2.
Highly vascular , constantly changing mineralised
connective tissue.
Consists of cells (osteocytes) and intercellular
matrix.
Matrix : Composed of
a) Organic materials (40%) mainly
collagen fibres.
b) Inorganic salts rich in calcium and
phosphate.
Anatomy of Bone
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3.
Bone is made of two components:
1) Outer dense,compact / cortical bone.
- Forms the outer wall or supporting
structures.
- Supreme importance in providing strength.
2) Inner spongiosa / trabecular / cancellous
bone
- Forms the inner wall
- Provides additional strength to cortices and
support the bone marrow at the end of long bones.
Macroscopically
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4.
Two types:-
Woven / Immature bone:-
• Characterised by random arrangement of cells
and collagen,associated with period of rapid bone
formation,such as initial stage of fracture healing.
Lamellar / Mature bone:-
• Characterised by an orderly cellular distribution
and properly oriented collagen fibres. This constitutes
organised bone both cortical and cancellous.
Microscopically
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5.
Basic architectural unit of lamellar bone.
Consists of central Haversian canal which runs
longitudinally, is surrounded by concentric lamellar of bony
tissue.
Numerous lacunae intervene between the lamellae.
This lacunae communicate with each other and with central
canal by numerous radiating canaliculi.
The lacunae are filled with osteocytes and canaliculi contains
protoplasmic process of osteocytes and convey outwards the
nutritive materials.
The haversian canal communicate with medullary cavity and
with surface of bone by numerous oblique channels known as
Volkmann’s canal which consists of neurovascular bundle.
Osteon/haversian system
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7.
Osteoprogenitor cells: (osteogenic/pro-osteoblasts)
• Undifferentiated mesenchymal stem cells
• Can differentiate into osteoblast,chondroblast and fibroblast.
• Types: 1) Committed 2) Inducible
Osteoblasts:
• Basophillic, cuboidal, mononuclear cell.
• Derived from marrow stromal cells by differentiation of pre-
osteoblasts.
• Synthesize major protein of bone- type 1 collagen, osteocalcin and
osteonectin.
• Control mineralisation of bone by secretion of ALP.
• Recent evidence suggest osteoblasts control osteoclastic function
by secretion of PG’s and IL-6 and IL-11.
Bone cells
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8.
Osteocytes:-
• Derived from osteoblasts,when they get incacerated in the matrix
which they secrete and get burried deep within the bone.
• Occupy spaces in matrix called as lacunae.
• Secrete ALP to maintain calcification.
Osteoclasts:-
• Large , multinucleated giant rounded cells.
• Numerous mitochondria and lysosomes.
• Osteoclasis – help in removing of living bone.
• Osteoclastic resorption release bone matrix protein and cytokines
which stimulate osteoblast production and bone formation.
Other cells:- Reticular cells, Endosteal cells and Fibroblasts.
Bone cells cont…
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9.
Made up of:- a) Outer layer of fibrous and elastic tissue.
b) Inner Cambium layer
Functions:-
• Serves as a limiting membrane for bone.
• Outer fibroblast layer provides fibrous attachment to
subcutaneous connective tissue,muscles,tendons and
ligaments.
• Inner cambium layer contains pools of undifferentiated
cells tha support bone formation during embryogenic and
post natal growth.
• Helps in fracture healing by forming periosteal callus.
Periosteum
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12.
Fracture is a break in the structural
continuity of bone.
The healing of fracture is in many ways
similiar to the healing in soft tissue wounds
except that the end result is mineralised
mesenchymal tissue i.e. BONE.
Fracture healing starts as soon as bone
breaks and continues modelling for many
years
Introduction
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13.
Bone is unique in its ability to repair itself.,it can
completely reconstitute itself by reactivating
processes.
Bone repair is a highly regulated process that can
be seperated into overlapping histologic,bio-
chemical & bio-mechanical stages.
The completion of each stage initiates the next
stage and this is accomplished by a series of
interactions and communications among various
cells and proteins located in healing zone.
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14.
Pathology & Staging
In 1975, Cruess and Dumont proposed that fracture
healing may be considered to consist of three
overlapping phases: an inflammatory phase, a reparative
phase, and a remodeling phase
In 1989, FROST proposed the stages of fracture healing
five stages.
stage of haematoma
stage of granulation tissue
stage of callus
stage of modelling
stage of remodelling
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15.
