1 Physical Agents. 2 Inflammation and Tissue Repair.

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Physical Agents

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Inflammation and Tissue Repair

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Common Causes of Inflammation Sprains, strains, and

contusions – Soft Tissue

Edema Fractures Foreign Bodies Autoimmune

Diseases (Rheumatoid Arthritis)

Microbial Agents (bacteria)

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

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

Cardinal signs of InflammationSign Cause

Heat Increased vascularity

Redness Increased vascularity

Swelling Blockage of lymphatic drainage

Pain Physical pressure and/or chemical irritation of pain-sensitive structures

Loss of Function Pain and swelling

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Inflammation Phase

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

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

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

Cellular Response– Basophils release histamine– Macrophages are involved in phagocytosis

& producing collagenase

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Inflammation Phase

Immune Response– Lymphocytes & phagocytes– Increased vascular permeability– Stimulates phagocytosis– Stimulates WBC activity

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Proliferation Phase

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

Collagen ProductionFibroblasts produce collagen1. 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

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

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

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

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 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 Local Factors

– External Forces Physical agents/modalities can affect

the healing process– Movement

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 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 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

Yet, proteogylcan content is low & thus predisposed to degeneration

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Healing of Specific Musculoskeletal Tissues 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

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 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 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)