A Thesis Entitled a Parametric Study of Physiological Changes To
A Thesis
entitled
A Parametric Study of Physiological Changes to Develop a Finite Element Model of Disc
Degeneration
by
Leonora A. Felon
Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Master of Science Degree in Bioengineering
Dr. Vijay Goel, Committee Chair
Dr. Scott Molitor, Committee Member
Dr. Mohamed Samir Hefzy, Committee Member
Dr. Patricia R. Komuniecki,
Dean College of Graduate Studies
The University of Toledo
December 2010 ii An Abstract of A Parametric Study of Physiological Changes to Develop a Finite Element Model of Disc
Degeneration
by Leonora A. Felon Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Master of Science Degree in Bioengineering
The University of Toledo December 2010
Finite Element spine models have been created to simulate disc degeneration in the
past; however they have not taken into account physiology and how other levels are
affected by a change at another level. Here in lies the problem with those models.
Several models were created to explore how physiological changes change an
experimental validated L3/S1 spine model. Physiological conditions taken into
account included Poisson’s ratio of nucleus, tearing of the annulus and
physiologically relevant compressive loads on the spine. Much was learned through
this process and a final set of three models were created and biomechanically
evaluated. The model with the greatest degeneration was also “graded” based on
clinical grading schemes and studies. The model was capable of simulating motion
similar to cadaver studies done by others. It showed increased pressure in the disc and
loading on the facets as the model was farther degenerated. Finally, based on the
clinical grading schemes and studies, the large degenerated disc model was
determined to be a grade IV degeneration of the L4/5 disc.
iii
For my ever supporting parents, Darrell & Karen, and all my family and friends who encouraged me along. For all the moms in my life who kept on me to finish, thank you.
iv
Acknowledgements
This thesis would not have been possible without the help and support of my advisor, Dr. Goel, and all my lab mates. I thank them for their help and entertainment over the years.
I’d like to thank my family for all the love and support for my education over the years, especially my parents, who have showed me what love and devotion look like. I’d like to thank my brothers of Theta Tau and sisters of the UT softball team. You definitely made my college experience better and more educational than just book learning and I thank you for that. I love that I can count some of my best friends as my brothers and sisters. Also thank you to all my friend moms who kept nagging at me to finish; Kate,
Christine, Mother Ana, Mrs. Tkacz and all my church ladies. Finally, thank you to God who has given me more talents than I deserve and for guiding me on how to use them to his glory.
v Contents
Abstract iii
Acknowledgments v
Contents vi
List of Tables x
List of Figures xvi
1 Introduction 1
1.1 Chapter Overview 1
1.2 Back Pain 1
1.3 Treatment Options 2
1.4 Degenerated Disc Basics 4
1.5 Scope of Study 5
1.6 Overview of Chapters 6
2 Literature Review 7
2.1 Chapter Overview 7
2.2 Aging Spine 7
2.3 Spinal Disorders 8
2.3.1 Vertebral body degeneration 8
vi 2.3.2 Disc Degeneration 9
2.3.3 Osteophytes 12
2.3.4 Facet Joint Degeneration & Osteoarthritis 12
2.3.5 Spinal Stenosis 13
2.3.6 Other degenerative conditions 14
2.4 Diagnosis 14
2.5 Treatment Options 15
2.5.1 Conservative 15
2.5.2 Decompression 16
2.5.3 Fusion Surgery 19
2.5.4 Non-Fusion Options: Spinal Arthosis & Dynamic 22
Stabilization
2.6 Spinal Arthosis 23
2.6.1 Total disc replacement 23
2.6.2 Facet replacement technologies 26
2.7 Dynamic stabilization 26
3 Methods & Materials 29
3.1 Chapter Overview 29
3.2 Initial model: nuclear changes alone 29
3.3 Examination of Physiological elements 31
vii 3.3.1 Constant Load with Nuclear Changes, Variable Tear Types 31
& Amount
3.3.2 Constant Tear Amount with Nuclear, Tear Type and 32
Load Changes
3.3.3 More Tears and their locations & patterns 33
3.3.4 Worst case scenarios 37
3.4 Degenerated Models: small, medium & large 39
4 Results 42
4.1 Chapter Overview 42
4.2 Initial model: nuclear changes alone 42
4.3 Examination of Physiological elements 46
4.3.1 Constant Load with Nuclear Changes, Variable Tear Types 46
& Amount
4.3.2 Constant Tear Amount with Nuclear, Tear Type and 55
Load Changes
4.3.3 More Tears and their locations & patterns 57
4.3.4 Worst case scenarios 59
4.4 Degenerated Models: small, medium & large 60
5 Conclusions & Discussion 79
5.1 Chapter Overview 79
5.2 Initial model: nuclear changes alone 79
viii 5.3 Examination of Physiological elements 80
5.3.1 Constant Load with Nuclear Changes, Variable Tear Types 80
& Amount
5.3.2 Constant Tear Amount with Nuclear, Tear Type and 82
Load Changes
5.3.3 More Tears and their locations & patterns 82
5.3.4 Worst case scenarios 83
5.4 Degenerated Models: small, medium & large 84
References 86
A Spine Anatomy 97
A.1 Vertebras 97
A.2 Intervertebral Disc 103
A.3 Ligamental Tissue 104
A.4 Muscular Tissue 110
B Lumbar Biomechanics 118
ix
List of Tables
3.1 Material properties of model elements 31
3.2 Various daily activities and the loads seen at L4/5 disc (19) 33
3.3 Combinations of Circumferential & Radial Tears at various amounts 34 of total tearing
3.4 Combinations of Circumferential & Radial Tears at various amounts 34 of total tearing
4.1 Angular motion (deg) in various loading modes for 400 N preload 43 and 10.6 Nm of bending moment across L4-5 segment.
4.2 Maximum Von Mises Stress (N/mm2) in the Nucleus during various 44 loading modes for 400 N preload and 10.6 Nm of bending moment across
L4-5 segment
4.3 Maximum Von Mises Stress (N/mm2) in the Annulus during various 44 loading modes for 400 N preload and 10.6 Nm of bending moment across
L4-5 segment
4.4 Facet Loads (N) in various loading modes for 400 N preload and 10.6 45
Nm of bending moment across L4-5 segment
4.5 Contact area in various loading modes for 400 N preload and 10.6 46
Nm of bending moment across L4-5 segment
x
4.6 Foramen Space (mm) changes across L4-5 during various loading 46 modes for 400 N preload and 10.6 Nm of bending moment; Neutral is before the moment is applied with only the preload.
4.7 Disc height percentage change caused by varying percentage of 47 circumferential tears and various nuclear material property (possion’s ratio) changes
4.8 Disc height percentage change caused by varying percentage of both 48 tear types & various nuclear material property (possion’s ratio) changes.
4.9 Disc height percentage change caused by varying percentage of radial 49 tears and various nuclear material property (possion’s ratio) changes.
4.10 Disc height percentage change caused by each tear scenario and 50 amount of tears for only a possion’s ratio of 0.1.
4.11 Trend line equations relating percentage of disc height loss (x) to 52 amount of tears (y) for each possion’s ratio. Value within parenthesis is the R2 value of the equation.
4.12 Values of tears needed to reach 50% disc height loss for each trend 53 line, if it exists based on trend lines from Table 4.11.
4.13 Trend line equations relating possion’s ratio’s (x) to percentage of 55 disc height loss (y) for various amounts of tears. Value within parenthesis is the R2 value of the equation.
4.14 Values of possion’s ratio needed to reach 50% disc height loss based 55 on trend lines from Table 4.13.
xi
4.15 Percentages of disc height loss across various load conditions for 56 each set of tears at a constant amount and two nucleus pulposus possion’s ratio changes (0.1 & 0.25).
4.16 Trend line equations relating load and disc height loss for each set of 57 tear groupings at a constant amount and two nucleus pulposus possion’s ratio with R2 values of trend lines in parenthesis. Calculated load to 50% disc height loss for each trend line case.
4.17 Trend line equations (forced through origin) relating load and disc 57 height loss for each set of tear groupings at a constant amount and two nucleus pulposus possion’s ratio with R2 values of trend lines in parenthesis. Calculated load to 50% disc height loss for each trend line case. Final column shows difference between tables 4.16 & 4.17
4.18 Disc height loss results from the 12.5% torn row of tables 3.3 and 58
3.4 for each cluster/pattern type.
4.19 Disc height loss data in the turquoise set (last column of table 3-3) 59 of tear combinations at increasing percentage of tears within the annulus for each cluster/pattern.
4.20 Disc height loss data for the worst case scenarios. 60
4.21 Numerical values for the relative angular motion across L4/5 for 61 large degenerated disc model in various modalities of motion.
4.22 Numerical values for the relative angular motion across L3/4 for 62 large degenerated disc model in various modalities of motion.
xii
4.23 Numerical values for the relative angular motion across L4/5 for 62 medium degenerated disc model in various modalities of motion.
4.24 Numerical values for the relative angular motion across L3/4 for 62 medium degenerated disc model in various modalities of motion.
4.25 Numerical values for the relative angular motion across L4/5 for 63 small degenerated disc model in various modalities of motion.
4.26 Numerical values for the relative angular motion across L3/4 for 63 small degenerated disc model in various modalities of motion.
4.27 Numerical values for the maximum Von Mises Stress through out 67 the L4/5 annulus for small degenerated disc model in various modalities of motion.
4.28 Numerical values for the maximum Von Mises Stress through out 67 the L4/5 nucleus for small degenerated disc model in various modalities of motion.
4.29 Numerical values for the maximum Von Mises Stress through out 68 the L4/5 annulus for medium degenerated disc model in various modalities of motion.
4.30 Numerical values for the maximum Von Mises Stress through out 68 the L4/5 nucleus for medium degenerated disc model in various modalities of motion.
4.31 Numerical values for the maximum Von Mises Stress through out 68 the L4/5 annulus for large degenerated disc model in various modalities of motion.
xiii
4.32 Numerical values for the maximum Von Mises Stress through out 69 the L4/5 nucleus for large degenerated disc model in various modalities of motion.
4.33 Numerical values for the load on each facet across the L5/S1 72 functional unit for the all degenerated disc models in various modalities of motion.
4.34 Numerical values for the load on each facet across the L3/4 73 functional unit for the all degenerated disc models in various modalities of motion.
4.35 Numerical values for the load on each facet across the L4/5 74 functional unit for the all degenerated disc models in various modalities of motion.
4.36 Numerical values for contact area of each facet across the L3/4 75 functional unit for the all degenerated disc models in various modalities of motion.
4.37 Numerical values for contact area of each facet across the L5/S1 76 functional unit for the all degenerated disc models in various modalities of motion.
4.38 Numerical values for contact area of each facet across the L4/5 77 functional unit for the all degenerated disc models in various modalities of motion.
4.39 Numerical values for the foramen space across the L4/5 functional 78 unit for the all degenerated disc models in various modalities of motion.
xiv
A.1 Typical Cervical Vertebrae (C3-C7); C1 & C2 not included because 98 of their atypical shape; from source Grant’s Atlas of Anatomy (2)
A.2 Typical Thoracic Vertebrae (T1-T12); from source Grant’s Atlas of 99
Anatomy (2)
A.3 Typical Lumbar Vertebrae (L1-L5); from source Grant’s Atlas of 100
Anatomy (2)
A.4 Composition of intervertebral disc; from Basic Orthopaedic 104
Biomechanics & Mechano-Biology (4)
B.1 Limits and Representative Values of Ranges of Rotation of the 121 Lumbar Spine; reproduced from Clinical Anatomy of the Lumbar Spine (10).
xv
List of Figures
3-1 Cross-section of intact L3-S1 model; nucleus is colored yellow; 31 annulus is colored sky blue and all bone is colored bright green.
3-2 a) Checker board pattern: numbers represent elements, white blocks 35 remain untouched; b) visual depiction of removed elements in model for checker board pattern.
3-3 a) Outside to inside arrowhead pattern: numbers represent elements, 36 white blocks remain untouched; b) visual depiction of removed elements in model for arrowhead pattern.
3-4 a) Inside to outside arrowhead pattern: numbers represent elements, 36 white blocks remain untouched; b) visual depiction of removed elements in model for arrowhead pattern.
3-5 a) Bottom to top stripe pattern: numbers represent elements, white 37 blocks remain untouched; b) visual depiction of removed elements in model for stripe pattern.
3-6 a) Top to bottom stripe pattern: numbers represent elements, white 37 blocks remain untouched; b) visual depiction of removed elements in model for stripe pattern.
xvi
3-7 a) “X” pattern: numbers represent elements, white blocks remain 38 untouched; b) visual depiction of removed elements in model for “X” pattern.
3-8 Worst case scenario pattern #1 39
3-9 Worst case scenario pattern #2 39
3-10 Worst case scenario pattern #3 39
4-1 Sagittal section of ligamentous L3-S1 finite element model 43
4-2 Differences in L4/5 facet orientation (red[left]=Inf L4 & blue[right]= 43
Sup L5).
4-3 Comparison of the differences in the stress in both the annulus and 45 the nucleus
4-4 Bar graph comparing various amounts of circumferential tears and 47 various nuclear material property (possion’s ratio) changes.
4-5 Bar graph comparing various amounts of both tear types and various 48 nuclear material property (possion’s ratio) changes.
4-6 Bar graph comparing various amounts of radial tears and various 49 nuclear material property (possion’s ratio) changes.
4-7 Bar graph comparing the percentage of disc height loss for a 50 possion’s ratio of 0.1 for each tear scenario and amount of tears.
4-8 Trend lines of the varying amounts of circumferential tears effect on 51 the percentage of disc height loss at various possion’s ratio.
4-9 Trend lines of the varying amounts of radial tears effect on the 51 percentage of disc height loss at various possion’s ratio.
xvii
4-10 Trend lines of the varying amounts of a combination of both tear 52 types effect on the percentage of disc height loss at various possion’s ratio
4-11 Trend lines of varying possion’s ratio’s effect on percentage of disc 53 height loss at various tear amounts for circumferential tears.
4-12 Trend lines of varying possion’s ratio’s effect on percentage of disc 54 height loss at various tear amounts for radial tears.
4-13 Trend lines of varying possion’s ratio’s effect on percentage of disc 54 height loss at various tear amounts for both tear types
4-14 Graph with trend lines showing percentages of disc height loss 56 across various load conditions for each set of tear groupings at a constant amount and two nucleus pulposus possion’s ratio changes (0.1 & 0.25).
4-15 Graphical representation of disc height loss data at 12.5% torn. 58
4-16 Graphical representation of disc height loss data within the 59 turquoise set (last column of table 3-3) of tear combinations.
4-17 Side by side comparison of final degenerated disc models before 60 testing.
4-18 Graphical representation of relative angular motion across L4/5 for 61 large degenerated disc model in various modalities of motion.
4-19 Graphical representation of relative angular motion across L4/5 for 62 medium degenerated disc model in various modalities of motion.
4-20 Graphical representation of relative angular motion across L4/5 for 63 small degenerated disc model in various modalities of motion.
xviii
4-21 Graphical representation of relative angular motion across L4/5 for 64 all degenerated disc models in various modalities of motion.
4-22 Graphical representation of relative angular motion across L3/4 for 64 all degenerated disc models in various modalities of motion.
4-23 Graphical representation of the maximum Von Mises Stress through 65 out the L4/5 annulus for all degenerated disc models in various modalities of motion.
4-24 Graphical representation of the maximum Von Mises Stress through 66 out the L4/5 nucleus for all degenerated disc models in various modalities of motion.
4-25 Graphical representation of the maximum Von Mises Stress through 66 out L4/5 disc for the small degenerated disc model in various modalities of motion.
4-26 Graphical representation of the maximum Von Mises Stress through 67 out L4/5 disc for the medium degenerated disc model in various modalities of motion.
4-27 Graphical representation of the maximum Von Mises Stress through 68 out L4/5 disc for the large degenerated disc model in various modalities of motion.
4-28 Graphical representation of the load on each facet across the L5/S1 72 functional unit for the all degenerated disc models in various modalities of motion.
xix
4-29 Graphical representation of the load on each facet across the L3/4 73 functional unit for the all degenerated disc models in various modalities of motion.
4-30 Graphical representation of the load on each facet across the L4/5 74 functional unit for the all degenerated disc models in various modalities of motion.
4-31 Graphical representation of the contact area of each facet across the 75
L3/4 functional unit for the all degenerated disc models in various modalities of motion.
4-32 Graphical representation of the contact area of each facet across the 76
L5/S1 functional unit for the all degenerated disc models in various modalities of motion.
4-33 Graphical representation of the contact area of each facet across the 77
L4/5 functional unit for the all degenerated disc models in various modalities of motion
4-34 Graphical representation of the foramen space across the L4/5 78 functional unit for the all degenerated disc models in various modalities of motion.
A-1 Side View of the curvature of the Vertebral Column; from Anatomy 98
& Physiology for Dummies (1)
A-2 Cervical Vertebrae (2) 101
A-3 Thoracic Vertebrae (2) 101
A-4 Lumbar Vertebrae (2) 102
xx
A-5 Sacrum and Coccyx (2) 102
A-6 Intervertebral Disc Cross-Section (3) 103
A-7 A median sagittal section of the lumbar spine to show its various 105 ligaments. From Clinical Anatomy of the Lumbar Spine (5)
A-8 The posterior longitudinal ligament. From Clinical Anatomy of the 106
Lumbar Spine (5)
A-9 The ligamentum flavum at the L2-3 level, From Clinical Anatomy of 107 the Lumbar Spine (5)
A-10 The ventral and dorsal leaves of the intertransverse ligament. From 108
Clinical Anatomy of the Lumbar Spine (5)
A-11 The transforaminal ligaments. From Clinical Anatomy of the 109
Lumbar Spine (5)
A-12 The mamillo-accessory ligaments (MAL). From Clinical Anatomy 110 of the Lumbar Spine (5)
A-13 Psoas major (PM) and quadratus lumborum (QL). From Clinical 111
Anatomy of the Lumbar Spine (5)
A-14 The short, intersegmental muscles. From Clinical Anatomy of the 112
Lumbar Spine (5)
A-15 The common fascicles of multifidus. From Clinical Anatomy of the 114
Lumbar Spine (5)
A-16 The lumbar fibres of longissimus (longissimus thoracis pars 116 lumborum). From Clinical Anatomy of the Lumbar Spine (5)
xxi
A-17 The thoracic fibres of longissimus (longissimus thoracis pars 117 thoracis). From Clinical Anatomy of the Lumbar Spine (5)
A-18 The thoracic fibres of iliocostalis lumborum (iliocostalis lumborum 117 pars thoracis). From Clinical Anatomy of the Lumbar Spine (5)
xxii
Chapter I:
Introduction
1.1 Chapter Overview
The wide spread cost of low back pain is discussed as well as the treatment options for low back pain ranging from conservative to cutting edge. A major cause of low back pain, disc degeneration, is explored to see how it can be modeled in vitro.
