Current Trends in Bone Grafting

114 Pages·1989·4.209 MB·English

by  Ping-Chung Leung MB, BS, MS, FRACS, FRCS (Edin) (auth.)

Ping-Chung Leqng
Current Trends
in Bone Grafting
Foreword by Robert B. Duthie
With 67 Figures in 108 Separate Illustrations
Springer-Verlag Berlin Heidelberg New York
London Paris Tokyo
Ping-Chung Leung, MB, BS, MS, FRACS, FRCS (Edin)
Chinese University of Hong Kong
Faculty of Medicine
Department of Orthopaedic and Traumatic Surgery
Prince of Wales Hospital
Shatin, N_ T_, Hong Kong
ISBN-13: 978-3-540-50139-8 e-ISBN-13: 978-3-642-73970-5
DOl: 10_1007/978-3-642-73970-5
Library of Congress Cataloging-in-Publication Data
Leung, Ping-Chung, 1941- Current trends in bone grafting I Ping-Chung Leung;
foreword by Robert Duthie. p. em. Includes bibliographies and index.
ISBN-13: 978-3-540-50139-8
1. Bone-grafting. I. Title. [DNLM: 1. Bone and Bones - transplanation. WE 190 L653c]
RD123.L48 1989 617'.4710592 - dc19 DNLM/DLC 88-39970
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Dedicated to my colleagues,
without whose support and diligence this
work could not have come to fruition
Foreword
This succinct, up to date and interesting review of all aspects of
bone grafting is a happy blend of the practical and the experi
mental - both having been carefully researched and synthesised by
the author. Professor Leung has an international reputation for his
work, particularly in the field of vascularised bone grafting, and on
perusing this volume one clearly sees why. The bibliography at the
end of each chapter also helps to make the book a most valuable
addition to the international literature. It is a pleasure to read, and
to recommend it without hesitation to the young surgeon in train
ing as well as to the expert, both of whom will gain a great deal.
Oxford, October 1988 Robert B. Duthie
Table of Contents
1 In Search ofa n Ideal Bone Graft. . . . . . . . . . . . . . .. 1
Cortical and Cancellous Grafts . . . . . . . . . . . . . . . .. 1
Bone Physiology in Relation to Grafting . . . . . . . . . . .. 2
Fate of Bone Grafts .... . . . . . . . . . 3
Bone Substitutes . . . . . . . . . . . . . . . 7
Conclusion . . . . . . 8
The Ideal Bone Graft 8
References ..... . 9
2 Vascularised Bone Grafts . . . . . . . . . . . . . . . . . " 11
Introduction ......... . 11
Early Experimental Results . . 11
Vascularised Bone Graft . . . . 13
References .................... . 15
3 Vascular-Pedicled Bone Grafts . .............. . 17
Experimental Work ....... " .... . 17
Historical Development . . . . . .. . . . . . 18
Indications . . . . . . . . . . . . . . . . . . . 19
Muscle-Pedicled Grafts . . . . . . ..... . 19
Vascular-Pedicled Bone Grafts ............... . 26
Conclusion . . . . . . . 30
References .......... . 30
4 Vascular-Pedicled Bone Grafts and Hip Reconstruction ... 33
Vascular Anatomy of Iliac Crest .............. . 33
Preparation of Vascular-Pedicled Iliac Crest Graft .... . 34
Clinical Applications. . . . . . . . . . . . . . . . . . . . . . 36
Conclusion . . . . . . . . . . . . . . . . . . . . . . . 48
References .......................... . 49
X Table of Contents
5 Free Vascularised Bone Grafts 51
Introduction 51
Donor Site . 51
Indications . 56
Postoperative Considerations 69
Conclusion 69
References .......... 70
6 Free Vascularised Composite Bone Grafts . . . . . . . . .. 73
Introduction .................... 73
Thumb Reconstruction Using Second Toe . . . . 73
Thumb Reconstruction Using Wrap-around Flap 82
Finger Reconstruction . . . . . 84
Pincer Reconstruction . . . . . . . . . . . . . . 87
Double Finger Reconstruction ......... 90
Toe Transplantation for Congenital Anomalies 93
Composite Tissue Grafting for Bone and
Soft-Tissue Deficiencies in the Hand 95
Conclusion 97
References .............. 97
7 The Future . . . . . 99
Experimental Work 99
The Future 102
References ..... 103
8 Name Index ......................... 105
9 Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . 107
1 In Search of an Ideal Bone Graft
In 1915, Albee first introduced bone grafting technique into surgical practice [1].
