Chapter 9: Bone Healing

Primary Bone Healing

Complications of Bone Healing Treatment of
Nonunions
Fusion
Bone Grafting
Aseptic Necrosis Following 1st Metatarsal Osteotomy
Electrical Bone Stimulation Cartilage Healing
 BONE HEALING
Primary Bone Healing
The two basic requirements for primary bone healing are an intact
vascular supply to the bone and rigid stable fixation of the fracture
fragments. Primary bone healing consists of simultaneous remodeling
and formation of new bone at the fracture site. The intermediary phase of
fibrocartilage formation as seen in callus bone healing is actually bypassed,
as new bone is formed intentionally at the fracture margins. Primary
bone healing is the direct reconstruction of the fragment edges by
haversian remodeling. This is the same homeostatic mechanism that
occurs in the living intact osseous skeleton on a daily basis.

There are six phases of the reparative process:

1. Hematoma: will form between the fracture fragments immediately
after the injury up until 1-3 days
2. Organization of the hematoma: slow shrinkage of the hematoma
resorption of devitalized bone, periosteal and endosteal cells from
osteoblasts at wound edges, from 3-10 days
3. Formation of fibrous/cartilaginous callus: this time of this phase will be
directly proportional to the proper apposition of fracture fragments and
immobilization of the affected body part, from 10-40 days
4. Primary bone callus: the bone callus becomes denser and fracture
clefts fill in with bone matrix to bridge the fracture site, from 40-80
days 5. Absorption of the primary bone callus: transformation of this
material to secondary bone callus, from 80-120 days
6. Remodeling of new bone: responding to the stresses placed upon it,
after 120 days

NOTE* When compression and rigid fixation devices are utilized, bone will
repair across the fracture gap by direct primary bone repair, with bone
callus being minimal or nonexistent.
Healing at points of contact along the fracture surface begins with the advance
of a capillary bud from the haversian canal. This organized structure
advances in a linear direction and crosses the fracture line depositing
lamellar new bone along its path. The tip of the complex is a group of large
multinucleated cells that function as osteoclasts. They cut their way
through existing osteoid and cross the fracture line into the surface of the
opposite fracture fragment (called the cutting cone).
The osteoclasts are followed closely by a capillary loop as the cutting cone creates
a tunnel in the existing bone substrate. The wall of this tunnel is lined by cells
with osteoblastic activity. These cells produce a concentric pattern of new
lamellar bone as the cutting cone passes and this is loosely deposited along
the course of the haversian canal to exist as mature lamellar bone.
NOTE* Underlying diseases such as rickets, osteomalacia, Paget's Disease of
Bone, hyperparathyroidism, osteoporosis and osteitis fibrosa cystica may
all cause a delay in bone healing

Complications of Bone Healing

Without an intact vascular supply to bone or rigid stable fixation
problems occur: irritation callus or secondary bone healing, malunion,
delayed union, non-union or pseudoarthrosis.

1. Secondary bone healing Involves the formation of fibrous tissue

(Phase 3), primary bone healing does not.

2. Malunion is a misalignment of the fracture fragments along any of the

three body planes including axial rotations, caused by inadequate
reduction and inadequate immobilization.

3. Delayed union is the inability of the fracture to heal within an acceptable

time period.
a. Diagnosis is by radiographic evaluation
b. Treatment is by rigid external or internal immobilation
c. A good prognosticator for healing is the formation and evaluation of
the bone callus
d. Treatment involves stimulating bone callus formation and can be
enhanced by bone drilling, onlay grafts, external electric current and
magnetic field induction e. Bone scans are of little value in
differentiating delayed from non- unions

4. Non-union can be an end stage of a delayed union, due to

inaccurate reduction, interrupted or inadequate immobilization,
severe local trauma to soft tissue and blood supply in the fracture site,
impairment of bony circulation following open reduction, infection
with secondary osteomyelitis of bony fragments, loss of bony
substance and distraction of bony fragments, age, compromised host,
anemia or anticoagulant therapy.

