Biomechanics of Normal and Pathological Human Articulating Joints

374 Pages·1985·16.18 MB·English

by  J. C. Mulier (auth.)

Biomechanics of Normal and Pathological
Human Articulating Joints
NATO ASI Series
Advanced Science Institutes Series
A Series presenting the results of activities sponsored by the NATO Science
Committee, which aims at the dissemination of advanced scientific and technological
knowledge, with a view to strengthening links between scientific communities.
The Series is published by an international board of publishers in conjunction with the
NATO Scientific Affairs Division
A Life Sciences Plenum Publishing Corporation
B Physics London and New York
C Mathematical and D. Reidel Publishing Company
Physical Sciences Dordrecht and Boston
D Behavioural and Martinus Nijhoff Publishers
Social Sciences Dordrecht/Boston/Lancaster
E Applied Sciences
F Computer and Spri nger -Verlag
Systems Sciences Berlin/Heidelberg/New York
G Ecological Sciences
Series E: Applied Sciences - No. 93
Biomechanics of Normal and
Pathological Human Articulating
Joints
edited by
Necip Berme
Dept. of Mechanical Engineering
The Ohio State University
Columbus, Ohio, USA
Ali E. Engin
Dept. of Engineering Mechanics
The Ohio State University
Columbus, Ohio, USA
Kelo M. Correia da Silva
Gulbenkian Institute of Science
Oeiras, Portugal
1985 Martinus Nijhoff Publishers
Dordrecht / Boston / Lancaster
Published in cooperation with NATO Scientific Affairs Division
Proceedings of the NATO Advanced Study Institute on Biomechanics of Normal and
Pathological Human Articulating Joints, Estoril, Portugal, 20 June-1 July, 1983
ISBN-13: 978-94-010-8762-9 e-ISBN-13: 978-94-009-5117-4
DOl: 10.1007/978-94-009-5117-4
Distributors for the United States and Canada: Kluwer Boston, Inc., 190 Old Derby
Street, Hingham, MA 02043, USA
Distributors for the UK and Ireland: Kluwer Academic Publishers, MTP Press Ltd,
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Distributors for all other countries: Kluwer Academic Publishers Group, Distribution
Center, P.O. Box 322, 3300 AH Dordrecht, The Netherlands
All rights reserved. No part of this publication may be reproduced, stored in a
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photocopying, recording, or otherwise, without the prior written permission of the
publishers,
Martinus Nijhoff Publishers, P.O. Box 163, 3300 AD Dordrecht, The Netherlands
Copyright © 1985 by Martinus Nijhoff Publishers, Dordrecht
Softcover reprint of the hardcover 1s t edition 1985
v
TABLE OF CONTENTS
Preface VI
Clinical Aspects of Human Articulating Joints; J.C. Mulier 1
Consideratiorls in Joint Replacement; J.P. Paul 37
Significance of Mathematical Modeling; J.P. Paul
and N. Berme 43
Experimental Techniques, Data Acquisition and
Reduction; A. Cappozzo 53
Gait Analysis as a Tool to Assess Joint Kinetics;
T.P. Andriacchi and A.B. Strickland 83
Biomechanics of the Joints in the Leg; J.P. Paul 103
Biomechanics of the Joints in the Upper Limb; N. Berme,
G. Heydinger and A.E. Engin 115
Passive and Active Resistive Force Characteristics in
Major Human Joints; A.E. Engin 137
Kinematics of the Human Knee Joint; R. Huiskes, R. van Dijk,
A. de Lange, H.J. Woltring and Th. J.G. van Rens 165
Dynamic Modeling of Human Articulating Joints; A.E. Engin,
N. Berme and N. Akkas 189
Lubrication of Joints; J.P. Renaudeaux 215
Biomechanics of Muscles; K.M.C. da Silva 239
Electromechanical Properties and Electromagnetic
Stimulation of Bone; N. Guzelsu 267
Biomaterials; P. Lawes 285
VI
Design, Manufacture and Testing of Prosthetic Devices;
P. Lawes 313
Stress Analysis and Fixation Problems in Joint Replacement;
R. Huiskes 337
Standards for Joint Replacements; J.P. Paul 359
Short Contributions
1. Relationships Among Osteoarthrosis, Bone Mineral
Content, Age and Sex; R. Sumner 363
2. Influence of Hip Endoprosthetic Design on Stress
Distribution; A. Rohlmann, U. Mossner
and G. Bergmann 364
3. Theoretical and Experimental Analyses of the
Coupling of Endoprosthesis and Femur; M.M. Gola
and A. Gugliotta 364
4. Gait Analysis as a Diagnostic Tool; H. Ranu 365
5. A Simple Finite Element Model of the Meniscus;
A.A.H.J. Sauren, A. Huson, R.Y. Schouten and
J.C. Nagtegaal 367
6. Experimental Stress Analysis Using Epoxy Models
of the Human Pelvis and Femur, Before and After
Insertion of a Hip Prosthesis; H.A.C. Jacob 368
7. Experimental Valgus Instability of the Knee;
S. Nielsen, C. Kromann-Andersen and o. Rasmussen 369
8. Finite and Instantaneous Helical Axis Estimation
from Noisy, Discrete Landmark Measurements;
H.J. Woltring 369
9. On the Initiation of Spondylolysis Through
Mechanical Factors; H.A.C. Jacob and Y. Suezawa 370
10. Intra-Operative Measurement of Cancellous Bone
Strength; I. Hvid 371
11. On the Loosening of the Femoral Component of
Freeman Double-Cup Hip Prostheses -- A Biomechanical
Investigation; H.A.C. Jacob and A. Schreiber 372
List of Participants 373
Index 375
VII
PREFACE
The widespread occurrence of the various forms of arthritis
not only results in a great waste of manpower, but also causes
immeasurable pain and suffering for the patients. Due to the
limited understanding of its etiology, the currently available
treatments are directed at the effects of the disease rather than
its causes. The solutions available to the clinician at the
advanced stages of arthritis are frequently surgical and include
prosthetic replacement arthroplasty. Many advances have been made
in the last decade in the basic understanding of the kinematics and
kinetics of anatomical joints, as well as in the technology of
joint replacement. The NATO Advanced Study Institute held in
Portugal during June 20-July 1, 1983 addressed these topics and