Finally the scope of this study is described.
1.2 Back Pain
Within the US, back pain is a considerable problem, especially low pain back
(LBP). Over a life time 80-90% of all adults suffer from LBP. LBP is the leading cause of disability for persons under 45 years old. Similarly it’s the second leading cause of doctor visits and third leading reason for hospital admissions. Over all in the US alone the cost of back pain ranges from $20 to 75 billion and soars to over $100 billion worldwide. (1) Back pain is not a diagnosis -- it’s a symptom of an underlying condition.
Common back pain causes include nerve problems, disc problems, osteoarthritis, muscular problems, (2) arthritis, poor posture, obesity, psychological stress and disease or injury of internal organs (3)
1
1.3 Treatment Options
In the initial stages of LBP, the majority of the physicians advise conservative therapies like heat therapy, traction, exercise, osteopathic manipulation, and/or mobilization of the spine. In actue LBP, rest is necessary in conjuction with the various conservative therapies. If LBP starts to limit the daily activities of a patient for a prolonged period of time, the patient will become an ideal candidate for surgery.
Various surgical techniques have emerged over the years to treat spinal disorders.
However, no definite treatment modality exists for any disorder and treatment choices are highly specific to the surgeon involved. Continuous advancements are being made to understand the spine and its function in order to arrive at an optimal solution for the treatment of various spinal disorders. The present day aim is to find procedures, which are minimally invasive, tissue sparing, and better physiological restorating.
The generation of low back pain has been traditionally attributed to the abnormal motion at the degenerative joint. Eliminating the motion with joint arthrodesis (fusion) was deemed an effective treatment option. Fusion has had a success in providing temporary pain relief, but restoring the natural disc function with a fusion procedure has been impossible due to the destruction of the anatomy and loss of mobility at the segments involved. Measuring the success of a fusion procedure with the amount of fusion achieved might not be clinically relevant since the outcomes of fusion by itself have been good but do not correlate well with the clinical success. The drawbacks of fusion surgery include pain at the bone harvesting site, adjacent level degeneration, and variability in the success of fusion surgeries (4). In the long term, follow up of fusion,
2 adjacent level degeneration has been the major concern. Many clinical and biomechanical studies have shown that fusion at one segment affects the adjacent segments. It is not clear, if the adjacent segment degeneration is due to the iatrogenic production of a rigid motion segment or if it is the progression of the natural history of the underlying degenerative disease (5, 6, 7, 8).
Various non fusion technologies have emerged in recent times to replace the conventional fusion techniques. They aim at providing a more physiological solution to the problem. The various non fusion techniques include spinal arthroplasty (artificial discs), facet replacement devices, nucleus replacements, annulus repair, and dynamic stabilization systems.
The intervertebral disc and facet joints are the main load bearing structures in the spine and hence are most susceptible to mechanical wear and tear. Back pain arising from the degenerative disease could be discogenic or may be directly due to diseased facet joints. Advanced stage of disc degeneration or facet degeneration might call for a replacement surgery. Disc arthroplasty and facet joint replacement technologies aim at restoring the normal kinematics of the spine by acting as load bearing devices (9). The surgery for these devices is highly invasive. Replacing either the disc or the facet joint would be considered a partial joint replacement. Being load bearing structures there is also a possibility of wear of the device finally leading to osteolysis. There is also a lack of literature on the kinematic effect of these replacement technologies on remaining structures of the motion segments (9).
Nucleus replacement restores the disc height and maintains the normal biomechanical behavior and the range of motion. The indications for use of a nucleus
3 replacement device are loss of disc height and voluminous disc herniation for patients who have a relatively healthy disc. The advantage of using these devices is the ease of surgery when compared to fusion or total disc replacement.
Annulus repair is a mechanical solution to reinforce the annulus. Current technology uses autograft tissue or polymers to create a sealing mechanism. This technology can be used along with the nucleus replacement surgery to avoid recurrent herniation. There have been very little biomechanical studies on the nucleus replacement and annular repair technologies, and the possible complications of using these devices especially with nucleus replacement might be device migration or/and instability.
1.4 Degenerated Disc Basics
Low Back Pain can be caused or increased by several factors such as instability, degeneration, psychosocial, injury, age, biological and mechanical overloading (10,11).
Disc Degeneration (DD) can be a result of these and is related to LBP, however the root cause is unknown (12). It is known that many of these have cyclical causes and effects; such as DD can cause biological changes which can cause overloading and instability which can cause farther DD (13). As DD is a major cause of LBP that necessitates surgery, DD is listed as an “indication for use” of the majority of FDA spine implant product codes (14). These codes describe implants used throughout the entire spinal column as DD is a problem across all levels.
Disc Degeneration is a board term that describes the loss of the disc’s ability to maintain its height and function. There are several physiological changes to and damage to the disc that attributed to and indentified as signs of DD.
4
Within the Annulus Fibrous, several types of tears and/or lesions can be found and categorized. Circumferential (or concentric) tears are typical interlaminar delamination and are found prominently in the anterior periphery of the disc (12,15).
Radial tears are irregular radial fissures extending from the nucleus outwards through the annulus (12). These extensive defects are found most frequently in the posterior or postero-lateral aspects of the disc (12,15). Finally, Peripheral tears (or rim lesions) are a separation of the outer anterior annulus from the adjacent vertebral endplate and orient at right angles to the direction of the annulus fibers (12,15). Within the lumbar spine, concentric tears are most pronounced with L2/L3 having the highest frequency; however at the L4/L5 level concentric and radial tears occur with equal frequency (12).
In the Nucleus Pulposus, both proteoglycan and water content of the intervertebral disc decrease with disc degeneration (16). This loss of water volume results in decreased disc pressure and reduced disc height (17) which can lead to instability due to lax ligaments and changes in mechanical properties causing the degenerated disc to act more as a solid than a healthy fluid-like disc (17).
1.5 Scope of Study
In order to model disc degeneration, both biological and biomechanical elements need to be incorporated or else the model will be limited (18). The purpose of this study is twofold; 1) study the physiologically observed parameters of disc degeneration and their simulated material properties in order to create a degenerated model of 50% disc height loss, 2) once that model is created, the biomechanics of the degenerated model are to be compared to that of the intact. It is hypothesized that
5 multiple variables will need to be altered in order to create this significant disc height lost characteristic of disc degeneration. All of these alterations should be done under a physiologically relevant load seen in everyday activities to reach that 50% disc height loss.
An experimentally validated, three dimensional, ligamentous finite element model of the L3-S1 spine was used as a base model. Variables in this model were altered based on physiological changes of disc degeneration to decrease the overall disc height.
The variables examined and evaluated include loading conditions, disc material properties and disc integrity. The disc height was the deciding factor of evaluation of the variable conditions. Once acceptable disc height was met, the biomechanics of the final models were evaluated under standard loading conditions and compared to an intact model. In total three models were created and evaluated to simulate various stages of degeneration.
1.6 Overview of Chapters
Methods will describe the steps taken to develop a physiologically based disc degenerated model. Results will lay out the data collected from each step along the way.
Conclusions will state what was learned from each step and what lead to the final models. Appendix A gives background information on spine anatomy. Appendix B lays out lumbar spine biomechanics.
6
Chapter II:
Literature Review
2.1 Chapter Overview
This chapter reviews the various literature revolving around the understanding and study of the spine, its disorders and biomechanics and finally treatment options.
Topics include: spinal disorders, diagnosis and treatment options.
2.2 Aging Spine
As the spine ages, it is unavoidable that degenerative changes will occur to the bony structures and soft tissue of the spine. Degeneration often starts with biochemical alterations, then micro-structural, and gross structural changes of the spine, however the initial trigger is still uncertain. Between the third and fifth decades of life, major degenerative changes occur such as degeneration of the intervertebral discs and facet joints. There are several diseases brought about by aging including, but not limited to, osteoporosis, degenerative disc disease, facet degeneration, facet osteoarthritis, and spinal stenosis [20].
7
2.3 Spinal Disorders
The human spine is composed of highly specific tissues and structures, which together provide an extensive range of motion and considerable load carrying capacity [21].
Alteration of the form of these structures due to increasing age, injury, trauma or any other reason can have a profound influence on the quality of the life. Low back pain is generally associated with degenerative changes occurring in the spine. Mechanical property changes resulting from degeneration are likely contributors to lumbar spine instability that may lead to other pathologies. This instability may further be accelerated by injuries or deformities [10]. Vertebral body degeneration and ligament degeneration are degenerative diseases, which can occur with age [22]. Due to the spine’s three-joint complex (intervertebral disc and bilateral facet joints) which share the majority of the load transferred through the spine, degenerative changes of the spine can be initiated as disc degeneration or facet joint osteoarthritis [9,23].
2.3.1 Vertebral body degeneration
The vertebral body is made up of cancellous bone surrounded by a dense and solid cortical shell. The cancellous bone has individual trabeculae, which are oriented around the paths of principal forces and play a crucial role in the transfer of the compressive forces along the spine [23]. Osteoporosis and several morphological changes such as trabecular thinning, increased intratrabecular spacing and loss of connectivity between trabeculae are the various age related degenerative changes associated with the vertebral bodies. In osteoporosis, the bone becomes porous and there is a loss in the bone mineral density. As a result, bones become brittle, and hence are prone to fractures. Most often a
8 disease inflicted upon women, men can also lose up to 30% of bone density and women up to 50%, starting around age 40 [21]. Osteoporosis of the vertebrae may lead to vertebral compression fractures, collapse of the vertebrae, and a decrease in the vertebral height. As the loss in bone density reduces so does the ability of the vertebral body to withstand compression loads causing vertebral fractures to become prevalent. Persons with a decreased bone density of 0.05 g/cm3 have a 99% chance of vertebral fractures
[21].These fractures usually lead to severe back pain, nerve pain, or dysfunction, loss of height, or spinal deformities such as Kyphosis (severely stooped posture).
The vertebral endplates can be affected as well. Their main purpose is to evenly distribute the loads from the intervertebral disc to the underlying cancellous bone. With age, thinning of the endplates may occur, thus leading to vertebral fracture. On the other hand, extreme ossification of the endplates may hamper the nutritive supply to the intervertebral disc [21].
2.3.2 Disc Degeneration
The intervertebral discs play a very important role in mobility and load transfer through the spinal column. Any load through the spinal column is transmitted to the intervertebral disc from the vertebral body. The normal intervertebral disc is an isotropic structure. The jelly like nucleus pulposus acts like a fluid filled bag and swells under pressure. This pressure transmits as a circumferential tension to the annulus converting it to a load bearing structure. This whole setting acts as a shock absorber for the spine such that there is no high spot loading at any point and allows for complex motion to occur.
9
With degeneration, however the biomechanical properties of the disc are altered. Once degeneration sets in, the intervertebral disc goes through a cascade of degenerative changes resulting in the biomechanical alteration of the load transfer through the disc causing changes in the mechanical properties and composition of the tissue. A structural disorganization is seen due to which the hydrostatic mechanism might fail.
Even though, the exact pathogenesis of the degenerative process is still unknown [24], several factors that might cause degeneration are: aging, mechanical factors due to occupational exposure [25,26], abnormal loading conditions [24], and the loss of nutrition to the disc. Ala kokko, 2001, has found that disc degeneration might also be predetermined genetically [24].
There are different ways a degenerated disc can lead to low back pain, depending on if the degeneration occurs in the nucleus pulposus or the annulus. A degenerated annulus can have fissures, microscopic fragmentation of individual fibers. Annular tears at the corners of the vertebral body separating the annulus from the endplates (due to age, wear and tear), concentric cracks cavities, and radiating ruptures are seen [27,28]. Disc bulging may occur due to decrease in the radial tensile strength of the annulus. The degeneration of the nucleus occurs due to loss of water content, collagenation of the nucleus. Nucleus degeneration combined with the annular degeneration may cause disc herniation into the spinal canal causing low back pain due to nerve pinching. Thinning of the disc and a loss of disc also can occur in a degenerated disc. This loss of disc height combined with gradual ossification of the endplate and protrusion of the disc tissue causes stenosis, which again leads to back pain.
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Biomechanically the degeneration in the disc causes the depressurization of the nucleus, and an increase in the load transmitted through the annulus. Loading the annulus, unprotected by the supporting pressure of the nucleus, may cause an increase in the interlaminar shear stresses of the annulus [9, 8. Due to this, the principal areas of load transmission across the disc depend on the posture: in flexion, the anterior annulus, in extension, the posterior annulus. This abnormally high transmission of load through the different areas of annulus with change in posture may cause posture and activity related mechanical back pain [9]. This altered stress distribution in the disc may also lead to overloading of the spinal ligaments, muscles, and facet joints, possibly damaging these structures [12].
At a macromolecular and biological level, it has been seen that the activity of the cells can be regulated by growth factors, cytokines (proteins), and physical factors like mechanical stress. It has been suggested that under normal conditions, applied stress affects cellular activity and the disc remodels to build a matrix, which minimizes the stress [29]. In response to prolonged heavy mechanical stress, cells of the intervertebral disc may degenerate. Degeneration occurs after cellular activity producing extracellular matrix decreases or stops [20]. After the cellular changes begin, gross anatomic changes appear. The disc also thins as one ages due to a loss of water content [21, 31] causing a decrease in disc height. The material properties of the disc nucleus pulposus shift from
“fluid like” to “solid like” [21]. It can be deduced than that a degenerated disc can be repaired by reversing the mechanically damaging load environment. It has been found that degenerative changes in one disc affect adjacent levels adversely. In Kim et al it was shown with an FE model that intradiscal pressures increased in the disc immediately
11 above the degenerated level suggesting further degeneration will occur along the spinal column [31]. Loss of disc height, irregular end plates, sclerosis of the disc, and osteophyte formation, as well as facet joint osteoarthritis is often the result of disc degeneration [30].
2.3.3 Osteophytes
The presences of osteophytes may not cause pain, but the formation of osteophytes is an indicator for the development of osteoarthritis. Osteophytes show no gender bias and seem to increase in frequency with heavy physical activity levels [32]. Osteophytes can not only occur on the vertebral body, but also in the facet joints [33, 34].
2.3.4 Facet Joint Degeneration & Osteoarthritis
Posterior element degeneration is generally seen at the facet joints. The facet joints are clinically important since they are found to be a direct source of pain [23]. Facet blocks with anesthetic and cortisone, and even facet denervation procedures, have been recommended as treatment for patients with low back pain.
Facet joints are adversely affected by degenerative changes. Facet joints with osteoarthritis exhibit changes in swelling, stiffness, deformity, instability, a decreased range of motion, and a change in load-bearing [33]. These changes to the joints may cause significant changes to segmental motion throughout the spinal column [33] and changes in stress distribution and load sharing [32]. Biomechanically, the facet joints are important stabilizing structures, and carry about 18% of the total compressive load borne by a lumbar spine segment [23]. Facets also are mainly responsible for preventing large
12 extension rotation and shear [35]. Higher facet loads and stresses are seen in extension rotation and shear, which might lead to facet osteoarthritis or hypertrophy leading to spinal stenosis Degeneration of facet joints due mechanical factors like increased facet loading and wear, is called “the facet syndrome.”
Osteophytes have also been found during early stages of facet joint osteoarthritis and tend to decrease spinal motion [33, 34]. The loading path increases through adjacent discs due to facet joint destruction, which may accelerate disc degeneration [36]. Facet joint degeneration changes are almost always associated with disc degeneration [32, 34, 36,
37].
2.3.5 Spinal Stenosis
Spinal stenosis is the narrowing of the lumbar spinal canal that leads to compression of neural roots [38, 39]. Spinal stenosis often occurs during the fifth and seventh decades of life. There are several mechanisms which cause spinal stenosis. Degenerated discs collapse the intervertebral foramen thereby compressing the exiting nerve. Both inferior and superior facet hypertrophy cause central and lateral stenosis, which is the narrow of the lumbar spinal canal and intervertebral foramen, respectively [38]. Significant pain begins in the low back, radiating down the buttocks and is worsened by walking, exercising, or standing for persons suffering from spinal stenosis. Pain relief is often felt by sitting, leaning forward, or squatting [38, 39]. Non-operative treatments seem to offer no abatement of the symptoms [38, 40] and some type of surgical intervention usually prevails.
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2.3.6 Other degenerative conditions
Initial degenerative changes in the lumbar spine most commonly occur within the intervertebral disc. Disc degeneration and facet joint osteoarthritis are usually related, but usually disc degeneration precedes facet joint osteoarthritis [28, 37, 41]. Spondylosis, spondylolisthesis, and disc herniation may follow these degenerative changes in the segment. Spinal stenosis is defined as a pathological narrowing of the spinal canal or foramen and may occur simultaneously in multiple locations. This may occur with aging due to the thickening of ligaments (ligamentum flavum), disc degeneration, posterior osteophyte projection into the spinal canal and facet hypertrophy. The other diseases of the lumbar spine can be congenital (e.g., spinal bifida), tumors or can be caused due to a traumatic injury.
2.4 Diagnosis
It is of importance to diagnose the origin of low back pain to prescribe the most suitable treatment applicable. Imaging the spine has been a standard technique for diagnosis of various spinal disorders. Before the advent of the recent imaging techniques, plain radiographs or invasive techniques like discography were used to determine the patients eligible for surgery. Plain radiographs (usually the initial imaging because they are inexpensive) when taken in flexion/extension and oblique direction show the disc space height and changes in the endplates.
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Magnetic resonance Imaging and CT being non-invasive are now the popular tools to evaluate the disc degeneration disease. Magnetic resonance imaging is a better option since it does not involve radiation effects. In an MRI image the anatomical features like disc height, tears in the annulus and fissures in the nucleus, level of hydration in the nucleus can be represented. Vjevtic, 2001 described the MR depiction of different discovertebral lesions [42]. N. Tanaka et al., 2001 have shown correlation between the extent of intervertebral disc degeneration and MRI images [16].
