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This is to certify that the

thesis entitled

THE EFFECTS OF POST-SURGICAL LOADING ON THE BIOMECHANICAL
AND HISTOLOGICAL PROPERTIES OF THE RABBIT PATELLAR TENDON

Date

0-7 639

AFTER REMOVAL OF THE CENTRAL 10% AND 40%

presented by

JEFFREY L. ROBBINS

has been accepted towards fulfillment
of the requirements for

M. 3. degree in BIOMECHANICS

 

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87-5-93

MSU is an Affirmative Action/Equal Opportunity Institution

 

PLACE IN RETURN BOX to mow this chookout from your rococd.
TO AVOID FINES totum on ot bd‘oro dato duo.

DATE DUE DATE DUE DATE DUE

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

MSU Io An Affirm-tin Action/Equal Opportunity Institution
Walla-9.1

 

THE EFFECTS OF POST-SURGICAL LOADING ON THE BIOMECHANICAL
AND HISTOLOGICAL PROPERTIES OF THE RABBIT PATELLAR TENDON
AFTER REMOVAL OF THE CENTRAL 10% AND 40%

BY

Jeffrey L. Robbins

A THESIS

Submitted to
Michigan State University
in partial fulfillment of the requirements
for the degree

MASTER OF SCIENCE

Department of Biomechanics

1993

ABSTRACT
THE EFFECTS OF POST-SURGICAL LOADING ON THE BIOMECHANICAL

AND HISTOLOGICAL PROPERTIES OF THE RABBIT PATELLAR TENDON
AFTER REMOVAL OF THE CENTRAL 10% AND 40%

BY

Jeffrey L. Robbins

Complications of using the central one-third of the
patellar tendon as autogenous tissue for anterior cruciate
ligament reconstruction may result from excessive
hypertrophic scarring of the host patellar tendon. It is
possible that this damage is a result of increased stresses
generated in the host patellar tendon after removal of a
portion for ligament reconstruction. In the present
research, this hypothesis is tested by increasing the
stresses in the rabbit patellar tendon by removing the
central 10% and 40% of the tendon prior to subjecting the
animal to post surgical exercise on a treadmill. In
addition, one group of rabbits with the central 40% removed
had a stress shielding device implanted to protect the host
tendon from stresses during exercise. The biomechanical and
histological properties of the tendons with the central 10%
removed closely resembled those of the contralateral control
tendons. vThe tendons with the central 40% removed showed
significant hypertrophy and decreased material properties.
Stress shielding of the tendon prevented scar formation but

encouraged disuse atrophy of the tendon.

mmms

First and foremost, I thank Roger C. Haut, Ph.D., for
his guidance, expertise, and the support he has given me
throughout this project and my entire master's program. I
would also like to sincerely thank my parents, Leo and
Margaret Robbins, for their encouragement and support during
my graduate studies. Thank you Jennifer for your love,
caring, and support which has been greatly needed and
appreciated during this project.

I would like to thank the committee members for serving
on my thesis defense: Dr. Charlie DeCamp, Dr. Robert
Hubbard, and Dr. Roger Haut for the support they have shown
throughout my program and while preparing this thesis.

Just as important, I would like to thank the following
people for assisting in the completion of this thesis during
the twentieth century: Dr. Charlie DeCamp for his surgical
expertise, Jean Atkinson for her work with the rabbits,
Cliff Beckett for being available everytime I touched a
computer, Tom Cooper for his assistance on MRI, Jane Walsh
for her superior work on the histology slides, Tammy Haut
for all the work she has done for me over the last two
years, Hai Gu for the math model work, Sharon Husch and

Brenda Robinson for answering all my questions when asked.

iii

TABLE OF CONTENTS

Page No.
LIST OF TABLES ....................................... Vi
LIST OF FIGURES ...................................... Vii
Chapter
I. INTRODUCTION ................................. 1
II. SURVEY OF LITERATURE ......................... 7
Autogenous Tissues ......................... 10
Surgical Procedures ........................ 13
Clinical Relevance ......................... 15
Previous Animal Model Studies .............. l7
Structures of Tendons and Ligaments ........ 22
Biomechanics of Tendons and Ligaments ...... 24
Repair Mechanism ........................... 26
Immobilization versus Exercise ............. 28
Significance of Present Research ........... 33
III. MATERIALS AND METHODS ........................ 34
Tendon Preparation ......................... 34
Mechanical Test Preparation ................ 36
Pre-Conditioning ........................... 41
Tensile Tests .............................. 42
Microstructural Model ...................... 43
Magnetic Resonance Imaging ................. 45
Rabbit Studies ........................ 45
Human Studies ......................... 46
Histology .................................. 47
Fat Pads .............................. 47
Tendons ............................... 48
Statistics ................................. 49
IV. RESULTS ...................................... 50
Control Data ............................... 51
Tissue Dimensions .......................... 51
Structural Properties ...................... 54
Mechanical Properties ...................... 58
Microstructural Model ...................... 60
Histology .................................. 63
Fat Pads .............................. 63
Tendons ............................... 66
Magnetic Resonance Imaging ................. 72
Rabbit Studies ........................ 72
Human Case Studies .................... 72
Human Study ........................... 74

iv

V. DISCUSSION .................................... 78

VI. CONCLUSIONS ................................... 86
VII. REFERENCES .................................... 87
VIII. APPENDICES .................................... 96
Appendix A ................................. 96

Appendix B ................................. 100

Appendix C ................................. 104

Appendix D ................................. 108

LIST OF TABLES

Page

Table 1. Tissue Dimensions of Control and

Surgical Tendons ......................... 54
Table 2. Mechanical Properties of Control and

Surgical Tendons ......................... 55
Table 3. Structural Properties of Control

Surgical Tendons ......................... 58
Table 4. Curve Fitting Parameters for Tendons at 6

Weeks .................................... 63

vi

Figure

Figure
Figure
Figure

Figure

Figure

Figure
Figure
Figure

Figure

Figure
Figure
Figure
Figure
Figure
Figure
Figure
Figure
Figure

Figure

10.

11.
12.
13.
14.
15.
16.
17.
18.
19.
20.

LIST OF FIGURES
Page

ACL location in knee,and attachment sites.... 2
(Arnoczky)

Possible mechanism for injury to ACL(Kennedy).3
Load deformation curve for safety zones(Noyes)8
Graph human patellar tendon vs. ACL (Noyes)..ll

Stress strain curves for human ligaments
versus patellar tendon (Butler) ............ 12

Stress strain curves for most medial to

lateral subunits for human PT (Chun) ....... 13
Mechanics of central defect (Linder) ......... 20
Collagen molecule (Nordin/Frankel) ........... 23
Tensile response collagenous tissue(Noyes)...25

Fibroblast orientation in tendons and
ligaments (Nordin/Frankel) ................. 27

Homeostatic responses of soft tissues (Woo)..29
Homeostatic responses to activities (Woo)....30
Implanted stress shielding device ............ 35

Potted patella-patellar tendon-tibia complex.37

Tendon dimension measurements ................ 38
Patella-tendon-tibia complex ................. 40
Stiffness from load-deformation curve ........ 42
Tendon crimp organization .................... 44
Histogram of C.S.A ........................... 53
Histogram of structural stiffness ............ 56

vii

Figure
Figure
Figure
Figure
Figure

Figure

Figure

Figure

Figure

Figure

Figure

Figure

Figure

Figure

Figure

Figure

21.
22.
23.
24.
25.

26.

27.

28.

29.

30.

31.

32.

33.

34.

35.

36.

Histogram of tensile modulus ................. 59
Experimental data and model fit .............. 60
Estimated "toe" region and stiffness ......... 61
Estimated "toe" region and tensile modulus...62
Histologic representation of control fat pad.64
Histologic representation of infrapatellar

fat pad, 10% removed ....................... 65
Histologic representation of infrapatellar

fat pad, 40% removed non-hypertrophic ...... 65
Histologic representation of infrapatellar

fat pad, 40% removed ....................... 66
Histologic representation of infrapatellar

fat pad, 40% with stress shielding ......... 67

Histologic representation of cross section
of control tendon .......................... 68

Histologic representation of cross section
of 10% removed tendon ...................... 69

Cross section of non-hypertrophic tendon ..... 7O

Histologic representation of tendon with
40% removed and stress shielding device....71

Histologic representation of tendon with
40% removed and no device .................. 72

Control and test, T—l weighted image of
human with reconstructed central one-third.75

Control and test, T-l weighted image of
human with reconstructed central one—third.77

viii

I. INTRODUCTION

The knee is the most vulnerable of the large joints in
the body. Located between the two longest lever arms in the
body, it is often subjected to large mechanical forces and
motions. The functions of the knee include transmitting
loads, participating in motion, assisting in the
conservation of momentum, and providing a force couple for
activities that involve the leg. Kinematically, the knee
rotates primarily in the sagittal and transverse planes.
The sagittal plane, in which flexion and extension of the
leg occur, is the most dominant plane of motion. Secondly,
is the transverse plane of motion in which internal and
external rotation of the knee occurs causing the helical
screw axis phenomenon. Unlike the hip and shoulder, the
knee is primarily a hinged joint with rotation and sliding
that occurs during movement through its full range of
motion.

Frequently, the knee must sustain loads of two to three
times bodyweight. With the supporting structures of the
knee being composed primarily of soft tissues like tendons,
ligaments, and menisci, it is highly susceptible to injury.
These soft tissues are also important in maintaining normal

stability and alignment of the knee during motion.

Insufficiency of the ACL is the most common cause of
knee instability30. The ACL attaches to the posterior
femoral condyle and the anterior tibial plateau. The
primary biomechanical function of the ACL is to resist, in
various degrees of flexion, abnormal anterior displacement

of the tibia in relation to the femur (Figure 1).

 
   

 
  
 

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Figure 1: Location of the ACL in the knee and showing
attachment sites. (taken from Arnoczky, 1983)

Midsubstance tears of the ACL occur due to excessive loads
being quickly applied to the knee. These are usually caused
by a deceleration, or "cutting" action of the knee joint34.
Other mechanisms of injury causing failure of the ACL
include external rotation and abduction of the leg at the
knee joint, which occurs in skiing accidents (Figure 2), a
direct posterior blow causing an anteriorly directed force
on the tibia similar to the force generated during clipping
in football, and lastly, complete dislocation of the knee

joint caused by excessive hyperextension of the kneeso.

Isolated tear Anterior Cruciate
\

 

Figure 2: Possible mechanism for injury to the ACL
(taken from Kennedy, 1974)

Failure to repair a torn ACL will result in knee
instability, along with degenerative changes in the knee
joint, and an increasing possibility of subsequent cartilage
and menisci damage.

ACL reconstructions have been performed using a variety
of techniques and tissues, each with their advantages and
disadvantages. Whether the medial or central portion of the
patellar tendon is used for ACL reconstruction varies among
orthopaedic surgeons. However, the biomechanical properties
of the central one-third of the human patellar tendon are
superior to those of the medial one third. Its strength and
accessibility has made this one—third portion of the
patellar tendon the most common candidate for autogenous
reconstruction of the ACL3'25'28'33'47'69.

Todays trend of rehabilitation programs by most
physicians, following ACL reconstruction using the central
one—third of the patellar tendon, leans toward an aggressive
physical therapy regimen. Many programs developed today
consist of muscle strengthening and range of motion
exercises to accelerate rehabilitation and increase knee

66,73,88.

stability However, these accelerated

rehabilitation may cause increased stresses on the already
surgically traumatized host patellar tendon. Increased scar
formation, in addition to increases in cross-sectional area

of the host patellar tendon, have been seen in recent

studies involving animal mode1518'43, as well as, human

16,70_

subjects Clinical studies involving magnetic

resonance imaging have shown increases in cross-sectional
areas of the host patellar tendon, when compared to
contralateral controls 12 to 24 months after ACL
reconstruction using the central one—third of the patellar
tendon16'70.

This thesis will investigate the histological and
biomechanical changes of the rabbit patellar tendon observed
after removal of its central one—third. These changes
include a significant amount of hypertrophic scarring often
seen in the host tendon after exercise
rehabilitation16'18'43'54. It is hypothesized that
increased stresses generated in the host patellar tendon
during exercise rehabilitation may structurally degrade the
remaining patellar tendon. This in turn may cause an
increase in collagen synthesis to accommodate the decreased
material properties of the damaged host tendon.

The increase in stresses of the surgical patellar
tendon were accomplished by removing the central 10% and 40%
of the rabbit patellar tendon from different groups of
animals. The rabbits were subjected to a six week
rehabilitation program in which they were exercised on a
treadmill for approximately 10 to 15 minutes daily. In
addition, this thesis will present test data of a group of
rabbits which had a stress shielding device implanted, in
vivo, after removal of the central 40%. This augmentation
device will completely unload the host patellar tendon of

any stresses generated during exercise. -Finally, the amount

of hypertrophic scarring of the host patellar tendon will be
monitored with the use of magnetic resonance images taken
one week after surgery, and again at sacrifice.

In addition, included in this thesis is two case
reports presented on patients with quite different post—
surgical rehabilitation programs. The surgical and
contralateral legs of each patient were scanned by magnetic
resonance imaging six months after ACL reconstruction using
the central one-third of the patellar tendon. The objective
was to determine if the patient with a more accelerated
rehabilitation program incurred significantly more scar
tissue formation in the host patellar tendon when compared
to a patient that took a much less aggressive approach to

rehabilitation of the surgical limb.

