2. Inflammation
What is Inflammation
A vascular and cellular response to
trauma. Its purpose is to initiate the
healing of the injured tissue
The body’s attempt to dispose of micro-
organisms, foreign material and dying
tissues so that tissue repair can occur
An inflammatory response may result from
external or internal factors (infection)
Protects to the body by localizing and
removing the injuring agent
4. Signs of Inflammation
(Cardinal Signs)
Redness (Rubor):
Caused by blood vessel dilation (the arterioles)
Chemical mediators promote the vessel dilation
(contained in the capillary walls or endothelium
resulting in immediate response)
Histamine
Seritonin
Bradykinins
Prostaglandins
Note: a 1x increase in arteriole diameter yields a
4x increase in blood flow
5. Signs of Inflammation Cont.
Swelling (tumor)
Edema fluid varies with the stage of
inflammation
initially vessel permeability is only slightly altered
and no cells or protein escapes and the fluid is
mainly water and dissolved electrolytes (transudate):
like synovial fluid
As capillary permeability increases and plasma
proteins escape the extravascular fluid becomes
cloudy and more viscous. This is called exudate
(contains a large amount of leukocytes (called pus)
6. Causes of Edema/Swelling-
bleeding from torn vessels
cell death due to anoxia, allows fluid leakage
(permeability increases)
increased proteins raise extracellular osmotic
pressure, drawing fluids from the capillaries
Chemicals alter cell permeability to proteins
and fluid
Gravity may increase swelling (Capillary
filtration pressures)
8. Signs of Inflammation Cont.
Pain (bolar)
Results from irritation of nerve ending by
physical or chemical factors
Physical trauma may irritate pain receptors
Chemical mediators release when cell damage
occurs sensitize pain receptors
Trauma may result in cell anoxia because of
interference with blood flow due to capillary
damage
9. Signs of Inflammation Cont.
Warmth (calor)
The result of chemical activity and increased
blood flow in the injured area.
Loss of Function
May occur due to pain causing reflex guarding
or muscle spasm
spasm decreases metabolic activity and constricts
blood flow which causes more pain due to ischemia;
thus the pain/spasm cycle
10. Phases of the Inflammatory
Process
Phase I: Acute Phase ( 2 subphases)
Early (Acute): inflammatory response: lasts 2-4 days
Late (Sub-Acute): continue inflammatory phase
which is usually complete in 2 weeks
Phase 2: Tissue Formation (Proliferation)
Tissue rebuilding approximately 2-3 weeks
This does not include chronic inflammation
Phase 3: Remodeling Phase
Adapt to original tissue
Continues for up to 1 year post injury
11. Phase I: The Inflammatory Process
Early Phase
Insult occurs - may be internal (infection) or external
(trauma)
Vasoconstriction to decrease blood flow (first 10
minutes)
Vasodilatation
Late Phase
Tissue Repair
Regeneration
12. Phase I -Early Phase: Acute
Inflammation
C h e m ic a l M e d ia t o r s R e le a s e d ( C h e m o t a x is )
C u a s e s V a s o d ila t io n
I n c r e a s e s B lo o d , P la s m a , P r o t ie n s , P h a g o c y t ic m a t e r ia l
P r o t ie n s a r e I n c r e a s e d a t I n ju r y S it e
I n c r e a s e in p r o t ie n s c a u s e s o s m o t ic r e la t io n s h ip w it h p la s m a
H 2 O flo w s fr o m h ig h e r p r o t ie n s c o n t e n t ( in ju r y )
t o in t e r s t ia l flu id c a u s in g e d e m a / s w e llin g
S w e llin g / e d e m a a r e d e c r e a s e d b y ly m p h a t ic s y s t e m
I n ju r y
O n s e t
14. Phase I: Early Phase Inflammation -
Vasodilatation
Chemical mediators are released:
histamine, bradykinis, serotonin,
prostaglandin's - increase vascular permeability
released from mast cells and blood platelets
into traumatized tissue.
As fluid filtrates through “gaps in the
extravascular spaces this is called exudation.
15. Phase I- Early Phase: Vasodilatation
Cont.