a. Unless a non-union is aggressively treated, it will usually result in a

pseudoarthrosis; the difference between them is that an atrophic non-
union does not have the fibrocartilaginous surface seen in a
pseudoarthrosis
b. Time frame for a non-union is usually 8 months following the initial
fracture
c. Diagnosis is by radiographic evaluation revealing gapping at the
fracture site with no bone callus; in some cases the fracture ends will
begin to round off (atrophic or non-reactive pseudoarthrosis); or will
mushroom developing a flaring (hypertrophic or elephant foot type
pseudoarthrosis) and form a joint space with synovial fluid filling the
gap.
 NOTE* Hypertrophic non-unions can be either Elephant type (maximum
callus /hypertrophy-best chance for healing), Horsefoot type (moderate
callus/hypertrophy) and Oligotrophic type (minimal callus/hypertrophy-
least reactive) NOTE" Atrophic non-unions can be either Torsion
wedge type (butterfly fragment with unilateral healing), Comminuted
(gap+numerous pieces), Defect type (no osseous integrity) and
Atrophic type (rounded edges) no osseous integrity.
d. Pseudoarthrosis is classified as non-infected, previously infected or
actively infected; non-infected are further subclassified according to their
location, diaphyseal vs metaphyseal (most diaphyseal pseudoarthroses are
atrophic)
e. Radiological studies:
i. Serial x-rays should be taken spanning time demonstrating a lack of
progress.
ii. Tomograms studies and CT scans can provide information of the bone
callus and the healing process.
iii. Bone scans are used to differentiate hypertrophic vs. atrophic
nonunions/pseudoarthrosis whereby a (+) bone scan would indicate a
hypertrophic/elephant foot type; a (-) bone scan would indicate an
atrophic/nonreactive type since it is relatively avascular.
f. Treatment of hypertrophic pseudoarthrosis: rigid immobilation and
electrical bone stimulation (cathode is inserted in the operative site set at
20 microamps). Bone forms under electronegative conditions.

NOTE* Bone stimulation is either implantable/invasive or non-invasive. Neither

will work for a synovial pseudoarthrosis. Non-invasive devices will not work
where the fracture gap is wider than 1 cm., and do not use during pregnancy or
in the presence of a pacemaker. Invasive stimulators may be used with
pacemakers and when the fracture gap is greater than 1 cm., also do not use
during pregnancy. Types of stimulators: constant direct current (semi-invasive),
pulsed direct current (invasive), inductive coupling electromagnetic
stimulation (non-invasive), capacitive coupling electromagnetic stimulation.

Note* Implantable bone stimulators have no known contraindications or adverse

effects, however, it is recommended that they not be used in the presence of
active OM or pathologic fracture from malignant bone tumors.

g. Treatment of atrophic non-union/ pseudoarthrosis: must resect the

area involved and replace with new bone using rigid internal fixation for
approx. 16 weeks minimum
h. Metaphyseal pseudoarthrosis, because of its proximity to the joint
space cannot be easily tension banded or fixated with a plate
5. Previously infected pseudoarthrosis/open infected pseudoarthrosis
a. The infectious process within bone will respond much quicker to
antibiotics only in the presence of a stable fracture fragment (stabilizing
the fracture fragment stabilizes the vascular bed), therefore, it is proper
medical practice to maintain rigid internal fixation in the treatment of
osteomyelitis
b. The goals of treatment are to provide a wide surface contact between
the fracture fragments under high compression, using whatever means is
necessary
c. Dead bone and non-viable soft tissue is removed
d. When bone loss is identified, the defect is filled with decorticated bone
or pure autogenous cancellous bone graft
e. Metal implants and fixation devices should be left undisturbed as long
as they afford rigid immobilization of the fragments. As soon as a
sufficiently strong bony bridge develops both the fixation devices and
the remaining sequestered bone are removed

6. Assessment of fracture healing

a. Standard x-rays
b. Stress fluoroscopy
c. Tomography/CT scans
d. Intraosseous venography: intramedullary injection of Renografin-76,
with sequential x-rays taken at 30 second intervals to access the presence or
absence of medullary flow across the fracture
e. Signs and symptoms: pain, warmth and tenderness

