1. 1 Physical Agents

2. 2 Inflammation and Tissue Repair

3. 3 Common Causes of Inflammation Sprains, strains, and contusions Sprains, strains, and contusions –Soft Tissue Edema Fractures Fractures Foreign Bodies Foreign Bodies Autoimmune Diseases (Rheumatoid Arthritis) Autoimmune Diseases (Rheumatoid Arthritis) Microbial Agents (bacteria) Microbial Agents (bacteria) Chemical Agents (acid, base) Chemical Agents (acid, base) Thermal Agents Thermal Agents Irradiation (UV or radiation) Irradiation (UV or radiation)

4. 4 Common Causes of Inflammation

5. 5 Phases of Healing

6. Inflammation Phase (Days 1-6) Inflammation Phase (Days 1-6) Proliferation Phase (Days 3-20) Proliferation Phase (Days 3-20) Maturation Phase (Day 9+) Maturation Phase (Day 9+) Timeframe (days) is NOT absolute! Timeframe (days) is NOT absolute! 6

7. 7 Inflammation Phase Cardinal signs of Inflammation Cardinal signs of Inflammation SignCause Heat Increased vascularity Redness 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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9. 9 Inflammation Phase Vascular Response Vascular Response –Alterations in microvasculature & lymphatic vessels –Vasodilation & increased permeability

10. 10 Inflammation Phase –Histamine is released which causes vasodilation –Clotting process is activated –Bradykinin is released - pain –Prostaglandins promote increased permeability

11. 11 Inflammation Phase Hemostatic Response 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

12. 12 Inflammation Phase Cellular Response 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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15. 15 Inflammation Phase Cellular Response Cellular Response –Basophils release histamine –Macrophages are involved in phagocytosis & producing collagenase

16. 16 Inflammation Phase Immune Response Immune Response –Lymphocytes & phagocytes –Increased vascular permeability –Stimulates phagocytosis –Stimulates WBC activity

17. 17 Proliferation Phase Epithelialization – the reestablishment of the epidermis Epithelialization – the reestablishment of the epidermis –Uninjured epithelial cells migrate over the injured area and close the injury site

18. 18 Proliferation Phase Collagen Production 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

19. 19 Proliferation Phase Wound Contraction 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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21. 21 Proliferation Phase Neovascularization 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)

22. 22 Maturation Phase Can take longer than 1 year Can take longer than 1 year Density of fibroblasts, macrophages, myofibroblasts, & capillaries decreases Density of fibroblasts, macrophages, myofibroblasts, & capillaries decreases Scar becomes whiter as collagen matures & vascularity decreases Scar becomes whiter as collagen matures & vascularity decreases Remodeling of collagen fibers occurs as a result of collagen turnover 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 Muscle tension, joint movement, soft tissue loading, temperature changes, & mobilization are types of forces that affect collagen structure

23. 23 Chronic Inflammation Can be a result of acute inflammation Can be a result of acute inflammation Can also be a result of an altered immune response (rheumatoid arthritis) Can also be a result of an altered immune response (rheumatoid arthritis) Acute = ≤ 2 weeks Acute = ≤ 2 weeks Subacute = > 4 weeks Subacute = > 4 weeks Chronic = months or years Chronic = months or years Can result in increased scar tissue & adhesion formation Can result in increased scar tissue & adhesion formation –Can result in loss of function

24. 24 Factors Affecting the Healing Process Local Factors Local Factors –Type, Size and Location of the injury Well vascularized areas heal faster than poorly vascularized areas Well vascularized areas heal faster than poorly vascularized areas Smaller wounds heal faster than smaller wounds Smaller wounds heal faster than smaller wounds –Infection Infections alter collagen metabolism Infections alter collagen metabolism –Vascular Supply

25. 25 Factors Affecting the Healing Process Local Factors Local Factors –External Forces Physical agents/modalities can affect the healing process 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 Muscle tension, joint movement, soft tissue loading, temperature changes, & mobilization are types of forces that affect collagen structure

26. 26 Factors Affecting the Healing Process Systemic Factors Systemic Factors –Age The pediatric population usually heals faster than the adult and geriatric population The pediatric population usually heals faster than the adult and geriatric population –Disease Diabetes, RA, AIDS, cancer, PVD Diabetes, RA, AIDS, cancer, PVD –Medications Corticosteroids and NSAIDS (to a lesser degree) Corticosteroids and NSAIDS (to a lesser degree) –Nutrition Amino acids, vitamins, minerals, water, caloric intake Amino acids, vitamins, minerals, water, caloric intake

27. 27 Healing of Specific Musculoskeletal Tissues Cartilage 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 Yet, proteogylcan content is low & thus predisposed to degeneration

28. 28 Healing of Specific Musculoskeletal Tissues Tendons and Ligaments 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 For example, the MCL heals better than the ACL Note: Even after healing, the injured ligament is ~ 30% - 50% weaker than the uninjured ligament Note: Even after healing, the injured ligament is ~ 30% - 50% weaker than the uninjured ligament

29. 29 Healing of Specific Musculoskeletal Tissues Skeletal Muscle 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)

30. 30 Healing of Specific Musculoskeletal Tissues Bone 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) 3 wks – 4 months (depends) –Remodeling – complete healing (months – years to occur)