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21 Cards in this Set
- Front
- Back
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Cell Replication
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All tissues contain labile, stable and permanent cell populations.
Labile cells actively undergo mitosis Stable cells may be recruited into cell cycle by Mitogens Permanent cells are incapable of recruitment into cell cycle (terminally-differentiated cells) Both stable and permanent cells express tissue-specific gene productions Tissues that can regenerate after wounding contain unipotential or pluripotential stem cells |
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Cell Migration
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Cells are recruited and directed within the wound environment for healing to proceed by local chemotactic agents that are soluble, matrix associated and/or cell-cell contact
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Cell Differentiation
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Factors present within the wound environment also direct the differentiation of recruited cells into stable and permanent cells transforming the would healing environment into a mature tissue
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Labile cell
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Cells that are actively undergoing mitosis
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Permanent cell
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Cells that are incapable of recruitment into the cell cycle and express a differentiate phenotype and tissue-specific phenotype
Also called end or terminally-differentiated cells |
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Stable cell
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Cells not under going active mitosis
They are in G0phase Under appropriate signals, they could be recruited into the cell cycle to become labile cell |
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Primary union
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AKA Primary intention
Type of epidermal wound healing Well-apposed wound margins as found in many surgical wounds that can be sutured together and they are immobilized Heals faster but with the same mechanism as Secondary union |
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Secondary union
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AKA Secondary intention
Poorly apposed wound or not apposed wound margins Heals at a much slower rate, but with the same mechanism as Primary union Ex: ulcer or extraction site |
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Day 1 of Wound Healing
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Wounding lacerates vessels, exposing Type I collagen and ECM proteins
Platelets start to aggregate and degranulate its vessicles to start Clotting cascade causes blood clot formation and fibrin deposition Transglutamase cross-links fibrin, collagen and fibronectin stabilizing the wound environment and creates scaffold Acute inflammatory response is initiated Neutrophils are recruited to phagocytose invading bacteria Basal cells near wound no longer have cell adhesion molecules to cells next to them therefore it signals nucleus to expression protein to allow it to migrate along CT |
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Transglutamase
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Makes covalent cross-links in fibronectin-fibrin scaffold to stabilize the wound and allow neutrophils to enter
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Day 2 of wound healing
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Wound margins are elevated by underlying mitotic activity and tissue edema
PMN cellular infiltration is replaced by macrophage-monocytic cells which complete debridement of wound such as apoptotic PMN Vascular proliferation is seen at wound edges (angiogenesis) Increased permeability of invading capillary network leads to local tissue edema Clot begins to dehydrate Wound margins contract largely by action of myofibroblasts |
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Day 3 of Wound Healing
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Proliferation and migration of fibroblasts from surrounding tissue into the fibrin clot
synthesize an extracellular matrix similar to embryologic mesenchyme composed of fibronectin, primitive proteoglycans and type III collagens. Granulation tissue is seen clinically. Vital basal cells of the epithelium adjacent to the wound margins alter phenotype and begin to migrate over the new extracellular matrix at an approximate rate of 0.5 mm/day. |
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Day 4 of Wound Healing and Onwards
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Remodeling of the initial extracellular matrix by macrophages and fibroblasts occurs
Successive wave of cells begins to synthesize a mature ECM composed of primary Type I collagen Epithelial cells have abridged the wound margins and cell adhesion molecules have established contact Epithelial cells express Type IV collagen and make basement membrane, attach to the basement membrane and keratinocytes start to differentiate into mature epithelium Gradual loss of vascularity, increase in Type I collagen and formation of collagen crosslinks increases tissue strength Scar formation seen clinically |
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Day 1 of Osseous Fractures
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Trauma ruptures vessels in periosteum and endosteum exposing ECM proteins
Causes blood clot and fibrin formation Stabilization by fibronectin and Transglutimase cross-links Followed by acute inflammatory cell infiltration Interruption of vascular supply causes local necrosis of bone cells adjacent to fracture site |
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Day 2-4 of Osseous Fractures
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Acute inflammatory cell infiltration is replaced with chronic inflammatory cells
Blood clot is invaded by new capillaries and de-differentiate fibroblasts (mesenchymal cells if high oxygen levels) Monocyte cells fuse to form osteoclasts to resorb necrotic bone |
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Day 7 of Osseous Fractures
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Primitive woven bone is deposited beginning in well perfused area in wound periphery
In Areas of poor vascularization, cartilage is seen which may calcify Fractures bone segments are immobilized by primary callus formed by primitive woven bone and calcified cartilage |
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Day 14 of Osseous Fractures and onwards
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Primitive callus is remodeled into mature lamellar bone by cutting cones (invading osteoclasts, endothelial and osteoblast bone remodeling units)
Bone structure closely reflects loads placed on it - Wolfe's Law Complete remodeling with mineralization may require 10+ months |
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Cutting cones
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Osteoclasts, endothelial cells and osteoblasts that remodel the primitive callus in osseous fractures into mature lamellar/haversian bone
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What factors affect wound healing
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Type, size and location of wound
Presence of infection or residual bacterial products Movement of wound margins Age Metabolic diseases Drugs that affect inflammatory response Nutritional deficiencies |
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Wound dehiscence
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Reopening of wound margins
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Keloid formation
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Exuberant scar formation
May be genetically determined |