Instability can be interpreted as abnormal motion under normal physiological load. [9]
The exact relationship between mobility of the segment and disc degeneration, facet arthrosis has not been clearly established yet [33]. However Tanaka et al, 2001 have found from MRI studies that disc degeneration in early stages causes instability and in the later stages, the mobility decreases [16]. In spite of abnormal translation being seen radiologically in the cases of disc degeneration with spondylolisthesis, it is not always present in symptomatic disc degeneration. It is therefore very difficult to find any basis for the concept of abnormal movement or instability as a cause of back pain.
2.5 Treatment Options
2.5.1 Conservative
Conservative treatment of the low back pain involves using non-invasive techniques to restore the patient to a normal daily routine. While many surgical options are available and will be discussed, those alternatives should only be exercised in a worst case
15 condition. Non-invasive practices involve exercises, muscle manipulation, toning and physical therapy as well as medications may alleviate pain. In many cases of acute back pain, prescription of rest generally reduces the magnitude of the pain and decreases the recovery time. Several spinal braces are available for different disorders that may successfully treat some patients. Epidural steroid injections are an additional treatment, but are not found effective for distinct pathologies such as spinal stenosis or disc herniation [23]. When non-invasive procedures fail to relieve pain, surgical intervention occurs.
2.5.2 Decompression
Often decompression surgery is performed to relieve pain due to nerve compression from disc degeneration, spinal stenosis, facet hypertrophy, or other disease situations [23].
There are several different categories of decompression surgeries including laminectomy and facetectomy surgery will be discussed. During a laminectomy surgery, the lamina, spinous process, and all associated ligaments are can be removed to decompress the nerve root, however the facet joint is left intact. Different degrees of a laminectomy are performed depending on the patient’s condition. It can range from only a small section of the lamina being removed to a wide laminectomy, in which all the spinous process and ligaments are removed along with the entire lamina, while retaining the facets [43]. A facetectomy removes only the facet joint [43]. A laminectomy and facetectomy can be performed together to remove the entire group of posterior elements.
Several biomechanical investigations have been performed on spine stability after decompression surgery with conflicting results. Several investigators have found an
16 increased risk of slippage after surgery [44, 45]; however, Mariconda et al did not detect any slippage after a clinical trial [46]. Johnsson et al subjectively assessed patients following decompression surgery and grouped them based on postoperative results of good (no symptoms or slight residual pain, but clearly improved walking capacity) and poor (unchanged or increased pain after surgery) [44]. Slippage was found in both groups and 20% of all patients; mean slippage was 4.4 ± 3.3mm in the good group and 5.75 ±
3.6mm in the poor group. A general trend of decreased disc height was found in all groups dwell [44]. In Lee’s study, all patients with preoperative slippage had further postoperative slippage and 3.7% of all decompression patients developed postoperative slippage [45].
Postoperative movements in forward bending and axial rotation are discouraged after a decompression surgery due to a decrease in spinal stability [47]. In a finite element spine study by Zander et al, it was determined a facetectomy increases motion in rotation and annular disc stresses. After a wide laminectomy, motion increased in flexion, but little change was noted in bending and extension was noted [47]. In vitro biomechanical studies have found range of motion increases significantly in flexion and axial rotation due to facetectomies [48, 49]. Abumi et al determined the range of motion for different degrees of facetectomies and reported motion increases in rotation with increasing degrees of facetectomy with a complete bilateral facetectomy resulting in the greatest range of motion [49]. With any degree of bone removal for a facetectomy, flexion resulted in increased range of motion [48]. Pintar et al studied the motion of functional spinal units under compression and flexion. When a facetectomy was performed,
17 instability increased as the compression load increased. When the posterior ligaments were removed, further instability was noted [49].
In finite element studies of decompression surgeries showed that stresses increase greatly in the annulus and small loads increase displacement by large degrees with a facetectomy greater than 50% [50, 51]. Lee et al compared different laminectomy and facetectomy condition motions and found angular motion increases in axial rotation however removal of facets and posterior elements has the least effect in lateral bending [50]. When they examined a bilateral laminectomy and bilateral facetectomy model; motion increased considerably in flexion and extension. Motion increased greatly in rotation when only the facet joint was removed indicating the importance of the facets in limiting axial rotation.
Degenerated disc model resulted in less angular rotation than a normal disc. Annular stresses increase significantly in all motions except lateral bending [50]. Teo et al also found an increase in flexibility of a lumbar motion segment when different degrees of facetectomies were performed in a finite element model [51]. Flexibility increased significantly by 30% as compared to intact when a complete bilateral facetectomy was performed and an anterior shear load was applied. Facet loads also decreased as the amount of facet removed was increased [51].
Such increases in instability of the lumbar spine after decompression surgeries such as laminectomies and facetectomies often indicate the need for further intervention.
Following wide laminectomies or complete facetectomies, many authors suggest the need for fusion to reduce the resultant instability [43, 48, 50, 51].
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2.5.3 Fusion Surgery
Fusion surgery is the current gold standard of surgical treatment of most kinds of acquired or iatrogenic lumbar spine instabilities. The term “fusion” refers to fusing one or more of the vertebrae of the spine so that motion no longer occurs between them.
Instability was thought to be the main cause of the pain in the low back. Therefore fusion was indicated to be an appropriate solution.
The first fusion surgery was performed with bone arthrodesis in 1911 by Albee and Hibbs
[52]. Albee used tibial grafts between spinal processes to stabilize the spine. Hibb’s
"feathered" the lamina and decorticated the facet joints and then added morsalized bone derived from the local dorsal spinous processes. Hibb's technique represented the very first documented example of flexible stabilization utilizing autologous local bone for reconstructive purposes. Burns in 1933 (Anterior Lumber Interbody) and Briggs and
Milligan, Cloward and Jaslow (Posterior Lumbar Interbody Arthrodesis) added the interbody approach. In the 1930s metallic implants were first introduced [53]. Over the years, various fusion techniques have been adopted by surgeons, which include posterior lumbar interbody fusion (PLIF), transforaminal posterior lumbar interbody fusion (TLIF), anterior lumbar interbody fusion (ALIF), posterior lateral fusion (PLAT). PLIF and TLIF are known to be the more rigid constructs and more popular for active age groups than the ALIF. In addition, majority of the surgeons are more comfortable with the posterior or lateral approaches than the anterior approaches [54]. ALIF requires an incision on the front of the body and a second surgeon to gain access to the spine. Because of this the
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ALIF surgery is generally a longer more complex surgery with more surgery related risks.
Fusion has been a successful technique in decreasing intervertebral motion and for increasing the spinal stiffness in various spinal disorders including degenerative stenosis, instability due to decompression, and iatrogenic lumbar spondylolisthesis [55, 56, 57, 58,
59]. With the recent fusion techniques, successful fusion rates have approached 100%, but this has failed to translate into an increase in the successful clinical outcome [60]. The clinical outcomes after fusion appear to be quite inconsistent: a systematic review of mainly retrospective case series reported that satisfactory clinical outcomes ranged from just 16% to as high as 95%, with an average of around 68% [61]. In addition, a significant apprehension of adjacent segment disease in the long-term follow-up has always been a concern for the surgeons [9].
Chen et al, 2001 conducted a finite element study in order to evaluate the stress distribution of the adjacent disc to fusion in flexion, extension, lateral bending, and torsion. They found that the von Mises stress increase was larger in the upper adjacent segment to fusion than the lower adjacent segment [62]. However, Rohlmann A et al.,
2001 conducted a similar finite element study and found only a minor change in the adjacent segment stresses [8]. Chow et al, 1996, measured segmental mobility and intradiscal pressure in six cadaveric lumbar spine specimens before and after, single level
L4-5 and double level L4-5-S1 anterior interbody fusions. They found that there was an increase in the motion at the adjacent levels. Unforuntately no evidence of increasing loads at the adjacent segments was found [63].
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Cunningham BW et al., 1997, in an in vitro biomechanical testing in human lumbar spines analyzed the effects of spinal destabilization and instrumentation on lumbar intradiscal pressure [64]. They measured the intradiscal pressures using pressure needle transducers in three testing conditions; axial compression (0-600N), flexion, and extension. In response to destabilization and instrumentation, adjacent disc pressures increased as much as 45%, and operative pressure levels decreased by about 41-55%.
A review of literature on lumbar fusion reported the abnormal processes observed radiologically at the adjacent segment after spinal fusion to be: (i) disc degeneration, (ii) spondylolisthesis (iii) scoliosis, (iv) osteophyte formation, (v) stenosis, (vi) vertebral compression fracture, (vii) herniated nucleus pulposus, (viii) instability, (ix) hypertrophic facet arthritis [6].
Okuda S et al., 2004 conducted a study using radiology and found that there was no correlation between the degeneration of the adjacent segment and clinical results [65].
The study concluded that the development of adjacent segment degeneration maybe a part of the normal aging and degenerative process and not a direct consequence of altered stresses that arises due to lumbar fusion. It is still unclear whether the radiographic and clinical findings of adjacent segment instability and degeneration are a direct outcome of iatrogenic production of a rigid motion segment with spinal fusion, or whether this is a representation of the progression of the natural history of the underlying degenerative disease [6, 7, 8, 58]. From a biomechanical point of view, rigid spinal fusion is inherently a non-physiologic procedure. Fusion represents a less-than-optimal solution to the management of spine disorders for many patients, particularly those afflicted with multi-
21 level degenerative and genomic disorders. Many patients with rigid fusion develop incapacitating "transitional" degenerative changes at adjacent spinal segments and often need additional spine surgery. It is now well accepted that degeneration of the spine is often, but not invariably associated with pain. It has been noted that back pain is primarily related to position or posture, rather than movement of the lumbar spine. It has therefore been hypothesized that it is the abnormal pattern of loading that is associated with degeneration, rather than the abnormal movement itself [9]. Given that the precise position that provokes an abnormal loading pattern for any given patient is rarely known may explain why the results of fusing the spine in one position appear to be somewhat
“random” as regards clinical success [53, 66]. Surgeons are looking for alternative procedures to avoid or at least delay fusion especially, for young patients whose indications are considered promising for such alternative procedures [9].
2.5.4 Non-Fusion Options: Spinal Arthosis & Dynamic Stabilization
As the age group of the patients shifts to the younger population, fusion is an over- treatment for many patients in most cases yet the most effective currently available [4].
Therefore non fusion technologies are evolving to provide a more physiological solution to the problem at hand. The ideas of non-fusion systems range from replacing the disc with complete excision of the disc, replacing the disc while maintaining the annulus, or maintaining the disc with a controlled motion of the segment. Joint replacement systems
(total disc replacement, facet joint replacement) and dynamic stabilization systems are the current focus. These will be discussed in greater detail in separate sections of this chapter.
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2.6 Spinal Arthosis
2.6.1 Total disc replacement
The preservation of spinal motion while relieving pain is the wish for every patient and while fusion eliminates and stabilizes motion at the diseased level, it often causes future pain. In order to accomplish this artificial discs are being developed to restore natural motion to a diseased level. Spinal arthrosis has gained interest over the recent years due to the obvious disadvantages in the fusion surgeries, which include adjacent level degeneration and restriction of mobility of the patient. The main goal of spinal arthrosis is to restore normal mobility to the degenerated spinal segment and restore the disc height. Few discs are currently on market, but preliminary results appear promising. In some short term studies, pain was relieved and the implants were found relatively safe
[30].
A total disc replacement surgery involves surgical removal of the pain causing disc and replacement with a mechanical device, which would mimic the normal spine kinematics.
Indications for a total disc replacement are, advanced stage of disc disease, multiple level discectomy, or as a secondary procedure after a failed fusion surgery [4]. The contraindications include posterior facet joint disease (i.e. facet joint osteoarthritis, deformed facets and severe facet hypertrophy), prior spinal fusion, osteoporosis, spinal stenosis, and spondylolisthesis [46]. Little is understood about the role of facet joints with artificial discs. It has been found that artificial discs increase the range of motion [45, 48].
Such increases in motion most likely place increased stress and strain on the facet joint
23 possibly resulting in painful joints if the facet joints are degenerated or otherwise diseased [48].
The various artificial discs that have evolved for the lumbar spine are Charite, Prodisc II, and Maverick. McAfee et al. published a report of 60 prospective randomized cases in the US for a one level discogenic pain with a one third of the cases undergoing fusion surgeries and the other two-thirds Charite disc replacements. They looked for functional outcome measurements and found that the results were comparable to fusion surgeries
[67]. Another group concentrated on the complications after implantation up to 127 months after implantation of Charite artificial disc and reported the complications involved degeneration of other lumbar discs, facet joint arthrosis at the same or other levels, and subsidence of the prosthesis [68]. Cunningham et al., 2003, conducted an in vitro biomechanical study using eight cadaveric lumbar spine specimens to quantify the multidirectional intervertebral kinematics following total disc replacement arthroplasty
(Charite disc) compared to conventional stabilization techniques (fusion). They used, range of motion (ROM) and centers of intervertebral rotation as the parameters to quantify the kinematics of the spinal segment. When compared to the intact at the instrumented level, Charite increases the ROM by 44% in axial rotation, 3% in flexion and extension, and 16% in lateral bending. The fusion case reduced the motion by 80% in axial rotation, 93% in flexion and extension, and 83% in axial rotation. No significant changes were found at the adjacent levels [69]. Based on flexion-extension radiographs, the intervertebral centers of rotation were calculated and it was found that disc replacement with Charite preserves the normal mapping of segmental motion [69].
Dmitriev AE et al., 2005, conducted an in vitro investigation of cervical adjacent level
24 intradiscal pressures (IDP’s) following a total disc replacement arthroplasty. They concluded that artificial disc replacement does not affect the adjacent segment IDP’s
[70]. The early randomized clinical trials for comparison of fusion with disc replacement showed that disc replacement patients reported significantly less pain and disability [71].
The exact surgical implantation of the device is of primary concern because it might cause abnormal load distribution through the segment [72]. The subsidence of the artificial disc is also an issue [72]. The long term effect of wear debris in these designs is also a concern if implanted in a younger age group of patients. Hallab et al., 2003, did a study that highlighted the association between spinal implants particulate wear debris and increased potential for osteolysis. Ooij et al completed a clinical trial in which anterior migration of the disc, degeneration at other levels, subsidence of the prosthesis, facet joint arthrosis, and polyethylene wear occurred in several patients [68]. Development of facet joint hypertrophy may be increased resulting in spinal stenosis with the use of an artificial disc [73]. Guyer et al states that pain from the facet joint will not be addressed by an artificial disc, thus any facet joint disease should be considered a contraindication of artificial discs [73]. Dooris et al completed a finite element study on artificial discs and determined placing the disc more posteriorly increased the range of motion in flexion up to 44% more than intact depending on the amount of annulus retained during surgery
[74]. In extension, the motion increased up to 40% more than intact when little annulus was retained. Facet loads predicted by the FE model increased 150% over the intact loads when the disc was placed more anteriorly, clearly showing the importance of proper disc placement and the imperativeness of facet joints [74].
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2.6.2 Facet replacement technologies
A facet joint replacement or arthroplasty is done to replace the degenerative facets with an articulating prosthesis that would imitate the motion of the natural facet joint with the intent of preserving natural motion. In order to restore normal function at a diseased site, artificial facets may be an alternative to fusion or other surgeries for treatment of severe facet tropism, facet hypertrophy, arthritic or degenerated facet joints, spinal stenosis, after laminectomy and facetectomy surgeries, and in addition to artificial discs. Facet replacements must restore normal motion in all modes of flexion, extension, lateral bending, and axial rotation. They must perform well under shear and torsional loads and be able to bear 20 to 30% of the physiological load [75]. The prosthesis also should be easy to place in all patients and fix to the bone well to reduce the risk of loosening.
As the number of total disc replacement surgeries increase, the interest in facet joint replacement technology has in turn increased as well. Preliminary designs for the facet joint replacement are still in development. Since this concept is in the early stages, studies have to be taken up to understand the biomechanical issues involved in the design of facet joints. It has been estimated in the year 2010 to exceed $90 million with the average price per implant to be $7000 [20].
2.7 Dynamic stabilization
Spinal fusion surgeries aim at limiting the motion of the segment and restoring the stability. Spinal arthroplasty (artificial disc and facets) devices restore motion by sharing
26 the kinematics of the remaining joints of the spinal motion segment. Dynamic stabilization systems aim at altering favorably the movement and load transmission through the spinal motion segment [9]. There are several advantages of using dynamic stabilization systems over fusion and arthroplasty techniques such as: (i) Tissue sparing: most leave the disc and most ligaments in tack, plus no secondary incision for graft material; (ii) Can be used adjunctly with other non fusion technologies: Dynamic stabilization/motion preservation technologies can be utilized with total disc replacements and disc nucleus replacements; (iii) Ability to be performed posteriorly:
Familiarity of surgeons with the posterior approach is advantageous for accuracy purposes; (iv) Load sharing: This is an advantage over the total disc replacement and prosthetic disc replacement, which cannot be used for patients with significant posterior pathology.
The current indications for the use of dynamic stabilization systems are for younger patients with multisegment disc degeneration, stabilization of decompression surgeries, and adjacent to fusion to avoid adjacent level degeneration [4]. However, they cannot be used as a standalone implantation in cases where the disc is completely degenerated.
The hypothesis behind dynamic stabilization system is that control of abnormal motion and more physiologic load transmission would relieve pain and prevent adjacent segment degeneration. If the degeneration is not too bad, it is believed that once normal motion and load sharing transmission is restored, the damaged disc may start to repair itself more effectively. This belief is now being supported by the fact and conclusions from research.
Many clinical studies suggest that cells of the intervertebral disc respond favorably to
27 reduced but not eliminated mechanical loading through deposition of extracellular matrix proteins into the disc space [29, 76, 77]. In initial clinical trials with one such dynamic system (Wallis, Spine next, Inc) it was seen that the degenerated disc became re-hydrated over time [4].
The biomechanical goals of a dynamic stabilization system are to permit motion and to share load with the disc and the facets. The load sharing should be more or less uniform during the entire range of motion. Therefore the kinematics of the dynamic stabilization system should be similar to the healthy intact spine. In order for this to be achieved, the instantaneous axis of rotation of the dynamic device should optimally be located near the instantaneous axis of rotation of the intact segment [9]. Implant fatigue failure is seen in rigid systems due to psuedoarthrosis, since the rigidity of the implant does not permit any motion. Flexible stabilization may accommodate this movement and may avoid a fatigue failure. A closer look however needs to be taken at the kinematics of the dynamic stabilization before the fatigue life may be determined [9]. Research is still needed to answer the current main biomechanical questions of dynamic stabilization devices including long term implant failure implications.