II. SURVEY OF LITERATURE

The ACL provides approximately 86% of the total
resisting force to anterior displacement of the tibia on the

23.

femur Chen and Black26 estimate the tensile forces in

the human ACL during normal function range from 67 N for
walking, to as high as 630 N for jogging. Grood and Noyes4O
calculated values of 200-400 N for young humans and 80-160 N
for older humans, by assuming that the normal forces range
from one-tenth to one-fifth of the breaking loads.
Morrison62 estimated forces in the ACL to be 67 N for
ascending a ramp, and as high as 445 N for descending a
ramp. To provide a factor of safety, it is important that
the autogenous tissue strength is greater than the forces
that it will be subjected to during normal and strenuous

64'67 (Figure 3).

activities
It is also important to account for the weakening of
the graft, due to tissue incorporation, after implantation

24'60. For example, Noyes et

of the replacement tissue
al.,65 had found that patellar tendon grafts in primates
drop 15% of their pre-implantation strength by six weeks
after surgery. This decrease in strength of the autograft

is the primary reason that one-third of patellar tendon is

often used for ACL reconstruction.

Most studies on the fate of intra-articular ligament
reconstruction have shown the graft to have a prolonged
weakness that requires a year or more to regain structural
strength4'11'29. Experimental, and clinical, studies
suggest that the patellar tendon grafts do survive within
the joint and are functionally adequate replacements for the
ACL. The structural strength of the tendon is directly
related to its physical size and inherent mechanical
properties. Long—term survival of these grafts are

dependent on revascularization of the transplanted tissue.

 

SAFETY
2000.. FAILURE ZONES

1730N ULTIMATE
13891...) STRENGTH

INITIAL

FAILURE
paHMI
Ioafing

STRENUOUS
ACTIVITY

- FORCES
445 N UPPER LIMIT .

(100 lbs.) , NORMAL
ACTIVITY
FORCES

I I I I
5 10 15 20

ELONGATION (mm)

 

1500-«

FORCE

N
( ) 1000-*

    

500-

 

 

 

 

Figure 3: Hypothetical load-deformation curve for
safety zones of the anterior cruciate
ligament. (taken from Noyes, 1984)

Arnoczky, et al.,12 in a study which used the medial one-
third of the patellar tendon for ACL replacement in dogs,
found that by 6 weeks after surgery the grafts were
completely ensheathed in a vascular synovial envelope, and
histologically showed avascular necrosis.

The vascular anatomy of the cruciate ligaments in

11 and in rabbits81

dogs was studied using microangiography.
The microvascular anatomy of the infrapatellar fat pad and
the synovial membrane in both dogs and rabbits were found to
be quite highly vascular. The blood supply to the cruciate
ligaments in Arnoczky's study was found to originate
predominantly from the infrapatellar fat pad and synovial
membranes of the joint. Intrinsic revascularization of the
patellar tendon autograft progressed from the proximal and
distal portion of the graft towards the center. One year
after surgery the vascular and histological appearance of
the patellar tendon graft resembled that of the normal ACL.
In a recent study by Horibe, et al.,44 it was shown that the
primary blood supply to the reconstructed ACL comes
primarily from the bone marrow, and secondly from the
infrapatellar fat pad and synovial tissues. The importance
of getting nutrients and a blood supply to the graft tissue
cannot be overlooked. It is therefore necessary to consider

the effects of ACL reconstructive surgery on the

infrapatellar fat pad.

10

We

There are many types of collagenous tissues available
in the human body for intra—articular and extra-articular
ligament reconstruction. The human patellar tendon
properties are far superior to most structures in the area.
The human patellar tendon grafts are extracted as a bone—
patellar tendon-bone complex allowing bone to bone fixation
in the knee. The patellar tendon autografts also show a
strong ability to revascularize and survive within the knee
joint after ACL reconstructionll. Few studies discuss
injury to the patellar tendon after this surgical

17'61. Some disadvantages of ACL reconstruction

procedure
using the central one third of the patellar tendon include a
loss of quadriceps strength of 15-20% at two years post
surgery, and a decrease in full range of motion73'74.
A previous study looked at the mechanical properties of
human patellar tendon graftss4. In this study they found
that the central one-third of the human patellar tendon was
far superior to all other graft tissues in both strength and
structure. Their results indicate that the central and
medial one-third sections of the human patellar tendon are
175% and 163%, respectively, stronger than the mean strength
of the human anterior cruciate ligament (Figure 4). In
comparison, the semitendinosus and gracilis tendons have

only 75% and 49%, respectively, the strength of the human

anterior cruciate ligament.

ll

  
    

4000 f

MEDIAL PATELLAR
3000 - ’ TENDON-BONE UNIT
2000 -

ACL-BONE
UNIT

FORCE (N)

1000

 

 

 

. I l.

O 5 TO T5 20
ELONGATION (mm)

Figure 4: Graph of human patellar tendon vs ACL (Taken from
Noyes, Ref. 64)

Butler, et al.,22 also found that the maximum strain levels

at failure were approximately 13—15% for both the anterior

cruciate ligament and patellar tendon in humans (Figure 5).

The bone-patellar tendon-bone units of the patellar tendon

were also found to be three to four times stiffer than the

anterior cruciate ligament itself. This allows a factor of

l2

safety for the decrease in properties often seen during the

revascularization period.

 

 

64~ PT
48-4
m ACL
§ PCL
tn
LLI
CI:
’—
U)
LCL
16 .
0 1 I T I 1
0 5 IO 15 20 25
STRAIN 96

Figure 5: Stress-Strain curves for selected human ligaments
versus the human patellar tendon. (Taken from
Butler, Ref. 22)

Chun, et al.,27 tested the material properties of the human
patellar tendon in subunits. The human patellar tendon was
divided into six equally spaced fascicles of bone-patellar
tendon-bone units (Figure 6). The results indicate that the

lateral and central thirds of the human patellar tendon have

13

a modulus that is twice that of the most medial one—sixth of

the human patellar tendon.

70.0

“1.0
50.0
40.0

30.0

STRESS (MP8)

20.0

10.0

 

F‘IIIITITWIIITTITTIFIITITITTTTITIfl1

 

3;

 

D
D
O
O
N
O
B
In
D
O

STRAIN (96)

Figure 6: Stress vs. strain curves for the most medial (A)
to most lateral (F) subunits of human PT. (Taken
from Chun, 1989).

Surgical Procedure

In 1963, Jones outlined a surgical procedure for
reconstruction'of the anterior cruciate ligament. This
procedure uses the central one—third of the patellar tendon
as an autograft tissue, a procedure that is still currently

used by many physicians47'48. Butler, et

14
al.,30'45'51'59'70'74'82'88 and others are proponents of the
autogenous patellar tendon graft, citing it as a superior
substitute from a biomechanical standpoint. Its tensile
strength and durability as a scaffold allow for adequate
revascularization and subsequent proliferation of a new
ligamentous tissue.

The usual width of the patellar tendon graft ranges
from 10-13 millimeters, representing approximately one-third
of the existing tendon. The two primary concerns in A
selecting the width of the host tissue is to not disturb
patellofemoral tracking, and to prevent tissue rupture in
the remaining patellar tendon. Bonamo, et al.,17 has
documented cases of rupture of the patellar tendon after
removal of its central one-third. Sachs, et al.,71 has
documented patellofemoral problems, including flexion
contracture, and patellofemoral pain after removal of the
central one-third of the patellar tendon for ACL
reconstruction. On the contrary, a recent study indicates
patellofemoral contact pressures immediately after
harvesting of the central one-third patellar tendon showed
no significant alterations in patellofemoral contact
pressures or pressure distribution32.

Support for using the central one-third of the patellar
tendon currently comes from its superior biomechanical
properties and its lack of disturbing the patellofemoral
contact pressure321'32. Conversely, critics of using the

central portion of the patellar tendon cite problems ranging

15

from loss of quadriceps strength and failure to maintain
normal thigh circumference7l'74. While most experimental
studies focus on the strength and composition of the
intrarticular graft, few look at changes and effects of the
surgery on the patellar tendon itself. Clinically
documented loss of quadriceps strength and decreases in
range of limb motion have been suggested to be in part
related to inferior performance of the host patellar tendon

after removal of its central one-thirdlB.

glinicg; Relevange

Yasuda, et al.,88 performed quantitative evaluations of
knee instability and muscle strength after ACL
reconstruction using the central one—third of the patellar
tendon. Measurements were performed on 65 patients who were
followed for 3 to 7 years. The authors checked for knee
instability of each patient and found that 89% of the
patients had differences of less than 2.5 mm between
operated and non-operated knees. Quadriceps strength was
measured with Cybex testing equipment and was found to be
less than 50% the strength on the uninjured knee three
months post-surgery. In men, quadriceps strength returned
to only 85% at final follow-up. In women, quadriceps
strength was only 70% the strength of the non—injured leg at
final follow-up. The authors felt that although using the
central one-third of the patellar tendon achieves good

stability, quadriceps weakness occurs as a result of damage

16

to the knee extensor mechanism. Sachs, et al.,71 also
compared a group of patients with patellar tendon
autografts, to a group with semitendinosus autografts.
Again, the patellar tendon group had a significant reduction
in quadriceps strength at 1 year post-surgery. Tibone and
Antich74 performed a two year evaluation of patients who had
an intra-articular ACL reconstruction using the central one-
third of the patellar tendon. Again, a decrease of
approximately 15-20% of quadriceps strength was noted.

The current trend in rehabilitation is a more
aggressive approach to regain range of motion, and muscle
strengthening as soon as possible. Recently, Shelbourne and
Nitz73 looked at two groups of patients that were subjected
to different rehabilitation regimens. In their study two
groups were divided into an "aggressive" rehabilitation
group and a "passive" rehabilitation group. All 450
patients in the study had an autogenous ACL reconstruction
using the central one-third of the patellar tendon.
Quadriceps strength and knee laxity were the parameters
measured in the study. The results indicate that after a
one year rehabilitation program there still remained a
decrease in quadriceps strength of the surgical leg of
approximately 10% in both groups73.

Berg recently reported a case study that indicated
uniform hypertrophic scar tissue formation in a patient
eight months after removal of the central one—third of the

patellar tendon for autogenous reconstruction of a torn

17

anterior cruciate ligamentl6. Despite an active life style
and extensive physical therapy, the patient had a limited
range of motion, walked with a limp, and had a 1.5 cm of
measured thigh atrophy six months after surgery. Post—
operatively the patient had continuous passive motion and
was allowed partial weight-bearing after one month. Fearing
infrapatellar contracture syndrome, the knee was re—Opened
to find that the central defect had filled and the
infrapatellar fat pad was atrophic. Magnetic resonance
images of the knee indicated that the cross—section of the
patellar tendon had uniformly hypertrophied to approximately
twice that of the contralateral control tendon. The fat pad

was not distinguishable from the adjacent tissue.

W

A recent study by Burks, et al.,18 indicates that a
significant amount of hypertrophic scar tissue is observed
in the dog patellar tendon six months after removal of its
central one-third. While the mechanical properties of the
healing tendon are significantly less than controls, the
cross—section is found to be uniformly hypertrophic and
approximately 4.5 times larger than the contralateral
control tendons. The structural stiffness and tensile
modulus of the operated tendon within the physiologic range
were reduced to 70% and 33% of controls at 6 months post
surgery, respectively. The authors also found a shortening

of the patellar tendon of dogs three months after removal of

18

the central one-third of the patellar tendon. Upon gross
inspection it was found that in all tendons the defect was
filled completely with scar tissue. Histologically, at 3
and 6 months after surgery, a haphazard arrangement of
collagen was noted throughout the entire tendon cross
section, interwoven with more normal appearing patellar
tendon.

A study performed by Cabaud, et al.,24 in which the
medial one~third of the patellar tendon was removed from
dogs, had results that differed significantly than those of
Burks. Failure testing of control and operated tendons
showed slight decreases in strength and stiffness at 4
months. Cabaud found no abnormalities on gross inspection
except for thickening of the undersurface where the fat pad
had been dissected. Cross-sectional areas of the tendons
did not differ significantly from control tendons.

54 also investigated the

A recent study by Linder
removal of the medial one-third of the canine patellar
tendon. Linder's results also differed significantly when
compared to the results found by Cabaud. Linder found that
at six months post surgery the operated tendons using the
medial procedure had inferior structural and mechanical
properties and a large increase in cross-sectional area when
compared to controls. The suggested differences in test
results were that Linder's dogs were allowed unrestricted

activity immediately following surgery. In contrast,

Cabaud's dogs were immobilized for six weeks immediately

19

following surgery, thus allowing time for the patellar
tendon to develop sufficient scar tissue.

Recently Haut, et al.,43 studied the effect of
immobilization versus enforced exercise on the amount of
hypertrophic scarring of the host patellar tendon. The
animal models used in Haut's study were subjected to an
aggressive exercise rehabilitation, or pin immobilized,
after removal of the central one—third of the patellar
tendon. Haut, much like Burks, also found an increase in
cross-sectional area of 3.5 times in the operated tendons of
the exercised group of rabbits when compared to
contralateral control tendons three months after surgery.

