West Visayas State University – College of Medicine – Batch 2020

Block XV
Module 1 Orthopaedics
Lecture 1
8/ 6/ 18
Dr. Macelo Jaen, MD, FPOA, FPCS

TOPIC OUTLINE A. HISTORY

I. Orthopaedics NICOLAS ANDRE (1741)
A. History • First to propose the term “Orthopaedia” in a self-help
B. Etymology book he wrote for parents (“Orthopaedia: Or, The Art of
C. Subspecialties
D. Qualities of Bone Correcting and Preventing Deformities in Children”)
E. Stress curve • He just coined the word “Orthopaedia” but God has
F. Bone composition been practicing orthopedics when he pulled out a rib
II. Terms
from Adam (if you are to look into the Bible)
III. Fractures
A. Types
B. 5 key factors B. ETYMOLOGY
C. Fracture patterns • From the greek words:
D. Communition patterns “Ortho” = straight
E. Open vs Closed fractures
IV. Intrinsic bone quality “Paedis” = child
A. Normal • Referred to diseases/injuries to the bones and joints
B. Osteopenia • Referred to musculoskeletal diseases and injuries
C. Osteoporosis
D. Osteopoikilosis
E. Osteopetrosis
V. Displacement, angulation and rotation
A. Displacement
B. Angulation
C. Rotation
D. Additional terms
VI. Fracture classification
A. AO classification
B. Gustilo-Anderson-Mendoza Classification
VII. Fracture Healing
A. Components of bone healing
B. Prerequisites for bone healing Figure 1. Orthopaedics logo
C. Stages of fracture healing
D. Variables that influence fracture healing C. SUBSPECIALTIES
E. Methods of promoting fracture healing • Trauma
Review Questions • Cold Orthopaedics (Non-traumatic Cases)
References
Pedia (e.g. Inborn)
Adult (e.g. Arthritis, Infectious)
LECTURER BOOK REFERENCE OLD TRANS
Spine (e.g. Pott’s disease)
Hand (e.g. Cross-deformities, Polydactyly)
• Others:
I. ORTHOPAEDICS
• A surgical subspecialty Sports Medicine
• Maladies of the Musculoskeletal system (all structures Minimally Invasive Surgery (Arthroscopy)
attached to bones): Arthroplasty (Joint Replacement/Reconstruction)
Bones ─ No perfect implant so far
Joints ─ Replacement can now survive for up to 20
Ligaments years, in the past only 5-7 years.
Tendons Tumor
Muscles Foot and Ankle (Podiatric Medicine)
Peripheral Nerves of the limbs Shoulder
• Diseases and injuries of the MS system Ilizarov
• Injuries or diseases affecting the spine, pelvis and Ilizarov uses rings and bars as external fixtures for
extremities, concerning: limb lengthening or shortening
Diagnosis
Treatment D. QUALITIES OF BONE
• The bone is a dynamic tissue that responds to
Rehabilitation
specific stimuli
Prevention

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• Mechanical environment around the bone can induce In the elastic region, presence of stress does lead to
changes in structure deformity but the bone goes back to its original
Bones are dependent on soft tissues that surround shape. In the plastic region, it leads to deformity but
them. When you have an injury, you don’t entirely the bone may not go back to its original shape until a
concentrate on the injury to the bone but as well on failure point occurs. Then you will end up with
the injury to the soft tissues. fracture.
• The strength of the bone is related to the quality and
amount of collagen, mineral content (calcium), and F. BONE COMPOSITION
overall density. CELLS
If bones are underused, it may lead to osteoporosis. • Osteocytes
If bones are overused, it may lead to fractures. • Osteoblasts
• Osteoclasts
ANISOTROPIC
• Mechanical properties are different when load is EXTRACELLULAR MATRIX
applied in different directions • Organic (35 %)
• Cortical bone is weak in tension and shear, but Collagen (type I) 90%
tough under compression Osteocalcin, osteonectin, proteoglycans,
glycosaminoglycans, lipids (ground substance)
VISCOELASTIC • Inorganic (65%)
• Amount of deformation a material demonstrates prior Primarily hydroxyapatite Ca5(PO4)3(OH)2
to failure
• Bones exhibit both viscous and elastic characteristics
when undergoing deformation
Especially with children.