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Chapter III:
Methods & materials
3.1 Chapter Overview
The development process of physiologically based computer modeling of intervertebral disc degeneration is discussed and laid out. The process is shown be a sort of trial and error learning process to reach the goals of the project.
3.2 Initial model: nuclear changes alone
An intact experimentally validated L3-S1 Finite Element model was used as a base of the Degenerated Disc model. The intact model in cross section and its material properties can be seen in Figure 3-1 and Table 3.1 respectively. It was decided that the
L4-5 disc was to be the focus of the degeneration. As this is the lowest lumbar disc, it sees the most external forces as well as being defined with disc loading conditions from literature. The goal of this first attempt was to examine the loads needed to decrease the intact disc height by 50%. The Poisson’s ratio was the only material property altered in this step. The Poisson’s ratio of the L4-5 disc was changed from the normal 0.4999
(incompressible) to 0.1 which would relate to the loss of water content within the disc. In order to isolate the L4-5 disc and not to induce artificial changes to adjacent levels, the
29 bottom of L5 was fixed and load was applied to the top of L4. A compressive force was spread over the entire top of the vertebra. A 400N load was initially applied in this manner. The load was increased in a trial and error manner until the desired disc height decrease was reached. The disc heights were calculated by subtracting the Z coordinate of the nodes along the mid-line at the top and bottom of the L4-5 disc and compared to the original height to gain a percent loss. The displacements (x, y, z) for all the nodes were then calculated within ABAQUS and outputted to a text file. These displacements were added to the original nodes coordinates to find the new coordinates of the altered (or degenerated) model. Nodes along the plane of reflection needed to be altered farther to insure the nodes reflected properly. All the X coordinates of nodes along this plane were changed to zero. The poisson’s ratio of the nucleus pulposus was changed back to 0.25 to still simulate a loss of water content but not an extreme loss. Once the first generation degenerated disc model was created from the new node location, a biomechanical study was performed. The bottom of S1 was fixed and loads were applied to L3.A 400N compressive preload was applied first to simulate load from body weight, then 10.6Nm moments were applied to create extension, flexion, left bending and right rotation. Right bending and left rotation are unneeded since the model is fully symmetrical.
Displacements were found and used to find angular displacements for each level and over whole spine model. Stresses within the annulus and nucleus were found within ABAQUS and outputted as Von Misses stress diagrams. Facet loads and contact area were calculated as well using contact elements between the facet faces. Foreman space was calculated as well using node displacements within the foreman. The first generation degenerated model was compared to the intact model to find any differences.
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Table 3.1: Material properties of model elements Part Young’s Modulus Poisson’s (MPa) Ratio Cortical Bone 12000 0.3 Cancellous Bone 100 0.2 Posterior Bone 3500 0.25 Annulus (ground) 4.2 0.45 Annulus (fiber) 175 X Nucleus Pulposus 1 0.499 Anterior Ligament 7.8 (<12%), 20.0 0.3 Figure 3-1: Cross-section of intact (>12%) L3-S1 model; nucleus is colored Posterior Ligament 10.0 (<11%), 0.3 yellow; annulus is colored sky blue 20.0(>11%) and all bone is colored bright green. Ligamentum 15.0 (<6.2%), 0.3 Flavum 19.5% (>6.2%) Transverse 10.0 (<18%), 58.7 0.3 Ligament (>18%) Capsular Ligament 7.5 (<25%), 32.9 0.3 (>25%)
Interspinous 10.0 (<14%), 11.6 0.3
Ligament (>14%)
Supraspinous 8.0 (<20%), 15.0 0.3 Ligament (>20%)
3.3 Examination of Physiological elements
Given that some of the major physiological changes to the disc due to degeneration are a loss of water content in the nucleus and annulus lesions such as circumferential and radial tears, these elements must be examined step wise and independently to see how each contributes to the height loss seen in degenerated discs.
Once this is analyzed, this knowledge can help determine how much tear damage must occur for the disc to lose up to half the disc height under physiological relevant compressive loads.
3.3.1 Constant Load with Nuclear Changes, Variable Tear Types & Amount
The first step was to evaluate tear type, percentage of tears, nuclear Poisson’s ratio gradient (0.499-0.1) under a constant load of 1000N which corresponds to the load
31 the disc would see as a person rises from a chair without arm rests (19). As discussed in the introduction, the L4/5 level has an equal frequency of occurrence of circumferential and radial tears, plus the tears are each found in exclusive areas allowing for area distinctions for each tear. In order to incorporate this into the model, circumferential tears, radial tears and a 50/50 combination (known as the “Both” set) of the two tear types were created in increasing numbers within the annulus based on their physiologically observed locations. The tear sets were made in 2.5, 5, and 7.5% of the total disc elements for circumferential and radial tear. The Both set included a 10% tears model as well to evaluate that set farther. Tears were created by removing elements within the model of the disc in the given directions for each type. Each set of tears was run with each percentage under each load condition and nuclear change for a board variable systematic scientific evaluation with only one variable changed at a time to find the best combination of variables. The L4-5 disc was isolated in the same manner as the first generation setup. Disc heights were calculated the same as the first generation model setup. Graphs were created for all cases by setting height loss as the independent variable.
Trend lines were calculated with the best fit to relate the variables. The trend lines were used to find the best combination of variables that would lead to a disc height reduction of half the original value.
3.3.2 Constant Tear Amount with Nuclear, Tear Type and Load Changes
The next step was to evaluate a couple nuclear Poisson’s ratio changes and type tears under various loading conditions while keeping the tear amount constant. Loads of
700N, 900N, 1000N, 1200N, 1400N, 1850N, 2100N and 3400N were applied to models
32 whose L4-5 nuclear Poisson’s ratio was altered to 0.25 & 0.1. These loads correspond to loads seen in the disc during various everyday activities (Table 3.2). All three sets of tear types were evaluated under each load and Poisson’s ratio change. The L4-5 disc was isolated in the same manner as the first generation setup. Disc heights were calculated the same as the first generation model setup. Graphs were created for cases by setting height loss as the independent variable and load or ratio as dependent in sets of ratio or load respectively. Trend lines were calculated with the best fit to relate load and height loss under the various conditions.
Table 3:2: Various daily activities and the loads seen at L4/5 disc (19)
Activity Load (N) Standing 700
Twisting 900 Bending forward 20º 1200 Bending forward 20 with 22lb in each hand 1850 Lifting 44lb, back straight, knees bent 2100 Lifting 44lb, back bent, knees straight 3400 Sitting, 100, seat inclined and arm rest 400 Rising, without arm rest, max value 1000 Sitting forward bent 20, 100N each hand 1400 (from Nachemeson, 1963, 1965, 1975, 1987) Partial reproduction of table from Biomechanics in Ergonomics (tbl 14.1)
3.3.3 More Tears and their locations & patterns
Larger numbers of tears were created first in 50/50 combinations. Second, tear patterns were created by increasing the number of circumferential tears to radial while keeping the total number constant. Third tear patterns were created by increasing the number of radial tears to circumferential while keeping the total number constant. These three elements were created for several percentages planned out with percentages ranging from 12.5% to 25 % (Tables 3.3 & 3.4). The 12.5% set was run five times with increasing
33 circumferential tears and decreasing radial. The 12.5% set another five times with increasing radial tears and decreasing circumferential tears. This was done to determine which ratio of tears would create the most height loss. This determined ratio column was continued through the percentage gradient. The patterns and length of tears were taken into account as well.
Table 3.3: Combinations of Circumferential & Radial Tears at various amounts of total tearing (Increasing Circumferential tears) Num Pink Orange Yellow Green Turquoise % removed circum radial circum radial circum radial circum radial circum radial 12x5- 8x5, 13x5- 7x5, 14x5- 6x5, 15x5- 5x5, 16x5- 4x5, 12.5 112 60 3x4-52 65 3x4-47 70 3x4-42 75 3x4-37 80 3x4-32 14x5- 12x5, 15x5- 11x5, 16x5- 10x5, 17x5- 9x5, 18x5- 8x5, 15 134 70 4-64 75 4-59 80 4-54 85 4-49 90 4-44 16x5- 13x5, 17x5- 12x5, 18x5- 11x5, 19x5- 10x5, 20x5- 9x5, 17.5 157 80 3x4-77 85 3x4-72 90 3x4-67 95 3x4-62 100 3x4-57 20x5- 15x5, 22x5- 13x5, 24x5- 11x5, 26x5- 9x5, 25x5- 10x5, 20 179 100 4-79 110 4-69 120 4-59 130 4-49 125 4-54 22x5- 16x5, 24x5- 14x5, 26x5- 12x5, 28x5- 10x5, 30x5- 8x5, 22.5 202 110 3x4-92 120 3x4-82 130 3x4-72 140 3x4-62 150 3x4-52 25x5- 15x5, 27x5- 13x5, 29x5- 11x5, 31x5- 9x5, 33x5- 7x5, 25 224 125 6x4-99 135 3x4-89 145 3x4-79 155 3x4-69 165 3x4-59
Table 3.4: Combinations of Circumferential & Radial Tears at various amounts of total tearing ( Increasing Radial tears) Sky Blue Lavender Blue Aqua Rose Num circum radial circum radial circum radial circum radial circum radial % removed 4x5, 16x5- 5x5, 15x5- 6x5, 14x5- 7x5, 13x5- 8x5, 12x5- 3x4-32 80 3x4-37 75 3x4-42 70 3x4-47 65 3x4-52 60 12.5 112 8x5,4- 18x5- 9x5,4- 17x5- 10x5,4- 16x5- 11x5, 15x5- 12x5,4- 14x5- 44 90 49 85 54 80 4-59 75 64 70 15 134 9x5, 20x5- 10x5, 19x5- 11x5, 18x5- 12x5, 17x5- 13x5, 16x5- 3x4-57 100 3x4-62 95 3x4-67 90 3x4-72 85 3x4-77 80 17.5 157 7x5,4- 28x5- 9x5,4- 26x5- 11x5,4- 24x5- 13x5, 22x5- 15x5,4- 20x5- 39 140 49 130 59 120 4-69 110 79 100 20 179 12x5, 26x5- 13x5, 25x5- 14x5, 24x5- 15x5, 23x5- 16x5, 22x5- 3x4-72 130 3x4-77 125 3x4-82 120 3x4-87 115 3x4-92 110 22.5 202 7x5, 33x5- 9x5, 31x5- 11x5, 29x5- 13x5, 27x5- 15x5, 25x5- 3x4-59 165 3x4-69 155 3x4-79 145 3x4-89 135 6x4-99 125 25 224
Six patterns were designed to cause damage. For each pattern the integrity of the pattern was attempted to be maintained thru out all runs, for example lengths of tears were increased to fit total numbers. In the case of the arrow head patterns, the arrows were increased posterior & midline and anterior & laterally respectively. Pattern #1 (figure 3-
2) is a simple checker board. Patterns #2 and #3 (figures 3-3 & 3-4) are arrows pointing
34 in opposite directions. Patterns #4 and #5 (figures 3-5 & 3-6) are stripes oriented in opposite directions. Pattern #6 (figure 3-7) is a simple “X”. Sets were run for each pattern with each set of tear ratio for 12.5%. The turquoise column was run for each pattern across the remainder of the percentage gradient. This T pattern across the table was done to expedite the variable evaluation. Load was held constant at the physiologically relevant 1000N and the L4-5 nucleus’s Poisson’s ratio was held at 0.1. The L4-5 disc was isolated in the same manner as the first generation setup. Disc heights were calculated the same as the first generation model setup.
Clustering pattern #1 Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-2: a) Checker board pattern: numbers represent elements, white blocks remain untouched; b) visual depiction of removed elements in model for checker board pattern.
35
Clustering pattern #2 Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-3: a) Outside to inside arrowhead pattern: numbers represent elements, white
blocks remain untouched; b) visual depiction of removed elements in model for
arrowhead pattern.
Clustering pattern #3 Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-4: a) Inside to outside arrowhead pattern: numbers represent elements, white
blocks remain untouched; b) visual depiction of removed elements in model for
arrowhead pattern.
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Clustering pattern #4 Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-5: a) Bottom to top stripe pattern: numbers represent elements, white blocks
remain untouched; b) visual depiction of removed elements in model for stripe pattern.
Clustering pattern #5 Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-6: a) Top to bottom stripe pattern: numbers represent elements, white blocks
remain untouched; b) visual depiction of removed elements in model for stripe pattern.
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Clustering pattern #6 Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-7. a) “X” pattern: numbers represent elements, white blocks remain untouched;
b) visual depiction of removed elements in model for “X” pattern.
3.3.4 Worst case scenarios
A worst case scenario of tears model was created by inducing as many tears as possible within the disc with as many as their type and location would allow for (figure 3-
8). Two other models were created as well. In a second worst case the tear numbers were kept equal (figure 3-9). In a third worst case there were four more radial tears than circumferential tears (figure 3-10). Load was held constant at the physiologically relevant
1000N and the L4-5 nucleus’s Poisson’s ratio was held at 0.1. The L4-5 disc was isolated in the same manner as the first generation setup. Disc heights were calculated the same as the first generation model setup.
38
43.3% more radial 40.2% equal # of tears Circumferential tears Circumferential tears superior superior 4097 4081 4065 4049 4033 4017 4001 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201 6297 6281 6265 6249 6233 6217 6201
Radial tears Radial tears Superior Superior looking from inside nucleus out looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 Lateral edge mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-8: Worst case scenario Figure 3-9: Worst case scenario
pattern #1 pattern #2
37.0% more circum Circumferential tears superior 4097 4081 4065 4049 4033 4017 4001 5097 5081 5065 5049 5033 5017 5001 posterior 5297 5281 5265 5249 5233 5217 5201 edge 5497 5481 5465 5449 5433 5417 5401 Anterior towards 5697 5681 5665 5649 5633 5617 5601 edge nucleus 5897 5881 5865 5849 5833 5817 5801 wall 6097 6081 6065 6049 6033 6017 6001 6297 6281 6265 6249 6233 6217 6201
Radial tears Superior looking from inside nucleus out 4112 4111 4110 4109 4108 4107 4106 4105 5112 5111 5110 5109 5108 5107 5106 5105 5312 5311 5310 5309 5308 5307 5306 5305 mid line 5512 5511 5510 5509 5508 5507 5506 5505 lateral edge posterior 5712 5711 5710 5709 5708 5707 5706 5705 of nucleus 5912 5911 5910 5909 5908 5907 5906 5905 6112 6111 6110 6109 6108 6107 6106 6105 6312 6311 6310 6309 6308 6307 6306 6305
Figure 3-10: Worst case scenario pattern #3
3.4 Degenerated Models: small, medium & large
Once the best combination of factors was determined a model was created with those elements: 0.1 Poisson’s ratio within the nucleus and 43.3% tears in the annulus using a combination of radial and circumferential tears, which lead to 41% disc height loss. Two additional models were created using data obtained from the previous sections
39 that would serve as intermediate models between intact and the 41% disc height loss model. Models were created that had about 21% and 10% disc height loss, medium and small models respectively. The 21% disc height loss model required 10% tearing of both types of tears and a nucleus Poisson’s ratio of 0.3. The 10% disc height loss model required 2.5% tearing of both types of tears. The damaged models were loaded with
1000N compressive force using the L4-5 isolation process previously described. The displacements (x, y, z) for all the nodes were then calculated within ABAQUS and outputted to a text file. These displacements were added to the original nodes coordinates to find the new coordinates of the altered (degenerated) model. Nodes along the plane of reflection needed to be altered farther to insure the nodes reflected properly. All the X coordinates of nodes along this plane were changed to zero. An assumption with this model was made that all the ligaments connecting the L4/5 functional spine unit remodeled or were shorten to accommodate the height change. This was an unfortunate side effect as these ligaments most likely will not remodel this way in vivo; however do to the limitations of the software, it was necessary.
Once these physiologically degenerated models were created, a biomechanical study was performed for each model. The bottom of S1 was fixed and loads were applied to L3. A 400N compressive preload was applied first using a spring as not to induce artificial flexion, then 10Nm moments were applied to create extension, flexion, left bending and right rotation. Right bending and left rotation are unneeded since the model is fully symmetrical. Displacements were found and used to find angular displacements for each level and over whole spine. Stresses within the annulus and nucleus were found within ABAQUS and outputted as Von Misses stress diagrams. Foreman space was
40 calculated as well using node displacements within the foreman. Facet loads and contact area were calculated as well using contact elements between the facet faces. These small medium & large degeneration models were compared to intact to find any differences.
41
Chapter IV:
Results
4.1 Chapter Overview
The calculated results from the given models are given to show a follow of lessons learned from one model set to another. Finally the biomechanics are reviewed of final model.
4.2 Initial model: nuclear changes alone
In order to create a disc height loss of 50% by only changing the Possion’s ratio of the nucleus pulpous, a compressive load of 2700N was needed. The height loss at L4/5 triggered a change in facet gaps and the relative orientation of that level and levels above,
Figure 4-1. The most dramatic facet changes did occur at the L4/5 level (Figure 4-2) in the form of a larger gap between the surfaces of the facets and alterations to the orientations of the capsular ligaments. Following the biomechanical study, the angular motion across the L4/5 segment decreased in all motions when compared to the intact model (Table 4.1).
42
a) Disc Degenerated b) Intact model model
Figure 4-1: Sagittal section of ligamentous L3-S1 finite element model
a) Degenerated L4/5 disc b) Intact disc
Figure 4-2: Differences in L4/5 facet orientation (red[left]=Inf L4 & blue[right]= Sup L5).
Table 4.1: Angular motion (deg) in various loading modes for 400 N preload and 10.6 Nm of bending moment across L4-5 segment. Angular Motion (deg) Extension Flexion Rotation Bending Intact 3.4 4.6 2.4 4.7 DDD 1.7 4.4 1.6 2.6 Percent change -49.5 -3.8 -33.9 -44.9
Maximum stresses in both the Annulus and Nucleus of the degenerated disc increase as well, except in extension (Tables 4.2 & 4.3). The Nucleus showed the higher percentage of stress increase (Figure 4-3). High stress areas varied depending on the
43
material and motion. During extension the annulus saw maximum stress in spots along the superior posterior edge bilaterally, while the nucleus saw maximum stresses along its posterior edge superiorly with inferior spots. During flexion the annulus saw maximum stresses in anterior superior elements not quite directly on the edge of the disc, while the nucleus saw maximum stress anterior as well however inferiorly. During left bending maximum stress for both areas occurred along the left lateral edge however it occurs superiorly for the annulus and inferiorly for the nucleus similarly to flexion. During right rotation, maximum stress in the annulus occurs anteriorly spreading laterally along the superior edge, while the stress occurs along the anterior inferior edge within the nucleus.
