Table Of ContentK. Hirohata . K. Mizuno
T. Matsubara (Eds.)
Trends in Research
and Treatment
of Joint Diseases
With 112 Figures, Including 4 in Color
Springer-Verlag
Tokyo Berlin Heidelberg
New York London Paris
Hong Kong Barcelona
KAZUSHI HIROHATA, M.D.
KOSAKU MIZUNO, M.D.
TSUKASA MATSUBARA, M.D.
Department of Orthopedic Surgery
Kobe University School of Medicine
Chuo-ku, Kobe, 650 Japan
ISBN-13: 978-4-431-68194-6 e-ISBN-13: 978-4-431-68192-2
DOl: 10.1007/978-4-431-68192-2
On the front cover: Electron micrograph of shadow-cast of lesion in tendon, see Fig. 4/p. 54,
and Fixation of the osteotomized site, see Fig. 2/p. 87.
© Springer-Verlag Tokyo 1992
Softcover reprint ofthe hardcover 1st edition 1992
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Preface
A half century ago, orthopedic surgeons needed to specialize in only the
pathophysiology and treatment of the neuromuscular and skeletal systems
in order to treat patients. However, since then, surprising progress has
been made in medicine, and through the limitless avenues for research
orthopedics is now divided into many subspecialities, with terms such as
orthopedic pathology, orthopedic oncology, orthopedic rheumatology,
and orthopedic traumatology becoming commonplace. Interdisciplinary
studies in this and other related fields are now indispensible. As a result,
the half-life of the information accumulating yearly has been estimated at
five years. In times such as these, if one stubbornly adheres to treatment
alone, progress comparable to that in other fields will not be made. If one
opens an orthopedic textbook, it is easy to see that there are still many
diseases of undetermined etiology; in the last quarter of a century, there
has been no evidence of even one of these diseases' etiology having been
resolved internationally. This is a direct result of the ineptitude of basic
orthopedic research. Therefore, recently in the United States, Japan
and Canada, orthopedic research institutes and associations have been
established, and SIROT has been organized internationally.
This book contains the manuscripts presented by international and
Japanese speakers at the 5th Annual Meeting of the Orthopedic Research
Society of the Japanese Orthopedic Association, and the Second Inter-
national Cherry Blossom Conference of Rheumatology. The speakers
included not only orthopedic surgeons also but rheumatologists, bio-
engineers, chemists, anatomists, and immunologists of international
reknown. The gathering of speakers of this calibre, the level of interdis-
ciplinary approach, and a book such as this presenting their findings is
surely a first. I recommend this book highly to the new generation
of orthopedic surgeons, for the reason that orthopedic basic research
should not be the sole domain of Ph.Ds (chemists, immunologists, and
bioengineers). Basic research is an essential part of becoming of a leading
orthopedic surgeon; it is a basic aspect. On the occasion of the publication
of this book, I would like to thank the staff members of Springer-Verlag for
their dedication and support.
KAZUSHI HIROHATA
Chairman of Orthopedic Surgery
Kobe University School of Medicine
Kobe, Japan
Contributors
Apley, A.G. 81, 125 Puhl, W. 110
Balasubramaniam, P. 51 Reiner, A. 3
Bogoch, E. 3 Rizkalla, G. 3
Bryant, T. 29 Ruth, J.T. 99
Bucholz, R.W. 128 Saegusa, Y. 85
Cooke, T.D.V. 29 Schiinke, M. 20
Fehr, K. 41 Scudamore, R.A. 29
Fischer, R. 110 Schurman, D.J. 72
Hirohata, K. 85, 166 Shimizu, T. 85
Hiroshima, K. 142 Takakura, Y. 149
Ionescu, M. 3 Takashima, T. 166
Kaneda, K. 156 Tanaka, Y. 149
Kumagi, J. 135 Tillmann, B. 20
Lane Smith, L. 72 Uhthoff, H.K. 135
Matsubara, T. 85, 156 Wang, G.J. 59
Matsuno, T. 156 Wilde, A.H. 99
McCarty, D.J. 13 Wright, T. 116
Mizuno, K. 166 Ziff, M. 35
Poole, A.R. 3
Contents
Preface. . . . . . .. . . ... . . .. .. . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . v
