Transcript latest tissue healing - Elite Physical Medicine

Anatomy and Physiology of Bone,
Ligament, Muscle and tendon.
Physiology of injury and tissue
repair
The inflammatory response and
healing
Clinical considerations
Paul Thawley MSc
Learning objectives
Formulate a clear understanding of the
structure and form of bone, ligament and
muscle on a molecular and macro level.
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• Be able to demonstrate the relative reparative
mechanisms
• Understand the implications for the athlete
and clinical rehabilitation.
Musculoskeletal system
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Give the body its structural form – specialised
connective tissues
Protect vital organs
Promotes efficient movement despite forces
of gravity
Store salts and other substances needed for
metabolism
Produce red blood cells
Musculoskeletal system - joints
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Where bones interact
Synarthrosis – a joint that does not permit
movement, Skull in adults
Diarthrosis (synovial joints)
 Monoaxial: hinge or pivot joints
 Biaxial: gliding, sliding or saddle joints
 Triaxial: ball and socket joints
Ligaments
Joint capsule –synovial fluid
Joint structure
Bone structure
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Diaphysis
Epiphysis
Medullary canal
Periosteum
Cartilage
Types of Bone
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Lamellar Bone
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Collagen fibers arranged in parallel layers
Normal adult bone
Woven Bone (non-lamellar)
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Randomly oriented collagen fibers
In adults, seen at sites of fracture healing,
tendon or ligament attachment and in
pathological conditions
Bone Composition
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Cells
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Osteocytes
Osteoblasts
Osteoclasts
Extracellular Matrix
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Organic (35%)
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Collagen (type I) 90%
Osteocalcin, osteonectin, proteoglycans, glycosaminoglycans,
lipids (ground substance)
Inorganic (65%)
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Primarily hydroxyapatite Ca5(PO4)3(OH)2
Lamellar Bone
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Cortical bone
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Comprised of
osteons (Haversian
systems)
Osteons
communicate with
medullary cavity by
Volkmann’s canals
Lamellar Bone
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Cancellous bone
(trabecular or spongy
bone)
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Bony struts
(trabeculae) that are
oriented in direction of
the greatest stress
Woven Bone
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Coarse with
random orientation
Weaker than
lamellar bone
Normally
remodeled to
lamellar bone
Figure from Rockwood and Green’s: Fractures
in Adults, 4th ed
Osteoblasts
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Derived from
mesenchymal stem
cells
Line the surface of the
bone and produce
osteoid
Immediate precursor is
fibroblast-like
preosteoblasts
Picture courtesy Gwen Childs, PhD.
Osteocytes
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Osteoblasts surrounded
by bone matrix
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trapped in lacunae
Function poorly
understood
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regulating bone
metabolism in response
to stress and strain
Picture courtesy Gwen Childs, PhD.
Components of Bone Formation
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Cortex
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Periosteum
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Bone marrow
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Soft tissue
Prerequisites for Bone Healing
 Adequate
blood supply
 Adequate mechanical stability
Mechanisms of Bone Formation
Cutting Cones
 Intramembranous Bone Formation
 Endochondral Bone Formation
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Cutting Cones
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Primarily a
mechanism to
remodel bone
Osteoclasts at the
front of the cutting
cone remove bone
Trailing osteoblasts
lay down new
bone
Courtesy Drs. Charles Schwab and Bruce Martin
Intramembranous (Periosteal)
Bone Formation
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Mechanism by which a long bone grows in
width
Osteoblasts differentiate directly from
preosteoblasts and lay down seams of
osteoid
Does NOT involve cartilage
Endochondral Bone Formation
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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)
Blood Supply
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Long bones have
three blood supplies
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Nutrient artery
(intramedullary)
Periosteal vessels
Metaphyseal vessels
Periosteal
vessels
Nutrient
artery
Metaphyseal
vessels
Figure adapted from Rockwood and Green, 5th Ed
Vascular Response in Fracture
Repair
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Fracture stimulates the release of growth
factors that promote angiogenesis and
vasodilation
Blood flow is increased substantially to the
fracture site
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Peaks at two weeks after fracture
Mechanical Stability
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Early stability promotes
revascularization
After first month,
loading and
interfragmentary
motion promotes
greater callus formation
Mechanical Stability
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Mechanical load and small displacements
at the fracture site stimulate healing
Inadequate stabilization may result in
excessive deformation at the fracture site
interrupting tissue differentiation to bone
(soft callus)
Over-stabilization, however, reduces
periosteal bone formation (hard callus)
Stages of Fracture Healing
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Inflammation
Repair
Remodeling
Inflammation
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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
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Osteoinductive growth factors stimulate the
proliferation and differentiation of mesenchymal stem
cells
Repair
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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
Repair
Figure from Brighton, et al, JBJS-A, 1991.