Table 4.2: Maximum Von Mises Stress (N/mm2) in the Nucleus during various loading modes for 400 N preload and 10.6 Nm of bending moment across L4-5 segment Nucleus Ext Flex LB RR Intact 0.14 0.16 0.21 0.12 DDD 0.13 0.33 0.36 0.23 percent change -1.35 51.80 43.02 45.64
Table 4.3: Maximum Von Mises Stress (N/mm2) in the Annulus during various loading modes for 400 N preload and 10.6 Nm of bending moment across L4-5 segment Annulus Ext Flex LB RR Intact 0.93 0.90 1.13 0.66 DDD 0.76 1.42 1.78 0.87 percent change -23.19 36.60 36.56 24.15
44
Maximum Von Mises Stress in L4/5 Disc 2 Intact-Annulus DD-Annulus Intact-Nucleus DD-Nucleus 1.5
1
0.5 Von Mises (MPa) Mises Von
0 Ext Flex Motion LB RR
Figure 4-3: Comparison of the differences in the stress in both the annulus and the nucleus
The facets loads decreased in all motions except rotation, while the corresponding contact areas showed a slight increase (Tables 4.4 & 4.5). The foramen spaces across the board decreased (Table 4.6). Neutral was defined as the model after only preload but before the moment is applied.
Table 4.4: Facet Loads (N) in various loading modes for 400 N preload and 10.6 Nm of bending moment across L4-5 segment Right Left Facet Load (N) Extension Flexion Rotation Bending R L R L R L R L Intact 170.6 170.6 51.4 51.4 0.0 183.9 75.2 65.7 DDD 134.6 134.6 28.6 28.6 0.0 186.9 38.5 63.2 Percent Change -21.1 -21.1 -44.4 -44.4 0.0 1.6 -48.8 -3.8
45
Table 4.5: Contact area in various loading modes for 400 N preload and 10.6 Nm of bending moment across L4-5 segment Right Left Extension Flexion Rotation Bending R L R L R L R L Intact 1.43 1.43 1.70 1.70 0.00 7.25 3.02 1.43 DDD 1.48 1.48 1.90 1.90 0.00 3.58 0.75 5.45 Percent Change 3.4 3.4 11.3 11.3 0.0 -50.6 -75.3 281.2
Table 4.6: Foramen Space (mm) changes across L4-5 during various loading modes for 400 N preload and 10.6 Nm of bending moment; Neutral is before the moment is applied with only the preload. Foramen Space Extension Flexion Right Rotation Left Bending Neutral (mm) R L R L R L R L R L Intact 22.30 22.30 24.20 24.20 23.21 23.68 24.77 19.97 23.00 23.00 DDD 19.06 19.06 20.82 20.82 19.81 20.61 20.74 17.08 19.85 19.85 Percent Change -14.51 -14.51 -13.97 -13.97 -14.64 -12.97 -16.26 -14.49 -13.71 -13.71
4.3 Examination of Physiological elements
4.3.1 Constant Load with Nuclear Changes, Variable Tear Types & Amount
Circumferential tears (Table 4.7; Figure 4-4) alone constantly produced the highest disc height loss in all cases, except in the run of 2.5% tears where radial alone produced losses a bit greater. The combination of 50/50 circumferential and radial (Table
4.8; Figure 4-5) produced the second most disc height loss. Radial tears only constantly produced the least disc height loss (Table 4.9; Figure 4-6). For all but one case (radial
7.5%), a nuclear possion’s ratio of 0.1 produced the most disc height loss (Table 4.10;
Figure 4-7).
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Circumferential tears 0.10 30 0.20 0.30 0.40 25 0.499
20
15
10 Percentage of disc height loss height Percentagedisc of
5
0 0.0% 2.5% 5.0% 7.5% percentage removed
Figure 4-4: Bar graph comparing various amounts of circumferential tears and various nuclear material property (possion’s ratio) changes.
Table 4.7: Disc height percentage change caused by varying percentage of circumferential tears and various nuclear material property (possion’s ratio) changes Circumferential 0.10 0.20 0.30 0.40 0.499 0.0% 22.09 21.72 20.98 19.20 10.55 2.5% 24.43 24.03 23.21 21.23 11.56 5.0% 25.98 25.56 24.71 22.68 12.72 7.5% 27.67 27.22 26.30 24.11 13.95
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Both tears 0.10 30 0.20 0.30 0.40 25 0.499
20
15
10 Percentage of disc height loss Percentage 5
0 0.0% 2.5% 5.0% 7.5% percentage removed Figure 4-5: Bar graph comparing various amounts of both tear types and various nuclear material property (possion’s ratio) changes.
Table 4.8: Disc height percentage change caused by varying percentage of both tear types and various nuclear material property (possion’s ratio) changes. Both 0.10 0.20 0.30 0.40 0.499 0.0% 22.09 21.72 20.98 19.20 10.55 2.5% 22.99 22.61 21.83 19.96 10.88 5.0% 24.46 24.03 23.16 21.09 11.41 7.5% 25.06 24.61 23.70 21.55 11.80 10.0% 22.19 21.78 20.96 19.05 10.32
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Radial Tears 0.10 30 0.20 0.30 0.40 25 0.499
20
15
10 Percentage of disc height loss height Percentagedisc of
5
0 0.0% 2.5% 5.0% 7.5% percentage removed
Figure 4-6: Bar graph comparing various amounts of radial tears and various nuclear material property (possion’s ratio) changes.
Table 4.9: Disc height percentage change caused by varying percentage of radial tears and various nuclear material property (possion’s ratio) changes. Radial 0.10 0.20 0.30 0.40 0.499 0.0% 22.09 21.72 20.98 19.20 10.55 2.5% 25.06 24.61 23.70 21.55 11.80 5.0% 21.95 21.56 20.79 18.96 10.22 7.5% 22.10 23.36 20.88 18.98 10.19
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radial Tears with 0.1 NP Poisson's ratio 30 Circumferential both
25
20
15
10 Percentage of disc height loss height disc of Percentage 5
0 2.5% 5.0% 7.5% percentage removed Figure 4-7: Bar graph comparing the percentage of disc height loss for a possion’s ratio of 0.1 for each tear scenario and amount of tears.
Table 4.10: Disc height percentage change caused by each tear scenario and amount of tears for only a possion’s ratio of 0.1. Radial Circumferential Both 2.5% 25.06 24.43 22.99 5.0% 21.95 25.98 24.46 7.5% 22.10 27.67 25.06
Trend lines were added to determine values to lead to the 50% height loss goal.
Cubic functions presented the best fits for the data accumulated. First compared was percentage of tears (x) to percentage of height loss (y) for each tear type and possion’s ratio (Figure 4-8,4-9,4-10). The equations were found to have an R2 value of 0.99 or higher all fits within this set (Table 4.11). The values of the amount of tears needed to reach a 50% height loss for this set were calculated as well (Table 4.12). Unfortunately none of the equations for the 50/50 combination reached this value. The second thing compared was the nuclear possion’s ratio (x) to percentage of height loss (y) for each tear type and percentage of tears (Figures 4-11,4-12,4-13). The equations were found to have
50
an R2 value of 0.98 or higher all fits within this set (Table 4.13). The values of the nuclear possion’s ratio needed to reach a 50% height loss for this set were calculated as well (Table 4.14). None of the equations reached a positive possion’s ratio value.
Circumferential tears 50
45
40
35
30
25
20
15 Percentage of disc height loss Percentage 10 0.10 0.20 5 0.30 0.40 0.499 Poly. (0.10) 0 Poly. (0.20) Poly. (0.30) 0.0% 2.5% 5.0% 7.5% 10.0% 12.5% 15.0%Poly. (0.40) 17.5%Poly. 20.0% (0.499) percentage of tears Figure 4-8: Trend lines of the varying amounts of circumferential tears effect on the percentage of disc height loss at various possion’s ratio.
0.10 0.20 radial tears 0.30 0.40 0.499 Poly. (0.10) Poly. (0.20) Poly. (0.30) 50.00 Poly. (0.40) Poly. (0.499)
40.00
30.00
20.00
percentage of disc height loss height disc percentage of 10.00
0.00 0.0% 2.5% 5.0% 7.5% 10.0% 12.5% 15.0% percent of tears
Figure 4-9: Trend lines of the varying amounts of radial tears effect on the percentage of disc height loss at various possion’s ratio.
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Both tears 50 0.10 0.20 0.30 0.40 0.499 Poly. (0.10) 45 Poly. (0.20) Poly. (0.30) Poly. (0.40) Poly. (0.499) 40
35
30
25
20
15 Percentage of disc height loss 10
5
0 -20.0% -15.0% -10.0% -5.0% 0.0% 5.0% 10.0% 15.0% 20.0% percentage of tears Figure 4-10: Trend lines of the varying amounts of a combination of both tear types effect on the percentage of disc height loss at various possion’s ratio
Table 4.11: Trend line equations relating percentage of disc height loss (x) to amount of tears (y) for each possion’s ratio. Value within parenthesis is the R2 value of the equation. Radial Circumferential Both* y=99754x3-12349x2 y=9999x3- y=-21502x3+2263.8x2- 0.10 +365.25x+22.089 (1) 1385.4x2+122.03x+22.089 (1) 10.325x+22.106 (0.9973) y=114876x3-13360x2 y=9712.3x3- y=-21005x3+2205.8x2- 0.20 +377.61x+21.721 (1) 1355.2x2+120.28x+21.721 (1) 9.9441x+21.738 (0.9971) y=92069x3-11408x2 y=8685.4x3- y=-20036x3+2096.4x2- 0.30 +336.42x+20.98 (1) 1236.8x2+114.81x+20.98 (1) 9.4355x+20.997 (0.9966) y=80777x3-10022x2 y=6095.5x3- y=-17814x3+1849.2x2- 0.40 +294.34x+19.196 (1) 927.99x2+100.8x+19.196 (1) .2705x+19.214 (0.9954) y=46748x3-5769.6x2 y=-961.41x3 y=-11072x3+1232.5x2- 0.499 +164.87x+10.552 (1) +196.5x2+35.978x+10.552 (1) 14.836x+10.571 (0.9821) *includes 10% data points Equation (R2)
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Table 4.12: Values of tears needed to reach 50% disc height loss for each trend line, if it exists based on trend lines from Table 4.11. Radial Circumferential Both 0.10 11.328 16.619 never inter 0.20 10.707 16.855 never inter 0.30 11.585 17.553 never inter 0.40 12.016 19.780 never inter 0.499 14.090 never inter never inter
Circumferential Tears 50 0.0% 2.5% 5.0% 7.5% Poly. (0.0%) Poly. (2.5%)
40 Poly. (5.0%) Poly. (7.5%)
30
20 Percentage of disc height loss Percentage 10
0 -0.30 -0.20 -0.10 0.00 0.10 0.20 0.30 0.40 0.50 0.60 nuclear possion's ratio Figure 4-11: Trend lines of varying possion’s ratio’s effect on percentage of disc height loss at various tear amounts for circumferential tears.
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Radial Tears 0.0% 2.5% 50 5.0% 7.5% Poly. (0.0%) Poly. (2.5%) Poly. (5.0%) Poly. (7.5%)
40
30
20 Percentage of disc height loss height Percentagedisc of 10
0 -0.40 -0.30 -0.20 -0.10 0.00 0.10 0.20 0.30 0.40 0.50 0.60 nuclear possion's ratio Figure 4-12: Trend lines of varying possion’s ratio’s effect on percentage of disc height loss at various tear amounts for radial tears.
Both Tears 0.0% 2.5% 50 5.0% 7.5% 10.0% Poly. (0.0%) Poly. (2.5%) Poly. (5.0%) Poly. (7.5%) Poly. (10.0%) 40
30
20 Percentage of disc height loss Percentage 10
0 -0.30 -0.20 -0.10 0.00 0.10 0.20 0.30 0.40 0.50 0.60 nuclear possion's ratio Figure 4-13: Trend lines of varying possion’s ratio’s effect on percentage of disc height loss at various tear amounts for both tear types.
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Table 4.13: Trend line equations relating possion’s ratio’s (x) to percentage of disc height loss (y) for various amounts of tears. Value within parenthesis is the R2 value of the equation. Radial Circumferential Both
y=-550.41x3+367.95x2- y=-550.41x3+367.95x2- y=-550.41x3+367.95x2- 0% 79.289x+26.964 (0.9957) 79.289x+26.964 (0.9957) 79.289x+26.964 (0.9957) y=-607.38x3+402.96x2- y=-616.65x3+412.24x2- y=-578.35x3+386.65x2- 2.5% 86.99x+30.419 (0.9961) 88.702x+29.879 (0.9956) 83.314x+28.115 (0.9957) y=-553.34x3+369.29x2- y=-635.37x3+425.04x2- y=-608.66x3+405.22x2- 5.0% 79.677x+26.85 (0.9958) 91.551x+31.604 (0.9956) 87.418x+29.842 (0.9959) y=-271.13x3+103.01x2- y=-636.42x3+422.98x2- y=-607.38x3+402.96x2- 7.5% 7.8077x+22.291 (0.9817) 91.148x+33.274 (0.996) 86.99x+30.419 (0.9961) y=-543.79x3+361.03x2- 10% n/a n/a 78.028x+27.002 (0.9961)
Table 4.14: Values of possion’s ratio needed to reach 50% disc height loss based on trend lines from Table 4.13. Radial Circumferential Both 0% -0.154 -0.154 -0.154 2.5% -0.131 -0.131 -0.145 5.0% -0.154 -0.121 -0.133 7.5% -0.354 -0.114 -0.131 10.0% n/a n/a -0.156
4.3.2 Constant Tear Amount with Nuclear, Tear Type and Load Changes
As the load increased within a given set, the height loss increased as well for all sets (Table 4.15). A possion’s ratio of 0.1 produced a greater height loss when compared to its 0.25 counter part. A linear trend line was used to relate load and height loss within each set (Figure 4-14). The equations were calculated and found to have a nearly 1 R2 relationship for all sets (Table 4.16, column 2). The load necessary to reach the 50%
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height loss goal was calculated for each set (Table 4.16, column 3) and was found to lie between 1910N to 2330N of compressive force on the top of L4. Calculations for the equations were also done using a zero load equal zero height loss to force the equations through the origin. The equations still came up with nearly 1 R squared values but the equations still did not go through the origin and the final load values were not much different than the raw data lines (Table 4.17).
Table 4.15: Percentages of disc height loss across various load conditions for each set of tears at a constant amount and two nucleus pulposus possion’s ratio changes (0.1 & 0.25). both 0.1 both 0.25 circum 0.1 circum 0.25 radial 0.1 radial 0.25 700N 17.55 16.97 19.98 19.36 15.34 14.83 900N 22.56 21.82 25.13 24.38 19.82 19.17 1000N 25.06 24.23 27.67 26.84 22.10 21.36 1200N 29.91 28.95 32.70 31.72 26.70 25.81 1400N 34.64 33.53 37.66 36.53 31.33 30.28 1850N 45.24 43.81 48.58 47.12 41.52 40.19 2100N 51.02 49.41 54.68 53.00 47.04 45.54 3400N 80.90 78.35 86.67 83.95 74.76 72.44
Loss at various Loads with constant amount of tears 100.00
90.00
80.00
70.00
60.00 both 0.1 both 0.25 50.00 circum 0.1 circum 0.25 40.00 radial 0.1 radial 0.25 Linear (circum 0.1) 30.00 Linear (circum 0.25)
percent loss original from Linear (both 0.1) 20.00 Linear (both 0.25) Linear (radial 0.25) 10.00 Linear (radial 0.1)
0.00 0 500 1000 1500 2000 2500 3000 3500 4000 load (N) Figure 4-14: Graph with trend lines showing percentages of disc height loss across various load conditions for each set of tear groupings at a constant amount and two nucleus pulposus possion’s ratio changes (0.1 & 0.25).
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Table 4.16: Trend line equations relating load and disc height loss for each set of tear groupings at a constant amount and two nucleus pulposus possion’s ratio with R2 values of trend lines in parenthesis. Calculated load to 50% disc height loss for each trend line case. Eqn (R^2) 50% load (N) both 0.1 y=0.0234x+1.637 (0.9998) 2066.79 both 0.25 y=0.0227x+1.5492 (0.9998) 2134.40 circum 0.1 y=0.0246x+2.9919 (1) 1910.90 circum 0.25 y=0.0238x+2.9512 (0.9999) 1976.84 radial 0.1 y=0.0221x+0.2029 (0.9996) 2253.26 radial 0.25 y=0.0214x+0.1267 (0.9997) 2330.53
Table 4.17: Trend line equations (forced through origin) relating load and disc height loss for each set of tear groupings at a constant amount and two nucleus pulposus possion’s ratio with R2 values of trend lines in parenthesis. Calculated load to 50% disc height loss for each trend line case. Final column shows difference between tables 4.16 & 4.17 Eqn (R^2) 50% load (N) % diff both 0.1 y=0.0237x+1.0359 (0.9995) 2066.00 -0.03868 both 0.25 y=0.023x+0.9803 (0.9995) 2131.29 -0.1457 circum 0.1 y=0.0252x+1.8932 (0.9988) 1909.00 -0.09944 circum 0.25 y=0.0244x+1.8675 (0.9987) 1972.64 -0.21276 radial 0.1 y=0.0221x+0.1284 (0.9997) 2256.63 0.149386 radial 0.25 y=0.0214x+0.0802 (0.9998) 2332.70 0.09315
4.3.3 More Tears and their locations & patterns
The turquoise set of 12.5% produced the greatest disc height loss. The turquoise set has the most circumferential tears and the least radial tears compared to its counter parts within the 12.5% set. Overall as the number of circumferential tears increased, the height loss increased as well for almost all cluster patterns (Table 4.18; Figure 4-15).
Cluster patterns starting from Anterior and heading Posterior (cluster #2 & #5) had the highest disc height losses constantly. The turquoise set was continued for the rest of the
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percentage amounts and for each cluster pattern. As the total percent of tears increased so did the disc height loss (Table 4.19; Figure 4-16). The highest disc height loss was reached at 25% tears with the cluster pattern #5.