During World War II, the technique was used much more frequently, first for fa
ciomaxillary and then for orthopaedic surgery [2], with grafts being taken from
cancellous bone. Since then, bone grafting has become one of the fundamental
techniques used in bone and joint surgery. This technique is indicated for exam
ple, for
(a) filling of bone cavities,
(b) replacement of bone losses,
(c) delayed union and non-unions,
(d) fusion of joints and
(e) skull augmentations.
Obviously, it is most commonly used in filling bone gaps and in non-union of frac
tures.
Cortical and Cancellous Grafts
Although cortical bone is only used under special circumstances, there are many
ways of applying it. It may be inserted as an inlay, onlay or double onlay, or as
chips or osteoperiosteal strips [3]. Different shapes might also be used to 'latch' or
'bolt' two bone ends [4, 5]. Cancellous grafts are used in the treatment of delayed
union as chips [6], as a block [7, 8] or as strips [9].
Segments of limb bones from the fibula, rib or metatarsal may be used as
grafts, e.g. fibular graft for the femoral neck [10], arthrodesis of the hip joint using
a fibular graft to bridge the femur and the ischium [11], split grafts of rib for de
layed union [12] and metatarsal bone used to replace missing metacarpal [13].
In children where growth of epiphyseal plate is desirable, bone transplants
with growth plates have been attempted, although the subsequent activity of the
growth plate is doubtful. The proximal fibula, with the entire head, has been used
to replace distal radius and distal tibia [14, 15].
Whole-bone transfer has been done by Van Nes: in the 'turn-up' operation, the
tibia and fibula are transplanted to replace the femur excised for tumour [16]. In
composite tissue transfer, e.g. pollicisation and toe transfer, whole bones are graft
ed together with their soft-tissue coverings.
2 In Search of an Ideal Bone Graft
Bone Physiology in Relation to Grafting
The periosteum consists of two layers: a fibrous limiting membrane, called the
cambium layer, and a cellular osteogenic layer, the epiosteum. In children, the
cambium layer is composed of several layers of osteoblasts and contributes to
wards bone growth by adding diaphyseal width, adding bone length at the epiphy
seal plate and adding articular cartilage [17). The cambium layer shrinks down to a
negligible thickness when bone growth is completed.
The inner surface of cortical and cancellous bone is lined by the endosteum.
The endosteum of the tubular bones contributes little towards callus formation; by
contrast that overlying cancellous bone demonstrates a lot of cell proliferation in
the case of fracture. The inner callus of a tubular fracture is mainly formed by
marrow cells [18).
The blood supply of the bone comes via the periosteum and from nutrient ar
teries which penetrate the cortical bone to supply the marrow space. The direction
of blood flow through the cortical bone is centrifugal, but a proportion of the
blood returns to the marrow space via small sinusoidal channels, which are lined
with reticuloendothelial cells capable of converting into osteoblasts in response to
trauma or grafting.
