximal femur were then imported into
Abaqus (SIMULIA, Dassault Systems, Providence, RI) for finite element model development and
analysis.
The hemipelvis and proximal femur were modeled as 3D deformable shell bones (1.5 mm
thickness) with homogenous, isotropic, linear elastic materials having an elastic modulus of
50
17 GPa and a Poisson’s ratio of 0.30 (Anderson et al., 2005, 2008; Assassi & Magnenat-Thalmann,
2016; Bagwell & Powers, 2017; Chegini et al., 2009; Dalstra et al., 1995). A surface-to-surface,
finite sliding, hard contact algorithm was employed between the femoral head (primary surface)
and acetabulum (secondary surface) with a friction coefficient of 0.02. (Bagwell & Powers, 2017;
Chegini et al., 2009; Harris et al., 2012; Liu et al., 2016). The hemipelvis was constrained in 6
degrees-of-freedom while the femur was constrained in 3 rotational degrees-of-freedom allowing
for translation in all directions.
For each simulated squat condition, the position of the hemipelvis was held constant and
the femur was rotated about the center of the femoral head (as defined above) to match the 3D hip
joint kinematics at peak hip flexion. Quasi-static loading simulations were run for each squat
condition using the subject specific bone-on-bone contact forces estimated from the EMG-driven
hip joint model at the instance of peak hip flexion. Forces were applied at the center of the hip
joint in the superior-inferior, anterior-posterior, and medial-lateral directions in the pelvis
coordinate system. The primary outcome variable of interest was peak acetabular contact pressure.
Statistical Analysis
Peak acetabular contact pressure was compared between the non-cued and cued gluteal
activation squat conditions using a paired t-test (one-tailed). Similarly, secondary variables of
interest were compared between squat conditions using one-tailed paired t-tests: mean EMG
activation levels of gluteus maximus and gluteus medius over the descent phase of the squat, peak
hip flexion, hip internal rotation and abduction at the time of peak hip flexion, and the resultant
bone-on-bone contact forces at the time of peak hip flexion. Correction for multiple comparisons
were applied to p-values using the Holm-Bonferroni method. Effect sizes were calculated using
51
Hedges’ g and 95% confidence intervals were computed. All statistical analyses were performed
in R

