Physical Agents
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Inflammation and
Tissue Repair
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Common Causes of
Inflammation
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Sprains, strains, and
contusions
– Soft Tissue Edema
Fractures
Foreign Bodies
Autoimmune Diseases
(Rheumatoid Arthritis)
Microbial Agents
(bacteria)
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Chemical Agents (acid,
base)
Thermal Agents
Irradiation (UV or
radiation)
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Common Causes of
Inflammation
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Phases of Healing
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Phases of Healing
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Inflammation Phase (Days 1-6)
Proliferation Phase (Days 3-20)
Maturation Phase (Day 9+)
Timeframe (days) is NOT absolute!
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Inflammation Phase
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Cardinal signs of Inflammation
Sign
Cause
Heat
Increased vascularity
Redness
Increased vascularity
Swelling
Blockage of lymphatic
drainage
Pain
Physical pressure and/or
chemical irritation of painsensitive structures
Loss of Function
Pain and swelling
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Inflammation Phase
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Vascular Response
– Alterations in microvasculature &
lymphatic vessels
– Vasodilation & increased permeability
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Inflammation Phase
– Histamine is released which causes
vasodilation
– Clotting process is activated
– Bradykinin is released - pain
– Prostaglandins promote increased
permeability
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Inflammation Phase
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Hemostatic Response
– Controls blood loss
– Platelets migrate to the injury site and
promote clotting
– Fibrin and fibronectin enter the injured
area & form cross-links with collagen to
form fibrin lattice
– Fibrin lattice serves as the only source of
tensile strength during the inflammation
phase
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Inflammation Phase
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Cellular Response
– Plasma (consisting
of RBCs, WBCs, &
platelets) circulates
to injury site & can
cause hematoma or
hemarthrosis
– WBCs clear the site
of debris &
microorganisms
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Inflammation Phase
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Cellular Response
– Basophils release histamine
– Macrophages are involved in phagocytosis &
producing collagenase
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Inflammation Phase
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Immune Response
– Lymphocytes & phagocytes
– Increased vascular permeability
– Stimulates phagocytosis
– Stimulates WBC activity
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Proliferation Phase
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Epithelialization –
the reestablishment
of the epidermis
– Uninjured epithelial
cells migrate over
the injured area and
close the injury site
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Proliferation Phase
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Collagen Production
Fibroblasts produce collagen
1. Fibroblasts synthesize procollagen →
2. Procollagen chains undergo cleavage by
collagenase and form tropocollagen →
3. Multiple tropocollagen chains bind to
form collagen fibrils →
4. Cross-linking between collagen fibrils
form collagen fibers
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Proliferation Phase
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Wound Contraction
– Epithelialization covers the wound surface
– Wound contraction pulls the injury site
edges together
– Myofibroblasts attach to the margins of
the intact skin and pull the epithelial layer
inward
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Proliferation Phase
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Neovascularization
– The development of a new blood supply to an
injured area
– Angiogenesis – the growth of new blood vessels
– Vessels in the wound develop small buds that
grow into the wound area
– Outgrowths join with other arterial or venular
buds to form a capillary loop (give wound a
pink/red color)
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Maturation Phase
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Can take longer than 1 year
Density of fibroblasts, macrophages,
myofibroblasts, & capillaries decreases
Scar becomes whiter as collagen matures &
vascularity decreases
Remodeling of collagen fibers occurs as a
result of collagen turnover
Muscle tension, joint movement, soft tissue
loading, temperature changes, &
mobilization are types of forces that affect
collagen structure
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Chronic Inflammation
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Can be a result of acute inflammation
Can also be a result of an altered immune
response (rheumatoid arthritis)
Acute = ≤ 2 weeks
Subacute = > 4 weeks
Chronic = months or years
Can result in increased scar tissue &
adhesion formation
– Can result in loss of function
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Factors Affecting the
Healing Process
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Local Factors
– Type, Size and Location of the injury
 Well vascularized areas heal faster than
poorly vascularized areas
 Smaller wounds heal faster than smaller
wounds
– Infection
 Infections alter collagen metabolism
– Vascular Supply
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Factors Affecting the
Healing Process
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Local Factors
– External Forces
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Physical agents/modalities can affect the
healing process
– Movement
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Muscle tension, joint movement, soft tissue
loading, temperature changes, & mobilization
are types of forces that affect collagen
structure
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Factors Affecting the
Healing Process
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Systemic Factors
– Age
 The pediatric population usually heals faster
than the adult and geriatric population
– Disease
 Diabetes, RA, AIDS, cancer, PVD
– Medications
 Corticosteroids and NSAIDS (to a lesser
degree)
– Nutrition
 Amino acids, vitamins, minerals, water,
caloric intake
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Healing of Specific
Musculoskeletal Tissues
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Cartilage
– Limited ability to heal due to lack of
lymphatics, blood supply, & nerves
– In injuries that involve articular cartilage
& subchondral bone, vascularization is
improved & cartilage heals more
effectively
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Yet, proteogylcan content is low & thus
predisposed to degeneration
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Healing of Specific
Musculoskeletal Tissues
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Tendons and Ligaments
– Heal more effectively than cartilage because of
increased vascular supply
– Mobilization can help in the remodeling of
collagen fibers (must be progressed slowly)
– Ligament healing depends on: type of ligament,
size/degree of injury, & amount of loading
applied
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For example, the MCL heals better than the ACL
Note: Even after healing, the injured ligament is ~
30% - 50% weaker than the uninjured ligament
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Healing of Specific
Musculoskeletal Tissues
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Skeletal Muscle
– Muscle can be injured by blunt trauma
(contusion), excessive contraction, excessive
stretch, or muscle-wasting disease
– Muscle cells cannot proliferate but, in some
cases, satellite cells can form new muscle cells
(conflicting research)
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Healing of Specific
Musculoskeletal Tissues
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Bone
– Impaction – impact force > strength of bone
– Induction – osteogenesis is stimulated
– Inflammation
– Soft callus – union of bony fragments by fibrous or
cartilaginous tissue, increased capillary density, &
increased cell proliferation
– Hard callus – hard callus bone covers the fracture site
 3 wks – 4 months (depends)
– Remodeling – complete healing (months – years to
occur)
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