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leading to the formation of newly woven bone at
the edges.
At approximately 3 weeks, callus fills in between
the edges (starts as soft callus populated by
chondrocytes, which gradually calcifies into hard
callus by endochondral ossification); continued
bone formation by osteoblasts leads to bony edge
unification.
Remodeling phase (starting at 2-3 months and
continuing for years)
Woven bone is slowly replaced by the lamellar
bone according to the Wolff law; medullary canal is
restored.
“Clinical healing” (defined as the state of adequate
stability and resolution of pain to allow protected
motion) occurs in most bones by 4-6 weeks.
Radiographic healing may lag by 6 months.
Tendon Healing
Mechanisms of tendon healing
Intrinsic healing
Tendon’s innate capacity to heal (operative repair
aims to maximize this type of healing)
Mediated by tenocytes/fibroblasts that arise from
the tendon and epitenon
Relies on synovial diffusion for nutrition
Enhanced by mobilization
Extrinsic healing
Surrounding soft tissue’s tendency to repair
damaged tendon.
Infiltration of inflammatory cells and fibroblasts
overlying the sheath.
Immobilization leads to the formation of adhesions,
limiting range of motion (early mobilization
minimizes adhesions caused by extrinsic healing).
Phases of healing
Inflammatory phase (within first few days, peaking at
3 days)
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Tendon defect fills with hematoma, tissue debris,
and fluid.
Increased phagocytic activity clears necrotic
debris.
Proliferative phase (starting at approximately day 5
and lasting up to several weeks)
Fibroblasts are the predominant cell type,
proliferating from epitenon and endotenon.
Collagen deposited, vascular ingrowth occurs.
Strength of repair begins and increases at ~2-3
weeks; synovial sheath is reconstituted at 3
weeks.
Remodeling phase (starting at several weeks after
injury and lasting up to 1 year after)
Collagen fibers initially deposited perpendicular to
tendon axis realign to the long axis of the tendon
by 8 weeks.
Cartilage Healing
Avascular tissue without intrinsic healing potential
Healing initiated by damage to the surrounding tissue (eg,
perichondrium and subchondral bone)
Extra-articular cartilage vs intra-articular cartilage
healing
Extra-articular cartilage (eg, auricular and nasal)
injury
Tissue injury response generated by
perichondrium with fibroblast influx and scar
formation (but not true regeneration of cartilage)
Intra-articular cartilage injury
Superficial (without violation of subchondral bone)
—no blood-carrying progenitor cells are released,
thus no repair occurs.
Full-thickness (through cartilage and into
subchondral bone)—allows influx of progenitor
cells and formation of fibrocartilage. Fibrocartilage
is less organized, more vascular, less tolerant of
mechanical force, and more susceptible to
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degradation compared with normal cartilage.
Fibrocartilage eventually breaks down, resulting in
an arthritic joint.
Nerve Healing
Response to injury see Chapter 45: Nerve Injuries,
Neuromas, and Compression Syndromes for classifications
of nerve injuries.
Trauma to vasa nervorum and surrounding tissue leads
to inflammatory response.
If the injury is close to the neuron cell body, the entire
neuron may die (eg, brachial plexus avulsion injuries).
Typical injuries to nerves in peripheral locations (eg,
complex forearm laceration) will affect connective
tissues (Schwann cells) and the axon but not the actual
neuronal cell body.
*Wallerian degeneration: Schwann cells will die,
and the distal axon degrades. This can extend up
to 2 cm proximal to the injury site.
Axon degradation and clearing of debris takes 15-30
days and precedes nerve regeneration.
Axonal regrowth occurs in response to neurotrophins
(eg, brain-derived neurotrophic factors, ciliary
neurotrophic factor, and nerve growth factor) secreted
by target cells (postsynaptic neurons or muscle cells)
and by Schwann cells.
Macrophages secrete interleukins that induce
Schwann cell proliferation.
Schwann cells along the distal axonal tract express
laminins and adhesion molecules, which help guide the
regenerating axon.
Axonal sprouts from the proximal cut end must enter
the distal tract to regrow. If budding axons cannot cross
the gap, regeneration does not occur.
