You are on page 1of 100

Nasaktan ka na ba?

Gaano kalalim at katagal bago


gumaling ang sugat???

Wound Repair
Vergel John P. Ercia DDM

Etiology of tissue damage based on


origin

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

Etiology of tissue damage based on


contamination
1. Clean wound
2. Clean & contaminated wound
3. Contaminated wound

Etiology of tissue damage based on


the depth
Superficial wound = only epidermis
1. Partial thickness wound = epidermis
+ dermis.
2. Full thickness wound= epidermis +
dermis +
subcutaneous fats
3. Deep wound = epidermis + dermis
+
subcutaneous fats + exposed
muscles, bone connective tissue,

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

Three Phases of Wound


Healing
Inflammatory

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

Three Phases of Wound Healing


Inflammatory Phase
Proliferative Phase
Remodeling Phase

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.

Three Phases of Wound Healing


Inflammatory Phase
Proliferative Phase
Remodeling Phase

Maturation Phase

Random to organized fibrils


Day 8 through years
Type III replaced by type I
Wound may increase in
strength for up to 2 years
after injury
Collagen organization
Cross linking of collagen

REPAIR OF WOUND

GRANULATION TISSUE

Two main processes


a. ANGIOGENESIS
NEUROVASCULARIZATION
b. FIBROGENESIS

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

Vascular endothelial growth factor: elaborated by


mesenchymal cells as the receptors are present
on endothelial cells only.
Platelet derived growth factor, transforming
growth factor- , fibroblast growth factor are all
associated with cellular proliferation.

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.

STEPS AND DURATION OF WOUND HEALING

TYPES OF WOUND HEALING


healing by first intention also called as
primary union/primary intention.
healing by second intention also called as
secondary healing/secondary intention.

HEALING BY PRIMARY INTENTION


clean and uninfected
surgically incised
without much loss of cells and tissue
edges of wound are approximated by
surgical sutures.

Steps in primary wound healing


Initial hemorrhage: Immediately after injury, the space
between the surfaces of incised wound is filled with blood
which soon clots, and prevent further infection.
Acute inflammatory response: occurs within 24 hours of
appearance of polymorphs from the margins of incision.
Epithelial changes: basal cells of epidermis from both cut
margins starts proliferating and migrating towards
incisional space in the form of epithelial spurs. A well
approximated wound is covered by a layer of epithelial cell
in 48 hrs. the migrated epithelial cell separates the necrotic
cells and clot forming a scab which is cast off. The basal
cells countinues to divide. By 5th day new epidermis is
formed.

Organisation :by 3rd day, fibroblasts also invades the


wound area. By 5th day new collagen fibrils start forming
which dominate till healing is completed.
In 4 weeks a scar tissue with scanty cellular and vascular
elements, a few inflammatory cells and epithelialised
surface is formed.
Suture tracks: each suture track is a separate wound and
follows the same steps as in healing of primary wound.
When sutures are removed around 7th day, much of the
epithelialised suture track is avulsed.

PRIMARY HEALING

HEALING BY SECODARY INTENSION

Open with large tissue defects, at times infected


Extensive loss of cells and tissues, and
Wound is not approximated by sutures but is left open.
STEPS IN HEALING OF SECONDARY WOUND
Initial haemorrhage: as a result of injury the wound
space is filled with blood and fibrin clot which dries.
Inflammatory phase: there is initial acute inflammatory
response followed by appearance of macrophages which
clear off the debris.

Epithelial changes : Epidermal cells from both the margins proliferate


and migrate into the wound in the form of spurs till they meet in the
middle and re-epithelialise the gap completely.
Proliferating epithelial cells do not cover the wound completely until the
granulation tissue from the base has started fill the wound space. In this
way the pre-existing viable connective tissue is separated from the
necrotic material and clot on the surface forming the scab, which is cast
off.
Granulation tissue: Main bulk of secondary healing is by granulations.
Granulation tissue is formed by proliferation of fibroblasts and
neovascularisation. The newly formed granulation tissue is deep red,
granular and very fragile. With time, it becomes pale white due to
increased in collagen and decreased blood supply.
Wound contraction: this phase is not seen in primary healing. Due to
the action of myofibroblasts present in granulation tissue, the wound
contracts to one-third of its original size. It occurs during the formation of
active granulation tissue.