The events in the process of fracture healing can be
divided into 3 phases.
1. Inflammatory Phase
a) Stage of Haematoma Formation.
b) Granulation tissue formation.
2.Reparative Phase
a) Cartilage callus formation
b) Lamellar bone deposition
3.Remodelling Phase
a) Remodelling to original bone contour
Pathology & Staging
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16.
Inflammation begins
immediately after
injury and is followed
rapidly by repair.
After repair has
replaced the lost and
damaged cells and
matrix,a prolonged
remodelling phase
begins.
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17.
An injury that fractures bones damages not only
the cells,blood vessels and bone matrix,but also the
surrounding soft tissue including the periosteum
and blood vessels.
Immediately after fracture,rupture of blood vessels
results in hematoma which fills the fracture gap and
also the surrounding area.
The clotted blood provides a fibrin mesh which
helps seal off fracture site and allows the influx of
inflammatory cells and ingrowth of fibroblasts &
new capillary vessels.
Inflammation Phase
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19. The degranulated platelets and migrating inflammatory
cells release PDGF, TGF-BETA, FGF and other
cytokines,which activates the osteoprogenitor cells in the
periosteum,medullary cavity,and surrounding soft tissues
and stimulate the production of osteoclastic and osteoblastic
activity.
Thus by the end of first week,the hematoma is
organizing,the adjacent soft tissue is being modulated for
future matrix production.
This fusiform & predominantly uncalcified tissue called
soft tissue callus or procallus provides some anchorge
between ends of fractured bones but offers no structural
rigidity for weight bearing.
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20.
The inflammatory cells releases the cytokines that
stimulate angiogenesis.
As the inflammatory response subsides,necrotic
tissue and exudate are reabsorbed and fibroblasts
and chondrocytes appear and start producing a new
matrix,the fracture callus .
Electronegativity found in the region of fresh
fracture may also simulate the osteogenesis.
Reparative Phase
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22. The activated osteoprogenitor cells deposit sub-
periosteal trabeculae of woven bone oriented
perpendicular to cortical axis and within the medullary
cavity.
In some cases the activated mesenchymal cells in soft
tissue and bone surrounding the fracture line also
differentiate into chondroblasts that make fibrocartilge
and hyaline cartilage.
The newly formed cartilage undergoes enchondral
ossification forming a network of bone
In this fashion,the fractured ends are bridged by a
bony callus and as it mineralizes,the stiffness and
strength of callus increase to point where controlled
weight bearing can be tolerated.
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23.
As the callus matures and transmits weight-
bearing forces,the portions that are not physically
stressed are reabsorbed,and in this manner the callus
is reduced in size until the shape and outline of
fractured bone has been reestablished.
The medullary cavity is also restored.
Remodelling Phase
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27.
I).OPEN FRACTURES:-
Severe open fractures cause soft tissue disruption,
fracture displacement, and, in some instances,
significant bone loss.
Extensive tearing or crushing of the soft tissue
disrupts the blood supply to the fracture site, leaving
necrotic bone and soft tissue, impeding or
preventing formation of a fracture hematoma, and
delaying formation of repair tissue
1.Injury variables
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28.
II).SEVERITY OF INJURY:-
They may be associated with large soft tissue
wounds, loss of soft tissue, displacement and
comminution of the bone fragments, loss of bone,
and decreased blood supply to the fracture site.
Comminution of bone fragments usually indicates
that there is also extensive soft tissue injury.
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29.
Displacement of the fracture fragments and severe
trauma to the soft tissues retard fracture healing,
probably because the extensive tissue damage
increases the volume of necrotic tissue, impedes the
migration of mesenchymal cells and vascular
invasion, decreases the number of viable
mesenchymal cells, and disrupts the local blood
supply.
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31.
III).INTRA-ARTICULAR FRACTURES:-
Because they extend into joint surfaces and joint
motion or loading may cause movement of the
fracture fragments, intra-articular fractures can
present with challenging problems.
Most intraarticular fractures heal, but if the
alignment and congruity of the joint surface is not
restored, the joint may be unstable, and,in some
instances, especially if the fracture is not rigidly
stabilized, healing may be delayed or nonunion may
occur.
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32.
IV).SEGMENTAL FRACTURES:-
A segmental fracture of a long bone impairs or disrupts
the intramedullary blood supply to the middle fragment.
