Physical Agents

1. Physical Agents

2. Inflammation and Tissue Repair

3. 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) Common Causes of Inflammation

4. Common Causes of Inflammation

5. Phases of Healing

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

7. Inflammation Phase • Cardinal signs of Inflammation

9. Inflammation Phase • Vascular Response • Alterations in microvasculature & lymphatic vessels • Vasodilation & increased permeability

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

11. 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

12. 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

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

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

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

18. Proliferation Phase • Collagen Production Fibroblasts produce collagen • Fibroblasts synthesize procollagen → • Procollagen chains undergo cleavage by collagenase and form tropocollagen → • Multiple tropocollagen chains bind to form collagen fibrils → • Cross-linking between collagen fibrils form collagen fibers

19. 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

21. 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)

22. 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. 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

29. 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)

30. 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)