Professional Documents
Culture Documents
Wound Repair
Vergel John P. Ercia DDM
Mechanical
1.Abraded wound
2.Punctured wound
3.Incised wound
4.Cut wound
5.Crushed wound
6.Torn wound
7.Bite wound
8.Shot wound
Chemical
Acid & base
Radiation
Thermal
Burning & freezing
Special
Toxins & venoms
Abrasions. They occur when the skin is rubbed away by friction against
another rough surface (e.g. rope burns and skinned knees).
Avulsions. Occur when an entire structure or part of it is forcibly pulled
away, such as the loss of a permanent tooth or an ear lobe. Explosions,
gunshots, and animal bites may cause avulsions.
Contusions. Also calledbruises, these are the result of a forceful trauma
that injures an internal structure without breaking the skin. Blows to the
chest, abdomen, or head with a blunt instrument (e.g. a football or a fist)
can cause contusions.
Crush wounds. Occur when a heavy object falls onto a person, splitting
the skin and shattering or tearing underlying structures.
Cuts. Slicing wounds made with a sharp instrument, leaving even edges.
They may be as minimal as a paper cut or as significant as a surgical
incision.
Lacerations. Also called tears, these are separating wounds that produce
ragged edges. They are produced by a tremendous force against the body,
either from an internal source as inchildbirth, or from an external source
like a punch.
Missile wounds. Also called velocity wounds, they are caused by an object
entering the body at a high speed, typically a bullet.
Punctures. Deep, narrow wounds produced by sharp objects such as nails,
knives, and broken glass.
Contusions
Punctures
Avulsions
Crushed wound
Burns
Superficial
Partial thickness
Full thickness
Deep wound
Phases of Healing
Inflammatory (Reactive)
Haemostasis Inflammation
Proliferative (Regenerative/Reparative)
Epithelial migration
proliferation
Maturational (Remodeling)
Contraction
scarring
Remodeling
Maturation
Phase
Proliferative Phase
Remodeling Phase
Inflammatory Phase
Hemostasis and Inflammation
Days 4 - 6
Exposed collagen activates clotting cascade
and inflammatory phase
Fibrin clot = scaffolding and concentrate
cytokines and growth factors
Inflammatory Phase
Granulocytes
First 48 hours
Attracted by inflammatory mediators
Oxygen-derived free radicals
Non-specific
Inflammatory Phase
Macrophages
Monocytes
attracted to area by complement
Activated by:
fibrin
foreign body material
exposure to hypoxic and acidotic
environment
Reached maximum after 24 hours
Remain for weeks
Inflammatory Phase
Macrophages
Activated Macrophage:
Essential for progression onto
Proliferative Phase
Mediate:
Angiogenesis: FGF, PDGF, TGFa&b and TNF-a
Fibroplasia: ILs, EGF and TNF
Synthesize NO
Secrete collagenases
Proliferative Phase
Epithelization, Angiogenesis and
Provisional Matrix Formation
Begins when wound is covered by
epithelium
Day 4 through 14
Production of collagen is hallmark
7 days to 6 weeks
Epithelialization
Basal epithelial
cells at the wound
margin flatten
(mobilize) and
migrate into the
open wound
Basal cells at
margin multiply
(mitosis) in
horizontal direction
Basal cells behind
margin undergo
vertical growth
Proliferative Phase
Fibroblast
Work horse of wound repair
Produce Granulation Tissue:
Main signals are PDGF and EGF
Collagen type III
Glycosaminoglycans
Fibronectin
Elastin fibers
Tissue fibroblasts become myofibroblasts
induced by TGF-b1
Wound Contraction
Actual contraction with pulling of edges
toward center making wounds smaller
Myofibroblast: contractile properties
Surrounding skin stretched, thinned
Original dermal thickness maintained
No hair follicles, sweat glands
CONTRACTION OF WOUND
wound starts contracting after 2-3 days and the
process is completed by 14th day. During this period
the wound is reduced by approximately 80% of its
original size.
Factors responsible for wound contraction:
1. Dehydration due to removal of fluids by drying.
2. Contraction of collagen
3. Discovery of myofibroblasts.
Maturation Phase
REPAIR OF WOUND
GRANULATION TISSUE
OR
ANGIOGENESIS ( NEOVASCULARISATION)
Formation of new blood vessels at the site of injury takes
place by proliferation of endothelial cells from the margins
of severed blood vessels.
Newly formed blood vessels are more leaky accounting for
the more edematous appearance of new granulation tissue.
Blood vessels differentiate into muscular arterioles, thinwalled venules and true capillaries.
Angiogenesis takes place under the influence of :
1. Vascular endotheial growth factor
2. Platelet derived growth factor
3. Transforming growth factor-
4. Fibroblast growth factor
FIBROGENESIS
Newly formed blood vessels are present in an
amorphous ground substance .The new fibroblasts
originate from the fibrocytes as well as by mitotic division
of fibroblasts.
Fibroblast has functional and structural similarities to
smooth muscles cell called as myofibroblast.
Collagen fibrils appear by about 6th day. As maturation
proceeds, more and more of collagen is formed the
number of active fibroblasts and the number of new
blood vessels decreases.
This result in the formation of inactive looking scare
known as cicatrisation.
PRIMARY HEALING
PRIMARY
SECONDARY
CLEANLINESS
CLAEN
NOT CLEAN
INFECTION
NOT INFECTED
INFECTED
MARGINS
SURGICALLY CLEAN
IRREGULAR
SUTURES
USEAD
NOT USED
HEALING
SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME
LINEAR SCAR
IRREGULAR WOUND
COMPICATION
NOT FRQUENT
FREQUENT
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Steps
Immediately after the removal of the tooth from
the socket, blood fills the extraction site.