If there is severe soft tissue trauma, the periosteal blood
supply to the middle fragment may also be
compromised.,possibly because of this, the probability of
delayed union or nonunion, proximally or distally, may
be increased.
These problems occur most frequently in segmental
fractures of the tibia, especially at the distal fracture site.
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33.
V).SOFT TISSUE INTERPOSITION:-
Interposition of soft tissue, including muscle, fascia,
tendon, and occasionally nerves and vessels, between
fracture fragments compromises fracture healing.
Soft tissue interposition should be suspected when the
bone fragments cannot be brought into apposition or
alignment during attempted closed reduction.
If this occurs, an open reduction may be necessary to
extricate the interposed tissue and achieve an acceptable
position of the fracture.
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34.
VI).DAMAGE TO BLOOD SUPPLY:-
Lack of an adequate vascular supply can significantly
delay or prevent fracture healing.
Insufficient blood supply for fracture healing may
result from a severe soft tissue and bone injury or from
the normally limited blood supply to some bones or bone
regions.
For example, the vulnerable blood supplies of the
femoral head,scaphoid, and talus may predispose these
bones to delayed union or nonunion, even in the absence
of severe soft tissue damage or fracture displacement.
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35.
I)AGE:-
Infants have the most rapid rate of fracture
healing.
The rate of healing declines with increasing age up
to skeletal maturity, but after completion of skeletal
growth the rate of fracture healing does not appear
to decline significantly with increasing age, nor does
the risk of non-unions significantly increase.
The rapid bone remodelling that accompanies
growth allows correction of a greater degree of
deformity in children.
2.Patient Variables
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36.
II)NUTRITION:-
The cell migration and proliferation and matrix
synthesis necessary to heal a fracture require substantial
energy.
Furthermore, to synthesize large volumes of collagens,
proteoglycans, and other matrix macromolecules, the cells
need a steady supply of proteins and carbohydrates, the
components of these molecules.
As a result, the metabolic state of the patient can alter
the outcome of injury, and in severely malnourished
patients, injuries that would heal rapidly in well
nourished people may fail to heal.
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37.
III).SYSTEMIC HORMONES:-
A variety of hormones can influence fracture healing.
Corticosteroids may compromise fracture healing
possibly by inhibiting differentiation of osteoblasts from
mesenchymal cells and by decreasing synthesis of bone
organic matrix components necessary for repair.
Prolonged corticosteroid administration may also
decrease bone density and compromise the surgeon's
ability to achieve stable internal fixation, leading to
nonunion.
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38.
The role of growth hormone in fracture healing
remains uncertain.
Thyroid hormone, calcitonin, insulin, and anabolic
steroids have been reported in experimental
situations to enhance the rate of fracture healing.
Diabetes, hypervitaminosis D, and rickets have
been shown to retard fracture healing in
experimental situations.
Nicotine and nicotine products(cigarette smoking)
inhibits fracture healing.
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39.
I)FORM OF BONE(CORTICAL OR
CANCELLOUS):-
Healing of cancellous and cortical fractures differs
probably because of the differences in surface area,
cellularity and vascularity.
Opposed cancellous bone surfaces usually unite
rapidly., possibly because the large surface area of
cancellous bone per unit volume creates many points
of bone contact rich in cells and blood supply and
because osteoblasts form new bone directly on
existing trabeculae.
3.Tissue Variables
2/17/2015 39
40.
In contrast, cortical bone has a much smaller
surface area per unit volume and usually a less
extensive internal blood supply, and regions of
necrotic cortical bone must be removed before new
bone can form.
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41.
II)BONE NECROSIS:-
Normally, healing proceeds from both sides of a
fracture,but if one fracture fragment has lost its
blood supply, healing depends entirely on ingrowth
of capillaries from the living side or surrounding soft
tissues.
If a fracture fragment is avascular the fracture can
heal, but the rate is slower and the incidence of
healing is lower than if both fragments have a
normal blood supply.
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42.
If both fragments are avascular, the chances for
union decrease further.
Traumatic or surgical disruption of blood vessels,
infection, prolonged use of corticosteroids, and
radiation treatment can cause bone necrosis.
2/17/2015 42
43.
Bone necrosis after a severe open
tibia fracture with failure of soft
tissue coverage
2/17/2015 43
44.
III)BONE DISEASE:-
Fractures through bone involved with primary or
secondary malignancies usually do not heal if the
neoplasm is not treated.