DUCTILE
• Bone undergoes large amount of deformation prior to
failure
• Maximal stress under which an object is immune to
fatigue failure regardless of the number of cycles
Bones are generally able to be “deformed” without
losing toughness (not brittle)
E.g. When you continuously run : Femur/Tibia stress
fracture (could not be seen by plain and simple Figure 2. Cells of the Bone.
radiography)

E. STRESS CURVE

Figure 3. Bone Extracellular Matrix.

• Put load = No effect on characteristics
• Continue putting load = Deformation
• Continue putting load = Fracture, Failure (Failure Point)
In the elastic region, the bone maintains its shape.
However, as you continue to add load or stress, it will
reach a yield point where the bone undergoes a
degree of deformity in the plastic region.
II. TERMS
DISLOCATION
• Complete disruption of the normal relationship of the
joint
Abnormal displacement of articulating surfaces such
that these surfaces are not in contact
Most common: Shoulder and elbow (Radial head is
out of the elbow joint)

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 III. FRACTURES
A. TYPES
1. ACCORDING TO DISPLACEMENT
Undisplaced
• Check what bone is injured
• If X-ray unsure, palpate. If with pain, suspect fracture
which is bound to displace (surgery is the intervention)

Displaced
• COMPLETE
Complete cortical circumference is involved
Figure 4. Dislocation Fragments are completely separated

SUBLUXATION
• A partial or incomplete disruption in the normal
relationship of the joint
Alteration of joint alignment such that the articulating
surfaces incompletely approximate each other
Compare with the opposite joint; to visualize,
request X-ray of both sides; few mm difference is
important depending on the areas involved Figure 7.
• INCOMPLETE
Not fractured all the way through
“Only one cortex” involved
Also known as “Greenstick fracture” esp in young
children < 10 yrs old
In children, the periosteum is thick, hence it can’t
be completely separated; it acts like an internal
splint which also speeds up recovery
Includes torus fracture
Ligaments of children are stronger than the bone =
dislocation rare, fracture common
In adults, fracture rare, dislocation common
Occurs due to the viscoelasticity of bone

Figure 5. Subluxation.
Figure 8. Greenstick fracture.
FRACTURE
• Any break in the continuity of the bone Torus
• Bone bends and buckles
• Due to longitudinal compression on the soft bone
Occurs in the junction between the metaphysis
(cancellous bone--area of weakness) and diaphysis
(cortical bone--area of rigidity)
May occur with a strong cortical but weak cancellous
bone
Compression fracture from distal to proximal
(Telescoping of the strong over the weak area;
Figure 6. Fracture.
Cortical gets into cancellous)

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 Do not manipulate, just immobilize because it is Segment (Long bones)
undisplaced • Epiphysis – articulating surface; ends; “on top of the
Children: 2-3 weeks physis”
Adults: 6-8 weeks • Physis – growth center; radiolucent (appears black) in
Golden period: 6-8 hours a growing child, mistakenly labeled as fracture
Healing time: 6-8 weeks • Metaphysis – flaring (radiological sign of disorders
which cause narrowing of the diaphysis and widening
2. ACCORDING TO OPEN OR CLOSED FRACTURE of the metaphysis)
Open • Diaphysis
• Also known as “compound fracture” or “open air
fracture”
• A fracture in which the bone penetrates the skin
• There is contact with the outside environment
• Some define this as a fracture with any open wound or
soft tissue laceration near the bony fracture
• It needs special care because of presence of injuries to
soft tissues and high risk for infection (once a bone is
infected, it is forever infected)
• Antibiotics are prolonged (2 yrs. or longer)

