FRACTURE HEALING IN CORTICAL

AND CANCELLOUS BONE

(ADULT Vs CHILD)

MODERATERS: PRESENTED BY:

Dr.G.C Basavraj M.S (Ortho) Dr.PRAMOD.B.M
Professor and Unit Head PG IN ORTHOPAEDICS

Dr.Manjunath reddy M.S (ortho)

Asso.Professor DATE: 23/12/09
INTRODUCTION:

• Fracture is defined as a break in the continuity of

bone. Fracture results in loss of its mechanical
stability and also partial destruction of blood
supply.
• Healing means to make whole or sound again, to
cure, leaving a scar behind. But following fracture
a scar is not formed, instead a bone has formed a
new at the original fracture site. So rather than
bone healing the appropriate nomenclature
would be BONE REGENERATION
HISTORY :
Bones have broken since the beginning of humanity and have
been recognised and treated as long as recorded history.
• History of fracture and its knowledge dates back to Egyptian
mummies of 2700 B.C

• In 17th century Albrecht Haller, observed invading capillary

buds in fracture callus and taught that blood vessels are
responsible for callus formation.

• John Hunter, a pupil of Haller, described the morphologic

sequence of fracture healing.

• In 1873, Kolliker observed the role of multinucleated giant

cells, osteoclast to be responsible for bone resorption.
 HISTORY contd...
• In1939, Gluksman suggested pressure and shearing stresses
are possible stimuli for fracture healing.
• In 1961, Tonna and Cronkie demonstrated the role of local
mesenchymal cells in fracture repair.
ANATOMY OF BONE:
Bone is essentially a highly vascular, living,
constantly changing mineralized connective tissue.
It is remarkable for its hardness, resilience and
regenerative capacity, as well as its characteristic
growth mechanism

Macroscopically : living bone is white, with either

dense texture like ivory or honeycombed by large
cavites.
Bone made up of two components,
• Outer dense, compact / Cortical bone
• Inner spongiosa /trabeacular /Cancellous bone
BONE MACROSCOPY:
HISTOLOGY OF BONE

WOVEN BONE CORTICAL BONE CANCELLOUS BONE

Microscopically: Bone is classified as
• Woven / Immature bone : Characterized by
random arrangement of cells and collagen
,associated with periods of rapid bone
formation, such as in initial stage of fracture
healing
• Lamellar bone / Mature bone : Characterized by
an orderly cellular distribution and properly
oriented collagen fibres . This constitutes
organised bone both cortical and cancellous
HEVERSIAN SYSTEM:
 PERIOSTEUM

PERIOSTEUM: The bone is surrounded by

periosteum which is made up of an outer layer
of white fibrous and elastic tissue and inner
cambium layer which has a looser
composition, is more vascular and contains
cells with osteogenic potency. Another layer
the endosteum, lines the surface of cancellous
bone.
Functions of periosteum
• The periosteum serves as a limiting membrane for bone .
• The outer fibroblast layer provides fibrous attachment to
subcutaneous connective tissue, muscle, tendons and
ligaments.
• Inner cambium layer contains pools of undifferentiaited cells
that support bone formation during embrogenic and post
natal growth.
• Periosteum helps in fracture healing by forming periosteal
callus.
• Intact Periosteal hinge or sleeve may lessen the extent of
displacement of fracture fragments and it also can be used to
assist in the reduction
 Blood supply:
Bone derives its blood supply mainly from
• Nutrient artey

• Epipyseal/ Metaphyseal artries

• Periosteal artries

• Muscular, ligamentous and

capsular arteries
Bone cells:
1.Osteoprogenitor cells: (osteogenic/ proosteoblasts)
These are undifferentiated mesenchymal stem cells which under
appropriate conditions can differentiate into osteoblast, chondroblast
and fibroblast. In case of fracture, they divide by mitosis once or twice
and differentiate into osteoblasts.
Types:

Committed osteoprogenitor cells-committed in formation of bone tissue

Inducible osteoprogenitor cells – they differentiate depending on the

inducer into osteoblast/chondroblast/fibroblast.
2.OSTEOBLASTS:
They are basophilic,cuboidal,mononuclear cells about 15-
30micro meter forming the continuous monolayer over the
surface of bone. They are derived from marrow stromal cells by
differentiation of pre-osteoblasts .
They:
1.Synthesize major protein of bone
Type 1 collagen
Non collagenous protein – Osteocalcin
- osteonectin
2.Control mineralization of bone by secretion of
alkaline phosphatase
3.Recent evidence suggest osteoblasts control osteoclastic
function by secretion of prostaglandin , interlukin 6 and
interlukin 11.
3.OSTEOCLASTS:
Large, multinucleated gaint rounded cells having numerous
mitochondria and lysosomes. They help in removing of living
bone know as osteoclasis. They are found where active
erosions of bone and lie in direct contact with the bone
surface in pits termed “Resorption bays” or “lacunae of
howship”.
RESORPTION AND NEW BONE FORMATION
3.OSTEOCYTES:

Derived from osteoblasts, when they get incarcerated in

the matrix which they secrete and get burried deep with
in the bone. They occupy spaces in the matrix called as
lacunae. Canaliculi radiate from each lacunae and permit
diffusion. They secrete alkaline phosphatase to maintain
calcification
The Biology of fracture fixation:
Fracture in man heals or unites by two main ways:
A)Primary healing / Osteonal / Direct healing :
Bone formation occurs directly without any callus
formation. This occurs particularly in stable, aligned,
closely apposed fractures. It is roughly comparable to
healing of soft tissue by primary intention. Occurs both
in Cortical and Cancellous bones. Eg:plating done in
case of fracture both bone forearm
Rigid fixation “fools” the bone into “thinking”
Is wasn’t broken
Types of primary healing:
1.Contact healing/ Haversian remodelling : When there is
direct contact between the cortical bone ends, lamellar
bone forms directly across the fracture line , parallel to
long axis of the bone, by direct extension of osteons.

CUTTER HEAD
2.Gap healing: Osteoblats differentiate and start
depositing osteods on the exposed surfaces of
fragment ends, mostly without a preceding
osteoclastic resorption. In large gaps of 200micro
meter – 1mm, the cells fill the defect with woven
bone and haversian remodelling begins to deposit
the lamellar bone.
B) Secondary healing/ Indirect healing
It is usual type consisting of formation of callus either of
cartilaginous or fibrous. This callus is later replaced by
lamellar bone. It is comparable to healing of soft tissue by
filling of gaps with vascular granulation tissue.
Osteoinduction and Osteoconduction
• Osteoinduction is the first step in bone healing, it causes mesenchymal
cells to differentiate into various cells which then proliferate and
produce messenger substances which further stimulate the
messenchymal cells to differentiate. This good cycle continues till
healing.
• In osteoconduction, a scaffold of collagenous network has developed,
upon which the reparative cells produce callus and bone. It facilitates
bone deposition in an orderly fashion and helps the callus to bridge the
gap between the fragments.
• Allografts has powerful osteoinductive as well as osteoconductive
properties.
 The natural course of fracture
healing includes :
 Stabilisation of fractured bone fragments by
periosteal and endosteal callus formation and by
fibrocartilage differentiation.
 Restoration of continuity and bone union by
ossification
 Substitution of avascular and necrotic areas by
haversian remodelling
 Malallignment can be corrected to a certain extent,
by remodelling at fracture site.
 Functional adaptation.
STAGES OF FRACTURE HEALING:
1. STAGE OF HAEMATOMA
FORMATION:

•Following fracture the local marrow,

periosteum and adjacent soft tissue
as well as the living bone itself get
damaged.

• As a result there will be

accumulation of blood within the
medullary cavity, fracture ends and
beneath the periosteum .

• The ring of bone immediately

adjacent to each side of fracture
becomes ischaemic, deprived of
blood supply
•The fracture hematoma immobilizes the fracture and
the swelling hydrostatically splints the fracture.

•The fracture haematoma provides a fibrin scaffold that

facilitates migration of repair cells.

The hematoma provides 2 important factors:

•It provides small amount of mechanical stability of

fracture site.
•Hematoma brings the osteoblasts, and the
chondrocytes precursors to fracture site in large
numbers that being to differentiates into osteoblasts
and chondrocytes to begin producing matrix.
 2.Stage of granulation tissue
•Granulation tissue invades and
replaces the initial hematoma and
then differentiates into connective
tissue and fibrocartilage.

• Injured tissue and platelets releases

vasoactive mediators such as
serotonin and histamine cause blood
vessels to dilate and exude plasma,
leading to acute edema.

