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Transcript of Fracture healing
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Fracture Healing
By :
Monther Alkhawlany
GROUP D 2015
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What TO Cover Today :
ANATOMY OF BONE
PATHOLOGY OF BONE
MECHANISM OF BONE FORMATION
INTRODUCTIONT TO FRACTURE HEALING
TYPES OF FRACTUER HEALING
STAGE OF HEALING
FACTORS INFLUENCE ON FRACTURE HEALING
REGULATION OF BONE HEALING
COMPLICATION OF FRACTURE HEALING
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Types of Bone
A. Lamellar Bone
(Orderly cellular distribution)
Collagen fibers arranged in parallel layers
Normal adult bone
B. Woven Bone or immature bone (non-lamellar)
Randomly oriented collagen fibers
In adults, seen at sites of fracture healing, tendon or ligament attachment and in pathological conditions
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Lamellar Bone
Cortical bone
- Comprised of osteons (Haversiansystems) runs longitudinally
Osteonscommunicate with medullary cavity by Volkmann’s canals that run horizontally
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Haversian Systemosteon
Haversian
canal
osteocyte
Volkmann’s
canal
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Woven Bone
Coarse with random
orientation
Weaker than
lamellar bone
Normally remodeled
to lamellar bone
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Bone Composition Cells
Osteocytes
Osteoblasts
Osteoclasts
Extracellular Matrix
Organic (35%)
Collagen (type I) 90%
Osteocalcin, osteonectin, proteoglycans, glycosaminoglycans, lipids (ground substance)
Inorganic (65%)
Primarily hydroxyapatite Ca5(PO4)3(OH)2
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Osteoblasts
Derived from
mesenchymal stem
cells
Line the surface of the
bone and produce
osteoid
Immediate precursor is
fibroblast-like
preosteoblasts
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Osteocytes
Osteoblasts
surrounded by bone
matrix
trapped in lacunae
Function poorly
understood
regulating bone
metabolism in
response to stress
and strain
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Osteocyte Network
Osteocyte lacunae are connected by canaliculi
Osteocytes are interconnected by long cell processes that project through the canaliculi
Preosteoblasts also have connections via canaliculi with the osteocytes
Network probably facilitates response of bone to mechanical and chemical factors
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Osteoclasts
Derived from hematopoietic stem cells (monocyteprecursor cells)
Multinucleated cells whose function is bone resorption
Reside in bone resorption pits (Howship’s lacunae)
Parathyroid hormone stimulates receptors on osteoblasts that activate osteoclasticbone resorption
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Components of BONE Formation
Cortex
Periosteum
Bone marrow
Soft tissue
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Prerequisites for Bone Healing
Adequate blood supply
Adequate mechanical
stability
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Mechanisms of Bone Formation
A. Cutting Cones
B. Intramembranous Bone
Formation
C. Endochondral Bone
Formation
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Cutting Cones
Primarily a
mechanism to
remodel bone
Osteoclasts at
the front of the
cutting cone
remove bone
Trailing
osteoblasts lay
down new bone
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Intramembranous
(Periosteal) Bone Formation
Mechanism by which a long bone grows
in width
Osteoblasts differentiate directly from
preosteoblasts and lay down seams of
osteoid
Does NOT involve cartilage .
It mainly forms cancellous bone.
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Intramembranous Bone
Formation
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Endochondral Bone
Formation
Mechanism by which a long bone grows in length
Osteoblasts line a cartilage precursor
The chondrocytes hypertrophy, degenerate and calcify (area of low oxygen tension)
Vascular invasion of the cartilage occurs followed by ossification (increasing oxygen tension)
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Endochondral Bone
Formation
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Blood Supply
Long bones have four
blood supplies
1. Nutrient artery
(intramedullary)
2. Periosteal vessels
3. Metaphyseal vessels
4. Epiphysial vesselsNutrient
artery
Metaphyseal
vessels
Periosteal
vessels
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Nutrient Artery
Normally the major blood
supply for the diaphyseal
cortex (80 to 85%)
Enters the long bone via a
nutrient foramen
Forms medullary arteries up
and down the bone
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Periosteal Vessels
Arise from the capillary-
rich periosteum
Supply outer 15 to 20%
of cortex normally
Capable of supplying a
much greater
proportion of the cortex
in the event of injury to
the medullary blood
supply
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Metaphyseal Vessels
Arise from periarticular vessels
Penetrate the thin cortex in the
metaphyseal region and anastomose
with the medullary blood supply
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Vascular Response in
Fracture Repair
Fracture stimulates the release of growth
factors that promote angiogenesis and
vasodilation
Blood flow is increased substantially to the
fracture site
Peaks at two weeks after fracture
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INTRODUCTION
Fracture is a break in the structural continuity of
bone or periosteum.
