Inflammation And Repair Process 2023-24 PDF

INFLAMMATION AND REPAIR General Intervention Methods Academic Year 2023-2034 Degree in Physiotherapy USP-CEU SCHEME INFLAMMATION AND REPAIR PHASES 1.INFLAMMATORY PHASE 1.1-Vascular response 1.2-Hemostatic response 1.3-Cellular response 2.PROLIFERATIVE PHASE 2.1-Epithelialization 2.2-Collagen product...

INFLAMMATION AND REPAIR General Intervention Methods Academic Year 2023-2034 Degree in Physiotherapy USP-CEU SCHEME INFLAMMATION AND REPAIR PHASES 1.INFLAMMATORY PHASE 1.1-Vascular response 1.2-Hemostatic response 1.3-Cellular response 2.PROLIFERATIVE PHASE 2.1-Epithelialization 2.2-Collagen production 2.3-Wound contraction 2.4-Neovascularization 3. MATURATION PHASE CHRONIC INFLAMMATION FACTORS AFFECTING THE HEALING PROCESS: LOCAL AND SYSTEMIC 2 INTRODUCTION Tissue healing “Body’s replacement of destroyed tissue by living tissue” ▪ Regeneration: Specialised tissues are replaced by proliferation of surrounding undamaged specialised cells. ▪ Repair: Lost tissue is replaced by granulation tissue matured to form scar tissue. VERY IMPORTANT FOR PHYSICAL THERAPISTS!!! 3 COMMON CAUSES OF INFLAMMATION Soft tissue trauma Fractures Sutures Autoimnune diseases (rheumatoid arthritis) Microbial agents Chemical agents Thermal agents (burns or frostbite) Irradiation (UV or radiation) 4 INFLAMMATION AND REPAIR - PHASES INFLAMMATION: Prepares wound for healing. PROLIFERATION: Rebuilds damaged structures and strengthens wound REMODELLING/MATURE PHASE: Modifies scar tissue into its mature form. 5 INFLAMMATION AND REPAIR PHASES 1.INFLAMMATORY PHASE 1.1-Vasocontriction 1.2-Vasodilation 1.3-Clot formation 1.4-Phagocytosis 2.PROLIFERATIVE PHASE 2.1-Epithelialization 2.2-Fibroplasia/Collagen production 2.3-Wound contraction 2.4-Neovascularization 3. MATURATION PHASE 3.1- Collagen Synthesis/Lysis Balance 3.2- Collagen Fiber Orientation 6 INFLAMMATORY PHASE (1st to 6th / 9th days) It begins with a trauma/disease. It is protective response to destroy or isolate cells or agents that may be at fault/damaged. Normal and necessary for HEALING. 5 signs of VIRCHOW: ✓ HEAT ✓ REDNESS ✓ SWELLING ✓ PAIN ✓ LOSS OF FUNCTION 3 parts: 1. Vascular Response. 2. Hemostatic Response. 3. Cellular Response. 7 INFLAMMATORY PHASE 1. VASCULAR RESPONSE Bleeding phase. Characterised by: Hyperemia (local redness and increased temperature in acute inflammation area). Local swelling due to increased permeability and VD of local blood vessels and infiltration of fluid into interstitial spaces. Pain due to the pressure of the edema or irritation of pain sensitive structures by chemicals. 8 INFLAMMATORY PHASE 1. VASCULAR RESPONSE Physical disruption of the capillaries: hemorrhage, fluid loss, cell injury Transient vasoconstriction: mediated by norepinephrine in the first 5-10 min and then prolongued by serotonin. Dilation of the noninjured vessels close to the injured area: up to 1 hour 9 INFLAMMATORY PHASE 2. HEMOSTATIC RESPONSE Controls blood loss. PLATELETS play a role in: ▪ HEMOSTASIS → coagulation + ↑ blood viscosity ▪ THE CONTROL OF FIBRIN DEPOSITION ▪ FIBROPLASIA ▪ ANGIOGENESIS. 10 INFLAMMATORY PHASE 3. CELLULAR RESPONSE LEUKOCYTES and NEUTROPHILS: Clear injured site of debris and microorganisms BASOPHILS: Histamine (increased vascular permeability). MONOCYTES predominate for 24-48 hours after an acute injury. MACROPHAGES: ▪ the most important (cells) in the inflammatory phase and are essential for wound healing. ▪ play a major role in phagocytosis by producing enzymes (collagenase), ▪ play a role in localizing the inflammatory process and attracting fibroblasts to the injured area by releasing fibronectin. 11 SUMMARY OF INFLAMMATION PHASE There are 3 major consequences of the inflammatory phase: 1st. Fibrin and fibronectin enter the area of injury forming crosslinks with the collagen to create a fibrin lattice → limiting hemorrhage and fluid loss (initial strength) 2nd. Macrophages then begin to remove damaged tissue. 