• Macrophages and osteoclasts come

into the site to remove damaged and
necrotic tissue
• The precursor cells from the deep surface of
periosteum close to the fracture in the sensitized
and stimulated local mediator mechanism begin to
produce new cells that differentiate and organise to
provide new vessels, fibroblast, intercellular matrix
and supporting cells.

• Collectively they form granulation tissue which

grows forward, outside and inside the bone to
bridge the fracture.
 3.Stage of repair/callus
• The process of osteogenesis
continues and fracture callus
bridges the fracture site and its
subsequent transition to mature
bone takes place.
• The bone can be produced through
intramembranous/ endochondral
ossification or both.
• Nests of cartilage cells or their
precursors lay new osteoid tissue.
• The cells synthesize a matrix with
high concentration of type-1 collagen
fibrils, and then create condition that
promote deposition of cluster of
calcium hydroxyapatite crystals in
collagen fibrils.
• Later osteoblasts, release
“prepacked” calcium phosphates
complex into the matrix. As
mineralization proceeds, the bone
ends gradually become enveloped in
a fusiform mass of callus.
TYPES OF CALLUS:
•External bridging callus/periosteal callus

•Medullary callus

•Soft fibrous callus / Cartilagenous callus

•Hard calls
4.Stage of consolidation:

The woven bone that forms the primary

callus is gradually transformed by the
activity of the osteoblasts into more
mature bone with a typical lamellar
structure.
5. Stage of remodelling:
•The process occurs along with usual
deposition–resorption phenomenon.

•It is a gradual modification of the

fracture region under the influence of
mechanical loads until it reaches some
threshold of optimal shape, which
typically is similar to the shape it had
before the fracture.

• Angular deformities slowly

decrease/disappear as bone is laid
down on the concave surface and
removed from convex surface.
CHEMICAL MEDIATORS OF FRACTURE HEALING:
1.Fracture haematoma contains many messenger substances:
• Serotonin Histamine
• PG E 2 Thrombroxane A2
• Hormones Growth factors
• Bone morphogenic proteins (cytokines)

2.Growth factors:
• Transforming growth factor beta
• Fibroblast growth factor
• Platelet derived growth factor
3.Permiability factors:
• Protease – Plasmin , Kalikrein, Globulin permeability factor.
• Polypeptides –leucotaxime,Bradykinin,Kallidin
• Amines – Adrenalin, nor-adrenalin,Histamine
All these factors influence fracture healing in various process that
involves
– Increase capillary permeability
– Alteration in diffusion mechanism in intracellular matrix
– Cellular migration
– Proliferation & differentiation
– New blood vessel formation
– Matrix synthesis
– Growth & developmen
BONE MORPHOGENIC PROTIEN:
BMP was discovered by Marshall Urist in 1969. It is a group of growth factor
proteins within the transforming growth factor-b (TGF-b) superfamily of
growth factors.
More than twenty types of BMP have been recognized, but only BMP-2,
4, 6, 7, and 9 have been shown to have significant osteogenic properties.
FUNCTIONS:
These molecules have osteoinductive properties which provide signal
for differenciation of mesenchymal cells into osteoblasts and chondroblasts.
BMP molecules seem to induce bone formation in a stepwise fashion, with
individual BMP molecules functioning at different stages of osteoblastic
differentiation and osteogenesis
USES:
• 1.In enhancing fracture healing: Implantation of recombinant human BMP
(rhBMP) induces bone formation by causing the differentiation of
mesenchymal cells into chondroblasts and osteoblasts.
• 2.Spinal fusion: rhBMP-2 is one component in a system used during spinal
fusions for the treatment of degenerative disc disease.
FRACTURE HEALING IN CANCELLOUS BONE :
Cancellous bone even with an intact blood supply has in fact a very
restricted form of osteogenic activity. Healing process follows a different
pattern here. Many injuries of cancellous bone are intra articular hence
accurate reconstruction is essential in order to restore the congruity of
the articular surface

1.Cancellous bone heals by “CREEPING SUBSTITUTION” - New

blood vessels can invade the trabecular of cancellous bone
and bone opposition may take place directly on to the surface
of trabeculum.
2.Heals at the point of direct contact: Cancellous bone
certainly can unite very rapidly, but it unites rapidly
only at the points of direct contact

3.No bridging callus :

Cancellous bone unites only by contact, not by throwing out
callus. In other words a cut surface of cancellous bone even
with an intact blood supply does not throw out callus. Dense
attachment of periosteum to cancellous bone prevents callus
formation
4.No death of osteocytes : In comparing the healing of cancellous
bone with cortical bone it is to be noted that cancellous bone
there appears to be no death of the osteocytes in the cut edges
of divided trabeculae. This must be because of the blood supply
is good and large surface area of the trabecular spaces combined
with relatively thin trabeculae, keep the osteocytes nourished.