(R Core Team, 2021) with statistical significance set to p < 0.05 for all tests.
Results
On average, peak acetabular contact pressure was significantly lower in the cued gluteal
activation squats compared to the non-cued squats (4.0 ± 1.0 vs. 5.9 ± 1.9 GPa, p = 0.023; Table
4-2, Figure 4-2). Mean gluteus maximus activation during squat descent was significantly greater
in the cued gluteal activation squats compared to the non-cued squats (12.0 ± 4.0% vs. 4.8 ± 2.5%
MVIC, p < 0.0001; Table 4-2, Figure 4-3). Similarly, mean gluteus medius activation increased
significantly from 5.8 ± 4.1 % MVIC during the non-cued squat trials to 11.8 ± 6.0 % MVIC during
the cued squat trials (p = 0.009; Table 4-2, Figure 4-3).
Table 4-2: Comparison of outcome variables of interest between the non-cued and cued gluteal
activation squat conditions.
13
Non-Cued
Squat
Cued Gluteal
Activation
Squat
Hedges’ g
[95% CI] p-value
Gluteus Maximus
(% MVIC)
5 ± 2 12 ± 4
3.15
[1.52, 5.20]
< 0.0001
Gluteus Medius
(% MVIC)
6 ± 4 12 ± 6
1.39
[0.46, 2.48]
0.009
Hip Internal
Rotation (°)
9 ± 10 4 ± 8
1.0
[0.19, 1.90]
0.024
Hip Abduction (°) 26 ± 4 25 ± 7
0.15
[-0.51, 0.82]
1.0
Hip Flexion (°) 106 ± 16 104 ± 16
0.72
[-0.02, 1.52]
1.0
Resultant Hip
Contact Forces
(N/BW)
6.8 ± 4.6 9.3 ± 4.6
1.34
[0.43, 2.40]
0.009
Acetabular Contact
Pressure (GPa)
5.9 ± 1.9 4.0 ± 1.0
1.06
[0.24, 1.99]
0.023
52
Figure 4-2: Peak acetabular contact pressure (GPa) of each participant for the non-cued and cued
gluteal activation squat conditions. Peak contact pressure is located on the anterior-superior
acetabulum (anterior = right) for all participants.
Figure 4-3: Ensemble average time-series of gluteus maximus and medius muscle activation and
hip joint bone-on-bone contact forces for the two squat conditions. Shaded region = standard error.
No difference in peak hip flexion was observed between squat conditions (105.8 ± 16.1°
vs. 104.4 ± 15.8°, p = 1.0; Figure 4-4). On average, peak hip internal rotation was significantly
lower during the cued gluteal activation squats compared to the non-cued squats (3.8 ± 8.5° vs. 9.0
± 9.8°, p = 0.024; Table 4-2, Figure 4-4). Peak hip abduction during the non-cued squat trials (26.0
± 3.8°) did not differ from the cued activation squat trials (24.9 ± 7.0°) (p = 1.0; Table 4-2, Figure
4-1). The resultant bone-on-bone hip contact force at peak hip flexion was significantly greater in
the cued gluteal activation condition compared to the non-cued condition (9.3 ± 4.6 N/BW vs. 6.8
± 4.6 N/BW, p = 0.009; Table 4-2, Figure 4-3).
53
14
Figure 4-4: Ensemble average time-series hip angles for the two squat conditions. Shaded region
= standard error.
Discussion
Diminished use of the gluteal muscles during activities that require high degrees of hip
flexion has been recognized as potentially contributing to mechanical impingement in persons with
cam morphology (Cannon et al., 2020). The results of the current study demonstrate that increased
gluteal muscle activation during squatting reduces peak acetabular contact pressure in persons with
FAIS. On average, peak acetabular contact pressures were found to decrease by 32% with gluteal
cueing, lending credence to the importance of gluteal muscle function in reducing mechanical
impingement in persons with FAIS.
Reductions in acetabular contact pressure during the cued gluteal activation squat condition
was consistent with the observed reduction in hip internal rotation. Although the average
difference between squat conditions only was 5°, this change in rotation is significant from a
mechanical impingement perspective. For example, a previous modeling study by Jorge et al.,
reported that only 2.8° of internal rotation at 90° of hip flexion imposed greater acetabular cartilage
contact pressure compared to a no internal rotation condition (Jorge et al., 2014). The findings of
Jorge et al., and the current study highlight the detrimental impact of small degrees of hip internal
54
rotation in contributing to mechanical impingement and the potential benefit achieved by reducing
this motion during tasks that require high degrees of hip flexion.
Contrary to our hypothesis, hip abduction did not change during the cued squat trials
(Figure 4-4). It is possible that the initial stance position adopted by our participants (slightly
abducted) minimized the likelihood of hip adduction motion occurring. The abducted and
externally rotated stance position employed in the current study was chosen with the intent to
create initial clearance between the cam morphology and the acetabulum. It is possible performing
the squats with a neutral stance position may have resulted in changes in hip adduction and perhaps
greater differences in peak acetabular contact pressures between the cued and non-cued conditions.
Further research is necessary to evaluate the impact of gluteal activation while performing squats
with varying stance positions.
The observed reduction in hip internal rotation during cued squat trials was achieved with
only a modest increase in gluteal muscle activation. On average, gluteus maximus and medius
activation increased by 7% and 6% MVIC respectively, compared to the non-cued condition.
Given that the gluteus maximus is the primary hip external rotator, the observed change in hip
internal rotation between conditions likely was the result of the greater recruitment of this muscle
during squat descent. However, the posterior fibers of gluteus medius also act to externally rotate
the hip (Neumann, 2010) and likely contributed to the observed decrease in hip internal rotation.
The fact that the external rotator and abductor moment generating capacity of gluteus maximus
and medius decrease with increasing hip flexion (Neumann, 2010; Ward et al., 2010), highlights
the importance of maintaining gluteal muscle activation throughout entire descent phase of
squatting to minimize acetabular contact pressures.
55
Gluteus maximus recruitment during the non-cued squat trials was observed to be very low
during squat descent (<5% MVIC) and could be viewed as being insignificant from a force
development standpoint. Evidence of impaired gluteal function has been reported in persons with
FAIS, including reduced hip external rotator strength at 90° of hip flexion (Harris-Hayes et al.,
2014), decreased cross-sectional area of gluteus maximus and minimus (Malloy, Stone, et al.,
2019), and impaired contraction velocity of gluteus maximus (Seijas et al., 2016). Reductions in
gluteal muscle recruitment, force generating capacity, and muscle volume may be due to
arthrogenic muscle inhibition which has been proposed to contribute to the cyclical progression of
FAIS (Cannon et al., 2020; Freeman et al., 2013).
Reductions in peak acetabular contact pressure were observed even though resultant hip
joint bone-on-bone contact forces increased during the cued squat condition. The higher resultant
hip contact forces were the result of higher activation of all muscles with the cued condition,
indicating that while gluteal muscles were targeted, isolated recruitment did not occur. It is
possible that with practice and training, greater levels of gluteal activation could be achieved
without co-contraction thereby reducing potential negative consequences of elevated bone-on-
bone contact forces.
The results of the current study suggest that interventions aimed at promoting gluteal
muscle recruitment may be effective in minimizing impingement and acetabular contact pressures
during activities that require high degrees of hip flexion. There is evidence to suggest that gluteal
activation training has a carry over effect to functional tasks and that increases in gluteal activation
gained from training may be sufficient to reduce tissue loading to prevent (further) intra-articular
joint damage (Cannon et al., 2022). Additional work is needed to explore the efficacy of a gluteal