In contrast to the Burks study in which the length of the
operated tendons decreased by 10%, Haut found a 12%
lengthening of the operated patellar tendons in the
exercised animals. The tendons from the animals with the
pin immobilized legs showed very little scar formation in
the operated tendons. The surgical leg was immobilized by
inserting a Steinmann pin through the femur and tibial shaft
after removal of the central one-third of the patellar
tendon. The cross-sectional area of the immobilized tendons
were not found to differ significantly from control tendons.

Burks suggested that the knee is put at a double
disadvantage after ACL reconstruction because of patellar
tendon shortening and the decreased material properties of
the remaining tendon. Van Eijden, et al.,77 used a

mathematical model to look at the effects of changes in

20

length of the patellar tendon. They found that a short
patellar tendon increased proximal tendofemoral compression
pressures, increased anterior translation force on the tibia
near full extension, and indicated a greater muscle force
was needed to generate the same extensor moment toward
terminal extension. Burk's suggested this effect as a

possible reason for the clinical observations of decreased

quadriceps strength.

ORKNNAL CENTRAL
TENDON DEFECT
uncemuso uncsiweo

PI Fl

 

 

 

 

 

 

 

 

 

 

 

 

 

// // // //

Assume length and area oi each third l5 constant

F=F. Iii-IFl F=E +F,
8 =F,/E =F1/E =Ii/E <5 =Fn/E =F5/E
F, =2/5 F F,=2/3 F (67°/o INCREASE)
F1=2/5 F F5=1/3 F (67% INCREASE)
FS=IIS F
Figure 7: Mechanics of the tendon after removal of the
central defect. (taken from Linder, 1992)

One explanation for the observed hypertrophic scar

formation may be the mathematical concept developed by

21

Linder54 (Figure 7). This mathematical model considered the
variations in tensile stiffnesses across the thirds of the
patellar tendons. In the human patellar tendon the tensile
modulii of the central and lateral thirds are approximately
twice that of the medial one-third27. When the central one—
third of the patellar tendon is removed, as in Burk's study,
the stresses in the remaining two-thirds may become
excessive. Linder suggested that the increased stresses in
the remaining tendon after removal of the central one-third
may result in micro-damages of the remaining collagen
fibers. This overstressing may act as a stimulant for
fibroblasts to synthesize more new collagen fibers after
removal of the central one—third to compensate for the
detected increase in internal stresses.

This mathematical concept may explain the differences
observed in the immobilized and exercised tendons in the
previously mentioned study by Haut43. A previous study by
Frank, et al.,36 also found the collagen alignment in
ligaments of pin immobilized legs to be superior than non—
immobilized legs. Viidik, et al.,79 suggests that tension
in a tissue is likely to influence the alignment of its
components. The tendons of the pin immobilized rabbits were
subjected to low level isometric stresses throughout the
three month rehabilitation period. Therefore, these

uniaxial stresses may assist in the alignment of the newly

synthesized collagen fibers. These well organized fibers

22

may be the reason for the decreased amounts of hypertrophic

scar tissue observed in the pin immobilized tendons36'43.

e o T

The structure and chemical composition of ligaments and
tendons are almost identical in humans and in many animal
species such as rats, dogs, rabbits, and monkeys.
Therefore, extrapolations regarding these structures in
humans can be made from the results of studies on animal
specieslo.

Tendons and ligaments are constructed primarily of type
I collagen (75%) and elastin (15%), and a ground substance
composed of proteoglycans with some degree of cellularity.
Tendons and ligaments are subjected, under physiological
conditions, to stresses of approximately one-third of their
ultimate tensile strength. They are furthermore non-linear,
viscoelastic materials. The collagen fibers in tendons are
aligned in a nearly parallel orientation which makes them
suitable to withstand high, unidirectional, tensile loads.
Ligaments however, have collagen fibers that may be somewhat
less parallel, but are closely interlaced with each other.
The collagen molecule is synthesized by fibroblastic cells.
Collagen molecules are formed by three alpha chains combined
in a right hand triple helix which gives collagen its
rodlike shape. The size of the collagen molecule is
approximately 280 nm in length and 1.5 nm in diameter

(Figure 8). The collagen molecules aggregate in the

23

extracellular matrix to form microfibrils and then fibrils.
Cross links are formed between collagen molecules and it is
these cross links that gives strength to tissue and allows

them to function under mechanical stress.

 

 

OVERLAPZONE

 

 

 

 

 

 

I

I

i .
THOLEZONE MICROFIBRILS
t

r

l

l
A

 

 

 

 

 

 

 

_ J
PACKING OF r
MOLECULES t g —-
r—7 I
// \\\
/// \\\
COLLAGEN [14/ 280nm :73
MOLECULE ~ 1 r J

TRIPLE
HELD<

 

Schematic diagram of collagen molecule.
(taken from Nordin/Frankel, 1989)

Figure 8:

24

Since collagen alignment is more organized in tendons than
ligaments, tendons have a shorter deformation prior to
reaching the linear region when a tensile load is applied.
Recall, in Figure 3, the shift in tensile response between
the patellar tendon complex and the ACL64. This shift is
likely caused by differences in the alignment of the
constituent collagen fibers and content of these fibers

between the patellar tendon and ACL.

Biomecgagicg of Tendons and Ligaments

Biomechanical properties of collagenous tissue can be
described using a tensile response curve (Figure 9). The
initial concave portion of the curve, region I of the graph,
represents the "toe" region. The sequential uncrimping and
progressive recruitment of relaxed collagen fibers occurs in
this region. It is within the "toe" region that most
physiological activities and clinical diagnosis takes
place63. Haut and Little reported the "toe" region to have
a strain value between 1.5 and 4.0%. This is where tissue
preconditioning is often performed prior to tensile tests42.

Region II is the "linear region" of the curve. The
collagen fibers are further elongated in the linear region
until first significant failure occurs at the linear load
point63.

In region III, a maximum loading occurs in which a

series of small, sudden, force drops and fiber separations

occur until maximum force is reached. At this point a

25

catastrophic failure of the tissue occurs. Finally region
IV, the post-failure region, the tissue loses its load
carrying capability even though some fibers may still appear

to be intact.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

|

III:I/ I/IK| l(| y! I I I TI I III/ I

1'55) I'lll‘éll'l ll;|\l
/ I ‘I '
wt Ii:§ I |\| I I V I I : I! : II; tl

I'(/ I/lII|\ 'I ll ’Ipl

IIgf\. I"'|I(I.lII"I/I

l l/'/ I I I I \ I . I |(

. III...I)_II H lqu
elastmloaded. I ' l I H | I I\ '
collagen elnstlnloaded. . I I I

Unc'impmg some cottagonlondod I elnstlnloaded. ‘
I all collagen loaded 9'35"" loaded.
' some collagen Ialls

 

A

 

 

Load

 

 

ElongaHon

Figure 9: Tensile response of curve of a collagenous
tissue. (taken from Noyes, 1977)

26

W
When damage to a soft tissue occurs there are three
primary phases of repair13. They include inflammation,

fibroproliferation, and subsequent remodeling of the tissue.
Inflammation involves a series of cellular mechanisms that
produce an increase in vascular permeability and the
accumulation of leukocytes, mostly neutrophils, and
macrophages to begin the process of decontamination and
debribement of the woundl3. Manske and Gelberman58 found
that the surface layer of epitenon cells that migrate into a
laceration site assume a phagocytic role, engulfing debris
and old collagen fragments. Garner, et al.,38 indicated
that the epitenon cells also participate in collagen
synthesis. Within three days after injury there is a
migration of fibroblasts and endothelial cells into the
defect that occurs in response to chemotactic factors. The
fibroblasts began to proliferate and synthesize an abundant
matrix, mainly in the form of type III collagen. During the
final stages of healing there is a gradual shift from type
III collagen to type I collagen. The type I collagen is
then progressively cross linked to provide tensile strength.
Lindsay, et al.,55 documented the events that occur
after a laceration of the flexor tendon. Granulation tissue
from the synovial sheath migrates into the wound gap along
with fibroblasts derived from both extrinsic and intrinsic
cells from the epitenon and endotenon during the first days

after injury. Many of the cells proliferating to the injury

27

site have a phagocytic function. The fibroblasts in the
wound lie perpendicular to the long axis of the tendon and
by the fifth day actively secrete collagen. These fibrils
are initially disorganized and are primarily aligned in a
plane that is perpendicular to the axis of the tendon. The
fibroblasts in the wound eventually align themselves with
the long axis of the tendon, likely as a result of stress.

Fibroblasts in tendons and ligaments are arranged in
long parallel rows in the spaces between the collagen

bundles (Figure 10).

 

 

 

 

 

 

 

 

   

   

NEARUYPARALLEL
BUNDLES OF
COLLAGENIUBERS

PARALLELBUNDLESCW
COLLAGENIUBERS

%

HBROBLASTS

   

HBHOBLASTS
TENDON UGAMENT

Figure 10: Fibroblast orientation in tendons and ligaments
(taken from Nordin/Frankel)

28

Several tendon bundles form the tendon fascicle, which is
surrounded by endotenon, and a number of fascicles are
surrounded by epitenon to form a basic tendon unit. An
elastic sleeve called paratenon surrounds the unit.
Functional alignment of collagen is usually complete
after 2 months. Although scar tissue never achieves the
strength of the original tendon, the remodeling phase can be
influenced by load bearing and mechanical stimulation. The
ultimate tensile strength of a connective tissue, and the
mass average diameter of the constituent collagen fibrils
have shown a positive correlation. Parry, et al.,68
hypothesized that the ultimate size of the collagen fibrils
in a tissue is dependent on the amount of stress under which
the tissue functions. Consequently, large collagen fibril
diameters are predicted to have a greater tensile strength

than small diameter fibrils.

mm

The universal goal of all orthopaedic treatments is for
conditions involving ligamentous deficiency to reproduce or
replace, as quickly as possible, the unique properties of

35. A superior

the normal bone-ligament-bone complexes
system for ACL reconstruction would be to maximize graft
strength and durability, without affecting the biomechanics
of the joint. This theory also holds true for the host

patellar tendon.

29

Occrcasc tncrcbsc

._—*—
Stress SirtSI

+_.

thslotoq'Ic
ACTIVIIIC‘

Immobitiufion Excrcit‘t

 

MECHANICAL PROPEHIIES
MASS

VMDO

 

STRESS AHO STRAMI
DURAHON

Figure 11: Homeostatic responses of biological soft tissues
(taken from Woo, 1982)

In a stress induced and immobilized ligament model Woo
documents that a relationship exits between strain levels
and soft tissue homeostasis46'85. Whereas complete
immobilization results in a rapid reduction of tissue
strength, exercise tends to increase mechanical properties
and mass of the tissue85. Woo developed the curve shown in
Figure 11 that represents the stress and motion dependent
homeostatic responses of biological soft tissues. Figure 12
depicts the effects of immobilization, exercise, and

recovery on ligament properties and insertion sites. The

30

effects of immobility occur rapidly, and recovery of the
ligament substance with remobilization occurs within a
similar time frame. In contrast, the recovery curve for
ligament insertion sites illustrates slow change over a

prolonged period of time84.

 

    

 

 

Exercise
IOO' Q/———m""m————T ————————————— CMHWX

‘1 S ‘ I Immoo'mY Recovery (ligamenI subsIonceI
<1 I

£2 E? I

Z l

<Im " I

531' '5 I Recovery (Insertion sIIel
[LJ :2 I

EE 5 I

\UJ U 50 P I

_IQ. \ I

«g E I

%d 5 I

F- E I

L) -- I

:3 E I

E 2 I

m e: I

O I— 5 ’1 IL
0 Weeks Months
——-T'HMIE——*

Figure 12: Summarization of homeostatic responses subjected
to different activities. (taken from Woo, 1987)
During the course of treatment for injuries to
ligaments and tendons, immobilization is often used as part
of the rehabilitation process. The major drawback is that
immobilization simultaneously induces reduction of the
mechanical properties and disuse atrophy of the surrounding

2,8,84,85.

healthy tissues Studies have shown that short

31

term immobilization can have detrimental effects on
cartilage, tendon, ligament, and bone. Noyes demonstrated
that after 8 weeks of immobilization, twelve months of
remobilization was required before the ACL-tibia complex
structural properties returned to norma163.

During immobilization there is an increase in collagen
crosslinking that may play a role in the contracture process
that often occurs with immobilized tendon818'87. Previous
studies using pin immobilization have observed better
collagen alignment in healing ligaments than in the

36'43. In these studies the

ligaments of a mobilized group
rabbits surgical legs were pin immobilized to prevent joint
motion, but uniaxial stresses were present in the tendon
during the healing phase. As mentioned previously, it has
been suggested that collagen will align in the direction of

stresses79 .

The collagen alignment of the healing tendons
in both studies were superior than that of the non-
immobilized tendons. In a recent study Amiel, et al.,5'8'41
suggests that since ligament size and collagen mass change
minimally during the first stages of immobilization, the
observed structural weakening must be due to changes of the
ligament substance itself, and not solely to atrophy. It is
because of these forementioned reasons that immediate
remobilization of the limb following surgery is the protocol
called out by many physicians today.