Muscles innervated by the injured nerve will atrophy
(70% loss at 2 months). Some muscle fibers die at 612 months if there is no regeneration of nerve. Motor
endplates remain open for approximately 1 year
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(variable) before fibrosis develops, and reinnervation is
then unlikely.
*Once growth is initiated, axons extend by ~1 mm a
day.
PATHOLOGIC WOUND HEALING
Wound Failure (Skin, Subcutaneous Tissue, Fascia, Muscle)
Acute wound failure (dehiscence): postoperative
separation of the surgical incision
Occurs when the load applied to the wound exceeds
the strength of the suture line and provisional matrix
Most commonly happens at 7-10 days postoperatively,
can happen any time from day 1 to more than 20 days
after surgery
Chronic wound failure (nonhealing wounds)
Failure to achieve anatomic/functional integrity over 3
months.
Chronic wounds can development into squamous cell
carcinoma (aka Marjolin ulcer).
Associated physiologic derangements.
*Abnormal ECM dynamics: increased MMPs,
decreased TIMPs
Associated factors for acute and chronic wound failure
(see Table 1-1)
TABLE 1-1 Factors Affecting Acute and Chronic Wound
Healing
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*Radiation therapy leads to vascular fibrosis
(relative ischemia) and decreases mitotic potential
of fibroblasts (also consider possibility of
osteoradionecrosis of the bone).
Diabetes (microvascular and macrovascular diseases
leading to local ischemia; glycosylation of hemoglobin
impairs oxygen delivery; impaired neutrophil function;
peripheral neuropathy).
Advanced age (shortened inflammatory phase causing
decreased strength of healing).
Malnutrition.
Vitamin C
*Role in collagen cross-linking by
hydroxylation of proline and lysine.
*Lack of vitamin C leads to “scurvy”: low
collagen tensile strength manifests in
collagen-containing tissues (skin,
dentition, bone, and blood vessels) as
hemorrhage (petechiae and swollen
gums), loss of dentition, and impaired
bone healing.
Folate and vitamin B6 (pyridoxine): DNA synthesis
and cellular proliferation
Vitamin E: strong antioxidant and immune
modulator
Zinc: cofactor for numerous metalloenzymes and
proteins; necessary for protein and nucleic acid
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synthesis
Nutrition historically assessed in the acute phase
with prealbumin level (normal >17 g/dL, 3-day half-
life) and in the chronic phase with albumin level
(normal >3.5 g/dL, 20-day half-life)
More recent literature suggests that these are
more representative of inflammation than
nutrition.
Chemotherapy: Most detrimental agents are
doxorubicin, cyclophosphamide, methotrexate, bischloroethylnitrosourea (BCNU), and nitrogen mustard.
Glucocorticoids.
Inhibit the inflammatory phase and collagen
synthesis of fibroblasts, leading to decreased
wound strength
*Can reverse effect with oral vitamin A to
augment epithelialization and fibroblast
proliferation
Anemia by itself does not impair wound healing.
Bone
Types of bone healing pathology
Delayed union: When clinical healing is delayed
beyond the usual expected time with radiographic
evidence of inadequate osteocyte activity and deficient
callus formation.
Nonunion: When there is no evidence of clinical or
radiographic healing beyond the usual healing time,
often with a mobile area fibrous scar and interposed
tissue in the gap (pseudoarthrosis).
Factors detrimental to bone healing (see Table 1-1)
Tendon
Immobilization after primary tendon repair
Extrinsic healing predominates with tendon sheath
adhesion formation.
Disorganized collagen fibrils and decreased strength of
repair.
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Poor tendon healing can be attributable to gapping
from poor surgical technique.
Overuse tendinosis: painful condition beginning with
repetitive microtrauma to tendon without allowing
appropriate time to heal; characterized by degenerative
changes in tendon
Nerve
Neuroma—painful regrowth of nerve in a scarred area of
previous injury
Failure of axonal regeneration (regeneration decreases with
age)
Degeneration of sensory receptors (for sensory nerves)
Fibrosis of motor endplates (for motor nerves)
Cross-innervation (eg, facial synkinesis, gustatory sweating
[Frey syndrome])
SCARRING
NORMAL SCARRING
Visible scar is the normal end point for all full-thickness
skin injuries. No such thing as scarless surgery.
