Font size
WorksheetsWound Healing Pt.III
Total questions: 25
Worksheet time: 14mins
Phases of Wound Healing
Inflammatory phase
Proliferative phase
Maturation Phase
- After initial wounding, the blood vessels in the wound bed contract and a clot is formed.
Clot formation
Early Inflammation
Late inflammation
are small soluble molecules that bind to receptors on leukocytes causing their granulation tissue.
(a)
a mass formed by a network of fibrin threads.
(a)
- Characterized by production of polymorphonuclear neutrophils
- Begin to enter the wound site within six hours of clot stabilization
- The main role of PMNs is wound decontamination by phagocytosis by phagocytosis of bacteria
Clot formation
Early Inflammation
Late inflammation
- Presence of macrophages
- Reaches peak concentration by approximately third or fourth day
- They remain in wound until healing is completed
Clot formation
Early Inflammation
Late inflammation
- The wound is „rebuilt‟ with new granulation tissue
- Granulation tissue
- fragile structure composed of an extracellular matrix of fibrin, fibronectin, glycosaminoglycans, proliferating endothelial cells, new capillaries, and fibroblasts mixed with inflammatory macrophages and lymphocytes.
- Healthy granulation tissue is granular and uneven in texture; it does not bleed easily and is pink/red in color.
- Dark granulation tissue can be indicative of poor perfusion, ischaemia and / or infection.
Inflammatory phase
Proliferative phase
Maturation Phase
- Fibroblasts migrate into the wound site on the 3rd
day after injury and achieve their peak numbers
by approximately 7th day.
- As the number of macrophages declines and
fibroblasts population increases, the wound
transforms from granulomatous tissue to
- granulation tissue.
- Fibroblasts produce type Ill collagen initially and
as the wound matures type I collagen is formed.
Fibroblasts: Fibroplasia
Endothelial cells: Angiogenesis
Osteoblast: Osteogenesis
Cementoblasts: Cementogenesis
- Formation of new blood vessels at the site of injury takes place by proliferation of endothelial cells from the margins of severed blood vessels.
- The newly formed blood vessels are more leaky accounting for the more edematous appearance of new granulation tissue.
Fibroblasts: Fibroplasia
Endothelial cells: Angiogenesis
Osteoblast: Osteogenesis
Cementoblasts: Cementogenesis
- Begins 5 to 7 days after injury.
- There is conversion of granulation tissue to fibrous connective tissue and decrease parallelism of collagen to the plane of the wound.
- Maturation of the epithelial layer quickly follows formation of the epithelial seal.
Inflammatory phase
Proliferative phase
Maturation Phase
Scar strength is: in 1 Week
3%
20%
80%
Scar strength is: in 3 Week
3%
20%
80%
Scar strength is: in 12 Week
3%
20%
80%
- Osteoclasts act as an organizational unit to debride necrotic bone from the wound margin similarly as macrophages remove tissue debris from the clot.
- New bone formation is apparent about 6 days after surgery.
- Bone formation is categorized into two types
Fibroblasts: Fibroplasia
Endothelial cells: Angiogenesis
Osteoblast: Osteogenesis
Cementoblasts: Cementogenesis
- Begins 10 to 12 days after root end resection.
- The exact sequence leading to the formation of new cementum remains unidentified.
- Cementum covers the resected root end approximately 28 days.
Fibroblasts: Fibroplasia
Endothelial cells: Angiogenesis
Osteoblast: Osteogenesis
Cementoblasts: Cementogenesis
- Begins 10 to 12 days after root end resection.
- The exact sequence leading to the formation of new cementum remains unidentified.
- Cementum covers the resected root end approximately 28 days.
Fibroblasts: Fibroplasia
Endothelial cells: Angiogenesis
Osteoblast: Osteogenesis
Cementoblasts: Cementogenesis
The following are local factors except:
Infection,
Presence of necrotic tissue and foreign body, Poor blood supply
Venous or Lymph stasis,
Tissue tension,
Hematoma
Age, obesity, smoking
Vitamin deficiency,
Anemia
Large defect or poor apposition,
Recurrent trauma,
X-ray iradiated area
Bone formaton is categorized into two types and this type
- Woven bone formation
- Osteoblasts produce matrix vesicles through exocytosis of their plasma membrane.
- It begins with the deposition and growth of hydroxyapatite crystals in the pore regions.
- The crystals amalgamate to form spherulites whose union results in mineralization.
Matrix vesicle-based process
Osteoid secretion
Bone formaton is categorized into two types and this type
- Lamellar bone formation
- Osteoblasts secrete an organic matrix composed of longitudinally arranged collagen matrix fibrils.
- Mineralization occurs by mineral deposition directly along the collagen fibrils.
- The osseous defect is filled with bone tissue by 16 weeks after surgery.
Matrix vesicle-based process
Osteoid secretion
partial or total separation of the edges of the wounds
in short reopening of the wound
can be accidental or intentional
ex: when surgical sutures get infected the physician may need to surgically reopen the wound. It can also happen accidentally when the wound has not fully healed and reopened due to excessive movement or pressure near or on the site of the wound
Wound Dehiscence
Ulceration
hypertrophic scar
keloid
- these are open sores caused by poor blood circulation
- poor blood circulation can cause the wound not to heal properly making minors wounds that would normally heal quickly to not heal or heal longer which can lead the wound to develop into ulcers
ex: patients with diabetes have high glucose levels that damage the blood vessels and result in the poor blood circulation in the body and this causes wounds not to heal or heal longer than expected because the nutrients needed for the wound to heal is not delivered.
Wound Dehiscence
Ulceration
hypertrophic scar
keloid
- thicked raised scar
- contained within the site of injury
- occurs commonly in taut skin areas following skin trauma, burns or surgical incisions
- often regress completely with time
Wound Dehiscence
Ulceration
hypertrophic scar
keloid
- also known as overgranulation or proud flesh
- wounds cannot heal with hypergranulation because it limits the ability of epithelial cells to migrate across the wound bed
- it appears light red or dark pink, smooth, bumpy tissue form and it is moist, soft to touch and may bleed easily
- occurs when granulation tissue during the proliferative phase grows beyond the wound surface due to excessive moisture, friction and/or pressure
Hypergranulation tissue
Demoids
Formation of contractures
- Also known as aggressive fibromatosis
- a rare type of fibrous tumor with low-grade malignancy and high potential of recurrence
- caused by trauma, hormonal factors (estrogen) or may have a genetic associations (familial adenomatous polyposis & garner's syndrome
- can occur anywhere in the body
- It is formed when connective tissue cells develop changes in its DNA. These changes cause the ct cell to multiply rapidly, creating a mass of cell (tumor).
Hypergranulation tissue
Desmoids
Formation of contractures
- develops when normally stretchy (elastic) tissues are replaced by non-stretchy (inelastic) fiber-like tissue.
- fixed tightening of muscles, tendons, ligaments, or skin
- injury to and around a joint causes inflammation, which can lead to different structures sticking to each other, resulting in stiffness and limited motion
Hypergranulation tissue
Desmoids
Formation of contractures