The accumulation of excess fluid is called
edema (Swelling)
Vascular permeability due to action of the
histamine is short-lived, lasting less than 1 hour
16. Phase I: Early Phase Inflam. -
Lymphatic channels are blocked
Local lymphatic channels are blocked by
fibrin plugs formed during coagulation.
Obstruction of the local lymphatic
channels prevents drainage of fluid from
the injured site, thus localizing the
inflammatory reaction.
17. Phase I- Late Phase: Phagocytosis
Body’s cellular defense to remove toxic
material via lymphatic system
Phagocytosis: a process when
leukocytes capture and digest foreign
matter and dead tissue
1st line of defense: neutrophiles (in most
abundance from 1-3 days) - phagocytic
activity reaches maximum effectiveness
within 7-12 days
18. Phase I- Late Phase: Phagocytosis
Cont.
2nd line of defense: monocytes (which convert
into large cells called macrophages) and
lymphoctes consume large amounts of bacteria
and cellular debris. Monocytes are critical in
the initiation of tissue repair because the attract
fibroblasts
Macrophage
Bacteria
19. Phase I- Late Phase Phagocytosis
Cont.
Pus is the end result - it contains leukocytes,
dead tissue and phagogenic material
Prolonged puss accumulation can prevent
fibroplasia which begins the wound healing
Fibroblasts are connective tissue responsible
for collagen synthesis
Ligaments, joint capsule, tendon
Osteoblasts: responsible for bone synthesis
Fibroblast Macrophages
20. Phase I: Early Phase Inflammation -
Margination
When trauma occurs the endothelial wall
is disrupted exposing collagen fibers
creating a “stickiness”
WBC’s concentrate in the injury site to rid
the body of foreign substances and dead
(necrotic) tissue
21. Phase I- Late Phase: Margination
Cont.
As circulation slows, leukocytes migrate
and adhere to the walls of post-capillary
veinuels (for approx 1 hour)
The leukocytes pass through the walls of
the vessels (diapedesis) and travel to the
site of injury (Chemotaxis)
22. Phase I: Late Phase Blood Clotting
Ruptured vessels release Enzyme (Factor X)
Factor X reacts with prothrombin (free floating
in blood)
Thrombin then stimulates fibrogen into its
individual form fibrin
Fibrin grouped together to form “lattice”
around injured area
Fibrin lattice contracts to remove plasma and
compress platelets forming a “patch”
23. Phase I: Late Phase Blood Clotting
Factor X
Prothrombin
Thrombin
Fibrogen and
Thrombin Meet
Fibrin Monomer
Fibrin
Mesh
Fibrin Forms
Seal
24. Phase II: Regeneration:
The replacement of destroyed cells by
reproducing healthy cells adjacent to the
wound (humans capacity to regenerate
tissue is limited and further affected by
age and nutritional state).
25. Phase II: Stages of Regeneration:
Stage starts with periphery
Re-eptheliaization is proliferation of
peripheral epithelial tissue which then
migrates to the wound until the area is
covered.
Capillarization (Capillary buds
proliferate and connect forming new
capillaries which gives the red, granular
appearance to the scar (granular tissue)
26. Phase II: Stages of Regeneration:
Cont.
Fibroplasia occurs due to fibroblasts
which arises from undifferentiated
mesenchymal cells and migrate into the
area along fibrin strands and begin to
synthesize scar tissue.
Scar tissue is CT and mostly collagen and
mucopolysaccharides.
Fibroblasts secrete both, contributing tensile
strength to the repair.
Scar tissue very inelastic compared to
surrounding tissue.
27. Phase II: Stages of Regeneration:
Cont.
Vascularization - occurs with the
proliferation of collagen synthesis
Formation of blood vessels (angiogensis)
28. Phase II: Collagen Synthesis:
Occurs within 12 hours of injury to 6
weeks (average 3 weeks)
Type I: collagen: associate with muscular
tissue (larger and stronger fibers)
Type III collage: smaller fibers, less cross
linking and highly disorganized
(ligamentous, tendinous)
Type III with time is replaced by Type I
collagen
29. Phase II: Collagen Synthesis Cont.
Tissue Healing Times
Muscle : approximately 3 weeks
Tendon: 4-6 weeks
Extent of the tissue damage and vascularity will
aid in determining healing time
Age may also be a factor in healing
30. Phase II: Stages of Regeneration:
Cont.