Table 4.18: Disc height loss results from the 12.5% torn row of tables 3.3 and 3.4 for each cluster/pattern type. Pink Orange Yellow Green Turquoise Sky Blue Lavender Blue Aqua Rose Clus 1 27.41 27.74 28.16 28.44 28.69 24.96 26.06 26.48 26.80 27.12 Clus 2 28.09 28.49 28.89 29.08 29.21 26.30 26.70 27.05 27.51 27.84 Clus 3 25.54 25.91 26.58 26.64 27.16 23.72 24.15 24.58 25.13 25.43 Clus 4 26.92 27.47 28.04 28.37 29.00 25.32 25.25 25.96 26.08 26.39 Clus 5 29.29 29.45 29.54 29.82 29.79 26.19 27.25 27.85 28.46 28.74 Clus 6 27.96 28.15 28.30 28.49 28.91 25.32 25.79 26.40 27.06 27.74 Increasing Circumferential; Decreasing Radial Increasing Radial; Decreasing Circumferential
12.5% tears with varying tear ratios 30
29
28
27
26
25 Pink Orange 24 Yellow Green Turquoise Sky Blue 23 Lavendar Blue
Percentage of disc height loss Aqua Rose 22 1 2 3 4 5 6 Cluster type
Figure 4-15: Graphical representation of disc height loss data at 12.5% torn.
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Table 4.19: Disc height loss data in the turquoise set (last column of table 3.3) of tear combinations at increasing percentage of tears within the annulus for each cluster/pattern. 15% 17.5% 20% 22.5% 25% cluster 1 29.57 30.15 31.29 33.86 34.90 cluster 2 29.91 30.73 32.33 34.43 35.91 cluster 3 27.77 28.82 30.45 32.97 34.10 cluster 4 30.60 32.12 34.90 36.22 37.22 cluster 5 31.02 33.18 36.33 37.91 38.19 cluster 6 29.22 30.09 31.34 34.12 35.08
Increasing Tear amounts at similiar ratio of tear types
40.00
38.00
36.00 15% 34.00 17.50% 20% 32.00 22.50%
30.00 25%
28.00 Percentage of disc height loss Percentage
26.00 1 2 3 4 5 6 Cluster type
Figure 4-16: Graphical representation of disc height loss data within the turquoise set (last column of table 3.3) of tear combinations.
4.3.4 Worst case scenarios
The worst case scenario cases ended up as 37%, 40.2% and 43.3% for the more circumferential, equal tears, and more radial tears respectively. The 43.3% tears yielded the highest disc height loss (Table 4.20).
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Table 4.20: Disc height loss data for the worst case scenarios. % tears % height loss more radial 43.3% 41.10 equal tears 40.2% 40.19 more circum 37.0% 38.46
4.4 Degenerated Models: small, medium & large
b) Large a) Intact c) Medium d) Small Figure 4-17: Side by side comparison of final degenerated disc models before testing.
The first thing examined for each model (Figure 4-17) was the angular motion at the affected level (L4-5) and the level above (L3-4). Angular motion at L4-5 for the large DD model increased at every motion (Figure 4-18; Table 4.21). The largest change occurred in bending motion. Angular motion at L3-4 for the large DD did not show a single trend (Table 4.22). Angular motion at L4-5 for the medium DD model continued the increase trend for flexion & extension, but the motion decreased for rotation & bending (Figure 4-19; Table 4.23). Angular motion at L3-4 for the medium DD has an overall increased motion trend however in flexion and rotation was slight (Table 4.24).
The angular motion at L4/5 trend for the small DD model was a decrease in motion for all the motions except extension which saw an increase (Figure 4-20; Table 4.25).
Angular motion at L3-4 for the small DD has an overall increased motion trend however
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in flexion and rotation was slight (Table 4.26) similar to the medium model. When comparing all three DD models at the L4-5 level, extension is the only motion that is consistently above the intact (Figure 4-21). However all the motions show a general increase as the degeneration level increased. When comparing the three DD models at the
L3-4 level, there appears to be not much difference across the range of degeneration
(Figure 4-22).
Relative Angular Motion Across L4/5 for Large DD model Intact 9.0 DDD
8.0
7.0
6.0
5.0
4.0
3.0
Angular Angular Motion (degrees) 2.0
1.0
0.0 Extension Flexion Rotation Bending Motion
Figure 4-18: Graphical representation of relative angular motion across L4/5 for large degenerated disc model in various modalities of motion.
Table 4.21: Numerical values for the relative angular motion across L4/5 for large degenerated disc model in various modalities of motion. L4/5 Angular Motion (deg) Extension Flexion Rotation Bending Intact 3.44 4.81 2.52 5.14 DDD Large 4.81 7.34 2.79 8.48 Percent change 39.89 52.67 10.91 65.07
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Table 4.22: Numerical values for the relative angular motion across L3/4 for large degenerated disc model in various modalities of motion. L3/4 Angular Motion (deg) Extension Flexion Rotation Bending Intact 3.35 4.65 2.31 4.67 DDD Large 3.39 4.40 2.27 4.81 Percent change 1.29 -5.40 -1.75 3.02
Intact Relative Angular Motion Across L4/5 for Medium DD model DDD
6.0
5.0
4.0
3.0
2.0
Angular Angular Motion (degrees) 1.0
0.0 Extension Flexion Rotation Bending Motion
Figure 4-19: Graphical representation of relative angular motion across L4/5 for medium degenerated disc model in various modalities of motion.
Table 4.23: Numerical values for the relative angular motion across L4/5 for medium degenerated disc model in various modalities of motion. L4/5 Angular Motion (deg) Extension Flexion Rotation Bending Intact 3.44 4.81 2.52 5.14 DDD Medium 3.81 4.88 2.32 4.45 Percent change 10.72 1.52 -8.08 -13.30
Table 4.24: Numerical values for the relative angular motion across L3/4 for medium degenerated disc model in various modalities of motion. L3/4 Angular Motion (deg) Extension Flexion Rotation Bending Intact 3.35 4.65 2.31 4.67 DDD Medium 3.44 4.65 2.31 4.98 Percent change 2.58 0.07 0.04 6.69
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Intact Relative Angular Motion Across L4/5 for Small DD model DDD 6.0
5.0
4.0
3.0
2.0 Angular Angular Motion (degrees) 1.0
0.0 Extension Flexion Rotation Bending Motion
Figure 4-20: Graphical representation of relative angular motion across L4/5 for small degenerated disc model in various modalities of motion.
Table 4.25: Numerical values for the relative angular motion across L4/5 for small degenerated disc model in various modalities of motion. L4/5 Angular Motion (deg) Extension Flexion Rotation Bending Intact 3.44 4.81 2.52 5.14 DDD Small 3.63 4.24 2.27 4.27 Percent change 5.51 -11.87 -10.06 -16.91
Table 4.26: Numerical values for the relative angular motion across L3/4 for small degenerated disc model in various modalities of motion. L3/4 Angular Motion (deg) Extension Flexion Rotation Bending Intact -3.35 4.65 2.31 -4.67 DDD Small -3.44 4.69 2.34 -4.96 Percent change 2.60 0.86 1.13 6.27
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Angular Motion for all Degenerated Models across L4/5 9 Intact DD Small 8 DD Medium DD Large 7 6 5 4 3
Angular Angular Motion (degrees) 2 1 0 Extension Flexion Rotation Bending Motion
Figure 4-21: Graphical representation of relative angular motion across L4/5 for all degenerated disc models in various modalities of motion.
Intact Angular Motion for all Degenerated Models across L3/4 DD Small DD Medium 6 DD Large
5
4
3
2 Angular Motion (deg) Motion Angular 1
0 Extension Flexion Motion Rotation Bending
Figure 4-22: Graphical representation of relative angular motion across L3/4 for all degenerated disc models in various modalities of motion.
Maximum stress within the L4-5 disc increased in both the annulus and the nucleus increased as the degeneration increased (Figures 4-23, 4-24), although in the small degenerated model showed an initial decrease compared to the intact model (Figure
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4-25; Tables 4.27, 4.28) for the majority of motions and locations (annulus & nucleus).
The medium degenerated model showed an overall increase across all motions and locations (Figure 4-26; Tables 4.29, 4.30). The large degenerated model showed the largest change (Figure 4-27/Table 4.31, 4.32). Its nucleus saw increases of 50% or higher for all motions and its annulus saw increases of over 35% for each motion.
Maximum Von Mises Stress in L4/5 Annulus 3.5 Intact Small DD Medium DD 3 Large DD
2.5
2
1.5
1 Von Mises (MPa) Mises Von
0.5
0 Ext Flex LB RR Motion
Figure 4-23: Graphical representation of the maximum Von Mises Stress through out the L4/5 annulus for all degenerated disc models in various modalities of motion.
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Maximum Von Mises Stress in L4/5 Nucleus
1.2 Intact Small DD Medium DD 1 Large DD 0.8
0.6
0.4 Von Mises (MPa) VonMises 0.2
0 Ext Flex LB RR Motion
Figure 4-24: Graphical representation of the maximum Von Mises Stress through out the L4/5 nucleus for all degenerated disc models in various modalities of motion.
Maximum Von Mises Stress in L4/5 Disc (intact vs small DD) 1.6 Intact-Annulus DD-Annulus 1.4 Intact-Nucleus DD-Nuclues 1.2 1 0.8 0.6 0.4 Von Mises (MPa) VonMises 0.2 0 Ext Flex LB RR Motion
Figure 4-25: Graphical representation of the maximum Von Mises Stress through out L4/5 disc for the small degenerated disc model in various modalities of motion.
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Table 4.27: Numerical values for the maximum Von Mises Stress through out the L4/5 annulus for small degenerated disc model in various modalities of motion. Annulus Ext Flex LB RR Intact 0.91 1.01 1.50 0.72 Small DD 0.88 0.73 1.01 0.72 percent change -3.61 -39.50 -48.28 -0.54
Table 4.28: Numerical values for the maximum Von Mises Stress through out the L4/5 nucleus for small degenerated disc model in various modalities of motion. Nucleus Ext Flex LB RR Intact 0.15 0.16 0.23 0.17 Small DD 0.16 0.18 0.20 0.10 percent change 6.12 13.09 -10.16 -63.78
Maximum Von Mises Stress in L4/5 Disc (intact vs Medium DD)
1.8 Intact-Annulus DD-Annulus 1.6 Intact-Nucleus 1.4 DD-Nucleus 1.2 1 0.8 0.6
Von Mises (MPa) VonMises 0.4 0.2 0 Ext Flex LB RR Motion
Figure 4-26: Graphical representation of the maximum Von Mises Stress through out L4/5 disc for the medium degenerated disc model in various modalities of motion.
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Table 4.29: Numerical values for the maximum Von Mises Stress through out the L4/5 annulus for medium degenerated disc model in various modalities of motion. Annulus Ext Flex LB RR Intact 0.91 1.01 1.50 0.72 Medium DD 1.13 1.53 1.55 0.91 percent change 19.13 33.80 2.99 20.46
Table 4.30: Numerical values for the maximum Von Mises Stress through out the L4/5 nucleus for medium degenerated disc model in various modalities of motion. Nucleus Ext Flex LB RR Intact 0.15 0.16 0.23 0.17 Medium DD 0.18 0.29 0.26 0.21 percent change 16.45 43.98 13.94 19.50
Maximum Von Mises Stress in L4/5 Disc (intact vs Large DD) 3.5 Intact-Annulus DD-Annulus Intact-Nucleus 3 DD-Nucleus 2.5
2
1.5
1 Von Mises (MPa) 0.5
0 Ext Flex LB RR Motion
Figure 4-27: Graphical representation of the maximum Von Mises Stress through out L4/5 disc for the large degenerated disc model in various modalities of motion.
Table 4.31: Numerical values for the maximum Von Mises Stress through out the L4/5 annulus for large degenerated disc model in various modalities of motion. Annulus Ext Flex LB RR Intact 0.91 1.01 1.50 0.72 Large DD 1.67 1.62 3.29 1.64 percent change 45.31 37.53 54.27 55.94
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Table 4.32: Numerical values for the maximum Von Mises Stress through out the L4/5 nucleus for large degenerated disc model in various modalities of motion. Nucleus Ext Flex LB RR Intact 0.15 0.16 0.23 0.17 Large DD 0.31 0.83 1.02 0.51 percent change 51.63 80.74 77.92 67.63
The location of the maximum stress was dependant on the motion simulated & the amount of degeneration. First, the stresses were examined in extension for the annulus for each model. The small model showed high concentrations of stress along the posterior inferior edge and superior posterior edge with some concentration along the anterior inferior edge. The medium model showed a similar trend however the bands of concentration were a bit wider and other high concentration hot spots occurred bilaterally on the superior posterior lateral sides. The large model had no bands of concentration just hot spots on the superior posterior edge. Second, the stresses were examined in extension for the nucleus for each model. The small model showed high concentration bands of stress along its posterior face while the medium model had several hot spots on its posterior face with stress bands radiating away from them. The large model similarly had hot spots, but all were along the posterior superior edge with concentration bands radiating across the superior surface and posterior face. Next, flexion was examined for each area with annulus first and nucleus second. The small model’s annulus showed high stress concentration along the superior anterior edge in the middle of concentration band with other bands along the posterior superior and anterior inferior edges. The medium model’s annulus showed three distinct high concentration bands along the superior anterior edge in the middle of a wider band and another concentration band along the
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inferior anterior edge. The large model’s annulus showed a high concentration band along the superior anterior in the middle of a thin band that spans whole anterior superior edge. For the small model, some bulging along the anterior surface could be seen and the high concentration of stress was in this bulge as well. Other radiating spots were seen around that high concentration area and on the superior surface and inferior posterior edge. The medium model’s nucleus was similar in pattern to the small except that it had bilateral hot spots on the superior edge. The large model’s nucleus saw a high concentration band along the anterior face in the middle of the face. Bending was the next motion to be examined and in this case left bending was only done due to the model’s symmetry. For the small model in the annulus, high stress concentration band was seen on the superior left side with a secondary hot spot on the right lateral edge, plus some bands around those two high areas and along the left interior edge. For the medium model in the annulus, high stress concentration was similar to the small of the left superior edge; however the right lateral spot disappeared to be replaced by a band along the left interior edge. For the large model, all the stress was concentrated along the left lateral superior edge. Moving to the nucleus for left bending, the small model had a large stress hotspot in the center of the superior face that traveled to the inferior with two smaller spots (both posterior and anterior) on the left lateral side. In the medium, the distribution changes drastically in the distribution from the small model. While the majority of the stress was concentrated to the left side, as well a singular hotspot was seen anteriorly and along the inferior left lateral edge. For the large model there was some definite nucleus collapse on the left lateral side along with a stress concentration. Finally rotation motion was examined specifically right rotation. For the small model’s annulus the stress was
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concentrated along the right side both superior and inferiorly plus a hotspot superior posterior right lateral area. The medium model’s annulus distribution is similar to the small model; however the superior posterior right lateral hot spot is smaller and a new hotspot arose directly opposite the first spot on the superior surface. Within the large model’s annulus during rotation, the distribution changes drastically. There is not a singular area of concentration of a wide band along the anterior superior edge from left lateral side to right lateral side with some spots along the posterior superior edge.
Facet loads were analyzed for the affected level (L4/5) and the levels above (L3/4) and below (L5/S1) as well. There was virtually no change at the L5/S1 level (Figure 4-28;
Table 4.33). Similarly there was not much of a change in the loads at the L3/4 level except for Bending (Figure 4-29; Table 4.34). For the degenerated (L4/5), the facet loads showed a difference based on the level of degeneration (Figure 4-30; Table 4.35).
Extension showed an overall trend of increasing facet loads with increasing degenerated despite a small decrease from intact to the small model. Flexion did not seem to follow a clear trend, but the large model did increase facet loads. Rotation also showed an increasing trend however the increase was slight. Bending also did not have a trend but the large model did increase facet loads bilaterally. The contact area of the facets followed a similar pattern for the levels above and below as the facet loads. Both showed little to no change compared to intact (Figures 4-31, 4-32; Tables 4.36, 4.37) which follows the loading trend. For the degenerated level the contacts areas showed some variation (Figure 4-33; Table 4.38). Overall the greatest changes were seen for the largest degeneration, however for most motions no change was even seen until the largest degeneration.
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The foramen space at the degenerated level was calculated and shown to decrease for all motions as the degeneration increased (Figure 4-33; Table 4.39). Neutral, defined as the point with only a preload and no motion yet applied, showed the same trend as well.
