Ch. 2
Tissue Healing
Introduction
• Tissue healing occurs and is influenced by
several factors
• There are three phases:
– Inflammatory response
– Repair/regeneration
– remodeling
Inflammatory Response
• Cells remove debris
• Cells create groundwork for repair and
regeneration phase
Repair/Regeneration Phase
• Cells restore the vascular and structural
integrity of injured structures
Remodeling Phase
• Healed tissue adapts to functional loading
• Gets stronger based on the stress that is
applied to it
• The three phases overlap one another
• Disruption of any one phase can cause an
unsatisfactory outcome
Types of Tissue
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Epithelial tissue
Connective
Muscle
nervous
Epithelial Tissue
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Composed of layers of cells
Protect organs
Secretions (glands)
Absorption ( lining of the stomach )
Connective Tissue
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Most abundant and variable tissue in the body
Attaching organs
Support/structure
Movement
Physical protection
Immune response, energy & mineral storage
Heat generation and transportation (blood,
etc.)
Connective Tissue
• Subtypes:
– Fluid connective tissue=blood and lymph
– Fibroconnective tissue=fat, tendons and ligaments
– Supportive connective tissue=cartilage and bone
Nervous Tissue
• Located in brain and spinal cord and nerves
• Electrically exciteable
• Used to transmit and respond to various
impulses and forms of information
Muscle Tissue
• Skeletal- striated or voluntary
• Cardiac – heart muscle
• Smooth- linings of organs and blood vessels
Common Injuries
Puncture and Laceration
Incision
Acute vs. Chronic
• Acute – single forcefull event (ACL tear)
• Chronic – occur over a period of time (Tennis
elbow)
Acute Injuries
• Contusions – bruises
• Strains – muscle or tendon injuries
• Sprains – ligamentous injuries
Contusions
• Caused by compressive forces
• or direct impacts and are graded by degrees
of trauma
• 1st degree-minimal swelling, no limits
• 2nd – pain, bleeding, moderate functional
limits
• 3rd-hematoma formation,sever limitations
Sprains and Strains
Fracture Classifications
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Greenstick
Transverse
Oblique
Spiral
Comminuted
Avulsion
Impacted
Depressed
Epiphyseal (Salter-Harris classification)
Peripheral Nerve Injuries
• Neuropraxia-least severe, transient and
reversible loss of nerve function
• Axontomesis- partial disruption, may cause
atrophy or weakness for 2 – 52 weeks
• Neurotomesis – complete severance of a
nerve resulting in permanent loss of function
Chronic Injuries
• Blisters – continuous friction
• Repetitive overload – tendinosis, tenosynovitis
• Chronic irritation –could cause neuralgia or
neuroma
Soft Tissue Healing
• Phase 1: Inflammatory Response
• Phase 2: Repair/Regeneration
• Phase 3: Remodeling/Maturation
Phase 1
• Signs and symptoms:
– Redness
– Heat
– Pain
– Swelling
– Loss of function
Phase 1 con’t
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Lasts 7-10 days
Initial damage is called “the primary injury”
Caused by a release of proteins at the injury site
Mast cells produce chemicals (histamines) which
promote vasodilation
• This causes the redness and heat
• Vessels become more permeable which
contributes to the swelling
Phase 1
• Mast cells also release chemicals that attract
neutrophils (immune cells) to come to the
injury
• Neutrophils clear debris and regulate the early
inflammatory process
• Injured area becomes ischemic and acidic
which may cause secondary damage to
otherwise healthy areas around the injury
Phase 1
• Neutrophils die and are ingested by
macrophages at the injury site
• When this happens the macrophages begin to
produce proteins that promote tissue repair
• Early scar tissue forms
• Early rehab should focus on pain
management, decreasing swelling, promote
tissue healing
Phase 1
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Immobilization or protection should be done
RICE
NSAIDS for decreased inflammatory symptoms
Short term analgesic
Phase 2: Repair/Regeneration
• Repair- articular cartilage, meniscus, spinal
cord (new tissue is not identical)
• Regeneration- bone, muscle, peripheral nerve,
blood vessels (heal with identical tissue)
• Patients are still swollen and pain with motion
• Blends with the inflammatory phase and
remodeling phase
• Day 7 to 21
Phase 2
• Fibrin clots form
• Fibroblasts proliferate near the injury
• Capillary proliferation occurs (more oxygen
needed)
• Fibroblasts produce fibronectin, collagens,
glycoproteins
• Fibronectin begins dormant followed by type
III collagen then to stronger type I
Phase 2
• Initially patient has structural deficiency
• Treatment – early controlled mobilization
• This aligns collagen with areas of physical
stress making it stronger
• Prevents atrophy
Phase 3: Remodeling/Maturation
• Lasts up to 24 months
• May have persistent swelling and pain with
motion
• Fibroblast activity decreases throughout this
phase
• Capillary density decreases
• Cellular matrix becomes more refined
Phase 3
• More type I and type III collagen fibers are
produced
