| SOFT-TISSUE HEASLING Cell Structure and Function - Metaplasia – conversion of one kind of tissue into a form that is nor normal for that tissue - Dysplasia – abnormal development of tissue - Hyperplasia – excessive proliferation of normal cells in the normal tissue arrangement - Atrophy – a decrease in the size of tissue due to cell death and resorption or decreased cell proliferation - Hypertrophy – an increase in the size of a tissue without necessary increasing the number of cells. - Necrosis = cellular death resulting from trauma - Stratum germinativum = responsible for new cell formation Cartilages Healing - Articular cartilage has limited capacity to heal because of little direct blood supply. - Cell division for new cartilage growth does nor occur in the adult - Hemarthrosis will destroy articular cartilage - Synovial fluid containing fibrinolysin slows the healing process - Ganglion cyst is a collection of a think fluid within a tendinous sheath or joint capsule Ligament Healing - Full ligament healing with scar maturation may take as long as 12 months. Skeletal Muscle Healing - Skeletal muscle healing and repair follow the same process as other soft tissue developing tensile strength according to Wolff’s law. Nerve Healing - If peripheral nerve regeneration occurs, it is at a rate of only 3~4 mm per day. - Neuronotomesis = The total nerve is disrupted - Axonotomeses = Outer nerve fibers are disconnected Modifying Soft-Tissue healing Management Concepts - Drugs to treat inflammation - Superficial thermal agents - Therapeutic modalities - Exercise and rehabilitation FRACTURE HEALING Acute Fractures of the Bone - Hematoma Formation - Cellular Formation - Callus Formation; 2 months to be completed - Ossification - Remodeling - Osteoclasts are cells that resorb bone during growth Management of Acute Fracture - Conditions that interfere with fracture healing o Poor blood supply o Poor immobilization o Infection Healing of Stress Fractures PAIN - Pain is one of the major indications of the presence of injury. - Inherent in pain - Anatomical structures - Physiological reactions - Psychological - Social Cultural - Cognitive factors Nociception - Pain receptors (nociceptors or free nerve endings) are sensitive to extreme mechanical, thermal , and chemical energy. Endogenous Analgesics - Stimulation of the periaqueductal gray area (PGA) of the midbrain and the raphe nucleus in the pons and medulla causes analgesia. Pain Categories - Pain Sources - Fast versus Slow Pain - Acute versus Chronic pain - Projected (Referred) Pain o Myofascial pain; Trigger points – Small hyperirritable areas within a muscle o Sclerotomic and dermatomic pain - Variations in Pain Sensitivity o Pain modulation o Pain assessment o Pain treatment o Heat and Cold o Induced analgesia o The gate theory o Acupuncture o Pharmacological agents Psychological Aspect of Pain - The bone marrow contains immature stem cells that differentiate into red and white blood cells and platelets |
| Tissue Response to Injury |
| THE INFLAMMATORY REPSONSE Acute Inflammation Phase 1; Acute phase - Redness - Heat - Swelling - Pain - Loss of function - Cellular death continues after initial injury because of the following; o Lack of oxygen caused by disruption of circulation o Digestive enzymes of the engulfing phagocytes that spill over to kill normal cells - Vascular response o First hour; Vasoconstriction; Decrease in the diameter of a blood vessel o Second hour; Vasodilation; Increase in the diameter of a blood vessel. § Exudate; Fluid with a high protein content and containing cellular debris that comes from blood vessels and accumulates in the area of the injury § Permeable; Permitting the passage of a substance through a vessel wall § The vadodilator theory of autoregulation suggests that metabolic byproducts increase blood flow by causing vasodilation in localized area - Cellular response o Mast cells; Connective tissue cells contain heparin (blood anticoagulant) and histamine o Leukocytes; Consist of two types – granulocytes (e.g., basophils and neutrophils) and agranulocytes (e.g., monocytes and lymphocytes) o Phagocytosis; Process of ingesting microorganisms, other cells, or foreign particles, commonly performed by monocytes (white blood cells) o Macrophages engulf large quantities of bacteria o Diapedesis is the process by which leukocytes squeeze through pores in the capillary wall - Chemical mediators o Histamine (Released by mast cells and platelets); Increased capillary permeability o Serotonin (Released by mast cells and platelets) o Bradykinin o Prostaglandins o Leukotrienes - Complement system o Leukocyte chemotaxis o Phagocytosis - Bleeding and exudate o Blood coagulation; Thromboplastin + Calcium = Prothrombin = Thrombin = Fibrinogen = Insoluble fibrin clot (+ Vitamin K) Phase 2; Repair Phase (Fibroplasis phase); Scar formation - Tissue repairs; o By resolution o By granulation tissue o By regeneration - Tissue repair depends on o Elimination of debris o Regeneration of endothelial cells o Production of fibroblasts - Fibroblasts become active during regeneration phase of the inflammatory response to begin building collagen Phase 3; Remodeling phase (up to 1 ~2 years) - Remodeling depends on the amount and type of scar tissue present - Synthesis; Process of forming or building up - Lysis; Process of breaking down Chronic Inflammation - Chronic inflammation can stem from repeated acute microtraumas and overuse. |
| Healing process |
| Inflammatory-Response phase (0-4 days) |
| Fibroblastic-Repair phase (2 days-6 weeks) |
| Maturation-Remodeling phase (3 weeks -2 years) |
| (Day) |
| Phases of the healing process and characteristics of each phase - time frames, physiological events |
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| 0 |
| 2 |
| 4 |
| 21 |
| 42 |
| 2 years |
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| Extent of injury (Macrotears & Microtears) - Edema - Hemorrhage - Poor vascular supply - Separation of tissue - Muscle spasm - Atrophy - Corticosteroids - Keloids and hypertrophic scars - Infection - Humidity, climate, and oxygen tension - Health, age, and nutrition |