wound repair

Wound Repair
 A thorough understanding of the biology of normal tissue repair is,
therefore, valuable for individuals intending to perform surgery.
 Tissue injury can be caused by pathologic conditions or by traumatic
events.

Wound Repair
CAUSES OF TISSUE DAMAGE
 Traumatic injuries can be caused by physical or chemical insults .

Wound Repair
Epithelialization
 Injured epithelium has a genetically programmed regenerative ability
that allows it to re-establish its integrity through proliferation,
migration, and a process known as contact inhibition.
 Any free edge of normal epithelium continues to migrate (by
proliferation of germinal epithelial cells that advance the free edge
forward) until it comes into contact with another free edge of
epithelium, where it is signaled to stop growing laterally.
 Wounds in which only the surface epithelium is injured ( abrasions)
heal by proliferation of epithelium across the wound bed from the
epithelium contained in rete pegs and adnexal tissues.

Wound Repair
Epithelialization
 Because epithelium does not normally contain blood vessels,
the epithelium in wounds in which the subepithelial tissue is also
damaged proliferates occur across any available vascularized tissue
bed and stays under the portion of the superficial blood clot that
desiccates (forms a scab) until it reaches another epithelial margin.
 Once the wound is fully epithelialized, the scab loosens and
is dislodged.

Wound Repair
Epithelialization
 An example of the rarely detrimental effect of the process of
contact inhibition controlling epithelialization occurs when an
opening is accidentally made into a maxillary sinus during tooth
extraction .
 If the epithelium of both the sinus wall and the oral mucosa is
injured, it begins to proliferate in both areas.
 The first free epithelial edge the sinus epithelium may contact oral
mucosa, thereby creating an oroantral fistula (an epithelialized tract
between the oral cavity and the maxillary sinus).

Wound Repair
Epithelialization
 Malignant epithelial cells have lost their feature of contact inhibition,
showing the value of the contact inhibition process.
 The process of re-epithelialization (secondary epithelialization) in
which an area of oral mucosa is denuded of epithelium (
unattached gingiva) and then left to epithelialize by adjacent
epithelium ( attached gingiva) creeping over the wound bed.

Wound Repair
Stages of Wound Healing
(1) Inflammatory stage .
(2) Fibroplastic stage .
(3) Remodeling stage .
Inflammatory stage.
 Begins immediately at the moment of tissue injury occurs and, in the
absence of factors that prolong inflammation, lasts 3 to 5 days.

Wound Repair
Inflammatory stage.
 Inflammatory stage has two phases: -
(1) Vascular phase.
(2) Cellular phase .
(1)Vascular phase.
 Vasoconstriction of disrupted vessels as a result of normal vascular
tone.
 The vasoconstriction slows blood flow into the area of injury,
promoting blood coagulation.
 After few minutes, histamine and prostaglandins E1 and E2,
elaborated by white blood cells, cause vasodilation and open small
spaces between endothelial cells, which allows plasma to leak and
leukocytes to migrate into interstitial tissues.

Wound Repair
Inflammatory stage.
(1)Vascular phase.
 Fibrin from the transudated plasma causes lymphatic obstruction,
and the transudated plasma— aided by obstructed lymphatic
vessels—accumulates in the area of injury, functioning to dilute
contaminants.
 This fluid collection is called edema .

Wound Repair
Inflammatory stage.
(1)Vascular phase (conclusion )
 Initial vasoconstriction.
 Vasodilatation (histamine and prostaglandins E1,E2)
 Migration of plasma and leukocytes to the interstitial tissue.
 Plasma accumulate at site of injury after fibrin block lymphatic flow.
 Fluid collection in the interstitial tissue is called.. edema

Wound Repair
Inflammatory stage.
(1)Vascular phase.
Cardinal signs of inflammation:-
 Redness (erythema): due to vasodilation
 Swelling (edema): due to transudation of fluid
 Pain: due to histamines, prostaglandins+edema
 Warmth: due to vasodilation
 Loss of function: due to histamines, prostaglandins+
edema

Wound Repair
Inflammatory stage.
(2) Cellular phase. of inflammation is triggered by the activation of
serum complement by tissue trauma.
 Complement-split products, particularly C3a and C5a, act as
chemotactic factors and cause polymorphonuclear leukocytes
(neutrophils) to stick to the side of blood vessels (margination) and
then migrate through the vessel walls (diapedesis).
 C3a and C5a
 Small cleavage fragments released by complement activation, are
potent mediators of inflammation.
 They are anaphylatoxins and act as cell activators with nanomolar
affinity, exerting their functions through binding to specific receptors.