SECONDARY WOUND HEALING


(various cells involved)

Difference between primary and


secondary union of wound
FEATURES

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

i
t
e
k
c
o
s
f
o
n
o
e
i
l
n
t
o
p
c
i
a
t
m
r
n
a
t
e
x
x
t
e
e
n
i
d
n
e
d
a
z
n
f
i
l
o
o
a
c
i
g
e
c
n
s
e
i
l
p
y
a
s
b
e a
g
n
i
l
a
e
h

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

Clot forms a temporary scaffold upon which


inflammatory cells migrate.
Epithelium at the wound periphery grows over the
surface of the organizing clot.
Osteoclasts accumulate along the alveolar bone
crest setting the stage for active crestal resorption.
Angiogenesis proceeds in the remnants of the
periodontal ligaments.

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

Extraction socket is filled with


granulation tissue and poorly
calcified bone forms at the wound
perimeter.
Surface of the wound is completely
re-epithelialized with minimal or no
scar formation.

Active bone remodeling by deposition and


resorption continues for several more weeks.
Radiographic evidence of bone formation does not
become apparent until the sixth to eighth weeks
following tooth extraction.
Due to the ongoing process of bone remodeling the
final healing product of the extraction site may not
be discernible on radiographs after 4 to 6 months.

FACTORS AFFECTING WOUND HEALING

Local factors

Systemic factors

INFECTION

NUTRITIONAL FACTORS

LOCATION OF THE WOUND

AGE OF THE PATIENT

IMMOBILISATION

SYSTEMIC INFECTION

PHYSICAL FACTORS

ADMINISTRATION OF
GLUCOCORTICOIDS
UNCONTROLLED DIABETES

FACTORS AFFECTING WOUND


HEALING
LOCAL FACTORS
INFECTION:
it has been demonstrated that wounds which is completely protected from
bacterial irritation heal considerably more rapidly than wounds which are
exposed to bacteria or other mild physical irritation.
LOCATION OF THE WOUND:
wounds in the area in which there is a good vascular bed heal considerably
more rapidly than the area in which is relatively avascular.

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.

local temperature in the area of wound influences the rate of


healing. Thus, in environment hyperthermia, wound healing is
accelerated while in hypothermia it is delayed.
circulatory factors: anemia has been reported to delay wound
healing. Similarly dehydration also delays 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

HEALING OF EXTACTION WOUND


IMMEDIATE REACTION FOLLOWING EXTRACTION

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.

FIRST WEEK WOUND


Within the first week after tooth extraction, proliferation of
fibroblasts from connective tissue cells in the remnants
of the periodontal ligament is evident, and these
fibroblasts have begun to grow into the clot around the
entire periphery.
Clot forms the scaffold on which the cells associated with
healing process may migrate. It is the temporary
structure.
Epithelium at the periphery of the wound grow over the
surface of the organizing clot.

Osteoclasts accumulate along the alveolar bone


crest setting the stage for active crestal resoption.
Angiogenesis proceeds in the remnants of the
periodontal ligaments.

SECOND WEEK WOUND


During the second week, the blood clot continues to get
organized through fibroplasia and new blood vessels that
penetrate towards the center of the clot.
Trabeculae of the osteoid slowly extend into the clot from
the alveolus, and osteoclastic resoption of the cortical
margin of the alveolar socket is more distinct.
The remnants of the periodontal ligament gradually
undergo degeneration and are no longer recognizable.

THIRD WEEK WOUND


As healing continues into the third week , the original clot
appear completely organized by mature granulation
tissue and poorly calcified bone at the wound perimeter.
The surface of the wound is re-epithelised with minimum
or no scar formation.
Very young trabeculae of osteoid bone forms around the
entire periphery of the wound from the socket wall.

The original cortical bone of the alveolar


socket undergoes remodeling so that it is
no longer consist of such a dense layer.
The crest of the alveolar bone is rounded
off by osteoclastic resoption.

FOURTH WEEK WOUND


During the fourth week the wound begins the final stage
of healing, in which there is continued deposition and
remodeling resorption of he bone filling the alveolar
socket.
Much of this early bone is poorly calcified, as is evident
from its general radiolucency on the radiograph.
Radiographic evidence of bone formation does not
become prominent until the sixth or eighth week after
tooth extraction.

HEALING AFTER EXTRACTION OF TOOTH

immediate reaction after extraction


second week after extraction
third week after extraction
4-six to eight weeks after extraction( complete
healing)

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.

condition derives its name from the fact that


after the clot is lost the socket has a dry
appearance because of the exposed bone.
commonly associated with difficult and traumatic
extractions like the removal of impacted third
molars.
destruction of the clot is caused by the
proteolytic enzymes produced by bacteria or
local fibrinolytic activity.

