Wound healing involves two main processes - regeneration and repair. Regeneration replaces lost tissue with identical cells while repair replaces tissue with fibrous scar tissue. There are several stages of wound healing including inflammation, demolition of dead tissue, and granulation tissue formation. Factors that can influence wound healing include location of the wound, vascular supply, infection, nutrition, and medications. Potential complications are infection, abnormal scarring, excessive contraction that causes deformity, and delayed or non-healing of fractures.

1. Wound Healing

2. • learning objectives:
• Describe the process of healing
• Specify the patterns of wound healing
• Factors influencing wound healing
• Discuss complication of wound healing
• Understand fracture healing

3. Definition:
• healing-bodies replacement of destroyed
tissue by living tissue
process of healing
• two processes:
-regeneration-by similar tissue
-repair (scar)-by connective tissue (fibrosis)

4. • tissue damage inflammation removal of
dead tissue and injurious agent replacement
by: fibrous tissue (scaring) or specialized
tissue (regeneration) healing
• healing by regeneration or repair is
determined partly by:
– the type of cell or
– destruction or intactness of stromal frame
work of the organ.

5. types of cells:
• a .labile cells-have continuous turnover
• excellent replicative capacity e.g. skin, mucosal
cells
• b. stable cells-lower level of replication and few
stem cells.
• undergo division following injury
e.g. smooth muscle cells, fibroblasts, osteoblasts,
endothelial cells , hepatocytes
• good replicative capacity
• c. permanent cells-non dividing cells
e.g.- neurons, striated muscle cells, cells of lens

6. • regeneration ( generare -bring to life)-
renewal of lost tissue in which the lost cells
are replaced by identical ones.
• regeneration involves two processes:
1. proliferation of surviving cells
2. migration of surviving cells

7. • the capacity of a tissue for regeneration
depends on:
1. proliferative ability
2. the degree of damage to stromal
framework
3. type and severity of damage
• NB: labile and stable cells proliferate
provided that framework intact.

8. • Repair (healing by connective tissue)
• repair-orderly process in which lost tissue is
replaced by scar (fibrosis).
• tissues with permanent cells and extensive
stromal injury heal by scar.
• begin with granulation tissue formation

10. • granulation tissue-is characterized by
proliferation of fibroblasts and in growth of
blood vessels in to the area of injury with
number of inflammatory cells.
• in granulation tissue formation there are 3
phases:
1. phase of inflammation-exudation
2. phase of demolition-digesting or
removing necrotic tissue
3. granulation tissue ingrowth

11. • fibroblasts-produce extra cellular matrix e.g.
fibronectine, proteoglycans, collagen(type1-
type 4)
• type 1 collagen is the major collagen of mature
scar tissue
• -it provides tensile strength of the matrix in a
scar.
• the tensile strength of the wound continuous to
increase many months after the collagen
content has reached a maximum.

12. Repair by CT(fibrosis)
• Occurs following tissue destruction with
damage to both parenchymal cells and
stromal framework.

13. Repair by CT(fibrosis)
Four components :
1.Formation of new blood
vessels(angiogenesis)
2.Migration and proliferation of fibroblasts.
3.Deposition of ECM
4.Maturation and organization of the fibrous
tissue ( remodeling ).

14. Angiogenesis
• Preexisting vessels send out capillary buds or sprouts to
produce new vessels.
Steps :
• Proteolytic degradation of the BM of the parent vessel to
allow formation of capillary sprout and subsequent cell
migration.
• Migration of endothelial cells toward the angiogenic
stimulus.
• Proliferation of endothelial cells, just behind the leading
part of migrating cells.
• Maturation of endothelial cells - inhibition of growth and
remodeling into capillary tubes.
• Recruitment of periendothelial cells i.e. pericytes and
smooth muscle cells.

17. Fibrosis
• Occurs within the granulation tissue frame
work of new b/d vessels and loose ECM.
Two processes
• Emigration and proliferation of fibroblasts
in the site of injury.
• Deposition of ECM.