Recently Yamamoto, et al.,87 installed an augmentation

device to completely stress shield the rabbit patellar

32

tendon. They found that after 6 weeks of stress shielding
there was a large increase in the number of fibroblasts
present in the patellar tendon after six weeks. Also, the
stress shielding decreased the tensile modulus to 9% of the
control tendons; whereas, Woo found a decrease of only 54%
of the control tendon modulus when the knee was immobilized.
Majima, et al.,56 also found that complete stress shielding
of the patellar tendon significantly decreased the
properties of the tissue while simultaneously increasing the
number of fibroblasts present.

Increased stress and motion, on the other hand,
increases the mass and strength of the tissue. The effects
of exercise on ligament strength are well

d1'19'53'75'76. Several studies show that

documente
increased stresses on collagen causes increased collagen
synthesi59'36'78'80. Mobilization during ligament healing
has shown to result in greater strength and stiffness upon
biomechanical testing31. Schaberg, et al.,72 suggests that
the larger cross-sectional area of the mobilized healing
ligaments leads to a higher structural stiffness when
compared to the stiffness of the stress immobilized
ligament. In contrast, Haut et al.,43 found a decrease in
stiffness of the non-immobilized versus pin immobilized

healing patellar tendons, although the cross-sectional areas

were 3.5 times that of the contralateral control tendons.

33

1 fi 9 f Pr nt e 9 ch

The reason for this study is based on the following
hypothesis. It is postulated that the increased stresses
developed in the remaining two-thirds of patellar tendon of
the exercise group in previous studies by Haut, et al.,43
and Burks, et al.,18 may have been caused a structural
breakdown of the remaining host patellar tendon. Possibly,
in addition to the degradation of the mature collagen their
was a simultaneous increase in immature collagen synthesis.
The newly synthesized immature collagen fibers are more
pliable, have reduced stiffness, and are randomly dispersed
which results in the tendon being inferior to resisting
tensile forces than a undisturbed tendon. Therefore, to
compensate for the lower structural properties of the newly
laid collagen, an increased amount collagen is produced
which results in an increase in the amount of hypertrophic
scar tissue.

If the data generated from this study supports this
hypothesis, it would be imperative that a augmentation
device be developed. This device would be required to allow
immediate remobilization of the knee, while simultaneously

protecting the host patellar tendon from excessive stresses.

III . MATERIALS AND METHODS

T n r r t n

Forty two Flemish giant rabbits, weighing 5.2 i 0.6 kg,
were divided into four groups. The first group consisted of
12 rabbits used for immediate sacrifice (time zero data) and
testing of the patellar tendon after removal of the central
10% and 40% of the patellar tendon. The contralateral limb
was used for control data. The second (n=8) and third
groups (n=5) consisted of animals with the central 10% and
40%, respectively, surgically removed from the patellar
tendon. The fourth group had 7 animals in which the central
40% of the patellar tendon was also removed, but in addition
a stress shielding device was implanted to protect the
remaining 60% of the patellar tendon from in vivo stresses
developed during treadmill exercise.

A pre-operation injection of Robinul V was induced
prior to surgery, at a doseage of 0.01 mg per kilogram of
bodyweight, to decrease secretions and maintain heartrate
during surgery. Intramuscular injections of 15 mg/kg of
bodyweight of Ketamine, and a 2 mg/kg of bodyweight of
Rompun were administered. The rabbits were maintained on 2%
Isoflurane for the duration Of the surgical procedure. The
rabbits were placed supine, with the right hind limb exposed

for surgery. The selected amount of the central patellar

34

35

tendon was then extracted in the following fashion. The
patellar tendon was exposed with a medial-longitudinal cut
through the skin and surrounding fascia layer. The width of
the patellar tendon was measured using a stainless steel
metric rule and then the central 10% or 40% of the patellar
tendon was sharply excised leaving the infrapatellar fat pad
intact. The stress shielding device consisted of a No. 40
monofilament line inserted medial to lateral through a 1.0
mm diameter hole located in the central region of the
patella and tibial tuberosity. The original length of the
tendon was measured. The monofilament line was tied on the
lateral side of the tibial tuberosity after the length of
the tendon was reduced by an average of 4.5 mm, as shown in

the diagram in Figure 13.

sntoldtng Device

 

Figure 13: Diagram showing implanted stress shielding device

36

The contralateral limb of all groups served as control data.
The tendon defect in all groups was left open. The
subcutaneous fascia was then closed using resorbable suture
and the skin closed with 4—0 nylon suture.

All three surgical groups were allowed one week of cage
activity following surgery and then were subjected to
magnetic resonance imaging (MRI). Upon completion of the
six week exercise program the rabbits were sacrificed with a
2 milliliter intravenous injection of Ecklemide and again

were subjected to MRI.

M ical T r n

Immediately following sacrifice the patella—patellar
tendon—tibia complexes from both the surgical and
contralateral limbs were extracted. The patella-patellar
tendon-tibia complexes were cleaned of all soft tissue
except for the patellar tendon. The fat pads were carefully
resected and placed in 10% buffered formalin for histology.
The tibia was cut off approximately four inches distally
from the tibial plateau using a reciprocating bone saw
(Stryker Inc.). A 1.0 inch inside diameter aluminum tube, 4
inches long with a .125 inch wall thickness was placed
vertically under a ventilator hood. A room curing
fiberglass resin (NAPA board Fiberglass reinforced resin
6371) was mixed with a compatible hardener and poured into
the tube until it was approximately three-quarters full.

The tibia was cleaned of fatty residue with alcohol. It was

37

then inserted into the epoxy filled tube until the tibial
insertion point of the patellar tendon was just above the
epoxy. Care was taken to ensure that the tendon did not
come into contact with the epoxy resin. The potted
configuration was allowed to harden at room temperature for
approximately 40 minutes. The tendon remained wrapped in

saline soaked gauze, throughout this procedure (Figure 14).

 

Figure 14: Potted patella-patellar tendon—tibia complex

38

The total time between potting and testing was approximately
1—3 hours.

Prior to testing the patellar tendon measurements were
made by a single examiner using vernier calipers (Figure
15). Width and thickness measurements were taken at three
locations along its length. The cross sections were assumed
rectangular and their averages were used to calculate the

average cross—sectional area.

 

Figure 15: Tendon dimensions measurements for C.S.A.

The cross—sectional areas of the time zero tendons with the
central 10% removed were measured as described above and
then the average cross-sectional area was decreased by 10%.
The time zero tendons with the central 40% removed were
measured in three places along its length and width as
previously mentioned. These dimensions were taken on both

the lateral and medial sections of remaining tendon and the

39

average cross—sectional area of both sections were added.
Tendon length was measured from the inferior pole of the
patella to the superior—posterior attachment of the tendon
on the tibia. The tendon was immediately wrapped in
physiological saline (0.9% NaCl) soaked gauze.

Prior to the mechanical tests the patella was potted in
a special stainless steel box-like grip (0.5 x 0.5 x 0.75
inches)18'54. The inside was sprayed with a silicone based
lubricant to allow easy removal of the potted patella after
tensile tests. The same epoxy resin hardener mix, described
previously, was used to secure the patella. The box was
nearly filled with the epoxy resin. The patella was then
pushed into the resin up to the anterior surface and the
front plate of the box was secured. The apex (inferior
pole) of the patella was allowed to rest against the bottom
of the box. A slot cut in the bottom of the box allowed the
tendon to pass through without restricting its motion. The
resin was allowed ten minutes to harden.

The tendon complex was then mounted into a specially
designed fixture which allowed alignment of the tendon along
the load axis (Figure 16). The fixture was composed of
three horizontal 1/4 inch stainless steel plates, a
vertically mounted rotating dish, and a 1/8 inch thick
plexiglass saline bath. The bottom plate was secured to the
base of the Instron machine. Screw drives were mounted
between each sets of plates to allow 2 dimensional motion of

the fixture. The x-y table configuration enabled the

4O

operator to precisely align the tendon with the axis of the

Instron actuator.

 

Figure 16: Patella-tendon—tibia complex mounted for testing

The rotating disc, located inside the bath, was secured by
three 1/4—28 stainless steel bolts. Its primary function
was to provide a secure mounted mechanism for the potted
tibia. A secondary function of the rotating disc was to
allow for angle changes between the tibia and load axis. An
inclusive angle of 110 degrees was used to simulate a
physiological loading configuration, and orient the patellar
tendon in tension without a tearing or cutting action at the
tibial tuberosity.

A standard servo—hydraulic tensile testing machine
(Instron model 1331) was used to mechanically extend the
preparation. The upper part of the loading mechanism

consisted of a 500 lb load cell mounted in line with the

41

actuator. Below the load cell a universal joint was used to
correct minor offsets in alignment of the tendon preparation
with the machine actuator. The box containing the potted
patella was connected to the load cell.

Physiological saline was heated to 37 degrees Celsius
by an external heat exchanger and pumped into the bath after
the specimen was properly aligned and secured. The patellar
tendon complex was allowed to equilibriate in the heated
saline for approximately five minutes prior to mechanical

testing.

Pr - i '

Viscoelastic properties of tendons are often used for
the understanding of its physiological function83. Specimen
preconditioning was performed on each specimen in this study
prior to failure testing. A 1.5 N preload was applied to
the patella-patellar tendon—tibia (PPT) complex prior to
cyclic testing. The specimen was then cycled at 3% strain
(3% of the tendons original length) with a one hertz,
haversine function, for 20 cycles. A standard linearly
variable displacement transducer (accurate to 0.016 mm) with
the Instron actuator measured the grip to grip deformation;
A Nicolet oscilloscope and compatible disk drive
continuously stored the load and deformation data at a rate
of 100 samples per second. The data generated was not

analyzed in this study.

42

Tensile Tests

The specimen was allowed to stabilize for two minute
following the pre-conditioning cycles. The tendon complex
was then failure tested at a nominal rate Of 100% strain per
second. Continuous load and deformation data were collected
and stored in the same manner as the cyclic tests at 1000
samples per second. The mechanism of failure in the PPT
complex was visually determined and documented.

Force versus deformation plots were generated from the
failure experiments. The structural parameters documented
in each experiment were the maximum load and time to peak
load. The stiffness in the linear range was then calculated
from the load—deformation plots (Figure 17). The tensile
modulus was calculated as the product of the stiffness times

the ratio of initial length to cross sectional area.

2800 —«
2400 -
2000 -‘ Maximum Force

I800 — A

1200 --

Force (NI

Terminal

800 - Stillnoss

400 llonuntiun at I-oIIIIIn

 

 

 

Elongation (MM)

Figure 17: Stiffness recorded from load—deformation curve

43

M t ur 1

Most studies describe the structural and mechanical
properties of tendons and ligaments in the linear range of
the tensile response curve. However, it is documented that
most physiological activity occurs at much lower strain
levels. Strain imposed on the ACL during clinical
diagnostic tests is rarely thought to extend beyond the non—

20.

linear "toe" response Noyes suggests that the maximum

loading on the ACL for normal activities rarely exceeds 445
N64. A widely accepted value for the amount of strain
placed on tendons and ligaments during normal physiological
activities is 2—4% strain37'49. As shown on most stress-
strain response curves, these low strain levels are usually
included in the "toe" region.

A mathematical model, previously developed by
Belkoffls, based on Lanir52, was implemented to help
quantitatively describe the "toe" region of load—deformation
curves generated from the failure tests of the rabbit
patellar tendons. Belkoff's model was originally used to
model the tensile response of the human patellar tendon.

The mathematical model assumes a natural waviness
(crimp) of collagen fibers in a stress-free tendon. As the
tendon is deformed, the collagen fibers are sequentially
uncrimped, until fibers are straight. Once straightened,
the fibers are able to resist deformation and transmit load.

It is assumed that collagen fibers are straightened

gradually with elongation of the tendon such that the

44

distribution of slack lengths is described by a normal
Gaussian distribution function (Figure 18).

Using the Marquardt method, Belkoff's mathematical
model was used to curve fit the load—deformation data. With
this curve fitting procedure it was possible to calculate
two model parameters that help describe the toe region of
the curve, namely u (mu) and o (sigma). In the model the
value of 0 describes the mean amount of deformation required
to straighten 50% of the collagen fibers, whereas, 0

describes the standard deviation, or degree of dispersion,

in the collagen crimping.

 

 

 

 

 

 

 

 

 

 

Toe Heel Llnear
Region Region Region A
A.
A
v 'Y . V

, , . «mechanical
distribution response

function "

Stress

 

 

 

 

Stretch

Figure 18: Tendon crimp organization

45

Intuitively the model equation can be used to quantify the
realignment of collagen during tensile elongation. For
example, skin has a extremely unorganized collagen matrix
compared to ligaments, or tendons. This model would predict

14, compared to that of tendonls,

a large n and o for skin
because it would require a larger deformation to straighten
out the collagen fibers. With a more randomized

organization, the "toe" region would be less accentuated and

more gradually stiffening.