DRY SOCKET

FIBROUS HEALING OF EXTRACTION WOUND


occurs more frequently when the extraction is accompanied
by the loss of both the buccal and the lingual cortical plates
of bone and the loss of periosteum as well.
On a radiograph the lesion appears as a well circumscribed
radiolucent area in the site of a previous extraction wound .
no certain way of differentiating fibrous healing from the
residual infection like residual cyst or granuloma.
areas of fibrous healing consists of dense bundles of
collagen fibrils with occasional fibrocytes and few blood
vessels. The lesion is a fibrous scar tissue with little or no
evidence of ossification.

HEALING OF THE BIOPSY WOUND


The healing of a biopsy wound of the oral cavity is
identical with the healing of a similar wound in any other
part of the body and thus may be classified as either
primary healing or secondary healing.
PRIMARY HEALING OF BIOPSY WOUND
Primary healing or healing by first intension is that type
of healing which occurs after the excision of a piece of
tissue with the close approximation of the edges of the
wound.

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.

Endothelial cells of the capillaries begin to proliferate,


and small capillary buds grow out and across the wound
which eventually forms new capillaries filled with blood.
When there is close approximation of the edges of the
wound, the surface epithelium proliferates rapidly across
the line of incision and re-establishes the integrity of the
surface.
In due course of time the collagen fibrils coalesce and
contracts so that the biopsy wound appears as a linear
scar which can be depressed below the surface.

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

Healing by second intention or the healing of the open


wound occurs when there is loss of tissue and the edges
of the wound cannot be approximated.
In this type of healing process the wound granulates in
since the material, which fills the defect is the granulation
tissue.
E.g.: removal of a lesion from the palate or large lesion
of alveolar ridge heals by secondary intension since the
edges of the wound cannot be coapted.

Steps in secondary healing of biopsy wound


After the removal of the lesion the blood clot fills the defect
and the healing process begins.
Cellular proliferation begins around the periphery of the
wound.
The fibroblasts and the endothelial cells grow into the clot
along the fibrin strands.

Polymorphonuclear leucocytes, and later lymphocytes , and


mononuclear phagocytes migrate into the granulation tissue
from the adjacent vessels and tissues.
Large number of leucocytes also accumulate on the surface
of the wound.
As the granulation tissue matures, it becomes more fibrous
through condensation of collagen bundles, and the surface of
the granulation tissue becomes epithelised.
collagen fibrils coalesce and the lesion becomes somewhat
less vascular and eventually the evidence of the wound may
be a small depressed area of the mucosa.

Secondary wound healing in a biopsy site on


the palate

HEALING OF GINGIVECTOMY WOUND


EARLY HEALING PHASE
Healing of the gingivectomy wound takes place rapidly
regardless of whether the postoperative pack is used .
Healing of gingivectomy wound is basically similar to
healing of wound elsewhere in the body, but is
somewhat modified by special anatomy of the involved
region.

STEPS IN
WOUND

HEALING

OF

GINGIVECTOMY

Two days after the gingivectomy the surface of the tissue


is covered by a grayish blood clot, and beneath this clot
is histologic evidence of delicate connective tissue
proliferation.
Four days after the operation, the deeper portion of the
blood clot demonstrates considerable organization, while
the superficial portion exhibits dense numbers of
polymorphonuclear leucocytes entrapped in fibrinous
network.

There is proliferation of young capillaries and young


connective tissue cells into the base of the blood
vessels.
Infiltration of polymorphonuclear leucocytes in the
deeper connective tissue is present in varying degrees.
The epithelium has extended over a portion of the wound
below the necrotic surface layer of the clot, but above
the proliferating and organising connective tissue.

LATE HEALING PHASE


Continuation of the healing process is manifested by
condensation of the young connective tissue with nearly
complete organization of the clot after 8-10 days.
Clinically, the wound is red, granular in appearance and
bleeds rapidly.
Epithilization is usually complete within 10-14 days after
gingivectomy.

epithelium remains thin and begins to mature


and form rete pegs only after two week interval.
Healing of the interproximal tissue appears to
lag behind that adjacent to the labial or buccal
surfaces this is because the epithelium must
grow in front from the labial and the lingual
areas, a relatively greater distance.

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.

Three major phase occurs:


1) Reactive phase:
-fracture and inflammation
-granulation tissue formation
2) Reparative phase:
-callus formation
-lamellar bone deposition
3) Remodelling phase:

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.

The two new tissue grow in size until they meet


their counter part from other part of fracture.
This process is called as Callus formation.
Callus in Latin means overgrowth of hard skin.
Composed of varied amounts of fibrous tissue,
cartilage and bone.
The external callus consists of the new tissue
which forms around the outside of two fragments
of bone.
The internal callus is the new tissue arising from
the marrow cavity.