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.
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The essential event in fracture healing is the
creation of a bony bridge between the two
fragments which can be readily be built upon and
modified to suit the particular functional demands .
INTRODUCTION
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Fracture healing is a complex process
that requires the recruitment of
appropriate cells (fibroblasts,
macrophages, chondroblasts,
osteoblasts, osteoclasts) and the
subsequent expression of the
appropriate genes (genes that control
matrix production and organization,
growth factors, transcription factors)
at the right time and in the right anatomical location
INTRODUCTION
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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
five stages.
1- stage of haematoma
2- stage of granulation tissue
3- stage of callus
4- stage of modelling
5- stage of remodelling
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Types for Bone Healing
Direct (primary) bone healing
Indirect (secondary) bone
healing
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Direct Bone Healing
Mechanism of bone healing seen when
there is no motion at the fracture site (i.e.
absolute stability)
Does not involve formation of fracture
callus
Osteoblasts originate from endothelial
and perivascular cells
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Direct Bone Healing
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Components of Direct Bone
Healing
Contact Healing
Direct contact between the fracture ends allows healing to be with lamellar bone immediately
Gap Healing
Gaps less than 200-500 microns are primarily filled with woven bone that is subsequently remodeled into lamellar bone
Larger gaps are healed by indirect bone healing (partially filled with fibrous tissue that undergoes secondary ossification)
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Indirect Bone Healing
Mechanism for healing in fractures that have some motion, but not enough to disrupt the healing process.
Bridging periosteal (soft) callus and medullary(hard) callus re-establish structural continuity
Callus subsequently undergoes endochondralossification
Process fairly rapid -weeks
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For convenience, we describe fracture healing in terms
of the three phases recognized by Cruess and Dumont,
noting that the reparative phase combines several
processes
Inflammation
stage of haematoma formation
Repair
stage of granulation tissue
stage of callus formation
Remodelling
Stages of Fracture Healing
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Duration
The inflammatory phase peaks within 48
hours and is quite diminished by 1 week
after fracture.
The reparative phase becomes activated
within the first few days after fracture and
persists for 2-3 months.
The remodelling phase lasts for many years
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Inflammation
inflammatory phase is identical to the typical inflammatory response of most tissues to traumatic injury.
Vasodilation and hyperemia, presumably mediated by histamines, prostaglandins, and various cytokines, accompany invasion of the injury site by neutrophils, basophils, and phagocytes that participate in clearing away necrotic debris.
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CONT…
Disruption of blood vessels in the bone, marrow, periosteum, and surrounding tissue disruption at the time of injury results in the extravasation of blood at the fracture site and the formation of a hematoma
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 and differentiation of mesenchymal stem cells
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Reparative phase
The reparative phase, which usually begins 4
or 5 days after injury, is characterized by the
invasion of pluripotential mesenchymal cells,
which differentiate into fibroblasts,
chondroblasts, and osteoblasts and form a soft
primary fracture callus.
Proliferation of blood vessels (angiogenesis)
within the periosteal tissues and marrow space
helps route the appropriate cells to the
fracture site and contributes to the formation
of a bed of granulation tissue.
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Mesenchymal cells at the fracture site proliferate
differentiate and produce the fracture callus
Two types of callus :
1-Primary callus or Soft callus – forms in the central
region in which there is relatively low oxygen tension .
• The primary callus may consist of cartilage, fibrous tissue,
osteoid, woven bone, and vessels.
• If the primary callus is successful,
• healing progresses to the stage of bridging callus
or hard callus.
2- Hard callus – formed at the periphery of the
callus by intermembranous bone formation
CONT…
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Periosteal callus forms along the periphery of the fracture site
Intramembranous ossification initiated by preosteoblasts
Intramedullary callus forms in the center of the fracture site
Endochondral ossification at the site of the fracture hematoma
Chemical and mechanical factors stimulate callus formation and mineralization
CONT…
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Repair
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Remodeling
The biochemical composition of the fracture callus matrix changes as repair progresses.
The cells replace the fibrin clot with a loose fibrous matrix containing glycosaminoglycans, proteoglycans, and types I and III collagen
In many regions they convert this tissue to more dense fibrocartilage or hyaline-like cartilage.
With formation of hyaline-like cartilage, type II collagen, cartilage-specific proteoglycan and link protein content increase.
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Woven bone is gradually converted to lamellar bone
Medullary cavity is reconstituted
Stability of the fracture fragments progressively increases .
eventually clinical union occurs that is, the fracture site becomes stable and pain-free.