Treatment of Nonunions
The nonunion must be viewed as more than a fracture that has not healed.
There is often edema, pain, joint stiffness and deformity in the bone,
resulting in impaired function. Consequently, the first principle in the repair
of nonunions is the restoration of function. Treatment of nonunions follows
4 basic
I. Resection of useless tissue is required to allow healing
II. The osteogenic capacity must be augmented by bone grafting
III. The osteogenic capacity must be stimulated by electricity
IV. The bone has the capacity to unite but has had inadequate
immobilization, so the foot now should be adequately
immobilized during healing.
concepts:
1. Open nonunions vs. closed: When considering the above concepts one
must first consider whether the nonunion is open (with extensive soft tissue
damage) or closed.
a. Open nonunions are less frequent and more difficult to manage
b. Open nonunions frequently require multiple autogenous cancellous grafts
(poor vascularity so cortical is a poor choice).
c. Stabilization of an open nonunion is critical- can use external skeletal
fixators (stability with minimal trauma to surrounding soft tissues)
d. Following the above stages split/full thickness skin grafting can be
applied next over a bed of granulation tissue.
e. The type of treatment of a closed nonunion (most common) depends
upon the type and etiology, which as previously discussed is based on
vascularity
f. Proper evaluation of the nonunion is made via technetium scanning
g. Approx. 20% of nonunions require bone grafting
h. Electrical stimulation can be used but requires patient selection (satisfactory
position of bone fragments, no interposed soft tissue, and positive bone
scan)

Fusion
The basic concept of fusion is to eliminate motion where motion normally
occurs through primary bone healing. This is accomplished by removing
cartilagenous surfaces, obtaining anatomical apposition and utilizing some
form of rigid fixation to obtain primary bone healing. Primary bone healing
means membranous bone formation not endochondral bone formation,
without evidence of fibrous tissue, cartilage and no evidence of callus
formation. External callus is evidence of motion at the fusion site and
endochondral bone formation.
Fusion occurs quicker in cancellous bone where there are more osteons and.
better blood supply available than in cortical bone.

Bone Grafting
1. There are essentially two types available:
a. Autogenous (isograft): from the same person or twin
b. Allograft: from the same species- two types available fresh and lyophilized
2. Indications for bone grafting are: osteogenesis, Immobilization, and
replacement
a. Treatment of delayed and nonunions, and pseudoarthroses.
b. Augmentation of defects.
c. Facilitation of arthrodesis
d. Bone blocking procedures
e. Reconstructive procedures (for opening wedge and bradymetatarsia
procedures)
f. Autogenous grafting to treat OM

3. Cortical vs. Cancellous

 Cortical Cancellous
a. Denser........................................................................Less dense
b. Few viable cells...........................................................Many viable cells
c. Gives stability.............................................................Fills defects
d. Never revascularizes...................................................There are vascular
channels that unite at
the graft-host junction immediately
e. Does not facilitate osteogenesis...............................Facilitates
osteogenesis (by
osteoconduction and osteoinduction
f. Used with fixation devices........................................Not used with
fixation devices (soft)
g. Incorporation is slow.................................................Incorporation is fast
h. Incompletely repaired/incorporated.........................Completely replaced
by new bone
i. Allows for creeping substitution................................Allows for creeping
substitution
j. Fenestration of graft helpful (drill holes) ................Fenestration not done
if made parallel to long axis of bone
k. Radiolucency when healing (immediate)..................Radiodensity when
healing because it quickly revascularizes
l. Has haversion systems................................................No haversion systems