5.Has tendency for late collapse :

This lack of callus production by cancellous bone explains the
tendency to late collapse in the healing of fractures in cancellous
bone which have been distracted. Then after reduction of colle’s
fracture a hallow cavity is left in the cancellous end of the radius.
FRACTURE HEALING IN CORTICAL
BONE:
FRACTURE HEALING IN CHILDREN:
• Compared with the relatively static mature bone
of adult, the changing structure and function
both physiological and biomechanical of
immature bones make them susceptible to
different patterns of fracture .
• Fracture in children are more common and are
more likely to occur after seemingly insignificant
trauma. Damage involving specific growth
regions such as the physis or epiphyseal
ossification center may lead to acute and
chronic growth disturbances.
Anatomical region of the child’s bone :

Epiphysis : Ends of long bone

which ossifies from secondary
center called epiphysis.
At birth each epiphysis
consists of completely
cartilaginous called
chondroepiphysis. Cartilage
gradually ossifies until the
cartilagious area has been almost
completely replaced by bone at
skeletal maturity. External surface
of an epiphysis is composed of
either articular cartilage or
perichondrium. Perichondrium
blends into the periosteum
• Physis :
Physis or growth plate present between epiphysis and
metaphysic primary function of the physis is rapid integrated
longitudinal and latitudinal growth. It appear radiolucent on X-
ray. Ischemia of physis due to fracture can lead to growth
disturbances.
Four zones within the physis
1. The resting cartilage zone
2. The proliferating cartilage zone
3. The zone of hypertrophy and
4. The zone of calcification.
Metaphysis :
Epiphyseal end of diaphysis is known as metaphysis

Major characteristic are

• Decreased thickness of cortical bone
• Increased trabecular one
• Shows extensive considerable bone turnover compared
with other region of the bone.
• Metaphysis is the site of extensive osseous modelling
and remodelling.
• A torus (Buckle) fracture is most likely to occur in a
metaphysis region with a trabecular, fenestrated
compressible cortex
Diaphysis :
Shaft of long bone which ossifies from
primary centre.

At birth the diaphysis is composed of laminar

(fetal woven) bone. The developing
diaphyseal bone is extremely vascular.
Periosteum mediated, membranous bone
formation leads to over all enlargement of
diameter of shaft variably increased width of
diaphyseal cortices and formation of marrow
cavity.
Periosteum :
A child’s periosteum is thicker, more redily
elevated from the diaphyseal and metaphyseal
bone and exhibits greater osteogenic potential
than of an adult.
Attachment :
Periosteum is attached relatively loosely to the
diaphysis. It is firmly fixed to the metaphysis
subsequently attaches densely into the
peripheral physis, blends into the zone of ranvier
as well as the epiphyseal perichondrium.
 FRACTURES UNIQUE IN CHILDRENS:
1.Physeal Fractures
• 18-30% of pediatric fractures
• Common in adolescence peak age 11-12 yrs
• Usually occur in the upper limb
• Physis contains the zone of provisional
calcification, which is a relatively weak area
 Torus “Buckle” Fracture
• Common fracture
• Metaphyseal region secondary to a
compressive loading
• Cortex “buckles” resulting
in a stable fracture
 Greenstick Fracture
• Most common fracture pattern in children

• Incomplete fracture at metaphyseal-

diaphyseal junction

• One cortex remains intact

• Angulation and rotation common

• Often must complete the fracture to

achieve union
 Bowing Fracture
• Longitudinal force on the
bone which stops short of
fracture, but causes a
persistent plastic deformity