Closed
• Fracture with intact overlying skin
• How to determine if blood is from a fracture
(communicating or non-communicating) or simple soft
tissue injury with pin prick size injury:
Check blood quality under bright light: If with fatty
Figure 9. Segment.
globules, fracture.
Apply pressure: If bleeding does not stop, fracture
4. ACCORDING TO ANATOMIC LANDMARKS
3. ACCORDING TO LOCATION Neck
Request 2 views: AP and Lateral • Subcapital
A way of checking which bones are involved. Below the head; may lead to avascular necrosis
• Transcervical
Thirds (Long bones) May also lead to avascular necrosis
• Proximal Third • Basicervical
• Middle Third Below the base of the neck; blood supply from
• Distal Third circumflex artery may not be disrupted and therefore
no avascular necrosis
Anatomic orientation Intracapsular – synovial fluid has hemolytic enzymes
• Proximal > no hematoma > no healing
• Distal
• Medial Trochanter
• Lateral • Trochanteric
• Anterior • Intertrochanteric – crosses greater to lesser trochanter
• Posterior • Subtrochanteric – which is 5 cm or 2 inches distal to
the lesser trochanter; but doc said 3 inches
Anatomic landmarks
• Head Condyle (Humerus and Femur)
• Neck • Supracondylar
• Body/Shaft • Transcondylar
• Base • Intercondylar
• Condyle • Condylar
Medial
Lateral

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Malleolar
• Medial Spiral
• Lateral • Rotational configuration
• Has a transverse and oblique segment
Epicondylar • Easier to fix because of bone continuity
• Medial – flexors of the wrist are attached
• Lateral – extensors of the wrist are attached

5. ACCORDING TO EXTRA OR INTRAARTICULAR

• Extraarticular
• Intraarticular
Also known as osteochondral
“Fracture of necessity”
Fixed as perfectly as possible via open reduction
and internal fixation (ORIF) to prevent post- Figure 13. Spiral fracture.
traumatic arthritis
Avascular and Aneural: Cartilaginous lining gets Comminuted
nutrition from synovial fluid • Broken, splintered or crushed into more than 3 pieces
• Associated with open fracture; patient received great
amount of energy (gunshot, falling from a high building)
• Deal with the bone and surrounding soft tissues

Figure 10. Extra-articular or Intra-articular.

6. ACCORDING TO CONFIGURATION
Figure 14. Comminuted fracture.
Transverse
• Longitudinally across the bone Butterfly Fragment
• Associated with comminuted, the 3rd fracture is
relatively large

Figure 11. Transverse fracture.

Oblique Figure 15. Butterfly fragment.

• Angular fracture Segmental
• Apply screws proximal and distal, let bones slide on • Bone is broken in >2 separate places and the fracture
each other lines of each do not connect
• Isolated in terms of vascular supply
• Ends up with fracture healing
• Bone grafting is needed

Figure 12. Oblique fracture.

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 2. TORSION AND COMPRESSION
• Results in a spiral wedge fracture

D. COMMINUTION / PATTERN
1. TRANSVERSE (SIMPLE)
Pure bending forces
• Result in transverse fractures from tension on the
convexity and compression on the convexity, with the
neutral axis moving towards the fracture

Figure 16. Segmental fracture. Tensile forces

Avulsion • Tend to arise at soft-tissue insertions to cancellous
• Specific part of the bone is fractured bone
• Produces transverse fractures

Figure 17. Avulsion.
7. ACCORDING TO THE NATURE OF THEIR
CAUSATIVE FORCE
Repetitive force
• Cyclical loading with forces below the ultimate strength
of the bone
• Micro damage may occur with each cycle of load
Single force
• Single application of force produces a fracture pattern
characterized by the nature of the application of force
Forces may be direct or indirect
B. THE TYPE OF FRACTURE PRODUCED BY
FORCES ACTING ON BONE IS DEPENDENT ON
5 KEY FACTORS
• Load
• Rate
• Direction
• Bone properties – e.g shape, anatomical area
• Quality of bone
• Forces
C. FRACTURE PATTERNS
1. COMBINED BENDING AND COMPRESSION
• Bending force causes a transverse crack in tension
• Compression force causes an oblique fracture
• Results in a bending wedge or butterfly fracture
Bending wedge (butterfly) fragment occurs on
compression (concave) side, esp in high-energy
injuries
2. OBLIQUE (SIMPLE)
Pure compression forces
• Rare in the skeleton but lead to shear forces, and often
on to fractures at 45 degrees to the compressive load
• Shear lines are formed by buckling of lamellae and
oblique cracking of osteons, which occurs first at areas
of stress concentration in the bone, e.g. vessels or
resorption spaces, leading to oblique fractures
Uneven bending forces
• Also create oblique fractures
3. SPIRAL (SIMPLE)
• Oblique in 2+ views
Torsional forces
• Cause spiral fractures with 2 components:
One spiral fracture line around the circumference
of the bone at approximately 45 degrees to the
horizontal caused by a failure in tension
perpendicular to the crack
A vertical line linking the proximal and distal ends
4. COMMINUTED
• Broken, splintered, or crushed into > 3 pieces
Four-point bending
• E.g a car bumper striking a femur, creates
comminuted fractures
5. SEGMENTAL
• Bone broken in 2+ separate places; fracture lines do
not connect
Associated with problems in healing.
Four-point bending
• E.g a car bumper striking a femur, creates segmental
fractures