M ic nanc in
Rabbit Study

One week prior to surgery the rabbits were placed on
the treadmill for approximately 5-10 minutes daily. All
three surgical groups were allowed one week of cage activity
following surgery and then were subjected to magnetic
resonance imaging (MRI). The animals were anesthetized
prior to being placed in the MRI chamber with intramuscular
injections, per kilogram of bodyweight, of 35 mg/kg
Ketamine, 5 mg/kg Rompin, and 0.01 mg/kg Butorphenol. The
rabbit was placed in a supine position and positioned so a
small elliptical surface coil could be placed slightly above
the knees. A pulse repetition time (TR) of 1.0 second, an
echo time (TE) of 16.0 milliseconds, and 128 phase encoding
steps were used to produce relatively high signal—to-noise
(SNR) images. Other imaging parameters included a 100 mm

field-of—view (FOV), 3 mm slice thickness, and 3 mm

46

innerslice spacing. The slice spacing is measured from the
center of adjacent slices, so all slices were spatially
continuous. Total imaging time was approximately 8 minutes
and 30 seconds for each animal. All data was acquired on a
4.7 Telsa OMEGA CSI system equipped with S—250 Accustar
shielded gradients (Bruker Instruments, Fremont, CA). After
completion of the MRI the animal was given a intravenous
injection of 0.25 ml Yohimbine. The following day each
rabbit began a six week aggressive exercise program in which
they were required to run on a treadmill for approximately
10—15 minutes daily at a speed of 0.013 meters/sec. After
six weeks each rabbit was sacrificed and again subjected to

MRI.

Human Study

It was fortuitous that during the course of our animal
studies two surgical patients (N.L. and G.M.) were available
for a comparative analysis using MRI. Six months previously
both patients had undergone ACL reconstruction using the
central one-third of the patellar tendon. Each patient had
undergone quite different rehabilitation programs, varying
in degrees of aggressiveness, since their surgery.

The subjects were scanned in a 1.5 Tesla Signal
clinical imaging system (General Electric Medical Systems,
Milwaukee, WI). The patient's legs were placed in the
transmit/receive extremity coil and rotated laterally 15 to

20 degrees to facilitate visualization of the anterior

47

cruciate ligament. The surgical and contralateral limbs
were imaged using four pulse sequences from the standard
knee protocol used at Michigan State University. The first
images taken were axial T-l weighted, 5 mm thick slices.
The second and third image sets, sagittal and coronal views
respectively, were also T-l weighted. The fourth and final
acquisition consisted of multi-echo (balanced and T-2
weighted) 5 mm sagittal images.

The T—l weighted MR images showing the cross—section of
the patellar tendon at the level of the meniscus were
scanned (300 pixels/inch) using a Microtek scanner and
digitized using a public domain software program (Image
1.44) on a Macintosh II computer. From the digitized images
we approximated the ratio of the cross sectional areas of

the surgical and contralateral control patellar tendons.

Histology

Fat Pads

The infrapatellar fat pads were resected from the
patellar tendon immediately following extraction of the
patella-patellar tendon-tibia complex from the rabbit. Each
infrapatellar fat pad was placed, superior side down, on
filter paper with the orientation noted. The paper and fat
pad were then immersed in 10% phosphate buffered formalin.
After fixation the fat pad was trimmed into three sections,
two longitudinal and one cross section, and processed

according to standard paraffin procedures. Samples, 6

48

micrometers in thickness, were cut on a Microtome and

stained with hematoxylin and eosin.

Tendons

The patellar tendons from each rabbit were used for
histological analysis after failure testing. The tibial
heads were removed from the tibias with a reciprocating saw
(Stryker Inc.) immediately following failure tests. Each
was wrapped in 0.9% phosphate buffered saline soaked gauze,
inserted into plastic bags, wrapped tightly and stored
overnight at a temperature of 4 degrees Celsius. Adjacent
cross sectional samples from the mid-tendon area were
sectioned the following day for transmission electron
microscopy (TEM) and histology. The TEM specimens were
immediately fixed in Karnovsky fix (4% Paraormaldehyde, 5%
Glutaraldehyde) and sent for analysis. These samples are
currently being processed and these data are not included in
this thesis. The histology specimens were fixed in 10%
buffered formalin. After fixation, the patellar tendon
specimens were processed for routine histology, embedded in
paraffin, and sectioned on a rotary Microtome at a thickness
of 6 micrometers. The specimens were stained with
hematoxylin and eosin (H & E) and observed under a light
microscope. The specimens were also observed under
polarized light to identify the amount of mature collagen

present.

49

We

The statistical analysis used for this study was
performed on CRUNCH (Crunch Software Corp.). The results
are presented as mean i one standard deviation. Initially,
an ANOVA (Analysis of variance) was performed on each
variable to determine whether the sample means came from the
same populations. If a significant difference was noted (p
< 0.05) with the ANOVA, then post hoc tests were performed.
These tests make pairwise comparisons of the means. The
Student-Newman-Keuls test (S-N—K) was chosen for the post
hoc analysis. The S—N—K test compares the maximum and
minimum means for each variable between groups. If the
range is not significant then no further testing is

required.

IV . RESULTS

The rabbits with the stress shielding device did not
appear to have any gait abnormalities related to the device.
Two rabbits with the stress shielding device were excluded
from the study due to complications that occurred from a
broken device and a broken patella. After extraction of one
of the rabbit's patella-patellar tendon-tibia complexes, it
was noticed that the stress shielding device had become
untied sometime during the exercise program. Severe
hypertrophic scar tissue was observed throughout the
patellar tendon. The rabbit with the broken patella was
involved in the exercise program for nearly six weeks.

Three days prior to sacrifice the rabbit became lame and was
removed from the program. Inspection of the knee during
tissue recovery showed that the patella had fractured at the
location of the 1.0 mm hole. Visual inspection of the
patella showed that the hole had been drilled relatively
close to the inferior end of the patella. The increased
stresses generated during running probably caused the
patella to fracture. Biomechanical data could not be
generated, but the specimen was used for histological

analysis.

50

51

t D t
The post-hoc results for the time zero control tendon
data and six week control tendon data for this study showed
no significant difference in any comparisons made between
all the variables. These groups were then combined to
increase the statistical power of subsequent tests. All
test groups were compared to the two control groups

(combined) using the method of contrasts.

Tissue Dimengigng

The surgical tendons, upon gross inspection and
dimensional analysis of the cross-sectional area, of seven
rabbits in the 40% removed without the stress shielding
device group showed no signs of severe hypertrophic scarring
after completion of the six week exercise program. After
discussions with the animal technician, it was noted that
two of these rabbits developed "sore hooks" during the
exercise program and were unable to run a majority of the
time. The other two rabbits were classified as "poor
exercisers" and did not run well on the treadmill. The
reason the patellar tendons of the remaining three rabbits
in this group did not become hypertrophic cannot be
explained. The data from this group of animals was
considered outlier data and removed from the 40% without
stress shielding group. Analysis of these data proved to be

interesting, and relevant to this study, so this data was

52

categorized in a separate group. The new group is referred
to as the "40% removed without hypertrophic scar tissue."

The average length of the control tendons was 20.7 i
1.4 mm (n = 33), as shown in Table 1. The average length of
the tendons with the central 10% removed and the 40% without
hypertrophic scar formation did not differ significantly
from the control tendons after the six week exercise
program. However, the lengths of tendons with 40% removed,
with and without a stress shielding device, differed
significantly from control values. The tendons without
stress shielding increased in length, on the average, by 16%
while the stress shielded tendons decreased in length by 9%,
when compared to controls.

The average cross sectional area of the control tendons
was 14.6 i 1.8 mm2. The average thickness of the control
tendons was 2.00 i 0.15 mm and the average width recorded
was 7.25 i 0.60 mm. The average cross sectional area of the
tendons with the central 10% removed was not significantly
different than controls. The average cross sectional areas
of the tendons with the central 40% removed, with and
without stress shielding devices, as well as, the tendons
with the central 40% removed without hypertrophic scar
tissue were significantly larger than controls. These
increases were due to a significant increase in both the
width and thickness of the operated tendons. The cross
sectional area of the operated tendons with the central 40%

removed, and no stress shielding device, increased 3.0 times

53

in cross section when compared to contralateral controls.

In comparison the cross sectional area of the tendons with
the central 40% removed and with the stress shielding device
increased 1.5 times compared to controls. Similarily, the
cross—sectional area from the group of tendons with the
central 40% removed that did not develOp hypertrophic scar

tissue increased in cross section by 1.3 times compared to

controls (Figure 19).

C.S.A. (square mm)

 

 

 

 

50
40
30
20
IO
0 . 1
Time Zero 6 II eekS
Ilcauuoi 8 I036 Removed 10% Removal 9 um mm“ El 10:: "'70 51111
Figure 19: Histogram of cross—sectional areas
As expected, the time zero tendons with the central 40%
removed differed significantly from controls. The thickness

and cross—sectional area of these tendons were 70% and 60%
of controls, respectively. This was due to the removal of

the central portion of the patellar tendon at sacrifice.

Table :

Spocinnn

Control

10% Removed
(T=0 Wks)

10% Removed
(T=6 Wks)

40% Removed
(T=O Wks)

40% Removed
(T=6 Wks)

40% W/Device

40% W/O Scar

54

Tissue dimensions of control versus surgical

tendons (Data is presented as Mean

Length
(mm)

Thickness

(mm)
2.0
ifl.2

H-
OH
NKO

I+
ow
NH

H-
OH
-0
00’

H-
o

H-

O N
0 o
N Oi

2.3*
ifl.2

i l S.D.)

* Denotes value that is significantly different than control (p < 0.05)

Strugggrgl Properties

All tendon specimens were elongated in tensile tests

sufficiently to cause a mechanical failure of the patella-

patellar tendon-tibia complex.

The mean and standard

deviation values of the structural stiffness are shown in

Table 2. The structural stiffness was determined as the

slope of the linear region of the load-deformation curve.

55

Table 2: The mechanical properties of the control versus
surgical data

Specimen Stiffness Modulus
(NYnn) (Hrs)
Control 129.3 198.3
$26.7 $68.4
10% Removed 130.9 206.7
(T=0 Wks) $15.2 $61.9
10% Removed 144.3 183.3
(T=6 Wks) $20.6 $29.1
40% Removed 97.0* 213.7
(T=0 Wks) $23.4 $70.7
40% Removed 85.8* 49.1*
(T=6 Wks) $14.8 $10.2
40% W/Device 93.9* 68.2*
$32.9 $29 9
40% W/O Scar 138.1 159.0
$30.9 $60.6

* Denotes value that is significantly different than control (p < 0.05)

The control tendons had a average structural stiffness of
129.3 $ 26.7 N/mm. There was no significant difference in
structural stiffness between the tendons with the central
10% removed, at time zero and 6 weeks, and the tendons with
the central 40% removed without hypertrophic scar formation
when compared to controls. The two groups of tendons with
the central 40% removed, with and without stress shielding,
showed significant decreases in stiffness at time zero, and

6 weeks, when compared to controls (Figure 20).

56

Stiffness(N/mm)

180
160
140
120
100
80
60
40
20

 

Time Zero _ 6 Weeks

 

'Contml 810% Removed I40°/. Removed 3400/. W/Deveee 940% 370 Scar

 

 

 

Figure 20: Structural stiffnesses of tendons after 6 weeks.
Bar indicates One Standard Deviation.

The structural stiffnesses of the 40% removed tendons, with
and without stress shielding, were 73% and 66% of controls,
respectively. The time zero tendons with the central 40%
removed recorded a stiffness that was 25% less than the
control values. Additionally, these time zero tendons also
recorded stiffness that was very similar to the stress
shielded tendons at 6 weeks.

The failure loads for the control tendons were, on the
average, 661.7 $ 175.9 N as shown in Table 3. There was no
statistically significant difference in failure load of the

tendons with the central 40% removed, and the tendons that

57

had the central 40% removed but did not develop hypertrophic
scar tissue, when compared to controls. In contrast, the
tendons with the central 10% removed and the tendons with
the stress shielding device were significantly different
than control values. The average failure load of the
tendons with the central 10% removed was, on the average,
73% of control values. The low average failure loads of the
10% removed tendons are due to one specimen failing in the
mid-substance area, on the lateral side only, at a
relatively low load. Additionally, two specimens failed by
patella avulsion at extremely low loads. Had these values
been treated as outlier data, then the failure loads of this
group would not be significantly different than controls.
The tendons with the stress shielding device failed, on the
average, at loads 57% of the failure loads of control
tendons. The mechanism of failure in approximately one-half
of the specimens in both groups was by mid—substance
failure.

Expectedly, the average energy at failure of these same
groups were significantly different than controls. The
energy at failure for the tendons with the central 10%
removed and the stress shielded tendons were, on the
average, 63% and 44% of controls, respectively.

The time zero tendons with the central 40% removed had
results that were similar to the tendons with stress
shielding. The failure load of the time zero, 40% removed

tendons, was only 8% larger than the stress shielded tendons

58

at six weeks. The energy at failure results show an
increase of 29% for the time zero, 40% removed tendons
compared with stress shielded tendons.

