Tissue Healing and Intro to Physical Agents

Cards (72)

  • Tissue Healing
    A coordinated & complex process that occurs in response to injury
  • Phases of tissue healing
    • Inflammation (Day 0-6)
    • Proliferation (Day 3-20)
    • Maturation / Remodeling (Day 9+)
  • Inflammation
    Immediate protective response to the injury of perfused tissue
  • Cardinal signs of inflammation
    • Calor (heat)
    • Rubor (redness)
    • Tumor (swelling)
    • Dolor (pain)
    • Functio laesa (loss of function)
  • Inflammatory phase
    1. Hemostatic response
    2. Vascular response
    3. Cellular response
    4. Immune response
  • Hemostatic response
    Controls blood loss when vessels are damaged
  • Vascular response
    Rapid transient vasoconstriction followed by vasodilation and increased permeability of capillaries
  • Prostaglandins
    Sensitize pain receptors, responsible for hyperalgesia
  • Cellular response
    Leukocytes (white blood cells) clear the injured site of debris and microorganisms
  • Immune response
    Macrophages present foreign antigens to T lymphocytes, T lymphocytes activate B cells, B cells make antibodies
  • Proliferation phase
    1. Neovascularization
    2. Collagen production
    3. Wound contraction
    4. Epithelialization
  • Neovascularization
    Development of new blood supply
  • Collagen production
    Fibroblasts lay down an extracellular matrix and produce collagen
  • Wound contraction
    Wound defect shrinks, facilitated by myofibroblasts
  • Epithelialization
    Uninjured epithelial cells migrate from margins of wound to cover the wound
  • Maturation phase
    1. Collagen turnover
    2. Collagen fiber orientation
  • Collagen turnover
    Balance between collagen synthesis and lysis, type III replaced by type I
  • Collagen fiber orientation
    Scar tissue attempts to mimic characteristics of the tissue it is healing, or is determined by internal and external forces
  • Chronic inflammation is excessive or prolonged expression of cardinal signs of inflammation
  • Acute vs chronic inflammation
    Acute: PMNs, platelets. Chronic: Macrophages, lymphocytes, plasma cells
  • Factors that may contribute to chronic inflammation
    • Repetitive mechanical trauma
    • Presence of foreign body
    • Lack of stimulus for repair
    • Inadequate perfusion
    • Use of cytotoxic agents
  • Localized chronic inflammation example
    Example: Osteoarthritis
  • Systemic chronic inflammation example
    Example: Rheumatoid arthritis
  • Factors affecting healing
    • Local factors
    • Systemic factors
  • Healing of cartilage
    • Limited ability to heal due to lack of vasculature & lymphatics
    • Injury to cartilage or cartilage + subchondral bone
  • Microfracture technique
    Clinical procedure to improve cartilage healing
  • Healing of skeletal muscle
    • Skeletal muscle cannot proliferate, scarring but not healing
    • Myositis ossificans - heterotopic bone formation
  • Healing of tendon
    • Repair potential is variable, depends on type of tendon and extent of damage
  • Cartilage injury
    • Cartilage
    • Cartilage + subchrondral bone
  • Microfracture
    Clinical Correlation for cartilage injury
  • Cartilage has low blood supply
  • Cartilage heals better with bone because bones are highly vascularized, allowing for formation of clots
  • Fibroclasts
    Tries to heal cartilage
  • Cartilage is made of Type 3 collagen
  • Skeletal muscle injury
    • Blunt trauma
    • Violent contraction
    • Excessive stretch
    • Muscle wasting
  • Skeletal muscle cannot proliferate, leading to scarring but not healing
  • Myositis ossificans
    Heterotopic bone formation (calcified hematoma), most common in quadriceps and biceps
  • Skeletal muscle cannot form new skeletal muscle cells
  • Muscle inflammation occurs within the muscle
  • Tendon repair
    • Variable repair potential
    • Depends on type of tendon
    • Extent of damage to tendon (& sheath)
    • Vascular supply
    • Duration of immobilization