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6. OTHERS Compressive force - results in shortening the
• Linear/Longitudinal Split – rare length of the bone
• Compression Tension - elongates the bone
• Impacted – e.g “Buckle/Torus” Torsion - causes twisting about its long axis
• Distracted Bending - causes to bow at the center.
• Avulsion Transverse fracture:
Bending due to progressive tensile failure
Starts from the outside of the bone
Oblique fracture:
Sheer failure in compression
Spiral fracture:
Failure in tension of the fibers on the surface of the
bone subjected to tension
Associated with rotational forces
Oblique transverse:
Combination of bending and compression (butterfly
fragment)

D. OPEN VS CLOSED
OPEN FRACTURE
• AKA “Compound fracture” (but this term is no longer
used)
• A fracture in which bone penetrate through skin;
• ”Open to air”
Check the bleeding. If there is presence of fat in the
blood, it is an open fracture.
• Fracture with any open wound or soft tissue laceration
near the bony fracture
• The break in the continuity of the bone communicates
with the outside environment
With infection, there could be failure of the bones to
unite.
No matter how small is the bone protruding, it is
considered an open fracture. It is better to overtreat as
open fracture.

CLOSED FRACTURE
• Intact overlying skin or soft tissue
• The break in the continuity of the bone does not
communicate with the outside environment

IV. INTRINSIC BONE QUALITY

A. NORMAL

Figure 18. Fracture pattern is related to the nature of force applied.

Source: Basic Orthopaedic Sciences.

The basic forces — compression, tension, torsion,

and bending — cause the bone to behave in
Figure 19. Normal Hand X-ray.
predictable ways.

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 B. OSTEOPENIA

Figure 20. Osteopenia. *Only a certain part of the body loses bone Figure 23. Osteopetrosis.
density. Source: Upclass Notes
V. DISPLACEMENT, ANGULATION AND ROTATION
C. OSTEOPOROSIS A. DISPLACEMENT
Generalized decreased density of bone • Extent to which fracture fragments are not axially
aligned
• Fragments are shifted in various directions relative to
each other
• Convention: describe displacement of distal fragment
relative to proximal

B. ANGULATION
• Extent to which fracture fragments are not anatomically
aligned
In an angular fashion
• Convention: describe angulation as the direction the
Figure 21. Osteoporosis. apex is pointing relative to the anatomical long axis of
the bone (e. g. apex medial, apex valgus)
D. OSTEOPOIKILOSIS
• Focal areas have increased density VALGUS VS. VARUS
• Multisclerotic foci Acceptable limits (accdg to Doc Jaen):
Sclerotic – more white on xray Tibia- up to 10 degrees
Litic – more black on xray Humerus – up to 30 degrees (due to soft tissues
covering the bone)

Figure 22. Osteopoikilosis.

E. OSTEOPETROSIS
• Increased bone density due to calcium and mineral
deposition
But the bone doesn’t become stronger. It becomes
more brittle.
Also known as “marble bone disease” because of
bone brittleness
There is a probability that you will end up with a
pathologic fracture (fracture associated with tumors
or any pathology in the bone).
Figure 24. Valgus and Varus angulation.
C. ROTATION
• Extent to which fracture fragments are rotated relative
to each other
• Convention: describe which direction the distal
fragment is rotated relative to the proximal portion of
the bone
Close reduction is done: immobilize fracture based
on position of proximal fracture segment
Other signs of fractures
Signs that manifest later; they should be
differentiated from tumors