Note* Corticocancellous grafts (from the iliac crest) gives the best
combination. It looks like the first metatarsal head. Cortical graft 4.
looses 80% of its strength immediately. The weakest point in the
cortical graft is at 8 weeks.
Autogenous bone
a. is the material for most situations, the advantages are: viable cells and
immunological compatibility
b. the disadvantages are: donor site morbidity, insufficient quantity,
increased OR time, additional risks arising from surgery at the donor site.
c. Soaking in sterile saline prior to use is detrimental; proper short-term
storage should be to place the graft in a closed container covered with a
moistened saline sponge without immersion.
d. Sources are: iliac crest (much bleeding and pain), fibula, and lateral
calcaneus (small amounts).
e. Procedure to remove graft from the calcaneus is as follows:
A lateral incision is made over the calcaneus, posterior to the neutral
triangle, avoiding the sural nerve and deepened by layers to bone. Drill
holes are made outlining a cortical window which is then removed with
a power saw. If cortical bone is not needed it is replaced on the lateral
side, after packing the defect with lyophilized bone and covering the
area with periosteum. Must keep the calcaneus nonweight bearing until
evidence of healing is present.

5. Lyophilized Allograft (bone bank bone)

a. To reduce the antigenicity and increase immunological compatibility the
dead bone is freeze dried; this reduces the moisture content to less than
5%

NOTE* It is important that potential donors do not transmit disease so must

be carefully screened by serological tests, autopsy, and blood and tissue
bacteriological cultures, before and at implantation surgery

b. Lyophilized allografts vs. autogenous isografts

Lyophilized Autogenous
Freeze dried/devoid of water Fresh/water present
Osteogenic precursor present Same
Non-cellular bony matrix Cellular bony matrix
Osteoinductive property is lost Osteoinductive property present
Requires good recipient bed Not as critical
Allows for healing by creeping Same
substitution
Unlimited amounts Limited amounts
No morbidity of donor site Morbidity of donor site
Less OR time Increased OR time
Try using autogenous first The preferred
material for repair of
nonunions, especially avascular nonunions

Note* Place lyophilized allografts in Ringer's lactate for 45 minutes prior to

use

c. No difference in post-op infection rate of lyophized grafts vs. autogenous

grafts

6. Healing of grafts is by creeping substitution, osteoconduction and

osteoinduction
a. Creeping substitution: the temporal and spatial repair activities whereby
new viable bone replaces necrotic bone.
b. Osteoconduction: the scaffolding effect of the bone graft that acts as a
conduit for migration of viable cells (allows creeping substitution to take
place). c. Osteoindudion : the presence of a bone morpheogenic protein
(inductor substance) that causes nonosseous tissue to become osteogenic.

7. Grafting techniques Include: cortical onlay, peg, inlay, and peg-in-hole

a. Papineau technique used to treat OM and infected nonunions: excision
of necrotic bone, cancellous bone grafting and skin coverage
8. Healing is monitored with x-rays, Tc-99 scans, tomograms and CT. A
gradual blurring of cortical margins occurs, with eventual crossing of the
trabecular pattern across the graft-host junction. Impending disaster is
signaled by sclerosis or dissolution of the graft.

Aseptic Necrosis of the First Metatarsal Head Following Osteotomy

Aseptic bone necrosis following metatarsal surgery can present itself.
Stripping
away too much periostium or allowing the bone to "heat up" by the
bone saw are potential sources. A diagnosis can be made by bone scans and
later x-rays, after the onset of pain, swelling, and erythema.
1. Etiology of bone necrosis:
a. Major trauma (osteotomy)
b. Minor trauma (contusion)
c. Steroid therapy
d. Arteritis
e. Occlusive PVD
f. Antecedent phlebitis
g. Post-irradiation
h. S/P renal transplant
i. Hyperuricemia/gout
j. Collagen vascular diseases (RA)
k. Sickle-cell disease
l. Alcoholism/pancreatitis
m. Hyperlipidemia
n. Osteoporosis/osteomalacia

2. Bone Circulatory Networks:

a. Nutrient artery
b. Endosteal artery
c. lntracortical systems
d. Metaphyseal-epiphyseal
e. Diaphyseal
f. Marrow capillaries
g. Periosteal
h. Venous pathw

3. Arterial Circulation: Six groups of vessels

a. Nutrient
b. Periosteal
c. Proximal metaphyseal
d. Proximal epiphyseal
e. Distal metaphyseal
f. Distal epiphyseal

