The document discusses tissue response to injury including the inflammatory response, cardinal signs of inflammation, and phases of the inflammatory response. It describes acute inflammation as having a short onset and duration with production of exudate and leukocytes, while chronic inflammation has a long onset and duration with extensive scar tissue. The three phases of the inflammatory response are the acute, repair, and remodeling phases.

1. Tissue Response to Injury

2. Inflammatory Response
• Acute Inflammation
– Short onset and duration
– Production of exudate, leukocytes
• Chronic Inflammation
– Long onset and duration
– Presence of extensive scar tissue

3. Cardinal Signs of
Inflammation
• Rubor (redness)
• Tumor (swelling)
• Color (heat)
• Dolor (pain)
• Functio laesa (loss of function)

4. Phases of the Inflammatory
Response
(3 separate phases)
• 1. Acute phase
• 2. Repair phase
• 3. Remodeling phase

5. Phase I: Acute Phase
• Initial reaction to an injury occurring 3
hours to 2 days following injury
• Goal
– Protect
– Localize
– Decrease injurious agents
– Prepare for healing and repair
• Caused by trauma, chemical agents,
thermal extremes, pathogenic organisms

6. • External and internal injury result in
tissue death and cell death
• Decreased oxygen to area increases cell
death
• Rest, ice, compression & elevation are
critical to limiting cell death

7. • First hour
– Vasoconstriction and coagulation occur to
seal blood vessels and chemical mediators
are released
– Immediately followed by vasodilation or
blood vessel
• Second hour
– Vasodilation decreases blood flow, increased
blood viscosity resulting in edema (swelling)

8. • Second hour (continued)
– Exudate increases (high concentration of
RBC’s) due to increased vessel permeability
– Permeability changes generally occur in
capillary and venules

9. • Cellular response
– Mast cells (connective tissue cells) and
leukocytes (basophils, monocytes,
neutrophils) enter area
– Mast cells with heparin and histamine serve
as first line of defense
– Basophils provide anticoagulant
– Neutrophils and monocytes are responsible
for small and large particles undergoing
phagocytosis - ingestion of debris and
bacteria

10. Phase II: Repair Phase
• Phase will extent from 48 hours to 6
weeks following cleaning of fibrin clot,
erythrocytes, and debris
• Repaired through 3 phases
– Resolution (little tissue damage and normal
restoration)
– Restoration (if resolution is delayed)
– Regeneration (replacement of tissue by same
tissue)

11. • Scar formation
– Less viable than normal tissue, may
compromise healing
– Firm, inelastic mass devoid of capillary
circulation
– Develops from exudate with high protein
and debris levels resulting in granulation
tissue
– Invaded by fibroblasts and and collagen
forming a dense scar and while normally
requiring 3-14 weeks may require 6 months
to contract

12. • Primary healing (healing by first intention)
– Closely approximated edges with little
granulation tissue production
• Secondary healing (heal by secondary
intention)
– Gapping, tissue loss, and development of
extensive granulation tissue
– Common in external lacerations and internal
musculoskeletal injuries

13. • Regeneration
– Related to health, nutrition and tissue type
– Dependent on levels of:
• debris (phagocytosis)
• endothelial production (hypoxia and
macrophages stimulate capillary buds)
• production of fibroblasts (revascularization
allows for enhanced fibroblast activity and
collagen production which is tied to Vitamin C,
lactic acid, and oxygen
–

14. Phase III: Remodeling
• Overlaps repair and regeneration
• First 3-6 weeks involves laying down of
collagen and strengthening of fibers
• 3 months to 2 years allowed for enhanced
scar tissue strength
• Balance must be maintained between
synthesis and lysis
• Take into consideration forces applied
and immobilization/mobilization time
frames relative to tissue and healing time

15. Chronic Inflammation
• Result of failed acute inflammation
resolution within one month termed
subacute inflammation
• Inflammation lasting months/years
termed chronic
– Results from repeated microtrauma and
overuse
– Proliferation of connective tissue and tissue
degeneration

