Transcript repair (healing)

REPAIR
DR: Gehan Mohamed
TYPES OF CELLS
Conteniously dividing cells (Labile): e.g
epithelium, haematopoietic (blood).
Quiescent (Stable): e.g hepatic, kidney and
pancreas as their cells divide when there is
need.
Non-dividing (Permanent): nerve cells and
skeletal muscle cells
REPAIR (HEALING)
Definition : Tissue repair involves replacement of damaged tissue with new
healthy living tissue.
Types
Usually involves two separate but coordinated components
A)
Regeneration:
healing by the same type of tissue cells from surrounding healthy living cells, this
occurs with in small damages of labile cells and stable cells for examples
liver cirrhosis and bone fractures
B) Fibrosis (scar tissue):
healing by granulation tissue (fibroblast with new capillaries formed) which
mature a vascular fibrous tissue (scar), this occurs in the healing process of
permanent cells and stable cells with high damage. for example
myocardial infraction and wounds
INTRODUCTION TO WOND HEALING
• The adult wound healing process can be
divided into 4 distinct phases:
•
•
•
•
The homeostasis phase
the inflammatory phase
the proliferative phase
the remodeling phase.
SEQUENCE OF EVENTS IN HEALING
Initial phase - Hemostasis
• Following vasoconstriction, platelets adhere to damaged
endothelium and discharge adenosine diphosphate (ADP),
promoting thrombocyte clumping, which dams the Wound
• The inflammatory phase 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. Fibrin provides the structural
support for cellular constituents of inflammation.
• This process starts immediately after the insult and may continue for a
few days
SEQUENCE OF EVENTS IN HEALING
Second phase - Inflammation
• Within the first 6-8 hours, the polymorphonuclear leukocytes (PMNs) or PNLs
“cleanse” the wound, clearing it of debris. The PMNs attain their maximal
numbers in 24-48 hours and commence their departure by hour 72
• As the process continues, 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.
• Many factors influencing the wound healing process are secreted by
macrophages. These include TGFs, cytokines and interleukin-1 (IL-1), tumor
necrosis factor (TNF)
SEQUENCE OF EVENTS IN HEALING
Third phase - Granulation
This phase consists of different subphases which 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
•
Angiogenesis is theThe formation of new vasculature which requires extracellular matrix and basement
membrane degradation followed by migration, mitosis, and maturation of endothelial cells
•
Re-epithelization occurs with the migration of cells from the periphery of the wound and adnexal
structures. This process commences with the spreading of cells within 24 hours. Division of peripheral cells
occurs in hours 48-72, resulting in a thin epithelial cell layer, which bridges the wound.
This succession of subphases can last up to 4 weeks in the clean and uncontaminated wound.
SEQUENCE OF EVENTS IN HEALING
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
• The collagen deposition in normal wound healing reaches a
peak by the third week after the wound is created.
• Contraction of the wound is an ongoing process resulting in
part from the proliferation of the specialized fibroblasts termed
myofibroblasts, which resemble contractile smooth muscle
cells.
TYPES OF HEALING
TYPES OF HEALING
TYPES OF HEALING
COMPLICATIONS OF THE HEALING
PROCESS
•
This process can go wrong and
produce an increase of
fibroblastic proliferation with a
resultant hypertrophic scar
•
Further exuberance can result in
keloid formation where scar
production extends beyond the
area of the original insult.
Conversely, insufficient healing
can result in atrophic scar
formation.
COMPLICATIONS OF THE HEALING
PROCESS
•
•
•
•
•
•
•
•
•
Weak scar: this may lead to hernia
Cicatrisation: contracture of the size of the scar
Implantation epidermiod cyst
Stump neuroma: following amputation causing a
painful coiled mass of nerves
Sinus: is a track of septic granulation tissue connecting
a cavity to the outside and has one blind end e.g.
pilonidal sinus
Fistula: is a tract of septic granulation tissue connecting
2 epithelial surfaces
Infection : leading to delayed healing
Rarely scars may develop squamous cell carcinoma
Ulcers: discontinuity of the covering epithelium or
muscle membrane
FRACTURES:
• Definition :Break in the bone.
TYPES:
• Simple / Compound .
• Single - Horizontal, oblique, spiral,
• Comminuted – multiple.
• Greenstick is a partial fracture common in
children.
TYPES OF FRACTURE:
Stages of wound healing
Remodeling
Vessel regression, Collagen remodeling
Proliferation
Reepithelialization, Angiogenesis, Fibrogenesis,
Inflammation
PMNs, Macrophages, Lymphocytes
Hemostasis
Fibrin clot, platelet
deposition
1D 3D
1wk
Time after injury
6wk
8wk
HEALING IN BONE:
•
•
•
•
•
1D - Hematoma formation (fibrin mesh)
3D - Inflammation
1W - Soft callus – granulation, matrix.
3-6W - Callus – ossification, woven bone
8+W - Re-modeling – absorb/deposit,
strength, lamellate.
COMPLICATIONS:
•
•
•
•
•
Delayed healing.
Non healing.
Joint involvement - ankylosis
Abnormal position – arthritis.
Bone necrosis – nutrient artery
• Pseudoarthrosis
FACTORS AFFECTING HEALING:
Local factors which delay healing:
• Mobilization of the fractured ends.
• Improper reduction – abnormal position.
• Infection. Debris, dead tissue in wound.
• Joint involvement.
Poor blood supply to area of injury.
FACTORS AFFECTING REPAIR:
General factors which delay healing :
-bad nutrition
Starvation Diabetes Corticosteroid therapy Chronic deblitating disease as T.B,malignancy
Old Age of patient.