Table 3: The structural properties of the control versus
surgical patellar tendons

Specimen Failure Energy at Failure
Load (N) Failure (J) Mode
Control 661.7 2.0 29/33 failed
$175.9 $1.1 by avulsion
10% Removed 707.0 2.2 4/6 failed
(T=0 Wks) $192.3 $1.5 by avulsion

10% Removed 481.0* 1.1 4/8 failed
(T=6 Wks) $156.7 $0.4 by avulsion

40% Removed 412.9* 1.2 0/8 failed
(T=0 Wks) $215.0 $0.8 by avulsion

40% Removed 509.9 1.9 6/6 failed
(T=6 Wks) $80.7 $0.6 by avulsion
40% W/Device 378.4* 0.9* 3/7 failed
$91.8 $0.5 by avulsion
40% W/O Scar 568.4 1.7 3/6 failed
$169.2 $1.2 by avulsion

* Denotes value that is significantly different than control (p < 0.05)

Mummies

The tensile modulus was derived from the linear region
of the tensile response curve after normalization of the
load-deformation data, as shown in Table 2. The average

modulus of the control tendons was 198.3 $ 68.4 MPa. Again,

59

the results of the tendons with the central 10% removed, at
time zero and 6 weeks, the tendons without hypertrophic scar
formation, and the time zero tendons with the central 40%
removed did not differ significantly from controls. In
contrast, the tensile modulus of tendons with the central
40% removed, with and without stress shielding, decreased
significantly from the control values (Figure 21). The
tensile modulus of the 40% removed, with and without stress
shielding, decreased by 34% and 25% of controls,

respectively.

Modulus (MPa)
300

250
200
150
100

50

 

Time Zero 6 Weeks

 

 

'Conlrol E um Removed 40% Removed E 40% W/Dew'ce Q 40% mo Scar

 

 

Figure 21: Tensile modulus of tendons after 6 weeks

60

Microgtructurgl Mode;
The mathematical microstructural model fit the

experimental data very well, especially in the toe region of

the load—deformation curve (Figure 22). The parameterll
was, on the average, .27 $ .06 mm for control tendons (Table
4). The value of u for tendons with the central 40% removed

was the only group significantly different than controls.
Statistical analysis of these tendons showed an increase in
u of 55% versus controls. Interestingly, two groups of
tendons had 0 values that were significantly different than

control values.

 

0.6

 

 

 

0.2“
0.1'
O \A I I T
O 1 2 3 4

Deformation (mm)

Figure 22: Experimental data and model fit

61

The tendons with the central 40% removed, as before, and the
tendons from the group with the central 40% removed that did
not show significant hypertrophic scarring had increased 0
values. The control tendons had an average 0 of .15 $ .08
mm _ This was approximately 35% less than the tendons with
the central 40% removed that did not develop hypertrophic
scar tissue, and 54% less than the tendons with the central
40% removed that showed significant increase in cross-
sectional area.

The n and O values were averaged for each group of
tendons after the 6 week exercise program. These values, in
addi tion to the average structural stiffness of each group,

were input back into the model equations and the estimated

"toe " regions and linear stiffnesses were plotted (Figure

 

 

23 ) ..
Structural Response of RP'I‘ ul 6 Weeks
250 __
_, Control
10% Removed
200 _
40% Removed
x
40% WIDcvlce
g '50 40% W10 Scar
’U
a
3
“)0
50-
(,1 V I I

 

 

 

0.2 0T4 0'.6 ofs i 1:2 1.4 l.6 L8 2
Deforumliou (mm)

Figure 23: Estimated "toe" region and structural stiffness

62

Accordingly, the same procedure was used with the average
tensile modulus for each groUp (Figure 24). These plots are
valuable in showing comparisons of the toe regions for each

group of tendons.

Mechanical Response of RI’T at 6 Weeks

 

 

16 ———

Coulrol
14- [0% Removed
12‘ 40% Removed

3K
40% \V/l)evice

40 % \V/O Scar

l0

 

Stress (MP3)
cc

 

 

 

2 3 5 '53
Slrahl(96)

I0

\Jd
mm
\D"

Figure 24: Estimated "toe" region and tensile modulus

The data shown in Table 4 suggests that the tendons
with the central 40% removed had a much larger "toe" region

than control tendons.

Table 4: Curve fitting parameters

63

for tendons at 6 weeks.

Swunnmn u G
Control 0.27 0.16
$0.08 $0.07
10% Removed 0.27 0.17
$0.12 10.07
40% Removed 0.49* 0.35*
$0.17* :0.1s*
40% W/Device 0.37 0.19
10.12 10.11
40% W/O Scar 0.36 0.25*
$0.16 10.09*

* Denotes value that is significantly different than control (p < 0.05)

IELSSKZLQKDL_il!u;;E!Ehll

A comparative analysis was made between the fat pads
extracted from the surgical knees, after six weeks of
exercise, and from the contralateral control knees. The
analysis of the fat pads was subjective and performed on two
longitudinal and one cross sectional samples taken from each
specimen. The specimens were evaluated on the fat cell
quality, amount of collagen present in the fat pad, and
amount of vascularity.

The control infrapatellar fat pads were primarily

composed of fat cells. Also present was small amounts of

64

collagen, randomly dispersed throughout the specimen, along

with a small number of visible blood vessels (Figure 25).

 

Figure 25: Histology of the control infrapatellar fat pads

The fat pads extracted from the surgical knees of rabbits
with the central 10% removed did not appear to be
significantly different than the contralateral control fat
pads in either collagen content or vascularity (Figure 26).
The rabbits with the central 40% removed that did not become
hypertrophic also did not appear to be significantly
different than their contralateral control tendons in either

collagen content, or vascularity (Figure 27).

X40

 

Figure 26: Histology of a infrapatellar fat pad with
the central 10% removed

 

Figure 27: Histology of a infrapatellar fat pad with the
central 40% removed that did not become
hypertrophic

66

In contrast, the infrapatellar fat pads from the group of
rabbits with the central 40% removed showed a small increase

in the amount of vascularity and collagen (Figure 28).

X40

 

Figure 28: Histology of a infrapatellar fat pad with the
central 40% removed
The infrapatellar fat pads from the surgical knees with the
stress shielding device differed significantly from all
other groups. These specimens showed large increases in
collagen content, amount of vascularity, and cellularity

(Figure 29).

W

A comparative analysis was made between the time zero
control tendons and the six week operated tendons. The
analysis was subjective and performed on the cross section

samples taken from both limbs“

67

 

Figure 29: Histology of infrapatellar fat pad from 40% with
stress shielding
These specimens were analyzed to determine if significant
differences in tissue quality and characteristics were
present. The control tendons of time zero, and 6 week, were
composed of primarily mature collagen, when observed under
polarized light. The cross sections of these patellar
tendons consisted of low cellularity tissue with long,
spindle shaped fibroblasts spaciously located throughout the

cross section (Figure 30).

68

 

Figure 30: Histology cross section of control tendon

The four specimens of the tendons with the central 10%
removed also was composed of "normal looking" tissue. Under
polarized light the tendon was composed primarily of mature
collagen, with relatively new collagen located in the
central defect. The central defects of these specimens were
completely filled with hypercellular tissue. The cells in
the defect were rounded in shape, rather than spindle shaped
that is often seen in normal tendon, and appeared to have
penetrated slightly into the mature collagen nearest the
defect (Figure 31).

The histology specimens of the three groups of tendons
with the central 40% removed varied significantly in tissue

quality. The patellar tendons that did not develop

69

 

Figure 31: Histology cross section of 10% removed tendon

hypertrophic scar tissue were superior in quality compared
to the other groups. These histology specimens showed
mature collagen in the locations of the original tendon.
The regions of mature collagen, similar to control tendons,
had relatively few spindle shaped fibroblasts randomly
located throughout two regions. The defect was partially
filled with hypercellular tissue that contained rounded
fibroblasts. The areas of mature collagen nearest the
defect showed signs of increased cellularity (Figure 32).
The specimens from the tendons that were stress

shielded showed two areas of normal appearing, mature

70

 

Figure 32: Histology cross section of tendons that did not
become hypertrophic
collagen, as seen under polarized light, along with the
defect being filled with hypercellular tissue. The soft
tissue in the defect appeared to have fat pad herniation
along with rounded fibroblasts. The tissue from the defect
appeared to partially encompass the two areas of mature
collagen. The two areas of mature collagen showed an
approximate twofold increase in the number of the
fibroblasts present within the boundaries. Although
increased in number, these fibroblasts maintained their size

and spindle shaped appearance (Figure 33).

71

X40

 

Figure 33: Histology of tendon with 40% removed and stress
shielding device

The 40% removed tendons that were not stress shielded
and scarred were composed of primarily immature and highly
disorganized collagen, when viewed under polarized light.
The entire cross section was composed of highly cellular
tissue with only rounded fibroblasts present throughout the
cross section. The defect area was not clearly visible due
to the increase in cellularity of the entire tendon. Fat
pad herniation was also present in the defect location in

some of these specimens (Figure 34).

mic " Tuna-i 11:!
Rabbit studies
The MR images taken of each rabbit was used to follow

the degree of hypertrophic scarring present in the surgical

72

 

Figure 34: Histology of tendon with 40% removed and no
device
patellar tendon. This data has not been analyzed and will

not be discussed in this study.

Human Case Studies
CASE REPORT 1:

A 15 year old female suffered a torn anterior cruciate
ligament while making a quick stop and pivot move during a
soccer game on July 27, 1992. The patient's knee had a
significant drawer motion when a Lachman test was performed
by the examining physician. The patient had no previous
knee injuries and was an active intramural athlete in
basketball, soccer, and volleyball. The patient's knee was
reconstructed on Aug. 12, 1992 with a central one—third

patellar tendon graft. The central defect was left open.

73

After 1 week of immobilization the patient was given a
functional leg brace and encouraged to maintain range of
motion. The leg brace was worn all day for 8 weeks. Weight
hearing was not encouraged until four weeks after surgery.
The patient performed quadriceps contraction exercises three
times a day, for 5 minutes each time, during rehabilitation.
Overall, an aggressive rehabilitation was not followed,
although weights were occasionally used by the patient. The
rehabilitation program was not monitored by a therapist. '
The patient experiences pain under the kneecap after playing
sports, especially after running. She also experiences pain
when she gets up from sitting for long periods of time, and
occasionally has difficulty in kneeling and extending the
leg. Also, the knee tends to swell after any type of

physical activity.

CASE REPORT 2

A 24 year old male patient suffered a torn anterior
cruciate playing basketball on May 15, 1992. The knee had
been subjected to a lateral blow while the knee was locked
and the leg was fully extended. The injured knee had
previously undergone two arthroscopic medial menisectomies.
The patient conservatively treated the injury for
approximately 3 months before MRI revealed a torn anterior
cruciate ligament. Surgical intervention and reconstruction
using the central one-third of the patellar tendon was

performed. The surgical limb was not subjected to

74

continuous passive motion following surgery. The patient
was encouraged to aggressively rehabilitate the surgical
limb. A soft cast was prescribed with limited motion and
weight-bearing being encouraged the day after surgery.
Quadriceps exercises were performed three times a day for
approximately 20 minutes per session beginning 1 week after
surgery. Weights were used during the rehabilitation
program. The patient was an active intramural athlete prior
to the injury. Limited running and hockey was resumed at
approximately 6 months. The patient was squat lifting 275
pounds 6 months after surgery. The patient often
experiences pain in the patellar tendon and medial portion
of the knee. His knee occasionally hurts when he gets up
from sitting for long periods of time or walks up stairs.

He also has difficulty kneeling.

Human Study

At six months post-surgery both patients were given MRI
scans. The axial MRI images of the female subject showed
that the defect was still observed in the central portion of
the host patellar tendon (Figure 36 a,b). The digitized MRI
images of the surgical and contralateral knees indicated a
slight (9.3%) increase in cross-sectional area when compared
to the contralateral control. T-2 weighted sagittal images
showed that the hypertrophy observed in the defect was not
caused by edema, hemorrhage, or fat. A uniform MRI response

was noted throughout the entire host tendon.

75

 

(b)

Figure 36: T-1 weighted image of a 16 year old female who
was reconstructed with a central one-third PT. After 6
months of minimal exercise the (a) control tendon and (b)
the surgical tendon showed the defect was filled an little
hypertrophic scar was evident elsewhere.

76

The digitized MRI images of the male subject indicated
that the cross sectional area of the host patellar tendon
had increased by 136% in comparison to the contralateral
control (Figure 37 a,b). T-2 weighted sagittal images
showed hypertrophy in the surgical tendon was not caused by
edema, hemorrhage, or fat. The tendon was uniformly
enlarged, and uniformly hypertrophic throughout its cross-
section. The infrapatellar fat pad in the surgical knee
appears to have become highly vascular and possibly

fibrotic.

77

 

Figure 37: T—l weighted MR image of a 24 year old patient
reconstructed with a central one-third PT. After 6 months
of aggressive rehabilitation the (a) control tendon and (b)
the surgical tendon which shows that the surgical defect was
still evident and significant scarring had developed

throughout the PT. Also, the infrapatellar fat pad was
altered.

V. DISCUSSION

The primary objective of the study was to determine if
the excessive hypertrophic scarring of the patellar tendon
often seen in animals, as well as in humans, after removal
of the central one-third of the patellar tendon was the
result of mechanical overstressing of the remaining host
tendon. This hypothesis was tested by surgical removal of
the central 10% and 40% of the rabbit patellar tendon. In
addition, one group with the central 40% removed had a
stress shielding device implanted to eliminate post-surgical
stresses in the host tendon.

Six weeks after surgery the tendons with the central
10% removed showed a small increase in cross-sectional area
and histologically appeared to be very similar to the
control tendons. Similarities in the structural and
mechanical properties of tendons with the central 10%
removed, when compared to the control tendons, suggests that
increased hypertrophic scar formation is not a physiological
response to the surgical "cutting" of the host tendon.
Furthermore, the slight increase in stress applied to the
remaining tendon actually results in a slight increase in
stiffness and a slight decrease in tensile modulus. This is

paralleled with a slight increase in cross-sectional area.

