Wound Healing And Tisue Regenration Flashcards
Healing
Healing is the body response to an injury in an attempt to restore normal structure and function.
It has 2 processes:
1. Regeneration: complete restoration of the original tissue
- Repair: healing by proliferation of connective tissue elements result in fibrosis and scarring
Steps of healing
- Injury induces acute inflammation
- Parenchymal cells regenerate
- Both parenchymal and connective tissue cells migrate and proliferate
- Extracellular matrix is produced
- Parenchyma and connective tissue matrix remodeling.
- Increase in wound strength due to collagen deposition.
Granulation tissue
Hallmark of healing
● Term comes from soft, pink, granular appearance when viewed from the surface of a wound
● Histology: Proliferation of small blood vessels and fibroblasts; tissue often edematous
Defects in collagen structures
Enhlers-Danlos Syndrome, osteogensis imperfecta,
Alport Syndrome (
Hereditary Nephritis,
deafness
dislocation of lens,
cataract.
Defects in collagen structures
Enhlers-Danlos Syndrome, osteogensis imperfecta,
Alport Syndrome (
Hereditary Nephritis,
deafness
dislocation of lens,
cataract.
Types of wound healing
Primary union/ healing by 1st intention
Secondary union/ healing by 2nd intention
Types of wound healing
Primary union/ healing by 1st intention
Secondary union/ healing by 2nd intention
Healing by 1st intention
involves healing of a clean uninfected, surgical
Incision, approximated by surgical sutures. Minimal death of epith. Cells, and CT. cells.
- Minimal disruption of epithelial BM continuity.
- The narrow incisional space fills with clotted blood containing, fibrin and blood cells → formation of Scab that covers the wound.
Steps of healing by 1st intention
Within 24 hours → Neutrophils appear at the margins of incision.
→ The epidermis of its cut edge thickens due mitotic activity of basal cells.
24 – 28 hours → spurs of epithelial cells migrate and grow along the cut margins of the dermis → depositing BM components.
→ Fuse at the centre producing a continuous but thin layer of epithelium.
By 3rd Day→ Neutrophils replaced by macrophages
→ Granulation tissue invades the incision space
→ Collagen fibres are now present in the margins
→ Epitheliazation continues → thickening
By Day 5 → Incision space filled with granulation tissue → Pink, soft granular appearance Histologically characterized by proliferation of new small BV (Angiogenesis or Neovascularization) and fibroblasts.
Neovascularization is maximal
Epidermis mature with surface keratinizing
2nd Week→ Accumulation of collagen
Proliferation of fibroblasts
Regression of vascular channels, oedema and leukocytes
By 1st month→ Scar formation
compose of a cellular CT devoid of inflammatory cells.
Tensile strength of the wound increases.
Takes months for tensile strength to get to maximum.
Healing by 2nd intention
Occurs where there is more extensive loss of cells and tissue
- e.g. infarction, inflammations, ulceration, abscess formation, surface wound that create large defects (severe Burns, cancrumoris)
Here the process is more complicated
- The large defect must be filled
- Regeneration cannot completely reconstitute the original architecture
- Abundant granulation tissue grows in from the margin to complete the repair.
Differences between 1st and 2nd union
- Large tissue defects with more fibrin and more necrotic tissue and exudates
- Inflammatory Rxn is more intense
- Much large amounts of granulation tissue are formed.
- Wound contraction occurs → Reduction in size of the area
- Healing starts from the base rather that edges
Mechanism of wound healing
Induction of an acute inflammatory process
2. Regeneration of parenchymal cells ( Labile, Quiescent or stable and permanent?)
3. Migration and proliferation of both Parenchymal and CT cells.
4. Synthesis of Extracellular matrix proteins
5. Remodeling of CT and parenchymal components
6. Collagenization
7. Acquisition of would strength
Bone healing
Stages:
➢ Haematoma formation – follows injury if periosteum is torn
➢ Acute Inflammation – Fibrin-rich exudates, increased WBC – Hyperaemia
➢ Demolition – Invasion by macrophages and osteoclasts – removing fibrin, RBC, Exudates, debris
➢ Formation of granulation tissue – Ingrowth of capillaries and mesenchymal cells
➢ Woven bone and Cartilage formation – mesenchymal cells differentiated to form woven bone or cartilage – forms hard material uniting the fractured ends – CALLUS
Collagen and ground substance are laid down to form OSTEOID
Undergo calcification to form Woven bone (In fractures that are immobilized like long bone)
In ribs, the mesenchymal cells behave like chondrocytes to form cartilage
Occurs by 10th day
In many fractures, both woven and cartilage are formed – serves to unite the ends
➢ Formation of lamellar bone – Adult bone
Woven bone is removed by osteoclasts – Vascular invasion
Cartilage disintegrates and are invaded by BV & osteoclasts
The provisional Callus is removed, osteoclasts laid down OSTEOID
Calcifies to form BONE
Collagen are arranged in orderly lamellar fashion (Haversian system)
➢ Remodeling – involves
Continued osteoclastic removal and osteoblastic laying down of bone
External callus – is slowly removed
Intermediate callus – converted to compact bone with Haversian system
Internal Callus – hallowed out to Marrow cavity
Abnormalities of fracture healing
I. FIBROUS UNION - Mesenchymal cells diff. to fibroblasts rather than osteoblasts
Common when there is free movement of fracture
II. MALUNION – Angulation/shortening
III. NON-UNION – interposition of soft parts into the fracture, preventing haematoma formation
IV. DELAYED UINON – causes of delade wound healing
Spontaneous Versus Pathological Fractures
Systemic factors affecting wound healing
1)Nutrition → lack of protein and vitamin C, def of Zinc → inhibit collagen synthesis and retard wound healing, def zinc,
2)Administration of glucocorticoids (have anti inflammatory effects while anabolic steroids enhance healing
3)Anaemia (inadequate leukocytes – Neutropenia) – delay wound healing
4)Age and Sex – old age and female sex – slower healing
5)Systemic diseases – DM