Subperiosteal new bone and fracture callus may
form,but the mass of malignant cells impairs or
prevents fracture healing,particularly if the
malignant cells continue to destroy bone.
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45.
Fractures through infected bone present a similar
problem.
Thus, healing of fractures through malignancies or
infections usually requires treatment of the
underlying local disease or removal of the involved
bone.
Depending on the extent of bone involvement and
the aggressiveness of the lesion, fractures through
bones with nonmalignant conditions like simple
bone cysts and Paget's disease will heal.
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46.
The most prevalent bone disease, osteoporosis,
does not impair fracture healing, but where there is
diminished surface contact of opposing cortical or
cancellous bone surfaces because of decreased bone
mass, the time required to restore normal bone
mechanical strength may be increased.
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47.
IV)INFECTION:-Infection can slow or prevent healing.
For fracture healing to proceed at the maximum rate,
the local cells must be devoted primarily to healing the
fracture.
If infection occurs after fracture or if the fracture occurs
as a result of the infection, many cells must be diverted to
attempt to wall off and eliminate the infection and energy
consumption increases.
Furthermore, infection may cause necrosis of normal
tissue, edema, and thrombosis of blood vessels, thereby
retarding or preventing healing.
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48.
Apposition of fracture fragments,decreasing the
fracture gap decreases the volume of repair tissue
needed to heal a fracture.
Restoring fracture fragment apposition is
especially important.
Fracture stabilization by traction, cast
immobilization, external fixation, or internal fixation
can facilitate fracture healing by preventing repeated
disruption of repair tissue.
4.Treatment Variables
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49.
Some fractures (e.g., displaced femoral neck and
scaphoid fractures) rarely heal if they are not rigidly
stabilized. Fracture stability appears to be
particularly important for healing when there is
extensive associated soft tissue injury, when the
blood supply to the fracture site is marginal, and
when the fracture occurs within a synovial joint
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51.
Treatment by closed methods:-
1.The process of fracture healing differs only when
the fractures are manipulated at the end of few
weeks after mobilisation even when before the
mineralisation starts.
2.Due to distraction of fragments.,the traction
forces tend to induce fibroblastic rather than
osteoblastic conversion in uncomminuted connective
tissue cells.
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52.
External callus is still the medium by which the
fragments are first bridged although it is often
reduced in quantity when compared with fixation by
external means alone.
In cases of fractures fixed with rigid
immobilizaton.,the modification in the healing
process are first noted by Dr.Danis in 1949 when he
observed radiologically that in rigidly fixed forearm
bones external callus did not form,but instead
fracture line gradually disappeared.
Healing progress for fracture
fixation done by plates and screws
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54.
He coined the term ‘SOUDRE AUTOGENE or
PRIMARY BONE HEALING’ to describe this type of
union.
When the fracture surfaces are rigidly held in
contact, fracture healing can occur without any
grossly visible callus. This type of fracture healing
has been referred to as primary bone healing,
indicating that it occurs without the formation and
replacement of visible fracture callus
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55.
When there is contact between the bone ends,
lamellar bone can form directly across the fracture
line by extension of osteons.
Osteoblasts following the osteoclasts deposit new
bone; and blood vessels follow the osteoblasts. The
new bone matrix, enclosed osteocytes, and blood
vessels form new haversian systems.
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56.
Where gaps exist that prevent direct extension of
osteons across the fracture site, osteoblasts first fill
the defects with woven bone. After the gap fills with
woven bone, haversian remodeling begins,
reestablishing the normal cortical bone structure, so
called ‘GAP HEALING’ and this inturn acted as a
conducting medium for the new osteones.
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57.
The main disadvantage of this method is the
damage which it inflicts on the medullary blood
supply.
In few cases where narrow implants are used and
reaming is not required.,vascular damage will be
minimal & rapid regeneration of blood vessels occur.
When bigger and wider implants are
used,vascular damage will be high and the
medullary blood supply is poor and for the fracture
healing to occur.,the sebsequent blood supply is
through the periosteal blood supply from the surrounding
soft tissue.
Healing in Intra-
medullary Fixation
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58.
1.Rockwood & Green’s-Fractures in Adults (VOL-
1)
2.Watson-Jones Fractures and Joint Injuries
3.Chapman’s Textbook Of Orthopaedics (VOL-1)
4.Campbell’s Textbok of Operative Orthopaedics
(VOL-3)
5.Robbin’s Textbook of Clinical Pathology.
References
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