Radiographic union occurs when plain radiographs show bone trabeculae or cortical bone crossing the fracture site, and often occurs later than clinical union .
Despite successful fracture healing, the bone density of the involved limb may be decreased for years
CONT…
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SUMMARY
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SUMMARY
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A. Age
B. Activity level including
1. immobilization
C. Nutritional status
D. Hormonal factors
1. Growth hormone
2. Corticosteroids
3. Others (thyroid, estrogen, androgen,
calcitonin, parathyroid hormone,
prostaglandins)
E. Cigarette smoking
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
I. Systemic factors or patient variables
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E. Diseases: diabetes,anemia,neuropathies,
tabes dorsalis
F. Vitamin deficiencies: A, C, D, K
G. Drugs: nonsteroidal antiinflammatory drugs
(NSAIDs), anticoagulants, factor XIII,
calcium channel blockers (verapamil),
cytotoxins, diphosphonates, phenytoin
(Dilantin), sodium fluoride, tetracycline
H. Other substances (nicotine, alcohol)
I. Hyperoxia
J. Systemic growth factors
K. Environmental temperature
L. Central nervous system trauma
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
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A. Factors independent of injury, treatment, or
complications
1. Type of bone
cortical or cancellous2. Abnormal bone
a. Radiation necrosisb. Infectionc. Tumors and other
pathological conditions
3. Denervation
II. Local factors or tissue variables
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
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B. Factors depending on injury or injury
variables
1. Degree of local damage
a. Compound fracture
b. Comminution of fracture
c. segmental fractures
d. Velocity of injury
e. Low circulatory levels of vitamin K1
2. Extent of disruption of vascular supply to
bone, its fragments (macrovascular
osteonecrosis), or soft tissues;
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
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3. Type and location of fracture (one or two bones, e.g., tibia and fibula or tibia alone
4. Loss of bone
5. Soft-tissue interposition
6. Local growth factors
7. Intraarticular fractures
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
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C. Factors depending on treatment
OR treatment variables
1. Extent of surgical trauma (blood supply, heat)
2. Implant-induced altered blood flow
3. Degree and kind of rigidity of internal or
external fixation and the influence of timing
4. Degree, duration, and direction of load-
induced deformation of bone and soft tissue
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
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5. Apposition of fracture fragments (gap,
displacement, overdistraction)
6. Factors stimulating posttraumatic
osteogenesis (bone grafts, bone morphogenetic protein,
electrical stimulation, surgical technique, intermittent venous
stasis ..
D- Factors associated with complications
1. Infection
2. Venous stasis
3. Metal allergy
VARIABLES THAT INFLUENCE
THE FRACTURE HEALING
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REST
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Regulation of Bone Healing
Growth factors
Transforming growth factor
Bone morphogenetic proteins
Fibroblast growth factors
Platelet-derived growth factors
Insulin-like growth factors
Cytokines
Interleukin-1,-4,-6,-11, macrophage and granulocyte/macrophage (GM) colony-stimulating factors(CSFs) and Tumor Necrosis Factor
Prostaglandins/Leukotrienes
Hormones
Growth factor antagonists
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Transforming Growth Factor
Super-family of growth factors (~34 members)
Acts on serine/threonine kinase cell wall receptors
Promotes proliferation and differentiation of mesenchymal precursors for osteoblasts, osteoclasts and chondrocytes
Stimulates both enchondral and intramembranous bone formation
Induces synthesis of cartilage-specific proteoglycans and type II collagen
Stimulates collagen synthesis by osteoblasts
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Bone Morphogenetic Proteins
Osteoinductive proteins initially isolated from demineralized bone matrix
Induce cell differentiation
BMP-3 (osteogenin) is an extremely potent inducer of mesenchymal tissue differentiation into bone
Promote endochondral ossification
BMP-2 and BMP-7 induce endochondral bone formation in segmental defects
Regulate extracellular matrix production
BMP-1 is an enzyme that cleaves the carboxytermini of procollagens I, II and III
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Bone Morphogenetic Proteins
These are included in the TGF-β family Except BMP-1
Sixteen different BMP’s have been identified
BMP2-7,9 are osteoinductive
BMP2,6, & 9 may be the most potent in osteoblastic differentiation Involved in progenitor cell transformation to pre-
osteoblasts
Work through the intracellular Smad pathway
Follow a dose/response ratio
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Timing and Function of Growth
Factors
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Fibroblast Growth Factors