When bone undergoes fracture or is grafted to a healthy bed, bone repair de
pends on the function of the osteogenic cells of the periosteum, marrow and end
osteum. The dividing cells responsible for the repair are called the osteoprogenitor
cells. These cells transform into preosteoblasts and preosteoclasts. The osteoblasts
deriving from the preosteoblasts synthesise collagen and mucopolysaccharide,
which surround the cells to form osteoid tissues, i. e. the matrix of the future bony
tissue. Calcification of the matrix usually follows at a later stage, after which the
osteoblasts become housed as osteocytes within lacunae. This process of osteogen
esis occurs when there is mitotic stimulation of the osteogenic cells or when there
is osteogenic induction of primitive connective tissue cells (reticuloendothelial
cells) [19, 20). The factors affecting the mitotic stimulus to repair include trauma
and, to a lesser extent, infection. Bone necrosis might produce biochemical reac
tions which, in experimental animals, are observed to be much more extensive
than the site directly involved.
When bone is grafted into susceptible tissues, bone formation is induced. It re
mains to be established whether this effect relies on the release of chemical sub
stances from the bone itself or whether it is the direct stimulation of the protein
content of bone.
The current picture of the process of biological calcifications portrays the cells
within the calcifying tissues as central factors controlling the deposition of mineral
crystals in the extracellular matrix. The initiation of calcification may be a mem
brane-associated phenomenon. The cell responds to hormones and second mes
sengers, and other changes in its environment, regulating the concentration of ions
within the extracellular matrix, and secreting macromolecules whose properties
determine the ability of the matrix to calcify. The mitochondria within the cells ac
cumulate calcium and phosphate, releasing these ions into the matrix as calcifica
tion progresses. Extracellular matrix vesicles, derived from the cells of some calci-
Fate of Bone Grafts 3
fying matrices, provide sites for initial mineral deposition in many tissues. Among
the macromolecules secreted by the cell, collagen provides the support for the hy
droxyapatite crystals, and proteoglycans serve to control the extent and progress
of mineralisation. The proteoglycans, glycoproteins, enzymes and the collagen it
self, along with the cells, determine the nature of the matrix, while phosphopro
teins, proteolipids and phospholipids may serve as hydroxyapatite nucleators or as
surfaces upon which apatite is deposited. But it is the interaction of many or all of
these factors that determines the process of biological calcification and controls
the properties of the calcified matrices [21-23].
Normal cortical bone is undergoing internal remodelling throughout life. In
this process, bone resorption matches bone accretion. The resorption process in
volves osteoclasts which may change into osteoblasts to facilitate the process of
bone accretion, through a mechanism which is still unknown. This process of
accretion and resorption is called remodelling and, while occurring in a more ex
aggerated manner in bone grafts, is known as creeping substitution [24].
Fate of Bone Grafts
Autograft
Most of the bone graft (cortical or cancellous) becomes necrotic after grafting. On
ly the most superficial layers survive to become a source of osteogenesis. Frag
mentation of bone is frequently performed to provide more exposed surfaces,
quicker reconstruction and greater resistance to infection. However, if the bone is
broken up too finely, it is no longer osteogenic and may even act as a foreign
body. Similarly, shavings and chips of cortical bone have little osteogenicity and
are of little value as grafting material.
The survival of the graft depends on the establishment of blood flow from the
surrounding tissues. When a graft is placed in its transplanted position, most of it
dies, except for the most superficial thin layer, the cells of which survive by obtain
ing direct nourishment from the surrounding tissues. For cortical bone graft, re
vascularisation is faster if the periosteum is removed; the process has to go via
necrotic Haversian canals [25].
Revascularisation of cancellous bone occurs quickly (in about 3 weeks) if the
graft is small. The optimal conditions for survival will be provided by placing the
bone graft in the closest contact with a vascular bed of bone and marrow and with
healthy muscle overlying it.
The formation of new bone must occur before union between the bone graft
and its bed is established. The osteogenesis of repair comes from the graft and its
bed. The cancellous graft from the iliac crest supplies a large trabecular endosteal
surface covered with osteogenic cells plus red marrow which is itself osteogenic
after transplantation. The fatty cancellous bone from long bones and from small
bones like the tarsus does not contain red marrow, and after necrosis, its fat con
tent might inhibit revascularisation. Worse still is the cortical bone, which contrib-