Contributors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . VI
Part I. Pathogenesis of Joint Diseases
Changes in the Extracellular Matrix of Articular Cartilage in Human
Osteoarthritis
A.R. POOLE, G. RIZKALLA, A. REINER, M. IONESCU, and
E. BOGOCH ................................................ 3
Pathophysiology of Osteoarthritis
D.l. MCCARTY. . . . . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Pathology of Osteoarthrosis
B. TILLMANN and M. SCHUNKE. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 20
Mechanical Factors in the Pathogenesis of Osteoarthritis
T.D.V. COOKE, R.A. SCUDAMORE, and T. BRYANT. . . . . . . .. . . . . .. 29
Immunopathology of Rheumatoid Synovium
M. ZIFF ................................................... 35
Interaction of Pannus to Rheumatoid Cartilage
K. FEHR................................................... 41
Mechanism of Collagen Breakdown by Local Infiltration of Steroids
P. BALASUBRAMANIAM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
Pathogenesis of Steroid-Induced Avascular Necrosis and Its Response
to Lipid Clearing Agent
G.l. WANG................................................ 59
Bacterial Adherence in Foreign Body Infection
D.l. SCHURMAN and L. LANE SMITH. . . . . . . . . . . . . . . . . . . . . . . . . . .. 72
Part II. Joint Surgery and Its Problems
The Evolution of Hip Replacement
A.G. APLEY . . . . . . . . . . . .. . . . . . .. . . ... . . . . . . . . . .. . . . . . . .. . .. 81
VIII Contents
Hip Reconstruction Supplemented with Chiari-Pelvic Osteotomy
K. HIROHATA, T. MATSUBARA, T. SHIMIZU, and Y. SAEGUSA .... . .. 85
Management of the Infected Total Knee Replacement by
Two-Stage Reimplantation
A.H. WILDEandJ.T. RuTH.................................. 99
Excimer Laser in Joint Surgery: Experimental Basis and
Clinical Experience
W. PUHL and R. FISCHER .................................... 110
Implant Debris from Total Joint Arthroplasties: Studies on the
Mechanisms Responsible, the Amounts of Debris Generated, and
the Implications in Loosening and Infection
T.WRIGHT ................................................. 116
Part III: Miscellaneous Conditions in Orthopaedics
How Should We Treat Fractures?
A.G. ApLEY ............................................... 125
Bone Graft Substitutes in Fracture Management: Basic Science and
Clinical Results
R.W. BUCHOLZ ............................................ 128
Embryology of Human Meniscus
H.K. UHTHOFFandJ. KUMAGI ................................ 135
Etiology of Congenital Dislocation of the Hip Joint
K. HIROSHIMA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 142
Pathogenesis of Hallux Valgus
Y. TAKAKURA and Y. TANAKA 149
Giant Cell Tumor of Bone: Current Controversies
T. MATSUNO and K. KANEDA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 156
The Etiology of Osteoporosis
K. MIZUNO, T. TAKASHIMA, and K. HIROHATA ................... 166
Index ....................................................... 181
Part I. Pathogenesis of Joint Diseases
Changes in the Extracellular Matrix of Articular
Cartilage in Human Osteoarthritis
A. ROBIN POOLE, G. RIZKALLA, A. REINER, M. IONESCU1, and E. BOGOCH2
Summary. Articular cartilage is carefully organized to impaired collagen fibril assembly although proteogly-
provide an articulating surface that provides almost can synthesis continues actively. Thus, the key to the
frictionless movement and the ability to absorb and survival of the cartillage is the protection and pres-
dissipate compressive load and resist tensile forces. ervation from damage of the inact type II collagen
The cartilage is organized into zones, the structures of fibrillar network. Clearly, there is no evidence of
which reflect the mechanical forces acting upon the impaired proteoglycan synthesis, but retention of
cartilage. Type II collagen, together with type IX and proteoglycans is prevented when collagen is damaged.