Remodeling
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Woven bone is gradually converted to lamellar bone
Medullary cavity is reconstituted
Bone is restructured in response to stress and
strain (Wolff’s Law)
Mechanisms for Bone Healing
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Direct (primary) bone healing
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Indirect (secondary) bone healing
Direct Bone Healing
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Mechanism of bone healing seen when there
is no motion at the fracture site (i.e. rigid
internal fixation)
Does not involve formation of fracture callus
Osteoblasts originate from endothelial and
perivascular cells
Direct Bone Healing
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A cutting cone is formed that crosses the
fracture site
Osteoblasts lay down lamellar bone behind
the osteoclasts forming a secondary
osteon
Gradually the fracture is healed by the
formation of numerous secondary osteons
A slow process – months to years
Components of Direct Bone
Healing
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Contact Healing
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Direct contact between the fracture ends allows healing
to be with lamellar bone immediately
Gap Healing
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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)
Direct Bone Healing
Figure from http://www.vetmed.ufl.edu/sacs/notes
Indirect Bone Healing
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Mechanism for healing in
fractures that are not rigidly
fixed.
Bridging periosteal (soft)
callus and medullary (hard)
callus re-establish structural
continuity
Callus subsequently
undergoes endochondral
ossification
Process fairly rapid - weeks
Local Regulation of Bone
Healing
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Growth factors
Cytokines
Prostaglandins/Leukotriens
Hormones
Growth factor antagonists
Implications for Rehabilitation
Stress fracture
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Partial or incomplete fracture of the bone that
occurs when repeated rhythmic submaximal
loads are applied to the bone
Failure or a crack in the bone
Difficult to spot on x-rays – bone scan/MRI
Treatment: protect from stresses/unload bone
Prevention strategies
Stress fracture
Implications for rehabilitation following bone injury
What are they?
• full repair
• Previous injury mechanism stress related
• Prolonged immobilisation
• conditioning
• Joint restriction altered biomechanics
• MM imbalance and risk of secondary injury
• Psych effects
Healing Soft Tissue
Ligament function
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Connect bone with bone
Augment the static mechanical stability of
joints
Prevent excessive or abnormal motion
Sensory source – protective and propioceptive
feedback; neuromuscular dynamic control of
stability
Ligament composition
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Cells (fibroblasts) 20%,
and ECM (collagen) 80%
90% of collagen is type 1
(10% type 3)
Crosslinking and quarterstaggered array
Less parallel arrangement
of collagen fibrils in
ligaments - can resist
forces in many directions
Ligament & tendon insertion
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4 zones of indirect insertion
Perforating fibres of Sharpey cross all 4 zones
Gradual change in structural properties results in increased
stiffness and decreased stress concentration minimising injury
at insertion sites
Ligament fibres insert oblique or orthogonal
Musculotendinous junction – aponeurosis
Blood supply is poor in both
 Ligament: insertion sites
 Tendon: paratenon, vincula
Grading of strains
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I - Spasm or cramp, stiff & sore, rapid recovery without loss of muscle
strength, managed conservatively.
 USS - normal or focal/ generalalized area of hyperechogenicity with or
without perifascial fluid
 MRI - oedema/hemorrhage/both with normal muscle morphology
II - Overuse, resolve with rest, include intrasubstance tear and partial
detachment of muscle from adjacent fascia or aponeurosis. Present with
pain and loss of function.
 USS - discontinuity of muscle fibers in echogenic perimysial striae,
hypervascular, intramuscular fluid.
 MRI - oedema/hemorrhage with tear and disruption up to 50%
III - Complete myotendinous or tendo-osseous tear with
avulsion/retraction. Due to violent contraction against firm resistance.
Early surgery may be required
 USS - complete discontinuity of muscle fibers, associated hematoma.
 MRI - complete tear with retraction
Ligament & Tendon healing
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Phase 1: inflammatory/haemorrhagic
 Haematoma – inflammatory response
 Cytokine mediated PMN’s, fibroblast and macrophage
migration
 Hours to a few days
Phase 2: proliferative
 New blood vessels
 Fibroblasts produce new matrix - collagen 3
 Weeks
Phase 3: remodelling
 Maturation and conversion of collagen 3 to 1
 Alignment of fibres
 Max strength at 6 months
Muscle structure
Myotendinous junction
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Shorter sarcomere
lengths
More organelles/cell
More synthetic ability
Interdigitation of cell
membrane
High degree of
membrane folding
VERY STRONG!
Muscle repair
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In complete tear, distal portion degenerates rapidly
Nerve supply needed for regeneration
More proximal injuries have a worse prognosis because
of greater muscle bulk denervation
Laceration results in scar formation. Myotubes
regenerate across the scar
Partial lacerations have better prognosis
Conplete laceration in muscle belly can recover approx.