16. Characteristics of Chronic
Inflammation
• Proliferation of connective tissue and tissue
degeneration
• Presence of lymphocytes, plasma cell,
macrophages(monocytes) in contrast to
neutrophils (during acute conditions)
• Major chemicals include
– Kinins (bradykinin) - responsible for
vasodilation, permeability and pain
– Prostaglandin - responsible for vasodilation
but can be inhibited with aspirin and NSAID’s

17. Factors That Impede Healing
• Extent of injury • Corticosteroids
• Edema • Keloids and
• Hemorrhage Hypertrophic Scars
• Poor Vascular • Infection
Supply • Humidity, Climate,
• Separation of Tissue Oxygen Tension
• Muscle Spasm • Health, Age, and
• Atrophy Nutrition

18. Soft Tissue Healing
• Cell structure/function
– All organisms composed of cells
– Properties of soft tissue derived from
structure and function of cells
– Cells consist of nucleus surrounded by
cytoplasm and encapsulated by phospholipid
cell membrane
– Nucleus contains chromosomes (DNA)
– Functional elements of cells (organelles)
include mitochondria, ribosomes, endoplasmic
reticulum, Golgi apparatus & centrioles

19. Soft Tissue Adaptations
• Metaplasia - transformation of tissue from one type to
another that is not normal for that tissue
• Dysplasia - abnormal development of tissue
• Hyperplasia- excessive proliferation of normal cells in
normal tissue arrangement
• Atrophy- a decrease in the size of tissue due to cell
death and re-absorption or decreased cell
proliferation
• Hypertrophy - an increase in the size of tissue without
necessarily changing the number of cells

20. Cartilage Healing
• Limited capacity to heal
• Little or no direct blood supply
• Chrondrocyte and matrix disruption
result in variable healing
• Articular cartilage that fails to clot and
has no perichondrium heals very slowly
• If area involves subchondral bone
(enhanced blood supply) granulation
tissue is present and healing proceeds
normally

21. Ligament Healing
• Follows similar healing course as
vascular tissue
• Proper care will result in acute, repair,
and remodeling phases in same time
required by other vascular tissue
• Repair phase will involve random laying
down of collagen which, as scar forms,
will mature and realign in reaction to
joint stresses and strain
• Full healing may require 12 months

22. Skeletal Muscle Healing
• Skeletal muscle cannot undergo mitotic
activity to replace injured cells
• New myofibril regeneration is minimal
• Healing and repair follow the same
course as other soft tissues.

23. Nerve Healing
• Cannot regenerate after injury
• Regeneration can take place within a nerve
fiber
• Proximity of injury to nerve cell makes
regeneration more difficult
• For regeneration, optimal environment is
required
• Rate of healing occurs at 3-4 mm per day
• Injured central nervous system nerves do
not heal as well as peripheral nerves

24. Modifying Soft-Tissue Healing
• Varying issues exist for all soft tissues
relative to healing (cartilage, muscle,
nerves)
• Blood supply and nutrients is necessary
for all healing
• Healing in older athletes or those with
poor diets may take longer
• Certain organic disorders (blood
conditions) may slow or inhibit the
healing process

25. Management Concepts
• Drug utilization
– Anitprostaglandin agents used to combat
inflammation
– Non-steroidal anti-inflammatory agents
(NSAID’s)
– Medications will work to decrease
vasodilatation and capillary permeability

26. • Therapeutic Modalities
– Thermal agents are utilized
• Heat stimulates acute inflammation (but works
as a depressant in chronic conditions)
• Cold is utilized as an inhibitor
– Electrical modalities
• Treatment of inflammation
• Ultrasound, microwave, electrical stimulation
(includes transcutaneous electrical muscle
stimulation and electrical muscle stimulation

27. • Therapeutic Exercise
– Major aim involves pain free movement, full
strength power, and full extensibility of
associated muscles
– Immobilization, while sometimes necessary,
can have a negative impact on an injury
• Adverse biochemical changes can occur in
collagen
– Early mobilization (that is controlled) may
enhance healing

28. Fracture Healing
• Potential serious bone fractures are part
of athletics
• Time is necessary for proper bone union
to occur and is often out of the control of
a physician
• Conservative treatment will be necessary
for adequate healing to occur