Both acidic (FGF-1) and basic (FGF-2)
forms
Increase proliferation of chondrocytes
and osteoblasts
Enhance callus formation
FGF-2 stimulates angiogenesis
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Platelet-Derived Growth Factor
A dimer of the products of two genes, PDGF-A and PDGF-B
PDGF-BB and PDGF-AB are the predominant forms found in the circulation
Stimulates bone cell growth
Mitogen for cells of mesenchymal origin
Increases type I collagen synthesis by increasing the number of osteoblasts
PDGF-BB stimulates bone resorption by increasing the number of osteoclasts
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Insulin-like Growth Factor
Two types: IGF-I and IGF-II
Synthesized by multiple tissues
IGF-I production in the liver is stimulated by Growth Hormone
Stimulates bone collagen and matrix synthesis
Stimulates replication of osteoblasts
Inhibits bone collagen degradation
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Cytokines
Interleukin-1,-4,-6,-11, macrophage and granulocyte/macrophage (GM) colony-stimulating factors (CSFs) and Tumor Necrosis Factor
Stimulate bone resorption
IL-1 is the most potent
IL-1 and IL-6 synthesis is decreased by estrogen
May be mechanism for post-menopausal bone resorption
Peak during 1st 24 hours then again during remodeling
Regulate endochondral bone formation
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Hormones
Estrogen
Stimulates fracture healing through receptor mediated mechanism
Modulates release of a specific inhibitor of IL-1
Thyroid hormones
Thyroxine and triiodothyronine stimulate osteoclasticbone resorption
Glucocorticoids
Inhibit calcium absorption from the gut causing increased PTH and therefore increased osteoclasticbone resorption
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Hormones (cont.)
Parathyroid Hormone
Intermittent exposure stimulates
Osteoblasts
Increased bone formation
Growth Hormone
Mediated through IGF-1 (Somatomedin-C)
Increases callus formation and fracture
strength
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Vascular Factors
Metalloproteinases
Degrade cartilage and bones to allow invasion of vessels
Angiogenic factors
Vascular-endothelial growth factors
Mediate neo-angiogenesis & endothelial-cell specific mitogens
Angiopoietin (1&2)
Regulate formation of larger vessels and branches
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COMPLICATIONS OF
FRACTURE HEALING
MALUNION
DELAYED UNION
NONUNION
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MALUNION
A MALUNITED Fracture is one that has
healed with the fragments in a non
anatomical position.
CAUSES1- INACCURATE REDUCTION
2- INEFFECTIVE IMMOBILIZATION
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MALUNION contd…
MALUNION CAN IMPAIR FUCNTION by :
1. ABNORMAL JOINT SURFACE
2. ROTATION or ANGULATION
3. OVERRIDING
4. MOVEMENT OF NEIGHBOURING JOINT MAY BE BLOCKED
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CHARACTERISTICS FOR
ACCEPTABILITY OF FRACTURE
REDUCTION
ALIGNMENT (MOST IMPORTANT)
ROTATION
RESTORATION OF NORMAL LENGTH
ACTUAL POSITION OF FRAGMENTS
(LEAST IMPORTANT)
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Operative treatment for most malunited
fracture should not be considered until 6 to
12 months but in INTRA ARTICULAR fracture
early operative treatment is needed.
Surgeon should look for before surgery—
OSTEOPROSIS
SOFT TISSUE
HOW MUCH FUNCTION CAN BE GAINED
MALUNION contd…
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ILIZAROV TECHNIQUE is BEST Simultaneous
restoration of :
ALIGNMENT
ROTATION
LENGTH
MALUNION contd…
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Delayed Union
The exact time when a given fracture
should be united cannot be defined
Union is delayed when healing has not
advanced at the average rate for the
location and type of fracture (Btn 3-6 mths)
Treatment usually is by an efficient cast
that allows as much function as possible
can be continued for 4 to 12 additional
weeks
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If still nonunited a decision should be made to treat the fracture as nonunion
External ultrasound or electrical stimulation may be considered
Surgical treatment should be carried out to remove interposed soft tissues and to oppose widely separated fragments
Iliac grafts should be used if plates and screws are placed but grafts are not usually needed when using intramedullary nailing, unless reduction is done open
Delayed Union cont…
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FDA defined nonunion as “established
when a minimum of 9 months has elapsed
since fracture with no visible progressive
signs of healing for 3 months”
Every fracture has its own timetable (ie
long bone shaft fracture 6 months,
femoral neck fracture 3 months)
Delayed Union cont…
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Delayed/Nonunion cont.
Systemic factors:
Metabolic
Nutritional status
General health
Activity level
Tobacco and alcohol use
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Local factors
Open
Infected
Segmental (impaired blood supply)
Comminuted
Insecurely fixed
Immobilized for an insufficient time
Treated by ill-advised open reduction
Distracted by (traction/plate and screws)
Irradiated bone
Delayed weight-bearing > 6 weeks
Soft tissue injury > method of initial treatment
Delayed/Nonunion cont.