Wound Contraction:
Wound contraction begins to occur in CT as the
myobroblasts (actin-rich fibroblasts) contract.
Myofibroblasts move toward the center of the
wound, helping reduce the size of the area to
be covered.
Outside-in
31. Phase III: Maturation/Remodeling
Phase
Purpose of this phase
Strengthen the repaired tissue
Firoblasts, myofobrpblasts & Macrophages
reduced to pre-injury state
Type III fibrin continues to be replaced by
Type I
32. Phase III: Maturation/Remodeling
Phase (day 9 onward)
Blends in with the repair phase, original
collagen fibers were randomly oriented.
During remodeling, the fibers become
more organized, parallel to the wound
surface which provides greater tensile
strength
The type of tissue involved will
determine the duration and extent of
remodeling activity
33. Phase III: Maturation/Remodeling
Phase Cont.
Strengthening of scar tissue continues
from 3 months to 1 year, but fully
mature scar in only 70% as strong as
intact tissue.
Motion will influence the structure and
functional capacity of scar tissue
(controlled stress increases functional
capacity, allows healing and reduces
adhesion formation).
35. Chronic Inflammation
Complications
Granuloma: large mass of weaker scar tissue
(usually due to large inflammation and activity
without regard to healing time)
Retardation of muscle fiber: with excessive
granuloma fibroblasts cannot reach damaged
tissue
Adhesions/contractures in tissue
Keloid/hypotrophic scars
36. Abnormal scarring:
Hypertophic scar or keloid scar.
Biological difference not well understood,
but clinically hypertrophic scar is
contained within the boundaries of the
original wound while a keloid scar extends
beyond the borders of the original wound.
37. Summary
O s m o t ic P r e s s u r e
R e s u lt e d e m a / s w e llin g
L y m p h a t ic C h a n n e ls b lo c k e d
V a s o d ia la t io n
C h m e ic a l M e d ia t o r s R e le a s e
M a r g in a tio n
P h a g o c y t o s is
I n f la m m a t io n
A p p r o x im a te T im e T a b le
7 - 1 0 d a y s
( A c u t e p h a s e 3 d a y s )
P h a s e I :
A c u t e P h a s e
A p p r o x im a t e t im e t a b le 2 - 3 w e e k s
R e g e n e r a t io n
S c a r t is s u e f o r m e d
C a p ila r iz a t io n
G r a n u la t io n
F ib r o b la s ts la y d o w n c o lla g e n
R e s o lu t io n
M in o r t o n o c e ll d e a t h
P h a s e I I :
T is s u e R e p a ir
O c c u r s f o r u p t o
1 y e a r
C a p illa r iz a t io n
R e p la c e m e n t o f T y p e I I I
c o lla g e n w it h T y p e I
C o lla g e n
P h a s e I I I :
M a t u r a t io n P h a s e
I n ju r y R e s p o n s e
W o n d H e a lin g
38. THE BIG QUESTIONS!
When do we use cold?
When do we use heat?
When do we use medications?
When do we use Electrical modalities?
39. Treatment Planning for Phases of
Tissue Healing
Phase I Phase II Tissue
Healing
Phase III:
Maturation
Control Active
Inflam. Limit
scope of Orig.
Injury
Encourage
Repair/
Replacement
Damaged Tissue
Encourage
Tissue
Remodeling and
Alignment with
Func. Stresses.
40. Treatment Planning:
Phase I Phase II Tissue
Healing
Phase III:
Maturation
Immobilization
Cold Modalities
Pulsed Ultrasound
Compression
Elevation
E-Stim
Contrast Baths
Compression
Devices
E-Stim
Pulsed/
Continuous US
Traction
Massage
Biofeedback
Heat Modalities
Heat Modalities
Continuous US
E-Stim
Massage
41. Treatment Planning: Maturation
Phase
Phase I Phase II Tissue
Healing
Phase III:
Maturation
Cryokinetics
Isometics
Controlled ROM
(CPM)
Proprioception
CV conditioning
Manual Therapy
Passive ROM
Active ROM
Progressive
Resistance Ex
Functional Ex
Cv Exercise
Overload
Resistance Ex
Proprioception Ex
Activity Specific
Functional Ex
Cv Exercise