78

79

The morphology of the host tendon, however, seemed to be
preserved. I

Linder suggested that with removal of the central one—
third of the patellar tendon, there is a 67% increase in
stress applied to each portion of the remaining tendon54.
The tendons of rabbits with the central 40% removed showed a
significant amount of hypertrophic scar, likely due to the
increased stresses in the host tendon. The increase in
cross-sectional area of the host tendon corresponded with
the human MR image for the aggressive rehabilitator, as well
as, a previous case study presented by Bergl5. However,
there were a group of animals with the central 40% removed
'that showed little or no increase in hypertrophic scar
formation. These rabbits were, for the most part,
classified as "poor" exercisers. I theorize that these
animals applied sufficient stress to prevent disuse atrophy,
yet did not apply excessive stresses on the healing tendon.
The appearance of these tendons during gross inspection
appear to be similar to the MR images of the human subject
that was a non-aggressive rehabilitator. These data suggest
that an optimum rehabilitation program likely exists.

Increases in cross-sectional area of the surgical
tendons, accompanied a decrease in structural and mechanical
propertiesof the host patellar tendon, after removal of the
central 40% of the patellar tendon, and paralleled the
results seen in previous studies. Haut, et al.,43 found a

28% decrease in the structural stiffness of the operated

80

tendons versus controls. In addition, the‘surgical tendons
increased in cross section by approximately 4.0 times the
control values. Similarly, Burks, et al.,18 found a
decrease of structural stiffness that was 20% of control
tendons, and a increase in cross section of 4.5 times the
control values. In this study, the structural stiffness of
tendons with 40% removed, with and without stress shielding,
decreased to 73% and 66% of control tendons, respectively.
The 40% removed tendons without the stress shielding also
had a cross-sectional area 3.0 times controls. Burks, et
al.,18 also found a 10% shortening in the surgical tendons
of dogs. The length of the surgical tendons in this study,
with the central 40% removed increased 16%, similar to
Haut's study. This lengthening may due to overstressing the
host tendon and subsequent damage. Conversely, the length
of the stress shielded tendons decreased 9% in length, and
increased 1.5 times in cross section compared to controls.
The decrease in length was most likely due to a contracture
process that often occurs in an immobilized, healing
tendons-7.

Amiel, et al.,5 suggests that with stress deprivation
there is a increase in collagen turnover in ligaments. With
a less mature collagen fiber being more pliable, there may
also be a reduced stiffness. The healing tissue is composed
primarily of newly synthesized, highly unorganized collagen,
with low material properties. Stresses applied it may

result in permanent deformation and lengthening of the

81

tendon. Eventually the newly laid collagen is aligned in
the direction of stress loading. These observations
correlate well with the results of this study for both the
40% removed, and the stress shielded tendons. I
hypothesized that the original mature collagen of the
tendons with the central 40% removed was overstressed during
exercise. This caused an increased synthesis of immature
collagen to help repair the ensuing microdamages. The
decreased mechanical properties of this newly synthesized
collagen then causes the host patellar tendon to increase in
cross-sectional area, so the total stiffness of the tendon
increases towards normal.

The tendons with the central 40% removed showed a
significantly increased "toe" region. The increased "toe"
region would suggest an increase in the amount of
unorganized collagen present within the composition of the
tendon. The decrease in tensile modulus also suggests that
these tendons are primarily composed of immature collagen.
This is also supported by the analysis of the histological
cross sections from these specimens. The "toe" region of
the stress shielded tendons was more similar to controls
than the group with the central 40% removed. Most likely
this was due to the larger amount of organized collagen
present in the stress shielded tendons, as seen
histologically under polarized light. The stress shielding
device may have protected much of the original tendon from

overstressing and subsequent microtrauma. However, the

82

decrease in modulus observed in these tendons was likely due
to the effects of disuse atrophy or stress deprivation.

The decrease in mechanical properties of the stress
shielded tendons with the central 40% removed was consistent
with a previous study by Yamamoto, et al.87 The tensile
modulus of rabbit tendons in Yamamoto's study decreased
9.0%, whereas, the tensile modulus of the stress shielded
tendons in this study decreased 34%, after six weeks of
stress shielding. The differences in results are probably
due to the central 40% being removed in the stress shielded
tendons for this study, while no surgery was performed in
the Yamamoto study. In addition to decreases in mechanical
properties, the cross-sectional area used in this study for
the normalization of load-deformation data included a
significant amount of unorganized, immature collagen that
probably was not load bearing during tensile failure. The
results of Yamamoto's study also showed an average increase
in cross section of 1.3 times larger than control tendons,
and a 15% decrease in length for the stress shielded
tendons. However, the cross sectional area of the stress
shielded tendons in this study was 1.5 times larger than
controls, and the initial length decreased by only 9% of
control values. The increase in cross—sectional area of the
stress shielded tendon in this study was due to the newly
laid scar tissue encompassing areas of original tendon.

Previous studies have shown that lack of joint movement

by pin immobilization results in better alignment of

83

collagen in a healing tendon36. Similarly, Schaberg
postulated in a study involving stress immobilized legs, and
non-stressed immobilized legs, that pin immobilization
prevents flexion and extension of the joint but allows
uniaxial longitudinal stresses which promote collagen
alignment72. Haut also found similar results in the
immobilized group of rabbits in his study. Haut used a
Steinmann pin immobilization technique, which probably
allowed newly laid collagen to align itself in the direction
of isometric stresses. In a recent study by Gomez, et
al.,39 rabbit MCL's were medially transected, permitted to
heal for 4 weeks, and then placed under increased isometric
tension for 8 additional weeks. Gomez found that there was
no significant difference in mechanical properties between
surgical and control MCL's after 12 weeks, and the newly
laid collagen in the defect area appeared to be well
aligned. Majima, et al.,56 found that the degree of stress
shielding affects the mechanical properties of the patellar
tendon. Majima concluded that complete stress shielding
significantly decreases the mechanical properties of
patellar tendon after six week356'57.
The scar formation in the central defect of the stress
shielded tendons in this study was relatively unorganized
according to the results generated from the mathematical
model. Most likely the lack of stress in the completely
stress shielded tendon made it difficult for the immature

collagen to align itself in any predominant direction.

84

Although the stress shielding device did not allow for any
stresses to be placed on the patellar tendon during collagen
synthesis, it did allow for normal range of motion of the
limb during the exercise program.

In many studies it is believe that exercise helps to
stimulate tendon remodeling and increase ligament
strength86. It is likely that this effect is shown in the
results of the tendons with the central 10% removed. Most
studies, however, focus on the clinical complications that
often occur after ACL reconstruction using the central one-
third of the patellar tendon, and do not consider the
possibility of overstressing the operated tendon during
physical rehabilitation. Although exercise has been shown
to increase strength of a normal ligament, or tendon, the
excessive stresses generated during exercise rehabilitation
may be detrimental to the already traumatized host patellar
tendon after removal of a central 40%.

A previous study by Majima, et al.,56 indicates that
partial stress shielding (at 30% of physiological loads)
results in no significant difference in the tensile strength
after six weeks. These data, along with the data presented
in the current study showing protection of the host tissue
from a proliferative response, would suggest that some
degree of augmentation may help protect the host patellar
tendon from excessive stresses during early exercise
rehabilitation. This augmentation device should allow full

range of motion to prevent disuse atrophy in the joint

85

tissues, while simultaneously sharing the forces applied to
the remaining portions of the host patellar tendon. The
extent of the load sharing should initially be high, and
decrease with time and the degree of healing. The device
used in this study was probably too stiff resulting in
complete shunting of loads from the tendon. An optimal
device would share loads with the host tendon. This would
protect the host tendon from excessive stresses, yet allow
development of newly formed collagen.

Future studies should consider using devices with
different stiffnesses to better control the amount of
loading on the tendon. The best scenario would probably be
a device that will ultimately decrease in stiffness as the
host tendon increases in stiffness by development of quality

repair tissue.

VI. CONCDUSIONS

1. The results for tendons with the central 10% removed
suggest that increases in cross-sectional area and decreases
in the structural and mechanical properties of surgical
tendons seen in earlier studies, are not a result of a

surgical "cutting" of the host patellar tendon.

2. Mechanical and histological results from tendons with
the central 40% removed are similar to the results from
previous studies by Burks et al18 and Haut et a143. Six
weeks after surgery the operated tendons show significant
increases in cross-sectional area and significant decreases
in the structural and material properties of the host
tendon. Excessive stress on the host tendon after surgery

results in complete remodeling of the host tissue.

3. The stress shielded tendons also showed a decrease in
stiffness, modulus, and original length six weeks after
surgery. These changes were probably due to disuse atrophy
resulting from a stiff augmentation device. However it

seemed clear that the host tendon morphology was preserved.

4. A number of animals, after having 40% portion of tendon
removed, showed little hypertrophic scar formation or change

in tendon morphology.

86

VII.

87

88

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APPENDIX A

96

97

Table 1:Tissue dimensions of the rabbit patellar tendon prior to
the six week rehabilitation program.

Control

Specimen Length Thickness C.S.A.
(nun) (nun) (nunz)
A2LF 19.220 1.350 8.720
AZRF 20.400 1.470 10.650
116CF1 21.250 1.930 16.550
23RBCF 20.510 2.040 14.320
88J1CF 19.920 2.090 13.690
GOlCF 21.500 2.110 15.570
FLICF 24.600 2.070 15 640
DEMCF 19.300 2.050 14.180
lean 20.840 1.889 13.670
Std. 1.730 0.302 2.680

JJflk Funmovmui

Specimen Length Thickness C.S.A.
(nun) (nun) (nunz)
JWZLF 21.500 1.560 9.300
CKZRF 19.020 1.880 13.650
23RBTF 19.610 2.010 16.800
88J1TF 20.52 2.020 14.460
GOITF 21.330 2.000 14.100
FLlTF 24.600 2.070 15.640
lean 21.100 1.923 13.990
sec. 1.970 0.189 2.570

40% Removed

Specimen Length Thickness C.S.A.
(nun) (nun) (nunz)
BBSLF 19.700 1.260 6.170
BB9RF 18.470 1.180 7.580
CKZLF . 19.900 1.050 5.240
NTLF 20.850 1.390 8.960
NTRF 20.400 1.310 7.810
116F1 22.850 1.600 9 290
PETLTF 17.240 1.860 12.480
DEMTF 19.290 1.780 11.750
lean. 19.840 1.428 8.660

Std. 1.660 0.290 2.520

98

Table 2: Tissue dimensions of the rabbit patellar tendon after
completion of the six week rehabilitation program.

Control

Specimen Length Thickness C.S.A.
(mrn) (mm) (mmzl
RSO43CF 19.680 1.960 13.450
GB4CF 21.730 2.170 16.170
CKJOFCF 19.750 2.120 14.460
BGJ3CF 21.320 1.969 13.430
GHlCF 19.810 1.967 13.790
9207C? 19.610 1.926 13.350
JOEYCF 20.780 1.927 13.180
KNSCF 20.790 1.846 12.670
H3CF 20.590 1.680 13.020
JCKlCF 20.510 1.960 11.740
I4OCF 19.250 1.960 13.200
I9CF 19.380 2.010 16.040
ISSCF 22.410 2.083 15.000
ISZCF 19.620 2.163 15.750
I51CF 20.270 1.967 14.560
I4CF 21.740 2.076 16.740
I36CF 18.370 1.948 13.880
IBSCF 19.010 2.070 15.630
ENlOCF 19.130 2.133 14.890
CKBSCF 18.760 1.970 12.490
CKOKCF 20.770 2.126 16.310
ISOCF 20.600 2.177 16.720
161CF 22.280 2.080 16.310
lean 20.268 2.103 14.469
sec. 1.115 0.117 1.507

JJHBJReumnnmd

Specimen Length Thickness C.S.A.
- (mm) (mm) (m2)
RSO43TF 19.280 1.880 13.220
GB4TF 20.510 1.880 13.400
CKJOFTF 18.710 2.080 13.540
I4TF 23.100 2.100 16.870
I36TF 20.090 2.230 16.990
ENIOTF 17.360 2.180 15.830
CKOKTF 20.860 2.350 17.810
154T? 17.320 2.110 17.010
loan 19.650 2.101 15.584

Std. 1.930 0.162 1.898

99

Table 2: (Continued)

ddfibineulnned

Specimen Length Thickness C.S.A.
(nun) (nun) (nunz)
GHlTF 23.320 3.730 37.670
9207TF 24.710 3.970 42.150
I40TF 21.780 4.990 45.300
I35TF 22.570 3.980 41.020
IGOTF 28.450 3.770 46.670
lean. 24.170 4.090 42.560
sec. 2.630 0.520 3.570

40%‘W/Stress Shielding Device

Specimen Length Thickness C.S.A.
(nun) (nun) (nunZ)
JOEYTF 18.200 2.560 21.900
KNSTF 20.300 2.500 19.430
172TF 18.290 2.229 17.100
ISSTF 17.780 2.360 22.350
ISlTF 16.610 2.719 25.100
161TF 20.700 2.800 26.740
lean 18.650 2.528 22.103
sea. 1.560 0.214 3.543

40%‘W/O Hypertrophic Scar Formation

Specimen Length Thickness C.S.A.
(nun) (nun) (nunz)
3GJ3TF 22.170 2.410 18.870
H3TF 21.910 2.240 16.690
I9TF 19.360 1.990 15.470
CKBSTF 17.400 2.653 26.370
lean 20.210 2.320 19.350

Std. 2.260 0.280 4.890

APPENDIX B

100

101

Table 3: Structural properties of the rabbit patellar tendon
prior to the six week rehabilitation program.