• Tensile strength improves
• Rehab can increase the physical demands until
patients return to their activities of daily living
Fracture Healing
• Four phases:
– Inflammation
– Soft callus formation
– Hard callus formation
– Bone remodeling
Phase 1: Acute
• Lasts up to a week
• Hematoma formation, inflammation,
angiogenesis (new blood vessel formation),
soft callus formation
• Dominated by immune cells
• Phagocytic cells remove debris
• Platelets form clots
Phase 2: Repair/Regeneration
• Lasts 8 to 12 weeks
• Remodeling of scar tissue through cartilage
formation, calcification and bone formation
• Mesenchymal cells become cartilage cells
• Proliferate the soft callus
• Replace the scar tissue with cartilage
• Chondrycytes hypertrophy and release
chemicals to promote bone formation
Phase 2
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Osteoblasts produce new bone
Revascularization of the region occurs
Soft tissue is replaced by bone
Casting is used to allow time for a proper
callus to develop
Phase 3: Remodeling
• Starts during Phase 2 and continues for
several years
• Starts 21 days post fracture
• Woven bone replaced by cortical or trabecular
bone
• New bone is remodeled by osteoclasts and
osteoblasts based on mechanical loading
Fracture Management
• Treatment varies by :
• type of fixation
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No reduction
Closed reduction
Open reduction
Open reduction internal fixation (ORIF)
Location of fx
Involved bone
Mechanical loads
Surrounding soft tissue
Fracture Management
• ORIF
– Surgical fixation
– Uses metal implants to stabilize fx’s
– May allow rehab to begin within first week after
surgery ( edema control, wound management,
early motion)
– More aggressive rehab can begin in 6-8 weeks
Fracture Management
• Non-surgical fixation
– ROM delayed for 3 weeks
– Until callus has enough tensile strength to tolerate
movement
– At 6-8 weeks patient may begin strengthening
exercises and increase mechanical loads
– Upper extremity fx’s may begin ROM exercises
sooner because of smaller loads and fear of
atrophy
Delayed/Non Union Fx’s
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Nutritional deficiencies
Diabetes, anemia
Smoking
Pharmacological drug use
Pre-injury vascular status
Muscle around fracture
Inadequate immobilization
Infection
High energy fractures
Gap distance
Nerve injury
Delayed / Non Union Fx’s
• Susceptible areas
– Tibia
– Ulna
– Femoral neck
– Scaphoid (most common)
Peripheral Nervous Healing
• More proximal injuries result in greater losses
• Within 3 -5 days, axons distal to the injury
undergo a degenerative process called
Wallerian degeneration
• This is promote by immune cells, Schwann
cells(the cell that normally myelinate axons)
and the distal axon
Nerve Healing
• Produce proteins that produce and
inflammatory response and pain
• Schwann cells divide to create an optimal
environment for regeneration
• Surgical repairs can be helpful but are not
guaranteed
• Only one proximal branch will form a new
axon the others will degenerate
Muscle Healing
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Tissue trauma
Hematoma formation
Inflammatory cell reaction
Phagocytosis
Capillary regrowth
Scar formation
remodeling
Muscle Healing
• Must balance regeneration with scar formation
• Scar tissue is weak and only serves as a “scaffold”
for the healing process
• Site is still weak
• No active motion immediately after injury
• Could result in re-rupture
• However, prolonged immobilization could result
in atrophy
Muscle Healing
• What do you do?
Muscle Healing
• Early mobilization and motion may be started
within the first 24 hours
• It must be pain free to avoid overloading
• Pain is your guide
Tendon Healing
• Ruptured tendons often require surgery
• Once repaired the tendon ends can go
through their normal healing stages
Tendon Healing
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Hematoma formation
Platelet aggregation
Recruitment of inflammatory cells
Phagocytosis
Angiogenesis
Fibroblast proliferation
remodeling
Tendon Healing
• Tensile strength increases at 4 weeks
• Continues to improve up to 1 year
• Strength of tendon never returns to pre-injury
level
Factors Affecting Healing
• Healing process is variable
• Factors:
– Extensive trauma
– Blood supply
– Infection
– Diabetes
– Age
– nutrition
Critical Thinking
• In a rehab setting, patients want to return
ASAP. As a result, some patients do extra
exercises, stretch to a point of pain, or try
aggressive exercises (e.g. running) too early.
What are the potential hazards to this
approach? How would you explain your
concerns to the patient or athlete?
Critical Thinking
• Two patients that are 10 weeks post –fractures
are exercising next to each other. One of the
patients had a distal radius fracture and the other
had a scaphoid fracture. Both were treated
conservatively with immobilization. The patient
with the scaphoid fracture notices that she is still
not able to do a lot of the exercises her
counterpart is able to perform. She then asks
why she is not progressing at the same rate as the
other patient. How would you explain the
differences in their recovery?