 Neuotrophils release lysosomal enzymes to destroy bacteria, and
digest necrotic tissue.
 Clearance of debris is also aided by monocytes such as macrophages,
which phagocytize foreign and necrotic materials.
 With time, lymphocytes accumulate at the site of tissue injury.

Wound Repair
Inflammatory stage.
lag phase
 The inflammatory stage is sometimes referred to as the lag phase,
because this is the period during which no significant gain in
wound strength occurs (Due to little amount of collagen deposition ).
 The principal material holding a wound together during the
inflammatory stage is fibrin, which possesses little tensile strength .
Inflammatory (lag) stage of wound repair.
o Wound fills with clotted blood, inflammatory cells, and
plasma.
o Adjacent epithelium begins to migrate into wound .
o Undifferentiated mesenchymal cells begin to
transform into fibroblasts.

Wound Repair
Fibroplastic stage.
 Lasts for 2-3 weeks
 Strands of fibrin, which are derived from blood coagulation,
crisscross wounds forming a latticework on which fibroblasts begin
laying down ground substance and tropocollagen.
 The ground substance consists of several mucopolysaccharides,
which act to cement collagen fibers together.
 Fibroblasts secrete fibronectin protein .
Fibronectin functions.
 Helps stabilize fibrin .
 Assists in recognizing foreign material that should be removed by the
immune system .
 Acts as a chemotactic factor for fibroblasts .

Wound Repair
Fibroplastic stage.
 Fibrin network is also used by new capillaries, which bud from
existing vessels along the margins of the wound and run along fibrin
strands to cross the wound.
 Fibrinolysis occurs, which is caused by plasmin brought in by the new
capillaries to remove the fibrin strands that have become superfluous
 Fibroblasts deposit tropocollagen, which
produce collagen.
 Collagen is produced in excessive amounts
and is laid down in a haphazard manner.
 Despite the poor organization of collagen,
wound strength rapidly increases during the
fibroplastic stage, which normally lasts 2 to 3
weeks.

Wound Repair
Fibroplastic stage.
 If a wound is placed under tension at the beginning of fibroplasia, it
tends to pull apart along the initial line of injury.
 If the wound is placed under tension near the end of fibroplasia, it
would open along the junction between old collagen previously on
the edges of the wound and newly deposited collagen.
 Wound at the end of the fibroplastic stage will be:-
 Stiff due to an excessive amount of collagen .
 Erythematous due to high degree of vascularization.
 Able to withstand 70% to 80% as much tension as
uninjured tissue .

Wound Repair
Remodeling stage.
(wound maturation , wound contraction)
 Final stage of wound repair .
 During this stage, many of the previous randomly laid collagen fibers
are destroyed as they are replaced by new collagen fibers, which are
oriented to better resist tensile forces on the wound.
 Wound strength increases slowly, but not with the same magnitude
of increase seen during the fibroplastic stage.
Remodeling stage of wound repair.
• Epithelial stratification is restored .
• Collagen is remodeled into more efficiently organized patterns .
• Fibroblasts slowly disappear, and vascular integrity is re-
established.

Wound Repair
Remodeling stage.
 Wound strength never reaches more than 80% to 85% of the
strength of uninjured tissue.
 As wound metabolism lessens, vascularity is decreased, which
diminishes wound erythema.
 Elastin found in normal skin and ligaments is not replaced
during wound healing, so injuries in those tissues cause a loss of
flexibility along the scarred area

Wound Repair
Remodeling stage.
wound contraction.
- A final process, which begins near the end of
fibroplasia and continues during the early portion of remodeling .
- During wound contraction, the edges of a wound
migrate toward each other .
- -In a wound in which the edges are not or will
not be placed in apposition, wound contraction
diminishes the size of the wound.

Wound Repair
Remodeling stage.
wound contraction
 Contraction can cause problems such as :-
 Deforming and debilitating contractures if
wounds are not covered with skin grafts and
aggressive physical therapy is not performed.
 Sharply curved lacerations, who frequently
are left with a mound of tissue on the concave
side of the scar because of wound contraction
 Contraction can be lessened by placement of
a layer of epithelium between the free edges
of a wound.

Wound Repair
SURGICAL SIGNIFICANCE OF WOUND HEALING CONCEPTS
Adherence to surgical principles facilitates optimal wound healing :-
 Re-establishment of tissue continuity .
 Minimization of scar size .
 Restoration of function.
No wound in skin, oral mucosa, or muscle heals without scar
formation.
 The surgeon’s goal with respect to scar formation is not to prevent a
scar but, rather, to produce a scar that minimizes any compromise of
function and looks as inconspicuous as possible.