provided instruction on the advances in biomechanics of
diarthrodial joints. The proceedings of this Institute are
presented in this volume.
Many different areas of specialization contribute to the field
of joint biomechanics. Due to the complexity of each individual
topic, it was not attempted here to present a complete treatise of
each of these areas. Each chapter typically gives a review and a
flavor of the subject matter, as well as discussing the state-of
the-art advances in general or in specific research areas. Some of
the chapters, such as those on lubrication and muscle mechanics,
are more mathematically oriented than the others. Nevertheless,
the reader with a non-engineering background, I trust, would still
find most of the book informative and easy to read. On the other
hand, the engineering expert will benefit from the chapter on
clinical review, as well as from those that are not in his
immediate field of expertise.
I would like to thank my co-editors Dr. K. M. Correia da Silva
and Professor A. E. Engin for their contributions in organizing the
Advanced Study Institute, as well as for their input in shaping the
scientific program. I would also like to thank the lecturers of
the Institute for their presentations, and particularly for their
contributions to this book. Finally, special thanks go to my
family for their support, understanding and patience throughout the
time it took me to give uniformity to this volume.
Necip Berme
CLINICAL ASPECTS OF HUMAN ARTICULATING JOINTS
J.C. Mulier
Department of Orthopaedic Surgery,
University Hospital, 3041 Pellenberg, Belgium
1. INTRODUCTION
A human synovial joint has two essential characteristics: its
stability and its mobility which are both provided by a complicated
system of structures. If damaged, most of the tissues making up a
joint have the poss~bility to repair themselves. In more differ
entiated cells this function is less pronounced. Of all the
structures making up a joint, cartilage is the most vulnerable
tissue and the least able to repair itself. Practically all
serious acute or chronic joint damage ends with damage of the
cartilage. Although cartilage is able to grow and resist wear very
well under normal circumstances, it looses its function as soon as
excessive damage or wear occurs.
In most cases deterioration of joint cartilage starts with a
mixture of causes. For the sake of clarity the causes will be
discussed under two headings: a) pure mechanical causes, and b)
structural causes. In practice this separation exists only rarely.
1.1 Mechanical Causes of Joint Degeneration
Osteoarthritis (OA) is the term used for description of
degeneration or destruction of joints by mechanical reasons. It is
a slow progressive disorder, usually starting with very little
pain. The course of osteoarthritis is variable and unpredictable
since the factors causing it are so multiple and variable. In some
rare occurrences it becomes stationary. This happens in the case
after osteotomy for instance. Only about 5% of untreated patients
with osteoarthritis remain pain free. In osteoarthritis we always
find two pathological processes:
2 Mulier
a) Deterioration and detachment of the weight bearing
surface.
b) Proliferation of new osteoarticular tissue at the margins
and beneath the detached joint surface.
Most clinicians agree that: a) Under abnormally high
mechanical pressures osteoarthritis begins as a focal fibrillation
of the joint cartilage that leads to secondary remodeling of the
bony components of the joint. Fibrillation may remain silent for a
long period, but eventually cartilage will respond with gradual
wear. Particles loosen and act as deteriorating factors.
b) Osteoarthritis can also be caused by changes in stiffness of
subchondral bone. Cracks occurring in the bone as typically seen
in aseptic necrosis of the head of the femur lead to partial
overloading. Stress peaks in the cartilage cause fissures in the
bone with subsequent loosening and deterioration.
The structural disintegration of the osteoarticular cartilage
and its abrasion leads to the loss of the subchondral tissue of the
articular surface. This causes proliferative phenomena including
the formation of new cartilage at the surface and at the edges of
the osteoarthritic joint. Characteristically degradation of
cartilage is focal. It is therefore likely that degradation
results from short range enzymes released by affected chondrocytes
in their immediate neighborhood. The nature of the mechanical
signal for the chondrocytes to digest their own matrix is unknown.
Remodeling of bone is the alteration of the internal and
external architecture of the skeleton dictated by Wolff's law in
response to variation in mechanical loading (1). It involves
removal of bony tissue at certain points and laying down bone
tissue elsewhere.
Cartilaginous repair is biologically possible by:
a) Replication of articular chondrocytes.
b) Metaplasia (change of a cell of a certain type into a cell
of another type) of granulation tissue that proliferates
in the subchondral bone marrow and at the margins of the
j oint surf ace.
The traditional teaching that chondrocytes are incapable of
mitotic division has been disproven by cell culture studies.
Clusters of chondrocytes in fibrillated cartilage represent clones
of newly proliferated cells. But a degree of chondrolysis seems to
be a necessary condition for growth of these cells.
It is not known why cartilage becomes mineralized at the lower
layers and where it has been destroyed. It becomes mineralized
however, under certain pathological conditions. The osteogenesis-
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