CHAPTER 2

Anatomy of Bone and

Fracture Healing
TOPICS
• Anatomy of bone
• Growth of a long bone
• Blood supply of bones
• Fracture healing
•  Healing of cancellous bones
• Primary and secondary bone healing
• Factors affecting fracture healing

ANATOMY OF BONE
Bones may be classified into four types on the basis
of their shape i.e., long, short, flat and irregular. For
practical purposes, anatomy of a typical long bone
only is being discussed here.
Structure of a typical long bone: In children,
a typical long bone, such as the femur, has two
ends or epiphyses (singular epiphysis), and an
intermediate portion called the shaft or diaphysis.
The part of the shaft which adjoins the epiphysis
is called the metaphysis – one next to each epiphysis
(Fig-2.1). There is a thin plate of growth cartilage,
Fig-2.1 Parts of a child's bone
one at each end, separating the epiphysis from the
metaphysis. This is called the epiphyseal plate. At
maturity, the epiphysis fuses with the metaphysis
and the epiphyseal plate is replaced by bone. The
articular ends of the epiphyses are covered with
articular cartilage. The rest of the bone is covered
with periosteum which provides attachment to
tendons, muscles, ligaments, etc. The strands of
fibrous tissue connecting the bone to the periosteum
are called Sharpey's fibres.
Microscopically, bone can be classified as either
woven or lamellar. Woven bone or immature bone
is characterized by random arrangement of bone
cells (osteocytes) and collagen fibres. Woven bone
is formed at periods of rapid bone formation, as in
the initial stages of fracture healing. Lamellar bone or
mature bone has an orderly arrangement of bone cells
and collagen fibres. Lamellar bone constitutes all
bones, both cortical and cancellous. The difference
is, that in cortical bone the lamellae are densely
packed, and in cancellous bone loosely.
The basic structural unit of lamellar bone is
the osteon. It consists of a series of concentric
laminations or lamellae surrounding a central canal,
the Haversian canal. These canals run longitudinally
and connect freely with each other and with
Volkmann's canals. The latter run horizontally from
endosteal to periosteal surfaces. The shaft of a bone