56

activation training program to increase gluteal muscle recruitment, improve hip kinematics, and
reduce symptoms during functional tasks in persons with FAIS.
The results of the current study should be viewed in light of several limitations. First, the
finite element models quantified bone-to-bone interactions that did not include the cartilage or
labrum. Thus, absolute values for acetabular contact pressure are orders of magnitude higher due
to the stiff contact between shell bones than would be expected with the inclusion of cartilage and
labrum. It is possible that modeling the cartilage and labrum would alter the distribution of load
and change the observed differences between squat conditions. Second, we only examined patients
with cam FAIS. Whether or not our findings would apply to those with pincer FAIS, or a
combination of cam/pincer morphology remains to be seen. Third, we only present data at peak
hip flexion during squatting. Whether or not the cueing employed in the current study would result
in changes in acetabular contact pressures at various hip angles cannot be determined from the
current study design.
Conclusions
The results of the current study demonstrate that small increases in gluteal activation during
squatting can reduce peak acetabular contact pressure in persons with FAIS. The reduction in peak
acetabular contact pressure owing to gluteal activation could be attributed to a small but significant
reduction in hip internal rotation. Our findings highlight the importance of gluteal activation in
minimizing impingement in persons with FAIS and thereby providing a foundation for
interventions aimed at preventing the development and progression of FAIS.

