Cellular growth/differentiation & Regeneration and Repair Flashcards
(45 cards)
Anaplasia
total loss of differentiation as might occasionally be seen in malignant neoplasms
More than just an increased N/C ratio, the nucleus
Congenital / Developmental Change: Hypoplasia and Agenesis
- Hypoplasia – defective formation or incomplete development of a part
- Agenesis – absence/failure of formation
Pathological definition of Repair
deposition of collagen and other extracellular matrix components, causing the formation of scar
• “patches rather than restores”
Pathological definition of Regeneration
proliferation of cells and tissues to replace lost structures
• restores
What are the 5 overlapping processes involved in tissue repair.
- Hemostasis – Plts, coagulation
- Inflammation – PMNs, macrophages, lymphocytes, mast cells
- Regeneration – stem cells and differentiated cells (part of proliferation phase)
- Fibrosis – macrophages, granulation tissue (fibroblasts, angiogenesis), type II collagen (part of proliferation phase)
- Remodeling–macrophages,fibroblasts, converting collagen III to I
Inflammatory Phase
- Redness, swelling, pain, heat & inflammation
- Capillary permeability increases & fluid moves in
- Phagocytic cells come in to prevent infection and release GF
- GF’s recruit fibroblasts, which marks beginning of the proliferative phase
Proliferative Phase
- Begun by fibroblasts that secrete collagen and cause angiogenesis
- This leads to epithelialization, and causes granulation tissue to form
- Plasma leaks in, and epithelialization is the last of this stage
- Here a new surface area, similar to the old one, is formed
Remodeling Phase
- Remodeling begins after 3 weeks, and continues 6 moths or longer (tensile strength can be 70-80% at end of 3 months)
- Synthesis and lysis of collagen occurs simultaneously
Wound Healing - Primary Intention
Primary Intention (primary union) • Regeneration • Edges are approximated • eschar (scab) • Epidermal cells proliferate under scab • Dermal healing is by routine scarring
Wound Healing - Second Intention (secondary union)
- Occurs with failure of first intention t
- poor apposition or dehiscence
- Foreign material
- Extensive necrosis
- Infection
- More fibrin, more granulation tissue
- Wound contraction
Wound healing - Tertiary Intention
- Surgical
* Sutures are placed later to help approximate the tissue
Etiology of scar formation:
- When resolution fails in acute inflammation
- Ongoing necrosis and chronic inflammation (eg.chronic hepatitis cirrhosis)
- When cell necrosis cannot be repaired (eg.myocardial infarction)
Stages of scar formation
• Bleeding
• Preparation – removal of inflammatory debris and necrotic tissue by phagocytes
• Granulation tissue (highly vascularized
connective tissue)
• Fibronectin produced by fibroblasts
Granulation Tissue
- Formed by fibroblasts and vascular endothelial cells.
- Grossly it has a pink, soft, grainy appearance.
- It is often edematous
- Eventually it is converted to a pale avascular scar composed of fibroblasts, dense collagen III, fragments of elastic tissue and other ECM.
Repair - Scar
- Collagenation – tensile strength
- Collagen produced by fibroblasts
- Maturation – pale/lacking circulation
- Contraction and strengthening
- Myofibroblasts contract early
- Collagencontracts in late scars (type III becomes type I)
Factors causing defective scar forming
Deficiencies of vitamin B2, C, bioflavonoids and Zinc
Angiogeneisis
formation of new blood vessels (also called neovascularization)
• Branching of adjacent vessels
• Recruitment of endothelial progenitor cells
• From bone marrow
The collagen triple helix.
The individual α chains are left-handed helices with approximately three residues per turn. The chains are in turn coiled around each other following a right-handed twist. The hydrogen bonds which stabilize the triple helix (not shown) form between opposing residues in different chains (inter-peptide hydrogen bonding) and are therefore quite different from α helices which occur between amino acids located within the same polypeptide
Collagen Types:
(over 29) In the remodeling phase, type III collagen is laid down in granulation tissue, then converted to type I collagen
Type I
Most common, and is the strongest as it is located in bones, skin, tendons, fascia, cornea, teeth and mature scars.
Type II
little bit less strength seen in cartilage, vitreous humor, and nucleus pulposus
Type III
is even weaker as it is present in granulation tissue, embryonic tissue, uterus, blood vessels, and keloids.
Type IV
is the weakest is it only supports a row of epithelial cells as it’s found only in basement membranes.
Hydroxylation of collagen is mediated by vitamin C. What cofactor is required? What is cross-linking performed by?
Cross-linking of collagen is performed by lysyl oxidase; Copper is a required cofactor