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• Periosteal reaction RADIOGRAPHIC UNION:
A sign that suggests healing bone Slow bone trabeculae or cortical bone crossing the
• Callus/osteosclerosis fracture site and often occurs later than chemical
• Fat pad sign/”sail sign” union
Radiolucency anterior and posterior to bone due to Callous formation on the three (3) sides of the bone
hematoma formation under the periosteum
Subtle and usually above the elbow VI. FRACTURE CLASSIFICATION
Common in children as point of tenderness • Description of the fracture
• Severity of the fracture
• Mechanism of injury
• Guide for management
• Prognosis

A. AO CLASSIFICATION
• Arbeitgeimeinshaft fur Osteosynthesefragen
• A system of classification of fractures (1987)
• A comprehensive classification of long bones fractures
The system is based on well-defined terminology,
which allows the surgeon to consistently describe
Figure 25. Fat pad sign. the fracture in as much detail as required for the
Usually managed by immobilization clinical situation. This description is the key to
classification and forms the basis for the
D. ADDITIONAL TERMS alphanumeric code that allows documentation and
DELAYED UNION: research. – AO Foundation
• Failure of the bone to unite within the expected time The AO/OTA (Orthopaedic Trauma Association)
6-8 hours – Golden time for management fracture classification is essentially the only generic
6-8 weeks – start of healing or universal system in wide usage today.
In applying the OTA fracture classification system,
NON-UNION: there are five questions that must be answered for
• Failure to unite each fracture:
Absence of pain
(+) Motion (Pseudoarthrosis) WHICH BONE?
Blunting of ends on x-ray • The major bones in the body are numbered
Pencilling effect • Humerus – 1
Failure of callous to cross fracture line • Radius & Ulna – 2
e.g. For radius and ulna formerly union at 6 months, • Femur – 3
currently 3 months • Tibia/fibula – 4
• Spine – 5
Atrophic • Pelvis – 6
No callus is formed. This is often due to impaired • Hand – 7
bony healing, for example due to vascular causes • Foot – 8
(e.g. impaired blood supply to the bone fragments)
or metabolic causes (e.g. diabetes or smoking). WHERE IN THE BONE IS THE FRACTURE?
• Identifies a specific segment within the bone.
Hypertrophic • In most long bones, the diaphyseal segment (2) is
Callus is formed, but the bone fractures have not located between the proximal (1) and distal (3)
joined. This can be due to inadequate fixation of the segments or:
fracture, and treated with rigid immobilization. Proximal – 1
Midshaft – 2
MALUNION: Distal – 3
• Angulation • The tibia is assigned a fourth segment, which is the
• Malrotation malleolar segment (4).
• Shortening • Example: AO/OTA of a fracture of the midshaft of
• Lengthening the femur has a numeric classification of 32.

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WHICH FRACTURE TYPE?
For diaphyseal fractures:
• Type A fracture – simple fracture with two fragments
• Type B fracture – has some comminution, but there
can still be contact between the proximal and distal
fragments
• Type C fracture – highly comminuted or segmental
fracture with no contact possible between proximal and
distal fragments
For proximal and distal segment fractures:
• Type A fractures – extra-articular
• Type B fractures – partial articular (there is some
continuity between the shaft and some portion of the
articular surface)
• Type C fractures – involve complete disruption of the
articular surface from the diaphysis.
Figure 27. AO Classification of Fractures – Long Bones for adults.

WHICH GROUP DO THE FRACTURES BELONG TO?

• Divides the fractures according to more specific
descriptive details

WHICH SUBGROUP?
• Most detailed determination in the AO/OTA
classification system
• Subgroups differ from bone to bone and depend upon
key features for any given bone in its classification
• Subgroups intend to increase the precision of the
classification system

B. GUSTILO-ANDERSON-MENDOZA OPEN
FRACTURE CLASSIFICATION
• This system uses the amount of energy, the extent of
soft-tissue injury and the extent of contamination for Figure 28. AO alphanumeric numbering. Upclass Notes
determination of fracture severity.