type XI collagens, forms a fibrillar network through-
out the matrix which is secreted by the chondrocytes. Key words. Cartilage Osteoarthritis
The large aggregating proteoglycans and the smaller Proteoglycans - Collagen - Proteinases
proteoglycans interact directly or indirectly with this
fibrillar network. The collagen and the proteoglycans
can be degraded by metalloproteinases produced by Introduction
the chondrocytes. In osteoarthritis, early damage to
the collagen fibrillar network is seen at the articular
surface and in the upper mid-zone. It is accompanied General Organization of the
by a local loss of the large aggregating proteoglycan
Collagen Fibrillar Network and
and small proteoglycans. Large proteoglycans exhibit
Cartilage Proteoglycans
degradative changes at this stage. With further pro-
gression of disease, fibrillation of cartilage occurs and
Articular cartilage, lubricated by synovial fluid,
proteoglycans are lost and replaced by larger more
intact molecules with different glycosaminoglycan provides almost frictionless articulation in a
chains. Collagen damage now extends throughout the diarthrodial joint. The collagen fibrillar network
cartilage. There are also significant changes in the (Fig. 1), composed of type II collagen, to which
organization of the small proteoglycans, decorin and type IX and type XI collagens are bound, [1,2]
biglycan, in the osteoarthritic cartilage. Overall, a endows cartilage with its strength and hence its
major reorganization of proteoglycans occurs with net tensile properties. Its organization reflects the
collagen damage. We now know which proteases mechanical forces which act upon the cartilage:
degrade both the collagen and the proteoglycan and
ranging from predominantly shear forces at the
how their synthesis, secretion and activity may be
articular surface, where fibrils are thin and are
stimulated. The arthritis probably results from a
aligned parallel to the articular surface, to
mechanical stimulation of protease activity with
compressive forces within the cartilage in the
mid and deep zones (Fig. 2). Here, the fibrils are
thicker and arranged in a more random manner
I Joint Diseases Laboratory, Shriners Hospital for Crippled
although there is evidence for the arcading of
Children, Division of Surgical Research, Department of
fibrils, originally described by Benninghoff [3]
Surgery, McGill University, Toronto, Ontario, Canada
2 Division of Orthopaedics, Department of Surgery, and confirmed by others [4]. The calcified car-
Wellesley Hospital, Toronto, Ontario, Canada tilage (Fig. 2) acts as an intermediate zone,
4 A. R. Poole et al.: Changes in Osteoarthritis
Type II collagen fibril
(contains type XI collagen)
Oecorin core
HA OS
Fig. 1. Organization of type II collagen fibrils, containing type IX and type XI collagen, and aggregating
proteoglycans that bind to hyaluronic acid in the extracellular matrix of adult articular cartilage. Hyaluronic
acid (HA) interacts directly or indirectly with collagen fibrils in a periodic manner as shown by Poole et al. [32] .
It may bind to the basic NC4 domain of type IX collagen (shown as a globular terminal component). This
collagen is covalently bound to and has a periodic distribution on type II collagen. Decorin also binds to type II
collagen though its core protein [33] in a periodic manner. Its single dermatan sulfate chain (DS) is shown .
Biglycan, which is co-distributed with decorin, (AR Poole, A Reiner, M. Ionescu and pj Roughley, manuscript
in preparation, see Fig. 3) is not shown but it may also be bound to type II collagen. Intact aggrecan molecules
contain a G3 globular domain at the C-terminus. They are attached to HA via a globular N-terminal domain
called Gl. The G2 and G3 globular domain have no known function. Keratan sulfate (KS) and chondroitin
sulfate (CS) are bound to core protein as shown. Link protein stabilizes the interaction of G 1 with HA.
Degradation products of aggrecan are shown that remain bound to HA via the functional Gl domain. These
proteoglycans can bind 50 times their weight of water, leading to hydration of the extracellular matrix. In
reality this hydration is limited by the collagen fibrillar network. As a result these molecules exhibit a swelling
pressure which endows cartilage with its compressive stiffness. The figure is drawn approximately to scale.
(From [32], with permission).
sitting between the uncalcified articular cartilage calcified zone and of the tidemark occurs in
of the deep zone (bounded by the tidemark) more advanced disease.
and the subchondral bone. It appears to be The cellular organization of adult articular
formed by a process of endochondral ossifica- cartilage also reflects the differences in bio-
tion but normally remains uninvaded by capil- mechanical properties, structure, and metab-
laries. In osteoarthritis capillary invasion of the olism. At the articular surface, the cells are