Fig-2.2 Cortico-cancellous junction
is made up of cortical bone, and the ends mainly
of cancellous bone. The junction between the two,
termed the cortico-cancellous junction is a common
site of fractures (Fig-2.2).
Structural composition of bone: The bone is made
up of bone cells and extra-cellular matrix. The
matrix consists of two types of materials, organic
and inorganic. The organic matrix is formed by the
collagen, which forms 30-35 percent of dry weight
of a bone. The inorganic matrix is primarily calcium
and phosphorus salts, especially hydroxyapatite
[Ca10(PO4)6(OH)2]. It constitutes about 65-70 percent
of dry weight of a bone.
Bone cells: There are three main cell types in the
bone. These are:
a) Osteoblasts: Concerned with ossification, these
cells are rich in alkaline phosphatase, glycolytic
enzymes and phosphorylases.
b) Osteocytes: These are mature bone cells which
vary in activity, and may assume the form of an
osteoclast or reticulocyte. These cells are rich in
glycogen and PAS positive granules.
c) Osteoclasts: These are multi-nucleate mesen
­
chymal cells concerned with bone resorption.
These have glycolytic acid hydrolases, collage-
nases and acid phosphatase enzymes.
GROWTH OF A LONG BONE
All long bones, with the exception of the clavicle,
develop from cartilaginous primordia (enchondral
ossification). This type of ossification commences
in the middle of the shaft (primary centre of
ossification) before birth. The secondary ossification
centres (the epiphyses) appear at the ends of the
bone, mostly* after birth.
The bone grows in length by a continuous growth
at the epiphyseal plate. The increase in the girth of
the bone is by subperiosteal new bone deposition.
* The epiphysis of distal end of the femur is present at birth.
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Anatomy of Bone and Fracture Healing | 9
At the end of the growth period, the epiphysis
fuses with the diaphysis, and the growth stops. The
secondary centres of ossification, not contributing
to the length of a bone, are termed apophysis (e.g.,
apophysis of the greater trochanter). The time and
sequence of appearance and fusion of epiphysis has
clinical relevance in deciding the true age (bone age)
of a child. Sometimes, an epiphyseal plate may be
wrongly interpreted as a fracture.
Remodelling of bone: Bone has the ability to
alter its size, shape and structure in response to
stress. This happens throughout life though not
perceptible. According to Wolff's law of bone
remodelling, bone hypertrophy occurs in the plane
of stress.
BLOOD SUPPLY OF BONES
There is a standard pattern of the blood supply of a
typical long bone. Blood supply of individual bones
will be discussed wherever considered relevant. The
blood supply of a typical long bone is derived from
the following sources (Fig-2.3):
a) Nutrient artery: This vessel enters the bone
around its middle and divides into two branches,
one running towards either end of the bone.
Fig-2.3 Blood supply of a typical long bone
Each of these further divide into a leash of
parallel vessels which run towards the respective
metaphysis.
b) Metaphyseal vessels: These are numerous small
vessels derived from the anastomosis around the
joint. They pierce the metaphysis along the line
of attachment of the joint capsule.
c) Epiphyseal vessels: These are vessels which
enter directly into the epiphysis.
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d) Periosteal vessels: The periosteum has a rich
blood supply, from which many little vessels
enter the bone to supply roughly the outer-third
of the cortex of the adult bone.
Blood supply to the inner two-thirds of the bone
comes from the nutrient artery and the outer one-
third from the periosteal vessels.
FRACTURE HEALING
The healing of fractures is in many ways similar to
the healing of soft tissue wounds, except that soft
tissue heals with fibrous tissue, and end result of
bone healing is mineralised mesenchymal tissue, i.e.
bone. A fracture begins to heal soon after it occurs,
through a continuous series of stages described
below (Table–2.1).
STAGES IN FRACTURE HEALING OF CORTICAL BONE (FROST, 1989)
• Stage of haematoma
• Stage of granulation tissue
• Stage of callus
• Stage of remodelling (formerly called consolidation)
• Stage of modelling (formerly called remodelling)
Stage of haematoma: This stage lasts up to 7 days.
When a bone is fractured, blood leaks out through
torn vessels in the bone and forms a haematoma
between and around the fracture. The periosteum
and local soft tissues are stripped from the fracture
ends. This results in ischaemic necrosis of the
fracture ends over a variable length, usually only
a few millimetres. Deprived of their blood supply,
some osteocytes die whereas others are  sensitised
to respond subsequently by differentiating into
daughter cells. These cells later contribute to the
healing process.
Stage of granulation tissue: This stage lasts for about
2-3 weeks. In this stage, the sensitised precursor cells
(daughter cells) produce cells which differentiate
and organise to provide blood vessels, fibroblasts,
osteoblasts etc. Collectively they form a soft granulation
tissue in the space between the fracture fragments. This
cellular tissue eventually gives a soft tissue anchorage
to the fracture, without any structural rigidity. The
blood clot gives rise to a loose fibrous mesh which
serves as a framework for the ingrowth of fibroblasts
and new capillaries. The clot is eventually removed by

Table–2.1: Stages of fracture healing (Frost, 1989)

Stage of healing Approximate time Essential features

Stage of haematoma Less than 7 days Fracture end necrosis occurs.

Sensitisation of precursor cells.

Stage of granulation tissue Up to 2-3 weeks Proliferation and differentiation

of daughter cells into vessels,
fibroblasts, osteoblasts etc.
Fracture still mobile.

Stage of callus 4-12 weeks Mineralisation of granulation tissue.

Callus radiologically visible.
Fracture clinically united, no more mobile.

Stage of remodelling 1-2 years Lamellar bone formation by multicellular

unit based remodelling of callus. Outline
of callus becomes dense and sharply defined.

Stage of modelling Many years Modelling of endosteal and periosteal

surfaces so that the fracture site becomes
indistinguishable from the parent bone.