Figure 26. Open Bone Fractures

Figure 29. Gustilo classification

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 • Similar in many ways to soft tissue healing except that
the end result is mineralized mesenchymal tissue
• Starts immediately after fracture (usually 24 hrs from
fracture) but continues modeling for several years
• Essential event is the creation of a bony bridge
Hematoma is the most important part of fracture
healing

History:
• 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
Stage of hematoma
Stage of granulation tissue
Stage of callus
Stage of modelling
Stage of remodeling

PRIMARY (DIRECT CORTICAL, OSTEONAL OR

HAVERSIAN) BONE HEALING
• Anatomical reduction and interfragmentary
compression, absolute stability

SECONDARY (CALLUS) BONE HEALING

• Relative stability, strain or movement at fracture site
stimulates secondary healing
• Callus formation is expected with medullary nails

2 Discrete Processes:
• Periosteal bony callus (intramembranous
ossification)
Starts from outer cuff and grows inwards
• Fibrocartilaginous bridging callus
Starts from the inner edges of the fracture to its
middle

PERREN’S STRAIN THEORY OF FRACTURE

HEALING
• After any form of fixation or immobilization, a fracture
that is loaded will undergo some degree of movement
or strain
Figure 30. AO alphanumeric numbering. Upclass Notes • Combines relative stability provided by an implant
. (plate) with preservation of natural fracture biology to
VII. FRACTURE HEALING achieve rapid callus formation and fracture
INTRODUCTION consolidation.
• Fracture healing is a complex process that requires the • Fracture callus becomes increasingly stiff with time,
recruitment of appropriate cells (fibroblasts, from a gelatinous granulation tissue, to soft callus
macrophages, chondroblasts, osteoblasts, osteoclasts) and to subsequently hard bony callus
and the subsequent expression of the appropriate
genes (genes that control matrix production and A. COMPONENTS OF BONE FORMATION
organization, growth factors, transcription factors) at • Cortex
the right time and in the right anatomical location • Periosteum
• Bone marrow
• Soft tissue
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 B. PREREQUISITES FOR BONE HEALING
• Adequate blood supply
• Adequate mechanical stability
Stability depends on intra- and extra-articular
characteristics:
Intra-articular fractures are bathed in synovial fluid,
thus hematoma doesn’t occur due to hemolytic
enzyme presence, leading to non-union
C. STAGES OF FRACTURE HEALING
Figure 31. Stages of fracture healing.
STAGE I: INFLAMMATORY PHASE
• Immediately after injury; 10% of the healing process
• Hematoma formation occurs within the first 24-48 hours
• Peak: 48 hours and is quite diminished by 1 week after
fracture
• Death of osteocytes and other cells and tissues
• Inflammatory mediators from platelets, dead and
injured cells
• Blood vessel dilatation, edema
Hematoma and Inflammation
• Haematoma from ruptured blood vessels forms fibrin
clot.
• Migration of inflammatory cells into the haematoma
occurs, responding to local growth factors and
cytokines
• IL-1, IL-6, TGF-β (transforming) superfamily including
BMPs, PDGF (platelet), FGF (fibroblast), IGF (insulin
like)
• Inflammatory cells migrate (PMNs, macrophages,
lymphocytes) releasing cytokines that stimulate
angiogenesis
• Necrotic tissues and exudate resorbed
• Fibroblasts & chondrocytes appear (callous formation)
Supplementary Notes from Upclass
• Tissue disruption results in hematoma at the fracture
site
• Local vessels thrombose, causing bony necrosis at the
edges of the fracture
• Increased capillary permeability results in a local
inflammatory milieu:
• Osteoinductive growth factors stimulate the
proliferation & differentiation of mesenchymal stem
cells
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• Platelets release various signaling molecules:
transforming growth factor beta, PDGF, BMPs, growth
differentiation factors (GDFs)
• Chemotaxis, angiogenesis, neovascularization
• Necrotic tissues and exudate resorbed
• Fibroblasts and chondrocytes appear (callus formation)
• Cellular attachment to the extracellular matrix and
conductive substrate is a basic requirement for fracture
healing accomplished with integrins (Fibronectin)
• Fibronectin: found in the first 3 days; associated with
callus; greatest in the earliest stages of fracture healing
• Integrins: activate chemical pathways to the interior of
the cell (signal transduction); activates transcription of
various regulatory genes that control cell life cycle,
cellular shape or motility; acts with cellular growth
factors VEGF, epidermal growth factor, PDGF for