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Nonunited fractures form two
types of pseudoarthrosis:
Hypervascular or hypertrophic
Avascular or atrophic
Nonunion
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Hypervascular or
Hypertrophic:
1. Elephant foot
(hypertophic, rich in
callus)
2. Horse foot (mildly
hypertophic, poor in
callus)
3. Oligotrophic (not
hypertrophic, no
callus)
Nonunion
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Vascular or Atrophic
Torsion wedge
(intermediate fragment)
Comminuted (necrotic
intermediate fragment)
Defect (loss of fragment
of the diathesis)
Atrophic (scar tissue with
no estrogenic potential is
replacing the missing
fragment)
Nonunion
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Classification (Paley et al)
Type A<2cm of bone loss
A1 (Mobile deformity)
A2 (fixed deformity)
A2-1 stiff w/o deformity
A2-2 stiff w/ fixed deformity
Type B>2cm of bone loss
B1 with bony defect
B2 loss of bone length
B3 both
Nonunion
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Treatment:1. Elecrical
2. Electromagnatic
3. Ulrasound
4. External fixation (ie deformity, infection, bone loss)
5. Surgical
Hypertrophic: stable fixation of fragments
Atrophic: decortication and bone grafting
According to classification:
type A : restoration of alignment,compression
type B : cortical osteotomy, bone transport or lengthening
Nonunion
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Surgical guidelines:
Good reduction
Bone grafting
Firm stabilization
Nonunion
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Reduction of the fragments:
Extensive dissection is undesirable, leaving periosteum, callus, and fibrous tissue to preserve vascularity and stability, resecting only the scar tissue and the rounded ends of the bones
External fixator, Intramedullary nailing, Ilizarov frame
Nonunion
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Bone Grafting origins:
Autogenous “the golden
standard”
Allograft
Synthetic substitute
Nonunion
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Bone grafting techniques:
Onlay
Dual onlay
Cancellous insert
Massive sliding graft
Whole fibular transplant
Vascularized free fibular graft
Intamedullary fibular graft
Nonunion
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BONE GRAFTING
CRITERTIA FOR SUCCESSFUL BONE
GRAFT
OSTEOCONDUCTION
OSTEOGENICITY
OSTEOINDUCTION
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Nonunion of
tibial shaft
treated by
dual onlay
grafts
Dual onlay
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Massive sliding graft
GILL MASSIVE SLIDING GRAFT
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Whole fibular transplant
Bridging of bone defect
with whole fibular
transplant. A, Defect in
radius was caused by
shotgun wound. B and
C, Ten months after defect was spanned by
whole fibular transplant,
patient had 25% range
of motion in wrist, 50%
pronation and
supination, and 80% use
of fingers.
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Vascularized free fibular
graft
Posteroanterior and
lateral
roentgenograms
made 3 years after
fibular transfer,
showing excellent
remodeling with
fracture healing.
(From Duffy GP,
Wood MB, Rock MG,
Sim FH: J Bone Joint
Surg 82A:544, 2000
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Intamedullary fibular graft
Anteroposterior
roentgenogram of humerus
5 months after insertion of
fibular allograft and
compression plating with a
4.5-mm dynamic
compression plate revealing
evidence of bridging callus
formation and incorporation
of the allograft. (From
Crosby LA, Norris BL, Dao KD,
McGuire MH: Am J Orthop
29:45, 2000.)
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Nonunion cont..
Stabilization of bone fragments:
Internal fixation (hypertrophic #):
intamedullary, or plates and screws
External fixation(defects
associated#): ie Ilizarov
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Internal fixation
Roentgenograms
of patient with
subtrochanteric
nonunion for 22
years treated with
locked second
generation
femoral nail. A,
Preoperatively. B,
Postoperatively.
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Ilizarov
Bifocal osteosynthesis with Ilizarov
fixator after debridement of necrotic
segments, as recommended by
Catagni.
Monofocal osteosynthesis with
Ilizarov fixator for hypertrophic
nonunions with minimal infection, as
recommended by Catagni
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Factors complicating nonunion
Infection
Poor tissue quality
Short periarticular fragments
Significant deformity
Nonunion cont..
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Summary
Fracture healing is influenced by many
variables including mechanical stability,
electrical environment, biochemical factors
and blood flow
Our ability to enhance fracture healing will
increase as we better understand the
interaction between these variables
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BY :
Mὄᾗȶђἔʀ AłќђᾄᾧłᾄᾗƳ