50% of previous force generated by muscle
Surprisingly, not studied greatly and more work needed
Interaction: sprain & strain
Stages of Soft Tissue Healing
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When soft tissue is injured, it progresses
through three stages of healing
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Acute Inflammatory
Repair
Remodeling
Acute Inflammatory
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Stage 1: Acute Inflammatory
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When a body part is injured, cells within the
area die
This occurs because they are ripped apart and
also are being cut away from their food and
oxygen supply
Acute Inflammatory
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In this stage, an increased flow of blood
to the injured area brings cells and
chemicals to begin the healing process.
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This increased flow causes the swelling that is
often found in the injured area
Acute Inflammatory
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There are three main components found
in these chemicals and cells:
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Phagocytes.
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Leukocytes
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Which are specialized cells that engulf and eat up
the dead cells
Which are infection fighting white blood cells
Platelets
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Which carry blood clotting materials
Acute Inflammatory
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The acute stage lasts for about two days
after the initial injury
Repair
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Stage 2: Repair
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The area is now filled with the blood, cells,
and chemicals to rebuild the area to as near
normal as possible
The fibroblasts (fiber building cells) begin
building fibers across the area of injury
Repair
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Fibroblasts form the scar, which takes
from six weeks to as long as three
months, depending on the extent of the
injury
The fibroblasts also bring in scar tissue
that builds around the injured area
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These form around the area and allow the
athlete to move and regain physical activity
despite the fact that injury hasn’t completely
healed
Scar Tissue
Remodeling
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Stage 3: Remodeling
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Remodeling takes up to a year or more to
accomplish
It is the body’s way of building tissue strength
in the tendons, ligaments, and muscles to
withstand the stress applied to the body
during activity
Remodeling
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The length of time it takes to remodel an
injury depends on the extent of the injury
For an injury to be completely healed it
takes much longer than expected to not
feel the effects of the injury on the body
Healing Time
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The greater the injury to the tissue, the
longer the healing time
Healing time depends on the following:
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The
The
The
The
degree of the injury
location of the injury
blood supply to the injury
age of the athlete
Healing Time
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If blood supply to an area is poor the
healing process will take longer
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Ex: the eye and the meniscus
Other factors that slow the healing
process are poor nutrition, illnesses like
diabetes, medications, and infections
Healing Time
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One complication of healing is scar tissue,
if more tissue is laid down than is
necessary to repair the wound
Excessive scar tissue can delay healing
time and decrease the range of motion
that a joint or area can move
Some scar tissue forms deep within joints,
and may have to be surgically removed so
that proper movement can occur
Healing Time
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Large wounds, whose edges are far apart,
take longer to heal
Keeping the wounds closed with stitches
or skin closures will help healing
Healing Time
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If activity is resumed too soon after an
injury, healing time will be longer because
the early activity can cause more cellular
injury
It becomes important that the MDT takes
into consideration the risks of having an
athlete take part in an activity to early
Healing Time
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Corticosteroids
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These are chemicals made in the body that
help reduce inflammation
Synthetic corticosteroids can be used as
medications to help reduce inflammation
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It can however, increase healing time
Sprain
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Injury to ligaments
Graded 1-3
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Based on amount of
tearing/disruption to
ligament
Ankle, knee, elbow,
wrist
Ligament does not
shorten with healing
Limited blood supply
Grading of sprains
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Grade 1 Sprain:
 Few torn ligamentous fibers
 Mild joint pain reproduced on local palpation
 Firm endpoint with minimal laxity
 No joint instability
Grade 2 Sprain:
 Increased joint instability
 Joint swelling and pain
 Firm endpoint with some joint laxity
 Decreased function
Grade 3 Sprain:
 Complete ligamentous tear
 Minimal or no endpoint, gross joint laxity
 Unstable joint
Other overuse injuries
Spinal Disc Herniation (Sciatica)
Spinal Facet Syndrome (Pinched Nerve)
Sacroiliac Dysfunction
Iliotibial Band Syndrome
Plantar Fasciitis (Heel Spurs)
Shoulder Impingement Syndrome (Rotator Cuff Syndrome)
Patellofemoral Syndrome (Runner’s/Jumper’s Knee)
Lateral Epicondylitis (Tennis Elbow)
Medial Epicondylitis (Golfer’s/Pitcher’s Elbow)
Thoracic Outlet Syndrome
Scapulothoracic Syndrome (Shoulder Blade Pain)
Shin Splints
Traction apophysitis
Remember !
Effects of injury – short term
Rehabilitation implications
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Decreased physical strength
Altered neuromuscular patterning
Circulation and metabolic rates slow
Bone mineral density decreases
Collagen levels decrease in connective tissues
Reduced cardio-respiratory function
Reduced glycogen storage
Re-Injury
Remember sport specificity
Discussion
Think about my functional anatomy lecture on
the Knee, married with the last 90 minutes
covering physiology of repair.
Following athlete case study was 8wks pre China,
athlete was going and qualified.
• PCL rupture 100+ kg Judo fighter, 6 days post knee
arthroscopy
• The PCL was not reconstructed
• The clock was ticking
• what would your thought processes be and why?