29. • Bone undergoes constant remodeling
through osteocyte activity
• Osteocytes cellular component of bone
– Osteoblasts are responsible for bone
formation while osteoclasts resorb bone
• Cambium (periosteum)
– A fibrous covering involved in bone healing
– Vascular and very dense
• Inner cambium
– less vascular and more cellular.
– Provides attachments for muscle, ligaments
and tendons

30. Acute Fracture of Bone
• Follows same three phases of soft tissue
healing
• Less complex process
• Acute fractures have 5 stages
– Hematoma formation
– Cellular proliferation
– Callus formation
– Ossification
– Remodeling

32. Callus Formation
• Soft callus is a random network of woven
bone
• Osteoblasts fill the internal and external
calluses to immobilize the site
• Calluses are formed by bone fragments
that bridge the fracture gap
• The internal callus creates a rigid
immobilization early

33. • Hard callus formation occurs after 3-4
weeks and lasts 3-4 months
• Hard callus is a gradual connection of
bone filaments to the woven bone
• Less than ideal immobilization produces
a cartilagenous union instead of a bony
union

34. Ossification
• Ossification is complete when bone has
been laid down and the excess callus has
been resorbed by osteoclasts.

35. Remodeling
• Occurs following callus resorption and
trabecular bone is laid along lines of stress
• Bioelectric stimulation plays a major role
in completing the remodeling process
• The process is complete when the original
shape is achieved or the structure can
withstand imposed stresses

36. Acute Fracture Management
• Must be appropriately immobilized, until X-
rays reveal the presence of a hard callus
• Fractures can limit participation for weeks
or months
• A clinician must be certain that the following
areas do not interfere with healing
– Poor blood supply
– Poor immobilization
– Infection

37. • Poor blood supply
– Bone may die and union/healing will not occur
(avascular necrosis)
– Common sites include:
• Head of femur, navicular of the wrist, talus, and
isolated bone fragments
– Relatively rare in healthy, young athletes
except in navicular of the wrist
• Poor immobilization
– Result of poor casting allowing for motion
between bone parts
– May prevent proper union or result in bony
deformity

38. • Infection
– May interfere with normal healing,
particularly with compound fractures
– Severe streptococcal and staphylococcal
infections
– Modern antibiotics has reduced the risk of
infections
– Closed fractures are not immune to
infections within the body or blood
• If soft tissue alters bone positioning,
surgery may be required to ensure
proper union

39. • Gate Theory
– Area in dorsal horn of spinal cord causes
inhibition of pain impulses ascending to
cortex
– T-cells will transmit signals to brain
– Substantia gelatinosa functions as gate
determining if stimulus sent to T-cells
– Pain stimuli exceeding threshold results in
pain perception
– Stimulation of large fast nerves can block
signal of small pain fiber input
– Rationale for TENS, accupressure/puncture,
thermal agents and chemical skin irritants

40. • Pain assessment
– Self report is the best reflection of pain and
discomfort
– Assessment techniques include:
• visual analog scales (0-10, marked no pain to
severe pain)
• verbal descriptor scales (marked none, slight,
moderate, and severe)
• Pain Treatment
– Must break pain-spasm-hypoxia-pain cycle
through treatment
– Agents used; heat/cold, electrical
stimulation-induced analgesia,
pharmacological agents

41. • Heat/Cold
– Heat increases circulation, blood vessel
dilation, reduces nociception and ischemia
caused by muscle spasm
– Cold applied for vasoconstriction and
prevention of extravasation of blood into
tissue
– Pain reduced through decrease in swelling
and spasm
• Induced analgesia
– Utilize electrical modalities to reduce pain
– TENS and acupuncture commonly used to
target Gate Theory

42. Psychological Aspects of Pain
• Pain can be subjective and psychological
• Pain thresholds vary per individual
• Pain is often worse at night due to solitude and
absence of external distractions
• Personality differences can also have an impact
• A number of theories relative to pain exist and
it physiological and psychological components
• Athlete, through conditioning are often able to
endure pain and block sensations of minor
injuries