18. wound healing
• wounds can be-accidental or surgical
(intentional)
• to demonstrate the two basic processes (i.e.
regeneration & repair) we see skin wound
healing
• i.e. healing of the epidermis (regeneration)
& healing of the dermis

19. two patterns of wound healing
based on the amount of tissue damage:
1.healing by first intention(10 union))
2.healing by second intention(20 union)

20. 1. healing by 10 union
• wound edges are approximated by surgical
sutures and healing occurs with minimal
tissue loss.
• the 1st step is formation of scab-dehydrated
clotted blood containing fibrin & blood
cells.
• with in 24hours basal cells mitotic
activity thickened at the cut edge

21. • by day 3 there will be granulation tissue
formation
• 2nd week leukocyte infiltrate, edema and
increased vascularity have largely
disappeared.
• 1st month-scar tissue covered by an intact
epidermis
• NB: dermal appendages lost permanently

23. 2. secondary union
• more extensive cell and tissue loss large
defect e.g.-infarction, ulceration
• Abundant granulation tissue grows in from
the margin to complete the repair.
• the difference with 10 union
– more intense inflammation
– much granulation tissue formation
– there is more wound contraction
– it takes longer time

24. wound contraction
• -mechanical reduction in the size of the
defect to 70-80% of original size.
• it is done by myofibroblasts

26. factors affecting wound healing
• local factors
• systemic factors
local factors:
• type, size and location of the wound
• e.g.-wounds on the face heal fast
• vascular supply
• infection excessive granulation tissue
formation large deforming scar
• movement
• ionizing radiation

27. systemic factors:
• circulatory status
• infection
• metabolic status
• e.g.-poorly controlled DM delayed
wound healing
• DM atherosclerosis, diabetic neuropathy,
so interferes with normal blood supply or
predisposes to injury respectively.
• nutritional deficiencies
-ed protein ed collagen formation

28. • vitamin deficiency
e.g.- vit c decreased collagen synthesis scurvy
• -zinc deficiency decreased cell proliferation
(fibroblasts) ed collagen
• hormones
e.g.- corticosteroids -impair wound healing
-ed collagen synthesis
-anti-inflammatory effect.....
• anti-inflammatory drugs
e.g.- aspirin

29. complications of wound healing
• abnormalities in repair, regeneration and contraction
complication
• 1. infection
• 2. deficient scar formation
• complication- a. wound dehiscence incisional hernias
-b. ulceration
-dehiscence occurs in 0.5-5% of abdominal surgeries
-dehiscence can be due to:-inappropriate surgical
techniques, stress, or infection
Ulceration-defect in the continuity of an epithelial surface
• neuropathic ulcers-in varicose,DM,leprosy,30
syphilis(spinal involvement, tabes dorsalis)

30. • 3. excessive scar formation
• -failure in 'maturation arrest' or block in the
healing process
– keloid-exuberant scar that tends to progress and recur
after excision
• -frequent after burns
• -common on neck &ear lobes.
• hypertrophic scar-structurally similar to keloid
• but never gets worse after 6 months
• doesn't recur

31. Keloid

32. • 4. excessive contraction
• exaggeration of contraction contracture
(cicatrisation)
• results in sever deformity
• palms, soles, and anterior thorax are prone for
contracture (why?)
• follows burn injuries
• it can occur in hollow viscera stricture
• e.g.-urethra, esophagus
• palmar contracture- dupuytren’s contracture

33. fracture healing
• defect is filled by specialized bone forming
tissue ,unlike scar formation
• so bone is restored nearly to normal
bone structure
• bone is composed of calcified osteoid tissue
consists of collagen fibers embedded in a
mucoprotein matrix (osteomucin)

35. • based on arrangement of collagen fibers
there are two histologic types:
1. woven, immature or non-lamellar bone
-collagen bundles arranged irregularly
-less abundant osteomucin, less
calcium
2. lamellar or adult bone
-collagen bundles arranged in parallel
sheets

36. • stages in fracture healing (bone regeneration)
• stage 1-hematoma formation
• stage 2-inflammation
• - hematoma attain a fusiform shape
• stage 3-demolition
• -macrophages remove clot, fibrin, red
cells, exudate & debris
• -fragments of bones by osteoclasts
• stage 4-formation of granulation tissue
• -neovascularization, osteogenesis

37. • stage 5-woven bone& cartilage formation
- osteoblasts- produce both woven
bone and cartilage
-callus formation, initially soft but will
be hardened

38. • stage 6-formation of lamellar bone
-provisional callus removed, osteoid
formed and calcified bone
• -collagen fibers arranged in lamellar fashion
concentrically around blood vessels
haversian system formed definitive
lamellar bone merges with the last stage

39. • stage 7-remodeling
-osteoclastic removal &
osteoblastic lay down of bone material
• -external callus removed

40. Complications:
• Delayed healing
• Non healing
• Joint involvement - ankylosis
• Abnormal position – arthritis.
• Involucrum formation.
• Pseudoarthrosis