4. Radiological Classification of Bone Necrosis:

a. Stage
1: Pre-radiologic (avascularity/precollapsed)
i. The joint space/epiphyseal contour/trabeculae are WNL
ii. Joint space may be stiff and painful
b. Stage 2: Probable (revascularization phase with bone deposition and
resorption/collapsed)
i. Joint space/epiphyseal contour are WNL
ii. Altered trabecular pattern (osteoporotic/sclerotic/sclero-cystic)
c. Stage 3: Definite (bone healing phase/early and late degenerative arthritic
changes)
i. Joint space is WNL
ii. Epiphyseal contour is disrupted and flattened
iii. Trabecular collapse, arcuate sclerosis, cysts, and sequestrum
d. Stage 4 (phase of deformity)
i. Joint space narrowed (cartilage disruption)
ii. Epiphyseal collapse
iii. Trabecular destruction (sclerosis and cysts)
iv. Epiphyseal collapse

5. Clinical Signs and Symptoms:

a. Stage 1: Usually asymptomatic with minimal pain and/or stiffness
b. Stage 2: Usually significant pain and stiffness, but can be asymptomatic
c. Stage 3: Pain, stiffness, and limitation of motion, but can be
asymptomatic

6. Clinical Lab Findings:

a. Elevated ESR (nonspecific finding and not diagnostic)

7. Clinical Radiological Findings:

a. Bone scan: Early (pre-collapse)- localized cold scan
b. Bone Scan: Later- Hot

8. Differential Diagnosis:
a. Arthrosis
b. RSD
c. Infection

9. Treatment of Aseptic Necrosis:

a. Eliminate weight bearing
b. Peripheral vasodilators
c. Indomethacin
d. Avoid steroids
e. Core decompression, autogenous cancellous graft
f. Pedicle muscle graft, decompression, bone graft
g. Chilectomy, decompression or osteotomy, decompression
h. Joint replacement (prosthesis)
i. Arthrodesis

10. Recommendations/Precautions:
a. Preserve capsular and periosteal attachments
b. Accurate hemostasis, avoid tamponade
c. Caution with modified Austin osteotomies (long-arm), Offset V osteotomy,
and long Z osteotomies
d. Caution with distal subchondral osteotomies, especially in the elderly
e. Avoid hemi-implant in combination with distal osteotomy
f. Use stable fixation, protective ambulation
g. Use routine serial radiographs
h. Consider bone scan early

Electrical Bone Stimulation

The use of electrical energy in an effort to effect the healing of bone was
initially described in 1812. A variety of therapeutic devices are currently
available to provide electrical stimulation in the treatment of nonunions of
bone. The discovery of stress related and steady-state electrical potentials,
resulted in the hypothesis that Wolff’s law of bone was in effect mediated by
electrical impulses.
Therefore the application of exogenous electropositive currents to stimulate
osteogenesis is the basis for bone stimulation.
1. A variety of methods have been employed to develop exogenous
electrical
potentials:
a. Constant direct current:
i. EBI:
 Implantable
 Contraindicated in osteomyelitis
 Available in either 24 or 36 weeks life span
b. Pulsed direct current:
i. EBI:
 Used for a 6 hour treatment/day
ii. AME:
 3 hour treatment/day
 Has even distribution
c. Capacitively coupled electrical field
i. Bioelectron:
d. Low intensity ultrasound
i. Exogen®

Cartilage Healing
1. Normal Cartilage:
a. Consists of chondrocytes in a glycoprotein hydrated matrix that may
contain collagen and/or elastin
i. Type Il collagen
ii. Ground substance (glycosaminoglycans and water)
b. Nutrition is through synovial fluid (there is no blood supply to the
cartilage)

2. Healing phase:
a. Necrosis
b. Inflammation
c. Repair via metaplasia and replication

3. Types of injury:
a. Partial thickness: Usually these injuries do not heal, using shaving and
drilling of articular surface may lead to the development of fibrocartilage
ingrowth
b. Osteochondral heals via:
i. Type II collagen: similar to hyaline cartilage
ii. Type I collagen: fibrocartilage