Intact Facet Loads across L5-S1 in Degenerated model DD small 160 DD medium 140 DD large 120 100 80 60 Load(N) 40 20 0 RLRLRLRL
Extension Flexion Motion Right Rotation Left Bending
Figure 4-28: Graphical representation of the load on each facet across the L5/S1 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.33: Numerical values for the load on each facet across the L5/S1 functional unit for the all degenerated disc models in various modalities of motion. Facet Loads Extension Flexion Right Rotation Left Bending L5-S1 R L R L R L R L Intact 133.10 133.10 18.39 18.39 151.10 0.00 62.21 0.00 DD small 133.20 133.20 18.51 18.51 150.70 0.00 61.41 0.00 DD medium 133.50 133.50 18.56 18.56 150.90 0.00 61.52 0.00 DD large 134.60 134.60 13.01 13.01 149.80 0.00 60.33 0.00
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Intact Facet Loads across L3/4 in Degenerated model 180 DD small 160 DD medium DD large 140 120 100 80 60 40
Load (N) Load 20 0 R L R L R L R L
Extension Flexion Right Rotation Left Bending Motion
Figure 4-29: Graphical representation of the load on each facet across the L3/4 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.34: Numerical values for the load on each facet across the L3/4 functional unit for the all degenerated disc models in various modalities of motion. Facet Loads Extension Flexion Right Rotation Left Bending L3-4 R L R L R L R L Intact 159.60 159.60 40.88 40.88 170.20 0.00 68.00 67.10 DD small 160.70 160.70 41.39 41.39 171.40 0.00 71.22 66.83 DD medium 161.20 161.20 41.45 41.45 171.40 0.00 73.57 63.35 DD large 161.00 161.00 42.87 42.87 171.10 0.00 76.92 59.29
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Intact Facet Loads across L4/5 in Degenerated model DD small 200 DD medium DD large
150
100
50 Load Load (N)
0 R L R L R L R L
Extension Flexion Right Rotation Left Bending Motion
Figure 4-30: Graphical representation of the load on each facet across the L4/5 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.35: Numerical values for the load on each facet across the L4/5 functional unit for the all degenerated disc models in various modalities of motion. Facet Loads Extension Flexion Right Rotation Left Bending L4-5 R L R L R L R L Intact 176.80 176.80 32.53 32.53 168.30 0.00 82.77 68.70 DD small 167.60 167.60 27.29 27.29 165.10 0.00 61.39 52.69 DD medium 183.70 183.70 22.82 22.82 170.10 0.00 70.22 50.05 DD large 197.60 197.60 46.48 46.48 174.00 0.00 138.00 110.90
74
Intact Contact Area of Facets Across L3/4 for Degenerated Models DD small DD medium 6 DD large
5
4 ) 2
3 Area (mm Area 2
1
0 R L R L R L R L
Extension Flexion Right Rotation Left Bending Motion
Figure 4-31: Graphical representation of the contact area of each facet across the L3/4 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.36: Numerical values for contact area of each facet across the L3/4 functional unit for the all degenerated disc models in various modalities of motion. Contact Area Extension Flexion Right Rotation Left Bending L3/4 R L R L R L R L Intact 1.43 1.43 0.94 0.94 5.01 0.00 1.43 2.56 DD small 1.43 1.43 0.94 0.94 5.01 0.00 1.43 2.56 DD medium 1.43 1.43 0.95 0.95 5.03 0.00 1.43 2.57 DD large 1.44 1.44 0.95 0.95 5.05 0.00 1.44 2.58
75
Contact Area of Facets Across L5/S1 for Degenerated Models Intact 3.5 DD small DD medium 3 DD large
2.5 ) 2 2
1.5 Area (mm Area
1
0.5
0 R L R L R L R L Extension Flexion Right Rotation Left Bending Motion
Figure 4-32: Graphical representation of the contact area of each facet across the L5/S1 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.37: Numerical values for contact area of each facet across the L5/S1 functional unit for the all degenerated disc models in various modalities of motion. Contact Area Extension Flexion Right Rotation Left Bending L5S1 R L R L R L R L Intact 3.13 3.13 1.26 1.26 3.13 0.00 3.13 0.00 DD small 3.13 3.13 1.26 1.26 3.13 0.00 3.13 0.00 DD medium 3.13 3.13 1.26 1.26 3.13 0.00 3.13 0.00 DD large 3.13 3.13 1.26 1.26 1.85 0.00 3.13 0.00
76
Intact Contact Area of Facets Across L4/5 for Degenerated Models DD small DD medium 7 DD large
6
5 ) 2 4
Area (mm Area 3
2
1
0 R L R L R L R L
Extension Flexion Right Rotation Left Bending Motion
Figure 4-33: Graphical representation of the contact area of each facet across the L4/5 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.38: Numerical values for contact area of each facet across the L4/5 functional unit for the all degenerated disc models in various modalities of motion. Contact Area Extension Flexion Right Rotation Left Bending L4/5 R L R L R L R L Intact 1.43 1.43 1.70 1.70 5.35 0.00 1.43 3.02 DD small 1.43 1.43 0.94 0.94 5.35 0.00 1.43 3.02 DD medium 1.43 1.43 0.94 0.94 5.35 0.00 1.43 4.53 DD large 1.43 1.43 1.89 1.89 7.25 0.00 6.95 1.51
77
Intact Foramen Space Across L4/5 small DD 30 medium DD
25 large DD
20
15
10 Magnitude Magnitude (mm)
5
0 RLRLRLRLRL
Extension Flexion Right Rotation Left Bending Neutral Motion
Figure 4-34: Graphical representation of the foramen space across the L4/5 functional unit for the all degenerated disc models in various modalities of motion.
Table 4.39: Numerical values for the foramen space across the L4/5 functional unit for the all degenerated disc models in various modalities of motion. Foramen Right Left Space Extension Flexion Rotation Bending Neutral R L R L R L R L R L Intact 22.12 22.12 23.61 23.61 22.78 23.13 24.41 19.45 22.50 22.50 small DD 21.96 21.96 23.73 23.73 22.74 23.01 24.05 19.59 22.47 22.47 medium DD 20.76 20.76 22.53 22.53 21.48 21.92 22.87 18.29 21.23 21.23 large DD 19.56 19.56 21.07 21.07 20.03 20.75 22.84 16.09 19.92 19.92
78
Chapter V:
Conclusions & Discussion
5.1 Chapter Overview
The results of each model set are discussed and conclusions are made to lead to the next model set. The final model is biomechanically evaluated and graded based on clinical grading schemes and literature findings.
5.2 Initial model: nuclear changes alone
The modeling done in this step showed how one physiological change to one level could affect the rest of the model. In order to achieve the desired goal of 50% disc height loss a large load was needed. While the load of 2700N is not entirely outside the physiological realm, it is a higher load than those more associated with everyday activities. For example, activities such as standing and twisting can produce loads of
700N and 900N respectively, while lifting 44lb with a bent back and straight knees can produce a load of 3400N (19).
This degenerated model showed promise as well in the biomechanical evaluation. The motion data seemed to agree with Tanaka et al who said that motion increased with disc degeneration, but decreased again with higher grades of degeneration (16). Part of the characterizations of high degree degeneration includes
79 gross height loss (which was simulated with 50% height loss), loss of water content in the nucleus and defects within the annulus (11). It was concluded from this model and knowledge that nuclear changes alone would not achieve the desired gross height loss within the everyday physiological loading conditions. Therefore, in order to discover the best combination of nuclear changes, lesion or tear induction and load each variable was evaluated in the next series of models.
5.3 Examination of Physiological elements
5.3.1 Constant Load with Nuclear Changes, Variable Tear Types & Amount
The goal of this modeling set was to observe and evaluate how each physiological change affected the resulting disc height loss. Although circumferential tears alone created the steepest trend of height loss to percentage of tears slope, from literature it was known that both types of tears are present at the chosen level of degeneration. This showed the first compromise between mathematical predictions and biology. It can be concluded that the frequency of circumferential tears will have a greater effect on the height loss than the radial tears. This logically makes sense as the circumferential tears are located in the anterior portion of the disc and damage here would allow the disc to collapse plus the natural curve of the spine would force the damaged area to collapse as well. While the circumferential tears alone and the both tear sets showed trends of constant increase of height loss as the amount of tears increased, the radial alone actually showed a decrease of height loss as the amount of tears increased, which given the same logic given to circumferential alone it could be that the height loss was more in the posterior section of the disc giving the disc the opposite
80 wedging effect (posterior to anterior). It could be concluded therefore that a better location for height loss could be the center of the disc; however given the anatomical geometry of the endplates this could skew the results and the height loss was continued to be measured and categorized by the anterior midline height loss.
Throughout this set of modeling, it was shown that the lowest Poisson’s ratio consistently yielded that greatest height loss for all sets. Clearly a low Poisson’s ratio is needed to induce height loss.
The trend for the amount of tears was somewhat predictable except for radial tears alone, which was discussed earlier. Therefore it’s safe to conclude that an increased number of tears will be required to attain the 50% height loss goal.
In order to make educated conclusions of how best to proceed with the next stage of modeling, trend lines were calculated to see how each variable could be used to achieve 50% height loss. The trend lines ended up being a little misleading. The
Poisson’s ratio trends indicated that negative Poisson’s ratios would be best. While negative Poisson’s ratios are theoretically possible, they probably are not physiologically probable. No published data could be found to support a negative
Poisson’s ratio in the disc. The amount of tears trends also yielded confusing results.
The trend lines for the Both tear set never reached 50% and the singular tear types yielded percentages in the teens, which when evaluated later did not yield 50% height loss. Overall the trend lines did not give any more insight into the best combination of variables to reach 50% height loss, further proving the biology can be unpredictable.
81
5.3.2 Constant Tear Amount with Nuclear, Tear Type and Load Changes
The variable not altered, Load, in the second set of models was evaluated in this third set. Physiological loads were chosen. The goal of this set was to see if the load required to reach 50% height was within a physiological range given the tear types and
Poisson’s ratio if the total amount of tears was held constant. All three combinations of tears were still evaluated as to not bias the results and to keep the possibilities open for discussion. Lower Poisson’s ratios were chosen given the overwhelming conclusion from the previous model set that lower Poisson’s ratios were needed to produce greater height loss. The load trend lines created gave more insight and made more logical sense than the previous set. It was shown that the loads required fell within the physiologically reported loads by Nachemson via Goel et al (19). However the loads were more consistent with lifting a large weight which the average person does not do in everyday activities as is a goal of this study. It was concluded that more damage to the disc was needed to create the desired height loss. The load used in the second set of models,
1000N, was decided to be used from this point to show an established load for an everyday activity.
5.3.3 More Tears and their locations & patterns
This fourth set of models at first plan required 360 models to try all the combinations laid over. This seems extreme so the number is cut with a process of elimination. The set of 12.5% was run across all tear combinations and patterns to determine which set of tear combinations would yield the greatest height loss. The turquoise column fit this determination as it was the greatest height loss for all tearing patterns. It contained the most circumferential tears to radial tears ratio, which
82 confirmed the previous conclusion that the number of circumferential tears would influence the height loss the most. Because this ratio of tears showed the most promise for greatest height loss, this column of tests was completed for increasing percentage of tears again with the various patterns. The data did continue the trend of increasing height loss with amount of tears however these tear amounts differed greatly from those found in previous trend lines again confirmation the conclusion that biological models can be unpredictable. Even though this combination of tears showed promise, not even the highest amount of tears came close to a 50% height loss for any pattern of tearing. It was therefore concluded that more tears were needed all over the disc.
5.3.4 Worst case scenarios
Although it was shown that many tears were needed to reduce the height 50% under a physiologically relevant load, tears could not be just randomly placed. The tears therefore were placed in their tear specific physiologic locations. Unfortunately none of these worst case scenario models yielded a height loss of 50%. It can be concluded that a load of greater than 1000N is needed to induce 50% height loss under these conditions.
A secondary conclusion can be made that additional material property alteration can be done to the nucleus in the form of Young’s modulus to make the nucleus stiffer and/or to the annulus ground and fiber elements to make the annulus weaker in order to reach the
50% height loss at the everyday set load of 1000N. A height loss of 41% still could be considered a “gross” height loss as described in the categorization of the grades of degeneration (16).
83
5.4 Degenerated Models: small, medium & large
The lessons were learned from each set of previous section’s models in order to make the next set and to evaluate the role of the main variables on disc height loss. Even though the goal of 50% height loss was not meet, enough scenarios were generated to create a range of degenerated models to simulate various grades of disc degeneration.
Identifying the level of degeneration based on grading schemes could be difficult as there are several grading scheme available to compare the model. Each grading scheme has its own number of level and description of levels based on now the disc is observed. In one article in particular that was reviewed, four grading schemes alone were compared (78). Grading schemes are based on Macroscopic, Discographic,
Radiographic, Morphologic and Magnetic Resonance Imaging (MRI) Assessments. One of the main difficulties of grading an FE model comes in the point that many of these schemes described blurred or indistinct boundaries of the nucleus and annulus. By nature the boundaries of these areas in the FE model are still clear. Another element used to grade degeneration is the formation of osteophytes which the body will naturally create to stabilize an unstable joint. These are not present in the FE model, so any reference to them in the grading can not be used to assess the grade of the FE model.
Also none of the schemes quantify a number or percentage of damage due to lesions or tears in the disc. Therefore the best way to grade the model would be to compare motion data collected when discs are graded by specific schemes.
Tanaka et al graded cadaver disc models based on MRI and Morphologic
Assessments (16). Motion data was collected on single functional spinal units. The
84 motion data for the lower lumbar segments, L4/5 and L5/S1, was comparable to the
Large DD model created in this study. However it is still not clear whether the Large
DD model is grade IV or V based on this data. The motion data for the Large DD model within the standard deviation of both grades.
Fujiwara et al (33) used MRI assessment to grade cadaver disc models and performed motion testing. The cadaver models were separated into make and female data points. Based on the flexion, extension and lateral bending data, the Fujiwara data would suggest that the Large DD model to be grade III or IV.
Krismer et al (78) evaluated discs based on Macroscopic, Discographic, and
Radiographic Assessments. However only axial rotation and lateral bending data was collected and examined. They found virtually no difference across the grades in lateral bending for all grading schemes, which does not match the motion data created in this study. The rotation data however can point to a potential grade of the Large DD model.
The Krismer et al motion data was separated based on the assessment scheme. Two of the three schemes presented pointed towards the Large DD model being grade IV. The third assessment did not have any data points for its grade IV.
Given this motion data review from three independent researchers, it can be concluded that the Large DD model is a grade IV degeneration of the L4/5 disc.
85
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88) Nachemson A. Lumbar interdiscal pressure. Acta Orthop Scand 1960; 96:509.
89) Farfan HF et al. The effects of torsion on the lumbar intervertebral joints. J Bone
Joint Surgery 1970; 52A:468.
90) Schultz AB et al. Mechanical properties of human spine motion segment part I:
responses in flexion, extension, lateral bending, and torsion. J Biomech Eng 1979;
101:46-52.
91) Adams MA, WC Hutton, JRR Stott. The resistance to flexion of the lumbar
intervertebral joint. Spine 1980; 5:245.
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92) Tencer AF, AM Ahmed, DL Burke. Some static mechanical properties of the
lumbar intervertebral joint, intact and injured. J Biomech Eng 1982; 104:193-201.
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Appendix A
Spine Anatomy
A.1 Vertebras
Within the spinal column there are five distinct regions: cervical, thoracic, lumbar, sacral and coccygeal (Figure A-1). The five cervical are found within the neck and allow the head to rotate. The twelve thoracic are found within the chest and give posterior attachment location for the ribs. The five lumbar are commonly referred to as the small of back or lower back. It sees the most stress and can be a source of pain to a patient. The five sacral vertebras are fused to form the sacrum which forms joints with each side of the pelvis. The coccygeal vertebras are fused as well to form the coccyx or tail bone. It is the remnants of a tail, which has been eliminated through the course of evolution. Each region has a distinct curvature that helps the column absorb shock and distribute pressure felt by a person in daily life. Though the parts may look a little different based of the region, each vertebra has five basic parts: body, vertebral foramen, transverse processes, articular processes and spinous process. Comparison of these parts between the three mobile regions is shown in Tables A.1, A.2 & A.3.
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Figure A-1: Side View of the curvature of the Vertebral Column; from Anatomy & Physiology for Dummies (79)
Table A.1: Typical Cervical Vertebrae (C3-C7); C1 & C2 not included because of their atypical shape; from source Grant’s Atlas of Anatomy (80) Part Distinctive Characteristics Small and wider from side to side than anteroposteriorly; Body superior surface is concave and inferior surface is convex Vertebral foramen Large and triangular Transverse processes Transverse foramina (foramina transversaria); small or absent
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in C7; vertebral arteries and accompanying venous and sympathetic plexuses pass through foramina, except C7, which transmits only small accessory vertebral veins; anterior and posterior tubercles Superior facets directed superoposteriorly; inferior facets Articular processes directed inferoanteriorly; obliquely placed facets are most nearly horizontal in this region Short (C3-C5) and bifid (C3-C5); process of C6 is long but Spinous process that of C7 is longer (for this reason, C7 is called vertebra prominens)
Table A.2: Typical Thoracic Vertebrae (T1-T12); from source Grant’s Atlas of Anatomy (80) Part Distinctive Characteristics Heart-shaped; has one or two costal faces for articulation with Body head of rib Circular and smaller than those of cervical and lumbar Vertebral foramen vertebrae Long and strong and extend posterolaterally; length diminishes Transverse processes from T1-T12 (T1-T10 have transverse costal facets fro articulation with tubercle of a rib) Superior facets directed posteriorly and slightly laterally; Articular processes inferior facets directed anteriorly and slightly medially; plane of facet lies on an arc centered about vertebral body Long and slopes posteroinferiorly; tip extends to level of Spinous process vertebral body below
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Table A.3: Typical Lumbar Vertebrae (L1-L5); from source Grant’s Atlas of Anatomy (80) Part Distinctive Characteristics Body Massive; kidney-shaped when viewed superiorly Triangular; larger than in thoracic vertebrae and smaller than Vertebral foramen in cervical vertebrae Long and slender; accessory process on posterior surface of Transverse processes base of each process Superior facets directed posteromedially (or medially); inferior Articular processes facets directed anterolaterally (or laterally); mamillary process on posterior surface of each superior articular process Spinous process Short and sturdy; thick, broad and hatchet-shaped
As one moves inferior within the column, the vertebra take on slightly different shapes based on their location in the column (Figures A-2, A-3, A-4, A-5). While the sacral and coccygeal regions are fused together, within the cervical, thoracic and lumbar regions each vertebra is separated by a flexible disc. Along with the surrounding ligaments, the intervertebral disc, immediate inferior and superior vertebras are considered as a single motion segment or a functional spinal unit (FSU). Collectively the motion segments throughout the spinal column allow for large range of motion of the spine as well as a support structure for the other body structures a protection of the spinal cord.
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Figure A-2: Cervical Vertebrae (80)
A) Lateral View B) Superior View
Figure A-3: Thoracic Vertebrae (80)
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A) Superior B) Posterior C) Lateral View View View
Figure A-4: Lumbar Vertebrae (80)
A) Anterior View B) Posterior View
Figure A-5: Sacrum and Coccyx (80)
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A.2 Intervertebral Disc
The intervertebral disc has an intricate microstructure with unique mechanical properties that are essential to its ability to absorb and transmit forces as well allow motion and flexibility of the spinal column. The disc is an avascular structure which causes it to have very slow tissue turnover and repair rates. It is also mostly devoid of innervation. There are two distinct regions of the disc; the annulus fibrous and nucleus
nucleus annulus pulposus fibrous
Figure A-6: Intervertebral Disc Cross-Section (81) pulposus (Figure A-6). However as part of the natural aging process, the boundary between the two becomes less distinct. Consisting of several alternating orientated layers, the annulus fibrous provides strength in tension and a secure enclosure for the gel-like nucleus pulpous. The nucleus pulpous and annulus are mainly composed of water, collagen and proteoglycans (Table A.4). Due to it’s extremely high water content, the nucleus creates hydrostatic pressure which maintains the shape and flexibility of the disc as well as a resistance to compression.