biological action
• Arachidonic Acid metabolism: main control in
inflammation and immunity
• Fatty acid oxidation of arachidonic acid and produce
prostaglandin and leukotriene factors that activate and
degranulate platelets sustaining inflammatory reactions
• COX - 1 & 2 metabolize AA to prostaglandin G2 and
H2
• Enzyme 5 lipoxygenase metabolizes AA into various
leukotrienes which have chemotactic effect on
migrating neutrophils
• Leukotrienes: increases vascular permeability;
stimulate proinflammatory activities; stimulate
endothelial cell adherence and chemokine production
by mast cell
• Mast cell: increase phagocytosis which leads to edema
productions, interstitial fluid accommodation (5 LO
inhibitors) in asthma
STAGE II: STAGES OF CALLUS FORMATION
• Increased cellularity, with proliferation, differentiation
and soft callus
• Soft callus – 1 month neovascularization
• Callus is a combination of fibrous tissue, cartilage and
woven bone
• Intramembranous (bony/periosteal) callus = primary
callus response: type I collagen (osteoid) laid down
from periosteal osteoblasts in the cambium layer as
periosteal bony callus or woven bone.
• Hard callus but it does not bridge the fracture
• Proliferation, differentiation and matrix synthesis as
haematoma is replaced by granulation tissue
• Capillary in-growth (angiogenesis) and recruitment of
fibroblasts, mesenchymal cells and osteoprogenitor
cells
The periosteum plays an important role in this
process.
• Cell types involved include PMNs, macrophages and
then fibroblasts.
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• At necrotic bone ends, bone resorption is mediated by to woven bone by osteoblasts, the amount of type I
osteoclasts and removal of tissue debris by collagen is increased.
macrophages • Clinical union, as opposed to radiographic union, is
achieved when the fracture site has become stable and
Supplementary Notes from Upclass pain-free
• Early Callus Phase • Mesenchymal cells proliferate to produce fracture
7- 10 days callus made of fibrous tissue, cartilage and woven
Chondrogenesis bone
Continued revascularization, proliferation of • Hard callus initially formed by membranous ossification
chondroprogenitors and differentiation of • Bone gradually replaces cartilage by osteochondral
chondrocytes ossification
Proliferation of type II collagens as the initial • Mineralization ensues
structure of fracture callus
Mineralization controlled by proteoglycans TWO TYPES OF CALLUS:
• Late Callus Phase Primary callus
Mineralization of cartilaginous callus matrix • Aka soft callus
Reduced chondrocyte proliferation eventually • Forms in the central region in which there is relatively
undergoing apoptosis low oxygen tension
Mineral is laid down • Consists of cartilage, fibrous tissue, osteoid, woven
Endochondral ossification with calcified cartilage bone, and vessels
removed by chondroclasts • If successful, healing progresses to the stage of
Woven bone formation leads to function in 4-5 bridging callus or hard callus
weeks
Hard callus
STAGE III: REPARATIVE PHASE • Formed at the periphery of the callus by
• 40% of the healing process intramembranous bone formation
• New matrix formation • Woven bone is gradually converted to lamellar bone
• Osteoblasts from endosteal surface • Medullary cavity is reconstituted
• Most of cells from granulation that replaces hematoma • Stability of the fracture fragments stabilizes
• Mesenchymal cells proliferate to produce fracture • Clinical union occurs: fracture site becomes stable and
callus made of fibrous tissue, cartilage and woven pain-free
bone • Radiographic union: plain radiographs show bone
• Hard callous initially formed by ossification trabeculae or cortical bone crossing the fracture site,
• Bone gradually replaces cartilage by osteochondral and often occurs later than clinical union.
ossification • Despite successful fracture healing, the bony density of
• Mineralization the involved lamb may be decreased for years
• Clinical signs of union
• Radiographic signs of union

Supplementary Notes from Upclass

• Becomes activated within the first few days after
fracture and persists for 2-3 months
• Chemical and mechanical factors stimulate callus
formation and mineralization
• Periosteal callus forms along the periphery of the
fracture site:
• Intramembranous ossification initiated by pre-
osteoblasts
• Intramedullary callus forms in the center of the fracture
site:
• Endochondral ossification at the site of the fracture
hematoma
• Type II collagen produced by chondrocytes initially Figure 32. Callus formation.
predominates in the callus. As cartilage is transformed