Deposition of lamellar bone by replacing


hyaline cartilage and woven bone.
Replacement process is called
endochondral ossification.
Lamellar bone begins forming soon after
the collagen matrix of either tissue
becomes mineralized.
New bone is formed in the form of
trabecular bone.

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.

STAGES IN HEALING OF FRACTURE

COMPLICATIONS OF FRACTURE HEALING


DELAYED UNION OR NON UNION
This results when the calluses of the osteogenic tissue
over each of the two fragments fail to meet and fuse or
when endosteal formation of bone is inadequate.
FIBROUS UNION
The Fractured ends of fragments are united by fibrous
tissue, but there is failure of ossification.
LACK OF CALCIFICATION
This may occur in unusual circumstances of dietary
deficiency or mineral imbalance which is seldom seen
clinically.

HEALING AFTER REPLANTATION


Following replantation the clot forms between the root
surface and ruptured periodontal ligament.
Proliferation of the fibroblasts and the endothelial cells
occurs in the periodontal ligament remnants on the side
of the alveolar bone.
The reconnection of the periodontal ligament is evident
by the extension of collagen fibers from the cementum to
the alveolar bone.

Epithelium is reattached to the tooth at the end


of the first week.
Complete regeneration of the periodontal
ligament takes place between two to four weeks.
In the course of time, a number of teeth results
in resorption or ankylosis.

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.

During healing, compact and cancellous bone


forms around the implant together with variable
amount of fibrous marrow.
Implants do not have a direct contact with the bone
and a certain amount of bone marrow and soft
tissue are interposed between the bone and the
implant.
implant and the mucosal interface serve the similar
functions as the dentogingival.

connective tissue of the


mucosa forms the intimate
contact with the implant.
collagen fibers of the
connective tissue runs
parallel to the long axis of
the implant, and the
epithelium is attached to
the implant by means of
basal
lamina
and
hemidesmosomes.

OSSEOINTEGRATION OF IMPLANT

COMPLICATIONS OF WOUND HEALING


INFECTION
Wounds may provide a portal of entry to
microorganisms. Infections of the wound delay the
healing process. Systemic conditions such as diabetes
mellitus, immunosuppressive state etc. make the
individual prone to infection.

KELOID AND HYPERTROPIC SCAR


Keloids are overgrown scar tissues with no tendency
for resolution. They occur in wound, which heal without
any complications.

hypertrophic scar occur in wounds where healing is


delayed. These scars are more cellular and vascular.
Keloid and hypertropic scars are not seen in the
wounds of the oral cavity.
PIGMENTARY CHANGES
common in healing of wounds on skin and may appear
and may appear as hyperpigmented and hypopigmeted
areas.
In oral cavity hypopigmented scars are less common but
some lesions leave hyperigmentation while healing e.g.
lichenplanus, lichenoid reactions.

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.

Guidelines to be followed for an Uneventful healing


Asepsis-Failure to follow aseptic technique is a frequent
reason for the introduction of virulent microorganisms into the
wound.
Minimal trauma transformation of contaminated wounds into
infected wounds is also facilitated by excessive tissue trauma,
remnant necrotic tissue, foreign bodies, or compromised host
defenses.
meticulous surgical technique -most important factor in
minimizing the risk of infection is meticulous surgical technique,
including thorough dbridement, adequate hemostasis.
proper postoperative technique must be augmented by
proper postoperative care, with an emphasis on keeping the
wound site clean and protecting it from trauma.

Importance of healing from prosthodontic point of


view

In the absence of healing a definitive prosthesis cannot be fabricated.


Ideally a waiting period of 4 to 6 months is advisable after extraction since
there is increased resorption immediately following extraction.
Cases of abused tissue ,hyperplastic tissue and an abnormally contoured
ridge can compromise the success of replacement dentures.
alveolar ridge following tooth extraction undergoes a progressive,irreversible
resorption.
mandibular residual ridge is resorbed faster than the maxillary ridge,despite
the greater bone density of the mandible
more severe mandibular resorption may be due to the small area available
to support the mandibular denture
factors such as the menopause cause residual ridge resorption, but the
evidence supports a multifactorial cause.

Sequence of changes in shape of residual


ridges following tooth extraction
ridge at first becomes knife edged before
becoming flat and finally totally resorbed.
there are differences in the direction of ridge
resorption in different areas of the mouth.
in the anterior part of the jaws, it is vertical
and labiolingual.
posteriorly maxillary ridge resorbs vertically
and buccopalatally
while mandibular ridge is resorbed in a
vertical direction.

You might also like