macrophages, giant cells and other cells arising in
the granulation tissue.
From this stage, the healing of bone differs from that
of soft tissue. In soft tissue healing the granulation
tissue is replaced by fibrous tissue, whereas in bone
healing the granulation tissue further differentiates
to create osteoblasts which subsequently form bone.
Stage of callus: This stage lasts for about 4-12
weeks. In this stage, the granulation tissue
differentiates further and creates osteoblasts. These
cells lay down an intercellular matrix which soon
becomes impregnated with calcium salts. This
results in formulation of the callus, also called woven
bone. The callus is the first sign of union visible on
X-rays, usually 3 weeks after the fracture (Fig-2.4).
The formation of this bridge of woven bone imparts
good strength to the fracture. Callus formation is
slower in adults than in children, and in cortical
bones than in cancellous bones.
Stage of remodelling: Formerly called the stage
of consolidation. In this stage, the woven bone is
replaced by mature bone with a typical lamellar
structure. This process of change is multicellular
unit based, whereby a pocket of callus is replaced by
a pocket of lamellar bone. It is a slow process and
takes anything from one to four years.
Stage of modelling: Formerly called the stage of
remodelling. In this stage the bone is gradually
strengthened. The shapening of cortices occurs at
the endosteal and periosteal surfaces. The major
stimulus to this process comes from local bone
strains i.e., weight bearing stresses and muscle
forces when the person resumes activity. This stage
is more conspicuous in children with angulated
fractures. It occurs to a very limited extent in
fractures in adults.
HEALING OF CANCELLOUS BONES
The healing of fractured cancellous bone follows
a different pattern. The bone is of uniform spongy
texture and has no medullary cavity so that there is
a large area of contact between the trabeculae. Union
can occur directly between the bony trabeculae.
Subsequent to haematoma and granulation formation,
mature osteoblasts lay down woven bone in the
intercellular matrix, and the two fragments unite.
PRIMARY AND SECONDARY BONE HEALING
Primary fracture healing occurs where fracture
haematoma has been disturbed, as in fractures
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Anatomy of Bone and Fracture Healing | 11
Fig-2.4 X-ray of the fracture of the tibial
shaft showing callus formation
treated operatively. The bone heals directly, without
callus formatiom, and it is therefore diffcult to
evaluate union on X-rays. Secondary fracture healing
occurs in fractures where fracture haematoma is
not disturbed, as in cases treated non-operatively.
There is healing, with callus formation, and
can be evaluated on X-rays. It also occurs in
fractures operated without disturbing the fracture
haematoma, as in fractures fixed with relative
stability (e.g. comminuted fractures).
FACTORS AFFECTING FRACTURE HEALING
a) Age of the patient: Fractures unite faster in
children. In younger children, callus is often
visible on X-rays as early as two weeks after
the fracture. On an average, bones in children
unite in half the time compared to that in adults.
Failure of union is uncommon in fractures of
children.
b) Type of bone: Flat and cancellous bones unite
faster than tubular and cortical bones.
c) Pattern of fracture: Spiral fractures unite faster
than oblique fractures, which in turn unite faster
than transverse fractures. Comminuted fractures
are usually result of a severe trauma or occur in
osteoporotic bones, and thus heal slower.
d) Disturbed pathoanatomy: Following a fracture,
changes may occur at the fracture site, and may
hinder the normal healing process. These are:
(i) soft tissue interposition; and (ii) ischaemic
fracture ends. In the former, the fracture ends
pierce through the surrounding soft tissues, and
12 | Essential Orthopaedics

get stuck. This causes soft tissue interposition
between the fragments, and prevents the callus
from bridging the fragments. In the latter, due
to anatomical peculiarities of blood supply of
some bones (e.g. scaphoid), vascularity of one
of the fragments is cut off. Since vascularised
bone ends are important for optimal fracture
union, these fractures unite slowly or do not
unite at all.
e) Type of reduction: Good apposition of the
fracture results in faster union. At least half the
fracture surface should be in contact for optimal
union in adults. In children, a fracture may unite
even if bones are only side-to-side in contact
(bayonet reduction).
f) Immobilisation: It is not necessary to immobi­
lise all fractures (e.g., fracture ribs, scapula, etc).
They heal anyway. Some fractures need strict
immobilisation (e.g., fracture of the neck of the
femur), and may still not heal.
g) Open fractures: Open fractures often go
into delayed union and non-union (discussed
subsequently on page 21).
h) Compression at fracture site: Compression
enhances the rate of union in cancellous bone.
In cortical bones, compression at the fracture
site enhances rigidity of fixation, and possibly
results in primary bone healing.
Further Reading
• Frost HM:  The biology of fracture healing. An overview for
clinicians, Part I. Clinical Orthopaedics and Related Research.
Nov: 1989 (248): 283-293.
• Frost HM:  The biology of fracture healing. An overview
for clinicians, Part II. Clinical Orthopaedics and Related Research,
Nov: 1989 (248): 294-309.

  What have we learnt?

• There are different parts of a long bone such as diaphysis, metaphysis and epiphysis. There
are diseases which typically affect only some parts of the bones.
• Growing skeleton is identified by presence of growth plate.
• The structure of the bone is complex, made of the basic structural unit called osteon.
• Different bone cells have different functions.
• Fracture healing follows a series of stages.
• Fracture healing depends upon a number of factors.

Additional information: From the entrance exams point of view

Pathognomonic sign of traumatic and fresh fracture is crepitus.
Most common cause of non-union is inadequate immobilisation.
Markers of bone formation: Serum bone specific alkaline phosphatase
Serum osteocalcin
Serum peptide of type 1 collagen
Markers of bone resorption: Urine and serum crosslinked ‘N’ telopeptide
Urine and serum crosslinked ‘C’ telopeptide
Urine total free deoxypyridinoline
Rate of mineralisation determined by labelled tetracycline.