• Little remodeling

• Functional and cosmetic

deficits common
 FRACTURE REPAIR IN CHILDREN
Fracture healing in children follow same pattern of
adults but with some peculiarities :
PERIOSTEUM:
• In the contrast to adults the periosteum strips away easily
from the underlying bone in children. Allowing fracture haematoma to
dissect along the diaphysis and metaphysic and this is evident in the
subsequent amount of new bone formation along the shaft.
• Dense attachment of the periosteum into the zone of
ranvier limit subperiosteal hematoma formation to the metaphysic and
diaphysis
• In children because of osteoblastic activity, the periosteum
contributes significantly to new bone formation by accentuating the
normal process of membranous ossification.
 REMODELLING:
WOLLF’s LAW
Defination: The principle that every change in the form and the function
of a bone or in the function of the bone alone, leads to changes in its
internal architecture and in its external form.
Bone in a healthy person will adapt to the loads it is
placed under. If loading on a particular bone increases, the bone will
remodel itself over time to become stronger to resist that sort of loading.
The internal architecture of the trabeculae undergoes adaptive changes,
followed by secondary changes to the external cortical portion of the
bone
The remodelling phase is the longest phases and in
children may continue until skeletal maturation. Remodelling is better
in children compared to adult, This is in response to constantly changing
stress Patterns in children during skeletal growth and development.
REMODELLING:

3 yrs OLD CHILD

 ACCEPTABLE ANGULATION IN PAEDIATRIC
FEMORAL FRACTURES

AGE VARUS/ ANTEROIR/ ROTATION

VALGUS POSTERIOR

Birth to 2yrs 30 30

2-5yrs 15 20 Not acceptable

6-10yrs 10 15

11yrs to maturity 5 10
  
ACCEPTABLE ANGULATION IN PAEDIATRIC
FOREARM FRACTURES
SAGITAL PLANE
AGE BOYS GIRLS FRONTAL
PLANE
4-9 20 15 15

9-11 15 10 5

11-13 10 10 0

>13 5 0 0
VARIABLES THAT INFLUENCE FRACTURE
HEALING :
I) INJURY VARIABLE :
 OPEN FRACTURES

 INTRA ARTICULAR FRACTURES

 SEGMENTAL FRACTURES

 SOFT TISSUE INTERPOSITION

 DAMAGE TO BLOOD SUPPLY

II) PATIENT VARIABLES :
 AGE

 NUTRITION

 SYSTEMIC HORMONES

 NICOTINE
III) TISSUE VARIABLES :
 FORM OF BONE (Cancellous / cortical).

 BONE NECROSIS

 BONE DISEASE

 INFECTION
IV) TREATMENT VARIABLES
 APPOSITION OF FRACTURE FRAGMENTS

 LOADING AND MICROMOTION


 FRACTURE STABILIZATION

 RIGID FIXATION

 BONE GRAFTING

 DEMINARALIZED BONE MARROW

RECENT ADVANCES IN FRACTURE
HEALING:

• ULTRASOUND:
Low intensity pulsed ultrasound accelerates fracture
healing. It increases the aggrecan gene expression as well as
the concentration of intracellular calcium in fracture callus
chondrocytes. Hence it provides safe, non-invasive method
of facilitating healing of fractures.
• ELECTRIC STIMULATION:
Electric stimulation of bone has been taught to be an
effective and non invasive method for fracture healing and
treating fracture non union. Studies shows that electric field
generated helps in proliferation of bone cells.

Types

1. Direct electrical stimulation

2. Capacity coupling
3. Inductive coupling
• GROWTH FACTOR THERAPHY
Due to their ability to stimulate proliferation and differentiation
of mesenchymal and osteoprogenitor cells, growth factors such as
Tumour Growth Factor, Fibroblatic Growth Factor , Bone
morphogenic protein (BMP-2 and BMP-7) have shown great promise
for their ability to promote fracture repair .
• APPLICATION OF PLATELET RICH PLASMA
Injecting platelet rich plasma at fracture site helps in fracture
healing , The platelet α granules are rich in growth factors,such as
transforming growth factor-β, vascular endothelial growth factor, and
platelet derived growth factor that play essential role in fracture
healing.
• TISSUE ENGINEERING, STEM CEELS AND GENE THERAPIES
In past decade tissue culture and stem cells have been
implicated in enhancing fracture healing and articular cartilage
regeneration.
FRACTURE HEALING IS LIKE……
MAKING LOVE
•it’s quite natural
•may take considerable
time
•two components
•with good local blood
supply
•in close contact
•with a little movement