Post on 17-Dec-2015
transcript
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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)