1. Tissue repair involves regeneration of injured tissue or replacement by connective tissue scarring. It involves cell proliferation and interaction between cells and the extracellular matrix.
2. Tissues are divided into continuously dividing, stable, and permanent groups based on their ability to proliferate. Continuously dividing tissues like skin regenerate easily while permanent tissues like neurons cannot regenerate after injury.
3. Growth factors and the extracellular matrix play important roles in tissue repair by stimulating cell growth and movement. Repair occurs through regeneration in labile tissues and scarring in others when injury is too severe for regeneration.
• Tissue repair:restoration of tissue architecture and function after
an injury
• Occurs in two ways:
• Regeneration of injured tissue.
• Replacement by connective tissue (scarring)
4.
• Usually, tissuerepair involves both processes
• Involves cell proliferation, and interaction between cells and
extracellular matrix.
5.
• Many cellsproliferate during tissue repair:
• Injured tissue remnants.
• Vascular endothelial cells
• Fibroblasts
6.
Tissues of thebody are divided into three groups:
•Continuously dividing (labile) tissues.
•Stable tissues.
•Permanent tissues
7.
•Continuously dividing (labile)tissues
•Cells are continuously proliferating.
•Can easily regenerate after injury
•Contain a pool of stem cells
•Examples: bone marrow, skin, GIT epithelium.
•Stable tissues
•Cells havelimited ability to proliferate.
•Limited ability to regenerate (except liver!)
•Normally in G0, but can proliferate if injured.
•Examples: liver, kidney, pancreas…
11.
• Permeant tissue
•Cells can't proliferate
• Can't regenerate (So injury always lead to scar)
• Examples: Neurons, Cardiac muscles
THE EXTRACELLULAR MATRIX
•ECMis the network that surrounds cells. It is two forms: interstitial
matrix and basement membrane.
•ECM regulates proliferation, movement, and differentiation of the
cells living in it.
14.
REGENERATION
•Occurs all thetime in labile tissues
•Cells are constantly being lost and replaced
•If demand increases, supply increases easily
15.
•Occurs in limitedform in stable tissues
•Remove one kidney: the other one undergoes hypertrophy and
hyperplasia
•Remove half of the liver: it will grow back
16.
SCARRING
•If injury issevere, regeneration can’t happen
•So, fibrosis (a scar) replaces the injured tissue
17.
•Four components tothis process:
•New vessel formation (Angiogenesis).
•Fibroblast proliferation.
•Synthesis of collagen (Scar formation).
•Remodeling of the scar.
18.
•By 24 hours:
•Endothelialcells start proliferating
•Fibroblasts emigrate
•By 3-5 days:
•Granulation tissue present (blood vessels+ fibroblasts).
•Weeks later:
•Dense fibrosis (scar)
•Scar is remodeled over time
21.
Introduction to woundhealing
• Healing is a complex and dynamic process of restoring cellular structures
and tissue layers.
• The adult wound healing process can be divided into 4 distinct phases:
• The homeostasis phase
• the inflammatory phase
• the proliferative phase
• the remodeling phase.
22.
Sequence of eventsin healing
Initial phase - Hemostasis
• Following vasoconstriction, platelets adhere to damaged
endothelium and discharge adenosine diphosphate (ADP),
promoting thrombocyte clumping, which dams the Wound
23.
• The inflammatoryphase is initiated by the release of numerous
cytokines by platelets.
• Fibrinogen is cleaved into fibrin and the framework for
completion of the coagulation process is formed.
24.
Second phase -Inflammation
• Within the first 6-8 hours
• polymorph nuclear leukocytes (PMNs) “cleanse” the wound, clearing it of
debris , monocytes also exude from the vessels. These are termed
macrophages. The macrophages continue the cleansing process and
manufacture various growth factors during days 3-4.
25.
Third phase -Granulation
sub phases are: fibroplasia -matrix deposition - angiogenesis -
and re-epithelialization
• In days 5-7, fibroblasts have migrated into the wound, laying
down new collagen of the subtypes I and III
26.
• Angiogenesis .The formation of new vasculature requires
migration, mitosis, and maturation of endothelial cells
• Re-epithelization occurs with the migration of cells from the
periphery of the wound . Division of peripheral cells occurs in
hours 48-72, resulting in a thin epithelial cell layer, which bridges
the wound.
27.
Fourth phase -Remodeling After the third week, the wound
undergoes constant alterations, known as remodeling,
• This can last for years after the initial injury occurred. Collagen
is degraded and deposited in an equilibrium-producing fashion
28.
• Contraction ofthe wound is an ongoing process resulting in part
from the proliferation of the specialized fibroblasts termed
myofibroblasts, which resemble contractile smooth muscle cells.
29.
1. SKIN WOUNDHEALING
• First intention
• Second intention
31.
Healing by FirstIntention
•Occurs in small wounds that close easily
•Epithelial regeneration predominates over fibrosis
•Healing is fast, with minimal scarring/infection
•Example: Well-approximated surgical incisions
32.
Healing by FirstIntention: Timeline
• By 24 hours
• Clot forms
• Neutrophils come in
• Epithelium begins to regenerate
33.
• By 3-7days
• Macrophages come in
• Granulation tissue is formed
New blood vessels
Fibroblasts
• Collagen begins to bridge incision
• Epithelium increases in thickness
34.
• Weeks later
•Granulation tissue gone
• Collagen is remodeled
• Epidermis is full and mature, but without dermal
appendages.
38.
Healing by SecondIntention
• Occurs in larger wounds that have gaps between wound margins
• Fibrosis predominates over epithelial regeneration
• Healing is slower, with more inflammation and granulation tissue
formation, and more scarring
FACTORS AFFECTING WOUNDHEALING
Local factors
• Infection is the single most important cause of delay in healing.
• Mechanical factors, as early motion of wounds, can delay healing.
• Foreign bodies, such as fragments of steel, glass, or even bone
44.
• Size, location,and type of wound influence healing. Wounds in
richly vascularized areas, such as the face, heal faster than those in
poorly vascularized
45.
General Factors
• Age
•General state of health
• chronic diseases e.g. diabetes, rheumatoid arthritis etc.
• Drugs (steroids) and hormones
• General cardiovascular status
46.
• General dietarydeficiencies e.g. protein
• Specific dietary deficiencies
• Vitamin C
• sulphur-containing amino acids