Wound Repair
Factors That Impair Wound Healing
(1) Foreign material .
(2) Necrotic tissue .
(3) Ischemia .
(4) wound tension.

Wound Repair
1)-Foreign material.
Is everything the host organism’s immune
system views as “non-self,” as bacteria, dirt, suture material.
Basic problems of foreign materials :-
A. Bacteria can proliferate and cause an infection which destroy
tissue.
B. Nonbacterial foreign material acts as a haven for bacteria by
sheltering them from host defenses and thus promoting infection.
C. Foreign material is often antigenic and can stimulate a chronic
inflammatory reaction that decreases fibroplasia.

Wound Repair
2)- Necrotic tissue.
A. Its presence serves as a barrier to the ingrowth of reparative cells.
(prolonging the inflammatory stage ) .
B. Necrotic tissue serves as a protected niche for bacteria.
 Necrotic tissue frequently includes blood collects which is an
excellent nutrient source for bacteria.

Wound Repair
3)- Ischemia.
Decreased blood supply can lead to :-
A. Tissue necrosis .
B. Lessen the delivery to a wound of antibodies, white blood cells, and
antibiotics, which thereby increases the chances of wound infection.
C. Decreases the delivery of oxygen and the nutrients necessary for
proper healing.
 Ischemia can be caused by :-
 Tight or incorrectly located sutures .
 Improperly designed flaps .
 excessive external or internal pressure on a wound .

Wound Repair
4)- Wound tension.
 Tension in this case is anything tending to hold wound edges apart.
 If sutures are pulling tissues together forcefully, producing ischemia.
 If sutures are removed too early , wound under tension will probably
reopen and excessive wound scar formation and contraction appear
 If sutures are left in too long in an attempt to overcome wound
tension, the sutures ran will epithelialize, leaving permanent,
disfiguring marks.

Wound Repair
Types of Healing
 Healing occur by Primary, Secondary, and Tertiary Intention .
primary intention .
-The edges of a wound in which there is no tissue
loss are placed and stabilized in essentially the same anatomic
position they held before injury and are allowed to heal.
 Wound repair occurs with minimal scar tissue because the tissues
would not “perceive” that an injury had occurred.
 This method of wound repair lessens the amount of re-
epithelialization, collagen deposition, contraction, and remodeling
needed for healing.

Wound Repair
Types of Healing
Primary intention .
 Healing occurs more rapidly, with a lower risk of infection, and
with less scar formation than in wounds allowed to heal by secondary
intention.

Wound Repair
Types of Healing
Secondary intention
- Gap is left between the edges of wound . ( due to tissue loss )
 These situations require a large amount of epithelial migration,
collagen deposition, contraction, and remodeling during healing.
 Healing is slower and produces more scar tissue .
Examples of wounds that heal by secondary intention include :-
• extraction sockets .
• poorly reduced fractures .
• deep ulcers .
• Large avulsive injuries
of any soft tissue.

Wound Repair
Types of Healing
Tertiary intention:
 The healing of wounds through the use of tissue grafts to cover large
wounds and bridge the gap between wound edges.

Wound Repair
Healing of Extraction Sockets
 Removal of a tooth initiates the same sequence of inflammation,
epithelialization, fibroplasia, and remodeling seen in skin or mucosal
wounds.
 Sockets heal by secondary intention .
 Months must pass before a socket heals to the degree to which it
becomes difficult to distinguish from the surrounding bone when
viewed radiographically .
 The socket fills with blood, which coagulates and seals the socket
from the oral environment.
 Inflammatory stage occurs during the first week of healing.
 White blood cells enter the socket to remove contaminating bacteria
and begin to break down any debris such as bone fragments that are
left in the socket.
 Fibroplasia with ingrowth of fibroblasts and capillaries.
 Osteoclasts accumulate along the crestal bone during the first week
of healing .

Wound Repair
 The second week is marked by the large amount of granulation
tissue that fills the socket.
 Osteoid deposition has begun along the alveolar bone lining the
socket.
 During the third and fourth weeks of healing, epithelialization of
most sockets complete at this time.
 The cortical bone resorbed from the crest and walls of the socket,
and new trabecular bone is laid down across the socket.

Wound Repair
 4 to 6 months after extraction is the cortical bone lining a socket
usually fully resorbed .
 This is recognized radiographically by a loss of a distinct lamina dura.
 Bone fills the socket, the epithelium moves toward the crest and
eventually becomes level with adjacent crestal gingiva.
 Only visible remnant of the socket after 1 year is the rim of fibrous
(scar) tissue that remains on the edentulous alveolar ridge.

wound repair

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