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STAGE IV: REMODELLING PHASE
• 70% of the healing process
more of a natural process
• Replacement of woven bone by lamellar bone
• Resorption of unnecessary callus
Osteoclast plays a role
• Wolff’s law
• Increased mechanical stability
This process usually lasts for many years
Figure 33. Bone remodeling.
Figure 34. Bone Formation and Completion.
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Wolff’s Law
• Bone models and remodels in response to the
mechanical stresses it experiences so as to produce a
minimal-weight structure that is ‘adapted’ to its
applied stresses.
• If load on a bone increases, bone attempted to remodel
itself to become stronger for resisting that particular
load.
Cortical bone thickens
Cancellous bone architecture changes
• If a load on a bone decreases the bone will become
weaker due to normal bone turnover.
Electronegativity in the area of concavity will allow
more cells to get pinned in the area of negativity. In
the area where there is extensive callous formation
and no more stress, you will have electropositivity.
Osteoclasts will become active in that area so the
unnecessary callous formation will even out. But in
the area where there is a necessary increased bone
formation in order for bone to bear stress, then the
osteoblasts will play a role. They will add up and
deposit more bone. This is called the Wolff’s law.
“The bone adapts according to the demand of the
bone.”
FACTORS DISRUPTING HEALING PROCESS
• Displaced and comminuted fractures
• Infection
• Vascular insufficiency
• Inadequate minerals and vitamins
• Inadequate immobilization
Mnemonic: SPLINT
• Soft tissue interposition
• Position of reduction
• Location
• Infection
• Nutrition
• Tumor and Pathology
D. VARIABLES THAT INFLUENCE FRACTURE
HEALING
INJURY VARIABLES
• Open Fractures
• Severity of Injury
• Intra-articular Fractures
• Segmental Fractures
• Soft tissue interposition:
Feeling of “gritty sensation,” also known as
crepitus
• Damage to blood supply
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PATIENT VARIABLES B. Osteopenia
• Age C. Osteopetrosis
• Nutrition D. Osteopoikilosis
• Systemic Hormone:
Corticosteroids inhibit differentiation of osteoblasts 3.The following are prerequisites for bone healing
from mesenchymal cells except?
Growth hormone can improve healing A. It requires osteoclastic and osteoblastic activity with
Thyroid hormone, Calcitonin, Insulin and Anabolic or without chondrocytic activity.
steroids enhance rate of healing B. It requires constant blood supply and mechanical
Diabetes, hypervitaminosis D and rickets retard stability
healing C. Stability depends on intra and extra articular
• Nicotine characteristics
Delays bone healing; physicians usually require D. It requires appropriate genes at the right time and
patients to stop smoking and stop excessive drinking location
of alcoholic beverages (due to loss of minerals etc)
4. It refers to the term in which there is apex lateral
TISSUE VARIABLES angulation.
• Type of bone (cortical vs cancellous bone) A. Valgus
• Bone disease B. Vargus
• Bone necrosis C. Vagus
• Soft tissue D. Varus
• Infection
5. It is a quality of bone that causes a greenstick
TREATMENT VARIABLES fracture.
• Apposition of fracture fragments A. Anisotrophic
• Loading and micromotion (Ilizarov= 1mm/day) B. Viscoelastic
• Fracture stabilization C. Ductile
D. Stress resistant
E. METHODS OF PROMOTING FRACTURE HEALING
• Nutrition and metabolism
• Bone grafting
• Bone transport – Ilizarov
• Electrical fields – electronegativity Answers: B, C, A, D, B
• Ultrasound
• Laser
• Demineralized bone matrix
• Growth factors or cytokines
• Autologous bone marrow

REFERENCES
• Dr. Jaen’s Lecture
• Upclass Notes
• Rockwood and Green’s Fracture in Adults 8E (2015)
• Handbook of Orthopaedic Surgery 10E (1986)

REVIEW QUESTIONS
1. A Subspecialty in orthopedics that deals with
Rheumatoid arthritis.
A. Trauma
B. Cold
C. Immune
D. MIS

2. Also known as “Marble bone disease”

A. Osteoporosis
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