Control
Specimen Failure Stiffness Energy at
Load (N) (N/mm) Failure
(J)
AZRF 1032.00 166.00 4.20
116CF1 675.00 144.00 2.07
23RBCF 729.80 105.37 2.24
88J1CF 480.60 123.48 1.08
GOlCF 680.90 126.14 2.02
FLlCF 667.50 107.31 0.69
DEMCF 538.45 116.07 1.59
lean 678.41 126.91 1.99
see 164.57 21.59 1.13
llflbinemlnned
Specimen Failure Stiffness Energy at
Load (N) (NYmm) Failure
(J)
JWZLF 735.00 134.00 1.95
CKZRF 672.00 144.00 1.95
23RBTF 783.20 103.59 2.92
88J1TF 396.10 123.77 0.83
GOlTF 987.90 136.98 4.60
FLlTF 667.50 142.88 0.67
lean 706.95 130.87 2.15
sea. 192.32 15.22 1.45
dmflbinemlnnad
Specimen Failure Stiffness Energy at
Load (N) (NYmm) Failure
(J?
BB9LF 178.40 67.00
BB9RF 518.00 109.00 1.27
CKZLF 104.00 62.00 0.11
NTLF 248.00 96.00 0.39
NTRF 448.00 101.00 1.02
116F1 632.00 130.00 1.62
PETLTF 698.65 117.78 2.60
DEMTF 476.15 93.04 1.69
lean 412.90 96.98 1.24

Std. 214.99 23.37 0.84

 

2102

Table 4: Structural properties of the rabbit patellar tendon
after completion of the six week rehabilitation program.

Control
Specimen Failure Stiffness Energy at
Load (N) (NYmm) Failure
(.1)
RSO43CF 825.00 126.00 3.65
GB4CF 446.20 115.00 0.84
CKJOFCF 461.20 141.00 1.50
3GJ3CF 668.40 200.00 1.38
GHlCF 488.30 154.00 0.81
9207CF 428.50 123.00 0.98
JOEYCF 447.80 172.00 0.69
KNSCF 357.40 92.00 1.10
H3CF 502.30 148.21 0.96
JCKICF 718.50 198.11 1.69
140CF 738.70 104.80 2.68
19C? 856.60 171.23 2.94
159CF 574.05 112.13 1.89
152CF 874.43 81.28 4.04
151CF 338.20 121.09 0.89
14CF 743.20 174.95 1.10
136CF 654.15 103.33 2.07
135CF 734.25 94.30 1.86
sulocs 365.00 114.43 0.44
CKBSCF 910.00 116.07 3.29
CKOKCF 754.30 120.22 2.35
ISOCF 754.30 123.63 2.52
161CF 694.20 122.71 2.88
CABOCF 623.13 143.53 1.19
F04CF 814.10 99.47 3.78
R379CF 998.00 150.00 3.58
lean 645.01 131.72 1.97
see 187.27 31.78 1.10
lofislkemlnnad
Specimen Failure Stiffness Energy at
Load (N) (NYmm) Failure

(J1

RSO43TF 558.90 154.00 1.50
GB4TF 248.00 103.00 0.78
CKJOFTF 346.70 158.00 0.82
14TCF 678.63 145.99 1.58
136TF 654.15 162.37 1.15
ENIOTF 335.10 126.21 0.58
CKOKTF 536.23 142.75 1.12
154TF 490.00 162.28 1.47
lean 480.96 144.32 1.13

Std. 156.69 20.60 0.37

103

Table 4: (Continued)

40% Removed

Specimen Failure Stiffness Energy at
Load (N) (N/mm) Failure
(J?
GHlTF 439.40 84.00 1.23
9207TF 485.70 107.14 1.45
140T? 631.90 88.70 2.58
135T? 547.35 65.59 1.93
160TF 445.00 83.56 2.22
Mean 509.87 85.80 1.88
Std. 80.71 14.84 0.55

40%‘W/Stress Shielding Device

Specimen Failure Stiffness Energy at
Load (N) (Nme) Failure
(ET)
JOEYTF 215.60 133.60 0.28
KNSTF 317.50 51.00 0.93
172TF 421.10 108.00 0.92
159TF 362.68 85.33 1.05
151TF 416.08 121.54 0.16
161TF 411.63 50.64 1.53
F04TF 503.90 106.90 1.27
lean 378.36 93.86 0.88
Std. 91.79 32.90 0.50

40%‘W/O Eypertrophic Scar Formation

Specimen Failure Stiffness Energy at
Load (N) (Nme) Failure

(0?

3GJ3TF 508.70 148.00 0.81
H3TF 348.00 157.55 0.62
19TF 489.50 182.60 1.19
CKBSTF 596.30 112.60 1.92
CA80TF 612.90 98.29 1.96
R379BTF 854.80 129.40 3.83
lean 568.37 138.07 1.72

see. 169.20 30.88 1.17.

APPENDIX C

104

105

Table 5: Mechanical properties of the rabbit patellar tendon
prior to completion of the six week rehabilitation program.

Control

Specimen Tensile Modulus 96 Strain at
Strength (MPa) Failure
A2RF 96.90 316.00 36.56
116CF1 40.79 322.00 27.00
23RBCF 50.96 150.92 34.90
88J1CF 35.11 179.67 23.45
GOlCF 43.73 174.18 27.70
FLlCF 42.68 168.79 31.05
DEMCF 37.97 157.98 32.40
lean 52.45 209.94 30.44
Std 21.24 75.14 4.65

10% Removed

Specimen Tensile Modulus % Strain at
Strength (MPa) Failure
JW2LF 79.03 309.00 27.19
CKZRF 49.23 202.00 30.30
23RBTF 46.62 120.92 40.60
88J1TF 27.39 175.65 42.00
GOlTF 70.06 207.22 46.20
FLlTF 42.68 225.48 33.10
lean 52.50 206.71 35.57
Std. 18.89 61.91 7.45

40% Removed

Specimen Tensile modulus 3 Strain at
Strength (MPa) Failure
BB9LF 28.91 215.00 15.70
BB9RF 68.34 270.00 29.80
CK2LF 19.85 108.00 12.00
NTLF 27.68 214.00 15.10
NTRF 57.36 265.00 22.40
116F1 68.03 322 00 24.50
PETLTF 55.98 162.70 39.60
DEMTF 40.52 152.74 36.90
lean 45.83 213.68 24.50

Std. 19.10 70.73 10.26

106

Table 6: Mechanical properties of the rabbit patellar tendon
after completion of the six week rehabilitation program.

Control

Specimen Tensile Modulus 96 Strain at
Strength (MPa) Failure
RSO43CF 61.34 192.00 36.20
GB4CF 27.59 153.00 19.30
CKJOFCF 31.89 176.00 26.10
3GJ3CF 49.77 312.00 20.00
GHlCF 35.41 211.00 17.80
9207CF 32.10 162.00 25.90
JOEYCF 33.98 ' 336.00 14.85
KNSCF 28.21 167.00 21.30
H3CF 38.58 234.47 19.50
JCKlCF 61.20 345.93 22.75
I40CF 5.96 152.84 35.10
I9CF 53.40 206.88 33.10
IS9CF 38.27 167.52 26.00
ISZCF 55.52 101.25 49.00
ISlCF 23.23 168.58 22.90
14¢? 44.40 ' 227.21 23.40
I36CF 47.13 136.76 35.20
I35CF 46.98 114.69 40.80
ENIOCF 24.51 147.02 20.70
cxsscr 72.86 174.34 41.10
CKOKCF 46.25 153.10 21.80
ISOCF 45.11 152.32 32.20
IGlCF 42.56 153.97 37.90
CA80CF 33.55 168.67 22.60
F04CF 58.86 140.28 42.30
R379CF 62.85 200 00 31.20
lean 44.49 186.72 28.42
sea 13.25 61.68 9.03

10% Removed

Specimen Tensile modulus % Strain at
Strength (NPa) Failure
RSO43TF 42.28 211.00 27.20
GB4TF 18.51 166.00 24.10
CKJOFTF 25.61 227.00 21.00
14TCF 40.23 199.90 22.50
136TF 38.50 192.00 26.80
ENIOTF 21.17 138.41 19.90
CKOKTF 30.11 167.20 33.20
154TF 28.81 165.24 29.60
lean 30.65 183.34 25.54

Std. 8.91 29.10 4.52

107

cable 6: (Continued)

40% Removed

Specimen Tensile modulus % Strain at
Strength (MFa) Failure
GHlTF 11.66 53.00 26.90
9207TF 11.52 62.81 25.80
140TF 13.95 42.64 39.80
135TF 13.34 36.09 38.90
160TF 9.54 50.94 31.30
lean 12.00 49.10 32.54
Std. 1.73 10.22 6.56

40% WYStress Shielding Device

Specimen Tensile modulus % Strain at
Strength (MPa) Failure
JOEYTF 9.84 37.50 21.90
KNSTF 16.34 52.00 32 40
172T? 24.63 124.00 26.80
159TF 16.23 68.01 31.10
151TF 16.58 80.43 26 00
161TF 15.39 39.20 20.00
F04TF 17.55 75.94 26.70
lean 16.65 68.15 26.41
Std. 4.33 29.91 4.47

40%‘W/O Eypertrophic Scar Formation

Specimen Tensile modulus 3 Strain at
Strength (MPa) Failure
3GJ3TF 26.96 182.00 18.10
H3TF 20.85 206.82 15.70
19TF 31.64 228.51 24.90
CKBSTF 22.61 74.30 38.20
CABOTF 26.78 99.47 28.85
R379TF 25.52 163.00 36.20
lean 29.63 159.02 26.99

Std. 10.19 60.63 9.22

APPENDIX D

108

1139

Table 7: Curve fit parameters recorded from time zero tendons

Control
financial“: ll (3
AZRF 0.330 0.081
116CF1 0.263 0.314
23RBCF 0.237 0.166
88J1CF 0.245' 0.110
GOlCF 0.222 0.064
FLlCF 0.252 0.098
DEMCF 0.290 0.187
lean 0.263 0.146
sec. 0.037 0.087
IlOfislunnowlu!
sunscismenl u. (I
JWZLF 0.464 0.442
CK2RF 0.378 0.351
23RBTF 0.165 0.131
88J1TF 0.377 0.251
GOlTF 0.171 0.076
FLlTF 0.246 0.360
lean 0.300 0.269
Std. 0.124 0.142
440%51Remlrwedl

smumcinuln ll (3
BBSLF 0.189 0.320
BBQRF 0.537 0.433
CK2LF 0.255 0.291
NTLF 0.135 0.259
NTRF 0.228 0.173
116F1 0.563 0.169
PETLTF 0.182 0.074
DEMTF 0.265 0.102
lean 0.294 0.228

Std. 0.163 0.120

111)

Table 8: Curve fit parameters recorded on 6 week tendons.

Control
S:nu:inlun u. (S
GB4CF 0.197 0.219
CKJOFCF 0.369 0.147
3GJ3CF 0.393 0.168
GHlCF 0.222 0.125
9207CF 0.345 0.226
JOEYCF 0.198 0.117
KNSCF 0.286 0.105
H3CF 0.333 0.176
JCKlCF 0.419 0.137
I40CF 0.369 0.209
I9CF 0.199 0.085
ISSCF 0.318 0.191
ISZCF 0.216 0.043
ISlCF 0.150 0.104
I4CF 0.227 0.099
136CF 0.246 0.118
I35CF 0.286 0.286
ENIOCF 0.232 0.140
CKBSCF 0.177 0.121
CKOKCF 0.156 0.180
ISOCF 0.204 0.091
161CF 0.186 0.290
lean 0.260 0.153
Std 0.081 0.064
zlofiisemlrvIKi

sumacimmenl ll (5
RSO43TF 0.219 0.148
GB4TF 0.271 0.087
CKJOFTF 0.327 0.246
I4TF 0.387 0.249
136TF 0.233 0.195
ENIOTF 0.128 0.072
CKOKTF 0.456 0.216
IS4TF 0.114 0.134
lean 0.267 0.168

Std. 0.119 0.069

Specimen

GHlTF
9207TF
I40TF
I35TF
IGOTF

Std.

Specimen

JOEYTF
KNSTF
172T?
ISQTF
ISITF
I61TF

Std.

Specimen

3GJ3TF
HBTF
I9TF
CKBSTF

Std.

111

Table 8:

(Continued)

40% Removed

00000

00

4096 W/Stress shielding Device

000000

0

4096 VIC Eypertrophic Scar Formation

0000

O

p.

.534
.555
.222
.476
.671

.492
.167

u

.612
.350
.311
.347
.393
.226

.373
.130

u

.499
.359
.158
.230

.311
.150

00000

0

000000

O

0000

O

.392
.258
.143
.546
.407

.349
.154

.371
.190
.086
.205
.278
.072

.200
.114

.354
.358
.199
.140

.263
.110

BRRRIES

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