57
Chapter 5 – Summary and Conclusions
Mechanical impingement in persons with cam morphology increases localized loading on
the acetabulum leading to chondrolabral damage and perhaps the initiation of symptoms consistent
with FAIS (Beck et al., 2005; Kuhns et al., 2015). Impingement during dynamic tasks that involve
high degrees of hip flexion is influenced by the individual’s bony hip morphology and hip joint
kinematics (Griffin et al., 2016). Despite a substantial increase in knowledge of FAIS over the last
20 years, the pathomechanics of this condition remain uncertain and optimal treatment strategies
elusive. The first aim of this dissertation was to develop a theoretical framework of FAIS (Figure
1-1). Second, this dissertation sought to provide experimental evidence for two aspects of the
theoretical framework (structural and neuromuscular contributors to mechanical impingement)
utilizing subject-specific finite element modelling.
In Chapter 2, a synthesis of current literature on various aspects of FAIS was presented to
develop a hypothesis driven-theoretical framework of FAIS from a pathomechanical perspective
(Figure 1-1). The framework posits a pathological cycle in which concomitant changes at the joint
and neuromuscular level may act as both a cause and consequence of symptomatic impingement.
From a biomechanical perspective, the framework presents evidence that hip internal rotation with
the hip flexed is a primary contributory to impingement. However, mechanical impingement and
the contact pressures incurred are patient-specific and likely are modulated by multiple
morphological characteristics of the hip joint.
Neuromuscular control patterns directly influence hip kinematics associated with
mechanical impingement. Impaired performance of gluteus maximus and medius may limit the
ability of persons with FAIS to prevent hip internal rotation during dynamic tasks such as
58
squatting. Inhibition or disuse of the gluteal muscles leading to hip kinematics that accentuate
impingement is part of the framework that is potentially modifiable, offering an opportunity to
disrupt the cycle and impede the progression of FAIS.
The review of literature performed in support of the framework presented in Chapter 2
revealed two gaps in the existing knowledge of FAIS, thereby providing the impetus for the
experimental studies described in Chapters 3 and 4. The purpose of Chapter 3 was to determine
which bony characteristics of the hip joint are most influential in contributing to mechanical
impingement in persons with a cam morphology. Results revealed that multiple hip joint
morphological characteristics influence the magnitude of acetabular contact pressure sensitivity to
internal rotation in persons with cam morphology. Specifically, lower values of FNSA, acetabular
anteversion, acetabular inclination, and a deeper acetabulum were able to explain 65% of the
variance in sensitivity. Interestingly, the degree of cam morphology and LCEA were not
significant predictors of acetabular contact pressure with increasing degrees of internal rotation.
The finding of this chapter suggests that a more comprehensive assessment of an individual’s bony
pelvis and femur structure may improve characterization of FAIS.
The purpose of Chapter 4 was to assess the influence of gluteal muscle recruitment on
acetabular contact pressure during squatting in persons with cam FAIS. Results revealed that a
modest increase in gluteus maximus and medius activation was able to reduce hip internal rotation
on average 5°, and in doing so reduced acetabular contact pressure by 32%. Reductions in
acetabular contact pressure occurred despite no observed changes in hip abduction and an increase
in bone-on-bone contact forces during the cued gluteal activation squats. This chapter highlights
the importance of gluteal function in persons with FAIS and offers an evidence-based foundation
upon which specific training interventions can be designed.

59

Taken together, the findings of Chapters 3 and 4 highlight the complexity of the
pathomechanics underlying mechanical impingement and FAIS. Although the experiments
performed in Chapters 3 and 4 examined the structural and neuromuscular contributions to hip
impingement in isolation, these two factors simultaneously interact to influence impingement in
persons with a cam morphology. Bony hip morphology may predispose an individual to
impingement, but neuromuscular control can provide a means of preventing or promoting hip
kinematics that create impingement.
Examination of data from individuals who participated in both experimental studies
presented in Chapters 3 and 4 highlight the interaction of morphology and neuromuscular control
on influencing impingement. Participant ‘P07’ demonstrated high sensitivity to hip internal
rotation (Figure 3-3) owing to low femoral neck-shaft and acetabular anteversion angles. However,
increased gluteal activation in this participant was able to reduce hip internal rotation by 6° and
decrease peak acetabular contact pressure by almost 50% (Figure 4-2; 6.4 vs. 3.3 GPa). In contrast,
participant ‘P01’ (Figure 3-3) exhibited low sensitivity to hip internal rotation due to relatively
high acetabular anteversion and inclination angles as well as a shallow acetabulum. In this
participant, increasing gluteal muscle activation only reduced hip internal rotation by 2°.
Interestingly, peak acetabular contact pressure (3.3 GPa) did not differ between squat conditions
and was of low magnitude compared to other participants (Figure 4-2). Thus, gluteal activation
cueing to reduce hip internal rotation was not effective, but likely unnecessary in this participant.
It could be argued that gluteal activation may be more impactful for persons with at risk
morphology and offer an effective means to prevent and/or manage symptomatic development.