Factors That Lead to Less Conspicuous Scars
Older age
Lighter colored skin
Surgical incision as opposed to traumatic laceration
Placement of incision or laceration within (parallel to)
relaxed skin tension line
Minimal tension following closure (eg, eyelids)
Optimal surgical technique (eg, atraumatic manipulation,
skin edge eversion, and removal of suture in 5-7 days on
face)
PATHOLOGIC SCARRING
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Hypertrophic Scar
Definition: an abnormal wound healing end point in
response to trauma, inflammation, burn, or surgery
Raised, erythematous, and often pruritic.
*Remains within the boundaries of original wound.
Upregulated fibrogenic cytokines (TGF-β isoforms,
PDGF, and insulinlike growth factor 1 [IGF-1]) lead to
higher levels of collagen synthesis.
Etiology
Major factors
Extent/depth of trauma (most commonly with
burns)
Inflammation, infection
Prolonged open wound (>21 days, most
commonly with burns)
Contributing factors
Tension on wound
Darker skin tone
Natural history
Becomes apparent at ~6-8 weeks after injury
Worsens over 6 months
May cause contractures at joints
May take 1-2 years to mature (scar typically will
become less red, less tender, and less pruritic)
Histologic characteristics (under standard light
microscopy, hypertrophic scar and keloid are
indistinguishable)
Cigar-shaped nodules of blood vessels, fibroblasts,
and collagen fibers that are arranged parallel to
epidermis and oriented along tension lines vs normal
skin, which has the basketlike woven pattern of
collagen fibers
*Presence of α-smooth muscle actin producing
myofibroblasts (not present in keloids)
Primarily composed of well-organized type III collagen
Treatment approach
Nonoperative
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Pressure garments
Commonly used for hypertrophic burn scars
Induces local tissue hypoxia, reduces
fibroblast proliferation and collagen synthesis
Compression of 24-30 mm Hg to be effective
Silicone sheeting and topical silicone gel
Unclear mechanism of action—thought to
increase hydration of remodeling scar
Require application at least 12 hours per day
for at least 3 months to be effective
Corticosteroid injection
Surgical excision
Attention to atraumatic technique, excision of
inflamed tissue, avoidance of nidus for
inflammation (eg, trapped hair or unnecessary
deep resorbable suture), and tension-free closure.
Z-plasty tissue rearrangements to release
contractures.
May require graft or flap reconstruction for
coverage.
Fractional ablative CO2 laser can be helpful
adjunct as well as pulse dye lasers to remove the
redness of scars.
Keloids
Definition: an abnormal wound healing end point in
response to trauma, inflammation, burns, or surgery
May start as a raised, erythematous, and pruritic lesion
*Evolves into an enlarging mass that extends
beyond the original boundaries of the wound
Higher level of collagen synthesis compared with
hypertrophic scars due to upregulated fibrogenic
cytokines (TGF-β isoforms, PDGF, and IGF-1) and
increased number of receptors for these cytokines
within keloidal fibroblasts
*Increased fibroblast proliferation
*Absence of myofibroblasts and decreased density
of blood vessels in comparison to hypertrophic
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scars
Decreased expression of MMPs (that degrade ECM),
increased ATP
Etiology
Major factors
Darker skin tone
Genetic predisposition
Contributing factors
Age (peak just after puberty)
Hormones (keloids worsen during puberty and
pregnancy; postmenopausal women experience
softening and flattening of keloids)
Natural history: evolves over time without a significant
regression or quiescent phase
Histologic characteristics (under light microscopy,
hypertrophic scar and keloid are indistinguishable)
*Thick and large collagen fibers haphazardly
packed closely together comprised of both type I
and type III collagen
Treatment approach: Nonoperative and operative
interventions are required, and an extremely high rate of
recurrence persists (50%-80%).
Nonoperative
Pressure devices (eg, pressure clip for earlobe)
(preventative measure)
Silicone sheeting and topical silicone gel
(preventative measure)
Corticosteroid injection (recurrence 15.4%)
5-fluorouracil (5-FU) injection (chemotherapeutic
drug) (recurrence rate 19%)
Surgical
Attention to atraumatic technique, excision of
inflamed tissue, avoidance of nidus for
inflammation (eg, trapped hair or unnecessary
deep resorbable suture), and tension-free closure
Excision ± skin graft depending on the size of the
lesion
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