3rd. Finally, endothelial cells and fibroblasts are recruited and stimulated to begin dividing (sets the stage of proliferation phase) 12 PROLIFERATIVE PHASE (4-24 days) Involves: ▪ Epithelial Cells ▪ Connective Tissues provide strength to the injury site 4 simultaneous process: 1. Epithelialization 2. Collagen production 3. Wound contraction 4. Neovascularization. 13 PROLIFERATIVE PHASE EPITHELIALIZATION Reestablishment of the epidermis. Within a few hours of injury. Uninjured cells played the main role. Not STRENGTH to the tissue!!!!! 14 PROLIFERATIVE PHASE COLLAGEN PRODUCTION FIBROPLASIA It takes place in connective tissues Fibroblasts migrate to injured area First synthesize procollagen, which changes into tropocollagen and finally the collagen fibrils are formed to create collagen filaments to form collagen fibers. Cross-linking between collagen molecules provides further tensile strength to the injured area. 15 PROLIFERATIVE PHASE COLLAGEN PRODUCTION FIBROPLASIA GRANULATION TISSUE: new capillaries, fibroblasts, myofibroblasts (fibroblastic activity and fibronectin). ▪ As the amount of granulation tissue increases, the size of the fibrin clot gets smaller. ▪ Fibroblasts initially produce a thin, weak-structured collagen (collagen type III) → to tolerate early, controlled movement without disruption. ▪ By day 7: significant increase in the amount of collagen ▪ By day 12: the immature type collagen III starts to be replaced by collagen type I (more mature and stronger). 16 PROLIFERATIVE PHASE WOUND CONTRACTION (Picture frame theory) Wound contraction begins 5 days after injury: MYOFIBROBLASTS. As scar tissue matures, it develops pressure and tension sensitive nerve endings in order to protect the immature vascular system. During the proliferative phase the scar appears red and swollen due to: ▪ the increase in vascularity ▪ the increase in fluid ▪ the innervations of the healing site ▪ the relative immaturity of the tissue. 17 PROLIFERATIVE PHASE NEOVASCULARIZATION ANGIOGENESIS ▪ to supply oxygen and nutrients to the injured and healing tissue ▪ healing cannot occur without angiogenesis. ▪ Macrophages are responsible for signaling neovascularization ▪ Angiogenesis can occur by 3 different mechanisms: Generation of a new vascular network. Anastomosis to preexisting vessels Coupling of the vessels in the injured area. 18 MATURATION PHASE (Day 9 onwards) Changes in the size, form and strength of the scar tissue. The longest duration phase. It may persist for over a year beyond the initial injury. During this period: ▪ the number of fibroblasts, macrophages, myofibroblasts and capillaries decrease ▪ the water content of the tissue declines ▪ the scar becomes white in appearance as the collagen matures and the vascularity decreases. 19 MATURATION PHASE (Day 9 onwards) IMPORTANT: Fiber orientation and the balance of collagen synthesis and lysis. Synthesis and lysis (by enzyme collagenase) of collagen occur in a balanced way. During this phase, the collagen which is synthesized and deposited is predominant type I. Length and mobility of the injured area could be modified by the application of stress during the appropriate phases of healing: controlled application of tension can increase the tensile strength. 20 21 CHRONIC INFLAMMATION Acute inflammation No more than 2 weeks. Sub-acute inflammation Between 2 to 4 weeks. Chronic inflammation Last for months or years 22 FACTORS AFFECTING THE HEALING PROCESS LOCAL SYSTEMIC ▪ Type, size, location. ▪ Age. ▪ Infection. ▪ Diseases: ▪ Vascular supply. ▪ Diabetes ▪ External forces. ▪ Immunosuppression ▪ Movement. ▪ Circulatory ▪ Medication. ▪ Nutrition. 23 SUMMARY OF THE PROCESS 24 25 WOUND HEALING 26 27 BIBLIOGRAPHY Cameron MH. Physical Agents in Rehabilitation: From Research to Practice. Elsevier, 2012. Bélanger AY. Evidence-Based Guide to Therapetic Physical Agents. Elsevier Churchill Livingstone 2.002. Watson T. Electrotherapy: Evidence-Based Practice. Elsevier, Churchill Livinstone, 2008. Bélanger AY. Therapeutic Electrophysical Agents. Evidence Behind Practice. Lippincott Willians & Wilkins, 2014. 28