60

Clinical Implications
The theoretical framework proposed in Chapter 2 provides a pathomechanical perspective
clinicians may utilize during diagnosis and treatment of persons with FAIS. The framework details
a potential progression of FAIS and provides mechanistic evidence detailing cause-effect
relationships between changes at the joint and neuromuscular level. Surgical and non-surgical
treatment plans should consider each facet of this framework in determining how and where to
best intervene.
A comprehensive assessment of an individual’s hip joint morphology may improve early
detection of persons who are most likely to develop symptomatic femoroacetabular impingement
(i.e., FAIS) and those who may benefit most from operative versus non-operative treatments. As
noted in Chapter 2, there is a high prevalence of asymptomatic persons with a cam morphology. It
is possible that certain individuals do not have other structural features that predispose them to
impingement and elevate the likelihood of chondrolabral damage and progression of symptoms.
Alternatively, asymptomatic persons with a cam morphology may avoid kinematics that promote
impingement by means of sufficient gluteal muscle activation and other modifications to
movement, or they do not participate in activities that regularly incur impingement. Therefore, the
belief that a cam morphology always should be surgically resected should be viewed with caution.
It is possible that gluteal training interventions that can minimize impingement and
concurrent chondrolabral loading may improve prevention efforts and rehabilitation following
surgery. Gluteal activation training may increase recruitment of gluteal muscles during functional
tasks allowing for more advanced stages of training to resolve strength deficits and address
neuromuscular control and movement patterns. Previous studies have reported that hip kinematics
during functional tasks remain unchanged following surgical resection of the cam morphology and

61

chondroplasty or debridement of the cartilage and labrum (Lamontagne et al., 2011; Rylander et
al., 2013). Despite the removal of cam morphology, continually loading the soft tissues in a
structurally compromised region of the joint may increase the likelihood of early hip osteoarthritis.
Thus, interventions aimed at improving gluteal activation may be useful in the prevention of
osteoarthritis of persons with cam morphology, or for persons who have had a cam morphology
surgically resected.
The development of cam morphology is not well understood. It is generally accepted that
intense athletic activity involving high loading of the proximal femur in adolescence, when the
epiphyseal growth plate is open, contributes to the development of a cam morphology (Anwander
et al., 2018; Kuhns et al., 2015; Pettit et al., 2021; Roels et al., 2014). However, the specific
postures and loading scenarios that stimulate sufficient osteogenic activity at the femoral head-
neck junction is not known. It has been suggested that the kinematics creating impingement,
namely high degrees of hip flexion in combination with internal rotation and adduction, also are
responsible for cam morphology development (Roels et al., 2014). In this scenario, repetitive bony
abutment during high impact loading may stimulate bone formation of the areas in contact. It is
possible that appropriate gluteal muscle function to avoid impingement may also be important in
the prevention of cam morphology itself. Longitudinal studies would be needed to test this
hypothesis.
Directions for Future Research
The findings of this dissertation provide the impetus for future research in several areas of
FAIS. The findings of Chapter 3 suggest that multiple bony characteristics, beyond the cam
morphology, contribute to mechanical impingement. It is possible that certain acetabular and
femoral features place an individual at higher risk of symptomatic development. However, future

62

research is needed to better understand why some people with cam morphology develop symptoms
while others do not. As discussed above, uncertainty exists surrounding the development of cam
morphology, with only general understanding that intense physical activity in adolescence
increases the prevalence of cam morphology. Future research investigating the mechanical
stimulus to create a cam morphology is necessary to identify if specific postures and loading
scenarios are the mechanism of cam development and how activity may be modified in an attempt
to avoid cam development.
Chapter 4 presents evidence that gluteal muscle activation was able to minimize
mechanical impingement. Future clinical trials are needed to establish how gluteal training
influences symptomatic progression, pain, and function in persons with FAIS. In addition, the
combined findings of Chapter 3 and 4 suggest that certain patients may be more amenable to
specific interventions (i.e., conservative vs surgical). For example, gluteal activation may be less
effective in patients with certain morphological profiles and may benefit from a cam resection.
Alternatively, certain patients may benefit from a non-surgical approach including neuromuscular
training. Tailoring clinical interventions based on a better characterization of bony morphology
and muscular deficits may lead to improved outcomes in this population.
Further research also should be directed to improve our capabilities to model deep hip
flexion postures with cam morphology while including the cartilage and labrum. Jorge and
colleagues (2014) noted in their study (n = 1, subject-specific model) that at 90
o
of hip flexion the
finite element analysis stopped at 2.8
o
internal rotation due to a lack of convergence. This was
likely the result of the cam morphology penetrating the acetabular cartilage and/or labrum. Other
finite element studies that model the cartilage and/or labrum during deep flexion tasks often choose
the instance of 90
o
hip flexion to analyze (when the hip is likely abducted and externally rotated