Both intrinsic and extrinsic pathways of the
clotting cascade are activated.
The resultant fibrin meshwork containing
entrapped red blood cells seals off the torn
blood vessels and reduces the size of the
extraction wound.
Organization of the clot begins within the first 24
to 48 hours with engorgement and dilation of
blood vessels within the periodontal ligament
remnants, followed by leukocytic migration and
formation of a fibrin layer.
1 week
st
2nd Week
Clot continues to get organized
through fibroplasia and new blood
vessels that begin to penetrate
towards the center of the clot.
Trabeculae of osteoid slowly extend
into the clot from the alveolus, and
osteoclastic resorption of the cortical
margin of the alveolar socket is more
distinct.
3 Week
rd
Local factors
Systemic factors
INFECTION
NUTRITIONAL FACTORS
IMMOBILISATION
SYSTEMIC INFECTION
PHYSICAL FACTORS
ADMINISTRATION OF
GLUCOCORTICOIDS
UNCONTROLLED DIABETES
IMMOBILISATION:
If the wound is an area which is subjected to constant movement so
that formation of new connective tissue is continuously distrupted
(e.g.: corner of the mouth) , it will result in delayed wound healing.
PHYSICAL FACTORS:
severe trauma to tissues is obviously a determinant in rapid wound
healing.
SYSTEMIC FACTORS
NUTRITIONAL FACTORS:
Delay in the healing of wounds may occur in a person
who is deficient in variety of essential foods such as
proteins, vitamins,
especially vitamin A, D and B
complex.
AGE OF THE PATIENT:
Wounds in younger persons heals more rapidly than
wounds In elderly persons and the rate of wound healing
appears to be in inverse proportion to the age of the
patient.
SYSTEMIC INFECTION
Delays healing of wound.
ADMINISTRATION OF GLUCOCORTICOIDS
anti-inflammatory effect thus delays wound healing.
UNCONTROLLED DIABETES
Diabetics are more prone to develop infections thus
delayed wound healing takes place.
HAEMATOLOGIC ABNORMALITIES
There is delayed wound healing
After the extraction, the blood which fills the socket coagulates, red
blood cells being entrapped in the fibrin meshwork.
The resultant fibrin meshwork containing entrapped red blood cells
seals off the torn blood vessels and reduces the size of the
extraction of wound.
Within the first 24-48 hours after extraction there are alterations in
the vascular bed.
There is vasodilation and engorgement of blood vessels in the
remnants of the periodontal ligament and the mobilization of
leucocytes to the immediate area around the wound.
COMPLICATION OF HEALING OF
EXTRACTON WOUND
DRY SOCKET
FIBROUS UNION
DRY SOCKET
most common and painful complication in the healing of
human extraction wound is alveolar osteitis or dry socket.
a focal in which the blood clot has disintegrated or been lost.
condition is extremely painful without suppuration and the
presence of foul odor.
DRY SOCKET
When the edges of the wound are brought into contact and
held in place by sutures, the blood clots.
In a matter of hours numerous leucocyes are mobilized to
the area.
Connective tissue cells in the immediate vicinity undergo
transformation into fibroblasts , which in turn undergo mitotic
division, and the new fibroblasts begin to migrate into the
line of incision. These cells form thin collagen fibrils which
coalesce in general direction parallel to the surface of the
wound.
PRIMARY
HEALING OF
BIOPSY WOUND
Pictures 1-6 shows the
biopsy of the labial mucosa
and the wound is
approximated with the
sutures.
In this case the healing
occurs by primary
intension.
SECONDARY
WOUND
HEALING
OF
BIOPSY
STEPS IN
WOUND
HEALING
OF
GINGIVECTOMY
HEALING OF FRACTURE
IMMEDIATE EFFECTS OF FRACTURE
When fracture of a bone occurs, the haversian vessels of
the bone are torn at the fracture site along with the vessels
of the periosteum and the marrow cavity. This evokes acute
inflammation in the soft tissue adjacent to the fracture line.
Because of the disruption of the vessels, there is
considerable amount of blood in this general area and at the
same time there is loss of circulation and blood supply.
Reactive phase
Soon after fracture the blood vessels constrict,
stopping any further bleeding.
Within a few hours after fracture, the extravascular
blood cells forms a blood clot called as Hematoma.
All of the cells within the blood clot degenerate and
die.
Some of the cells adjacent to the fracture site also
die, but fibroblast survive and replicate forming a
loose aggregates of cells interspersed with small
blood vessels known as Granulation tissue.
Reparative phase
Days after fracture, the cells of the periosteum
replicates.
Periosteal cells proximal (close) to the fracture gap
develops into chondroblasts which forms hyaline
cartilage.
Periosteal cells distal (far away ) from the fracture
gap develops into osteoblasts which forms woven
bone.
Fibroblast with in the granulation tissue develops in to
chondroblasts which also forms hyaline cartilage.
Remodelling phase
the trabecular bone is replaced by
compact bone.
takes 3-5 yrs depending on factors like
type of fracture, age of patient, or general
condition of patients.
OSSEOINTEGRATION OF IMPLANTS
Osseointegration is a direct structural and functional
connection between ordered living bone and the surface
of the load carrying implant.
Factors that determine the outcome of the implant
treatment depend on the biocompatibility of the implants,
status of the host tissue, surgical technique, and the
loading condition.
After the implant insertion, a period of 10-12 weeks of
healing is required.
OSSEOINTEGRATION OF IMPLANT
CICATRIZATION
Cicatrization refers to late reduction in the size
of the scar in contrast to immediate wound
contraction. It a complication due to burns on the
skin.
IMPLANTATION CYSTS
Epithelial cysts may slide and get entrapped in
the wound and later may proliferate to form
implantation cysts.