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Table A.4: Composition of intervertebral disc; from Basic Orthopaedic Biomechanics & Mechano-Biology (82) Outer Annulus Inner Annulus Nucleus Fibrosus Fibrosus Pulposus Water (per wet weight) 65-75% 75-80% 75-90% Collagen (per dry weight) 75-90% 40-75% 25% Proteoglycans (per dry weight) 10% 20-35% 20-60% Other Proteins (per dry weight) 5-15% 5-40% 15-55%
A.3 Ligamental Tissue
Several ligaments are present along the spine to help hold its motion segments together and protect and limit motion. The spine ligaments consist of the posterior & anterior longitudal ligaments, supraspinous ligament, interspinous ligament and ligamentum flauvm (Figure A-7). The Anterior Longitudal Ligament (ALL) runs the length of the spine from the cervical to the sacral vertebra along the anterior portion of the vertebral bodies. The ALL attaches primarily to the anterior margins of the vertebral bodies, though it does attach secondarily to the concave anterior surfaces present in the lumbar spine. While there are some deep collagen fibres that blend into the periosteum of the concaved areas, the main body of the ligament bridges the concave and the area between is filled with loose areolar tissue, blood vessels and nerves (83) When the ALL spans the intervertebral discs, it is only loosely attached to the annuli fibrosi. The ALL’s primary function is to resist vertical separation of the anterior ends of the vertebral bodies meaning for example in the lumbar region if would function in extension movements resisting anterior bowing.
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Figure A-7: A median sagittal section of the lumbar spine to show its various ligaments. ALL-anterior longitudinal ligament. PLL-posterior longitudinal ligament. SSL- supraspinous ligament. ISL-interspinous ligament: v-ventral part; m-middle part; d-dorsal part. LF-ligamentum flavum, viewed from within the vertebral canal, and in sagittal section at the midline. From Clinical Anatomy of the Lumbar Spine (83)
Similarly to the ALL, the Posterior Longitudal Ligament (PLL) runs the length of the spine along the posterior of the vertebral bodies. The PLL attaches to the vertebra much differently than the ALL. Some fibres of the PLL mesh with the annuli fibrosi, but penetrate through the annuli to attach to the posterior margins of the vertebral bodies
(81) Generally the fibers of the PLL span at least two intervertebral discs. For example,
“starting at the superior margin of one vertebra, they (PLL fibers) attach to the inferior margin of the vertebra two levels above, describing a curve concave laterally as they do so” (83) (Figure A-8). Some of the longer superficial fibers can span up to five vertebra.
Because of its attachment the PLL can exercise its will over several interbody joints. Its main purpose however is to resist separation of the posterior ends of the vertebral bodies.
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Figure A-8: The posterior longitudinal ligament. The dotted lines indicate the span of some of the constituent fibres of the ligament arising from the L5 vertebra. From Clinical Anatomy of the Lumbar Spine (83)
The Ligamentum Flavum (LF) joins consecutive laminae of the vertebra together. The LF is bilaterally symmetrical and each side can be traced into two portions based on its inferior attachment. The superior end a given LF attaches to the lower half of the anterior surface of the lamina and the inferior aspect of the pedicle (Figure A-9).
The medial inferior portion of the LF passes to the back of the next lower lamina and attaches to the area located on the upper quarter of the dorsal surface of the lamina. The lateral inferior portion of the LF passes in front of the zygapophysial joint formed by the two vertebra and attaches to the anterior aspects of that joint. Due to it’s more elastic nature, the LF has been said to aid in restoring the flexed lumbar spine to its extended position as soft of an energy store, although the importance of its function to the mechanics of the lumbar spine for example are unknown.
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Figure A-9: The ligamentum flavum at the L2-3 level, A: posterior view. B: anterior view (from within the vertebral canal). The medial (M) and lateral (L) divisions of the ligament are labelled. The shaded areas depict the sites of attachment of the ligamentum flavum at the levels above and below L2-3. The silhouettes of the lamina and inferior articular processes behind the ligament are indicated by the dotted lines. From Clinical Anatomy of the Lumbar Spine (83)
The Interspinous Ligaments (ISL) connect adjacent spinous processes. Due to the way the fibers are configured, three parts can be identified within each ISL (ventral, middle & dorsal). The ventral fibers pass posterocranially from the dorsal aspect of the
LF to the anterior half of the lower border of the spinous process above. The middle fibers, which form the main part of the ligament, run from the anterior half of the upper border of one spinous process to the posterior half of the lower border of the spinous process above. Finally the dorsal fibers run from the posterior half of the upper border of the lower spinous process then passes behind the posterior border of the upper spinous process to form the Supraspinious Ligament (SSL). The SSL fibers lie on the midline of the body. It is most developed in the upper lumbar region. Since both the ISL and SSL
107 bridge the interspinous gap, they are charged with resisting the separation of the spinous processes and are involved in limiting flexion movements of the intervertebral joint.
Figure A-10: The ventral and dorsal leaves of the intertransverse ligament. D- dorsal leaf. V- ventral leaf. VR- ventral ramus of spinal nerve. MB- medial branch of dorsal ramus. From Clinical Anatomy of the Lumbar Spine (83)
There are also three sets of false ligaments: intertransverse ligaments, transforaminal ligaments and the mamillo-accessory ligaments. The Intertransverse
Ligaments (ITL) span the gap between consecutive transverse processes (Figure A-10).
They are formed by connective tissue that lacks distinct borders. The collagen fibers that form this tissue are not as densely packed and lack the regular orientation seen in true ligaments (83). The ITL are difficult to distinguish from extensions of the tendinous insertions of the segmental muscles and may actually be just that in some regions of the spine (84). However the ITL are most distinct in the lumbar region and can be isolated as membranous bands (84). Transforminal ligaments (TFL) are marrow bands of collagen fibers that span the outer end of the intervertebral foramen, which can be divided into five types based on their attachments (Figure A-11). TFL have an overall
108 occurrence of around 47% (83). TFL can be more correctly identified as bands of fascia but given their general location, they most likely can be viewed as a thickening of the ventral leaf of the intertransverse ligaments. TFL are most frequently found in the lumbar region (84). The final set of false ligaments is the Mamillo-accessory Ligaments
(MAL) (Figure A-12). The MAL are bundles of the collagen fiber of varying thickness that bridge the tips of the ipsilateral mamillary and accessory processes of each lumbar, it is not a true ligament because it connects two points on the same bone. The MAL serve no biomechanical function however they do serve a purpose by covering the medial branch of the dorsal ramus of spinal nerve that runs through the mamillo- accessory notch.
Figure A-11: The transforaminal ligaments. A: Superior and inferior corporotransverse ligaments. B: Superior transforaminal ligament. C: Middle transforaminal ligament. D: Inferior transforaminal ligament. From Clinical Anatomy of the Lumbar Spine (83)
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Figure A-12: The mamillo-accessory ligaments (MAL). MP- mamillary process. AP- accessory process. Note the foramina under the ligaments, through which pass the medial branches of the lumbar dorsal rami. From Clinical Anatomy of the Lumbar Spine (83)
A.4 Muscular Tissue
While ligaments are in place in the spine to limit or protect motion, there are several muscles to provide that motion to the spinal column. The muscles of the lumbar region specifically can be divided into three groups based on functionality: 1) Psoas major and psoas minor, 2) Intertrnsversarii laterals and quadratus lumborum, and 3) the lumbar back muscles.
Psoas major and minor cover the anterolateral aspects of the lumbar spine. Psoas major (Pmaj) originates in the anterolateral aspect of the lumbar spine descends over the edge of the pelvis and inserts into the lesser trochanter of the femur. While its principal
110 action is flexion of the hip, when the thigh is fixed it can act to flex the lumbar spine.
The Pmaj has several attachments to each vertebra of the lumbar spine (Figure A-13).
For each vertebra, it attaches to the medial half of the anterior surface of the transverse process, to the intervertbral disc, the margins of the vertebral bodies adjacent to the disc and to a fibrous arch that connects the upper and lower margins of the lumbar vertebral body. The psoas minor is an inconstant small muscle belly that originates from the T12-
L1 intervertebral disc and forms a very long narrow tendon that inserts into the region of the iliopubic eminence.
Figure A-13: Psoas major (PM) and quadratus lumborum (QL). At each segmental level psoas major attaches to the transverse process, the intervertebral disc and adjacent vertebral margins, and to the tendinous arch covering the vertebral body. The attachments of quadratus lumborum are to the iliac crest (A), the ilio-lumbar ligament (B), the transverse processes (C), and the 12th rib (D). From Clinical Anatomy of the Lumbar Spine (83)
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The intertransversarii laterals (IL) and quaratus lumborum (QL) connect and cover the transverse processes anteriorly. The IL can be divided into pars IL ventrales and IL dorsales. The ventral portion connects the margins of consecutive transverse processes, while the dorsal portion connects an accessory process to the transverse process below (Figure A-14). While the exact function of IL has not been determined experimentally, it can be ascertained that based on their attachments they act synergistically with the QL in lateral bending of the lumbar spine. The QL is a wide, basically rectangular muscle that covers the lateral two-thirds of the anterior surface of the L1 to L4 transverse processes. It originates from the inferior anterior surface of the
12th rib and inserts along the pelvis’s superior edge from the lateral iliac crest to the attachment point of the ilio-lumbar ligament.
Figure A-14: The short, intersegmental muscles. ITLV- intertransversarrii laterales ventrales. ITLD- intertransversarrii laterales dorsales. ITM- intertransversarrii mediales. IS- interspinales. AP- accessory process. MP- mamillary process. MAL- mamillo-accessory ligament. From Clinical Anatomy of the Lumbar Spine (83)
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The lumbar back muscle group lies behind the plane of the transverse processes and exerts action on the lumbar spine. Included in this group are muscles that attach directly to the lumbar vertebra as well as those that do not but that exert action on the lumbar. Based on their morphology this group can be divided farther into 3 subgroups:
1) short intersegmental 2) polysegmental and 3) long polysegmental muscles. The short intersegmental muscles include the interspinales and the intertransversarii mediales which can be seen in Figure A-14 above. The polysegmental muscles attach directly to the lumbar vertebra include the multifidus and the lumbar aspects of longisssimus and iliocostalis. The long polysegmental muscles generally do not attach to the lumbar region from the thoracic above although they do cross the lumbar region from the thoracic levels to find their attachments on the ilium and sacrum. These muscles include the thoracic components of the longissmus and iliocostalis lumborum.
The interspinales lie on either side of the interspinous ligament and connect consecutive spinous processes. They are meant to act in concert with the multifidus to produce rotation. The intertransversarii mediales start from the superior vertebra mamillo-accessory ligament to the superior portion of the mamillary process on the vertebra directly below.
The multifidus is the largest and most medial of the lumbar muscles. It consists of a repeating series of fascicles which start from the laminae and spinous processes of the lumbar vertebra and exhibit a constant pattern of attachments inferiorly (Figure A-
15). The multifidus’s main role is during rotation; however it does not produce the rotation. Its job is to oppose the flexion effect of abdominal muscles as they produce the
113 rotation. Therefore the multifidus acts more as a stabilizing muscle than a motion producing muscle.
Figure A-15: The common fascicles of multifidus. A: The laminar fibres of multifidus. B to F: The fascicles from the L1 to L5 spinous processes respectively. From Clinical Anatomy of the Lumbar Spine (83)
The lumbar aspects of the longissimus and iliocostalis lumborum are more accurately called the longissimus thoracis pars lumborum (LTPL) and Iliocostalis lumborum pars lumborum (ILPL) respectively. The LTPL (Figure A-16) is composed of five fascicles, each beginning from the accessory process and the adjacent medial end of the dorsal surface of the transverse process of a lumbar vertebra. The LTPL can help produce extension based on its vertical line of force. It can also aide in rotation due to its
114 horizontal vector although it is at a mechanical disadvantage due to its location near the axis of rotation. The ILPL consists of four overlying fascicles arising from each lumbar vertebra except for L5. It attaches superiorly at the tip of each transverse process.
Because of its vertical component, the ILPL helps with extension. Due to its horizontal component and position it is better suited than the LTPL for rotation. With both components of its force, it is well suited to work with the multifidus to oppose the flexion effect of abdominal muscles when they act on the trunk.
Figure A-16: The lumbar fibres of longissimus (longissimus thoracis pars lumborum). On the left, the five fascicles of the intant muscles are drawn. On the right, the lines indicate the attachments and span of the fascicles. From Clinical Anatomy of the Lumbar Spine (83)
The thoracic components of the longissimus and iliocostalis lumborum are more accurately called longissimus thoracic pars thoracic (LTPT) and iliocostalis lumborum pars thoracic (ILPT) respectively. The LTPT consists if 11 or 12 pairs of small fascicles starting from the ribs and transverse processes of T1 or T2 down to T12 (Figure A-17).
Due to its more oblique orientation, the LTPT allows for lateral bending of the thoracic column and indirectly therefore the lumbar column as well. The ILPT consists of 115 fascicles that arise from the lower seven or eight ribs (Figure A-18). Because the distance between the ribs and ilium does not shorten much when the trunk rotates but on the opposite of the body, rotation does increases this distance, the ILPT has little action in axial rotation, but serves better to de-rotate the rib cage and in turn the lumbar spine.
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Figure A-17: The thoracic fibres of longissimus (longissimus thoracis pars Figure A-18: The thoracic fibres of thoracis). The intact fascicles are shown iliocostalis lumborum (iliocostalis on the left. The darkened areas represent lumborum pars thoracis). The intact the short muscle bellies of each fascicles. fascicles are shown on the left and their The span of the individual fascicles is span is shown on the right. From indicated on the right. From Clinical Clinical Anatomy of the Lumbar Spine Anatomy of the Lumbar Spine (83) (83)
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Appendix B
Lumbar Biomechanics
While the biomechanics of the spine is unusual and sometimes difficult to predict due to the large number of articulations, it is also unique due to the intervertebral joints flexibility in all six degrees of freedom (82). The spinal column is the most complex part of the human musculoskeletal system (85). Because of this complexity, Lumbar biomechanics will be the focus since this is the section of study. In order to help quantify the spine’s mechanical response to loading and to evaluate possible implants and devices, several techniques have been developed, such as finite element modeling, advanced radiography, optoelectric tracking, in vitro analysis, MRI, detailed clinical reporting and biological characterization (86).
The spine’s natural loading and motions determine its biomechanics. Seeing as the number of muscles crossing in the lumbar section alone exceeds 180, plus each vertebra has its own set of six degrees of freedom (82), one can start to understand why spinal biomechanics is so complex. In order to simplify the motion, each type of loading will be focused on separate and apart from each other. Motions include compression, flexion, extension, axial rotation and lateral bending.
For axial compression, the spine is loaded along its vertical axis which is perpendicular to the discs. In the body, this load is a combination of upper body weight and posterior muscle tension where as for in vivo cadaveric testing a similar amount of
118 load is applied with a follower preload system and/or dead weights. These compressive forces can be much greater than an individual’s body weight during normal daily activities. Some activities can increase the load to over 6000N (87). Due to these large loads the spine can displace, which can be quantified by its stiffness coefficient. Soft tissue degeneration, segment level and size, and bone density are examples of factors that can affect this stiffness coefficient (86). The load is transmitted through the spine as a whole by the disc and facet joints. The disc and facet joints ability to transmit the force is greatly dependant on the structural integrity of each, the segment angulation and disc hydration. The disc carries the majority of the compressive load; however the facets may carry as much as 18% of the load (88). Facet loads may increase though due to a combination of loading conditions on the body and its posture while loading. Disc degeneration as well can affect facet loading.
Flexion, the largest range of motion for the lumbar spine, occurs in the sagittal plane as the anterior side of the vertebral bodies rotates around the pelvis towards the anterior thigh. As the spine flexes, the disc starts to form a wedge as the anterior portion compresses and the posterior portion is forced into tension. All the ligaments of the spine are put into tension except the Anterior Longitudal Ligament (ALL). The facets slide past each other without contacting (89). The spine’s stiffness during flexion has been reported to be about 0.8 Nm/deg (90). Although, failure of the functional spinal unit (FSU) may occur as moments reach as high as 50Nm, physiological moments may be as large as
100Nm (91). These large moments may be balances by muscular contraction that convert some of the moment into axial compression.
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Extension is the direct opposite of flexion and is limited by the facet joints. With elements left intact, stiffness has been reported at about 0.74 deg/Nm, while without the posterior elements, stiffness can lower to 1.1 deg/Nm (86, 92). The only ligament under tension during extension is the ALL while the disc reverses its wedge made by flexion.
Axial rotation results as the spine rotates about its longitudal axis and is in the same plane as the disc. Facet joints in the lumbar spine limit the range of motion. As one facet is under compression the opposite facet experiences tension. The rotational load shared by the ligaments and the disc. Ligaments share about 10% of the total spinal stiffness while the disc’s share is about 45% and yield loads up to 45Nm in axial rotation.
(91).
Lateral bending occurs in the coronal plane and causes the spine to bend to a given side. It can be seen as the lateral side of a vertebra reaches to meet the greater trochanter of the same side. A similar wedge is created as in flexion/extension except its turned 90° towards the side of bending. Lateral bending is resisted by several elements of an individual FSU, such as the intertransverse ligaments, facet capsular ligaments and lateral portions of the annulus. While the ligaments on the side to which the spine is bending are in compression and shortening, the opposite side is under tension and lengthening. Because of the orientation of the facets in the lumbar spine, bending produces slight coupled moment of flexion and axial rotation (90). As was the case with extension, if posterior elements are removed spine stiffness decreases. Lateral bending stiffness decreases from 2.07 Nm/deg to 1.15Nm/deg if the posterior elements are removed.
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Due to the numerous structures of and surrounding the lumbar spine, the range of
motion of the region can be naturally controlled. Unless pushed beyond its failure point, a
ligament in tension can only displace the distance between two points by its natural
length thus limiting the motion. Bony structures such as facers and spinous processes can
restrict motion by surfaces contracting each other. Typical ranges of motion within the
lumbar spine are listed below in Table B.1.
Table B.1: Limits and Representative Values of Ranges of Rotation of the Lumbar Spine; reproduced from Clinical Anatomy of the Lumbar Spine (83). Combined Flexion- One-Side Lateral Bending One-Side Axial Rotation Extension (±X axis (Z axis rotation) (Y axis rotation) rotation) Inter- Limits of Representative Limits of Representative Limits of Representative space Ranges Angle Ranges Angle Ranges Angle (degrees) (degree) (degrees) (degree) (degrees) (degree) L1-L2 5-16 12 3-8 6 1-3 2 L2-L3 8-18 14 3-10 6 1-3 2 L3-L4 6-17 15 4-12 8 1-3 2 L4-L5 9-21 16 3-9 6 1-3 2 L5-S1 10-24 17 2-6 3 0-2 1
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