63

during the squat) (Ng et al., 2019), or do not report the hip angles utilized (Chegini et al., 2009;
Hellwig et al., 2015; Ng et al., 2012). Therefore, how finite element models perform at maximum
degrees of hip flexion during squatting remains unknown.
Chapter 3 assessed hip internal rotation angles up to 15
o
which may be near the maximum
motion possible in persons with cam morphology when flexed to 90° (Diamond et al., 2015; Freke
et al., 2016). Although this degree of internal rotation occurs in-vivo, simulating this degree of
motion using FEA may be troublesome if the cartilage and labrum were included due to
convergence issues. The use of idealized geometries in some studies may limit convergence issues
in the finite element analysis but do not reflect subject-specific anatomy. To improve our
understanding of impingement in persons with FAIS, it is necessary to accurately model the
osseous formation (i.e., the cam morphology) that characterize the syndrome and bony structures
that influence impingement.
Refining finite element models to be more patient-specific is a necessary evolution for
future research in FAIS. The utilization of subject-specific geometry, movement kinematics, and
EMG-driven hip models in this dissertation are more patient-specific than many previous studies,
allowing for unique insight to be gained on morphological and neuromuscular contributors to
impingement. Further specificity such as individual geometry and material properties (of bone,
cartilage, labrum) and the inclusion of individual three-dimensional muscles in finite element
analyses (opposed to resultant forces) have been explored by some groups and will likely continue.
However, the increased cost (time, computation, and resources) versus the degree to which these
properties influence results will determine the usefulness of pursuing such specificity.

64

Conclusions
FAIS is a complex, multi-faceted syndrome. Over the last 20 years there has been an
increased understanding of various aspects related to the diagnosis, characteristics, and treatment
of this pathology. However, we find ourselves at a crossroads in terms of how this condition should
be diagnosed and managed moving forward. The results of this dissertation suggest that a more
comprehensive morphological assessment of an individual’s hip is necessary. Studies exploring
the efficacy of physical therapy-led prevention and treatment as well as optimal rehabilitation
protocols following surgery are necessary to optimize treatment of FAIS and avoid an increasing
number of hip arthroscopy procedures that may be deemed excessive and unnecessary in the future
(Kemp, Crossley, et al., 2014). The finding that increased gluteal muscle activation can reduce
acetabular contact pressure provides evidence for a potential strategy to minimize impingement
that will inform future training intervention studies. To advance our understanding and treatment
of FAIS, collaborative efforts across sub-disciplines of FAIS will be required to perform
mechanistic studies investigating optimal detection, prevention, and treatment of FAIS.

65

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Appendix A

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Figure A.1: Ensemble average time-series hip angles for the non-cued and cued gluteal activation squat conditions of every
participant (shaded area = standard deviation).

84

Figure A.2: Ensemble average time-series hip moments for the non-cued and cued gluteal activation squat conditions of every
participant (shaded area = standard deviation).

Abstract (if available)

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University of Southern California Dissertations and Theses

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Asset Metadata

Creator Cannon, Jordan (author)

Core Title Pathomechanics of femoroacetabular impingement syndrome: utilizing subject-specific modeling approaches to investigate the influence of hip joint morphology and neuromuscular control

School School of Dentistry

Degree Doctor of Philosophy

Degree Program Biokinesiology

Degree Conferral Date 2022-05

Publication Date 04/19/2022

Defense Date 03/03/2022

Publisher University of Southern California (original), University of Southern California. Libraries (digital)

Tag cam morphology,femoroacetabular impingement syndrome,finite element analysis,gluteus maximus,gluteus medius,hip,hip joint morphology,musculoskeletal model,OAI-PMH Harvest,patient-specific,squat,subject-specific

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Language English

Contributor Electronically uploaded by the author (provenance)

Advisor Powers, Christopher (committee chair), Kulig, Kornelia (committee member), Lewton, Kristi (committee member), McNitt-Gray, Jill (committee member), Rankin, Jeffery (committee member)

Creator Email cannonjo@usc.edu,cannonjord@gmail.com

Permanent Link (DOI) https://doi.org/10.25549/usctheses-oUC111022421

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