Wound healing

WOUND HEALING
By- Praveen kumar singh
PG student first year
Dept. of oral medicine & radiology

CONTENTS:
 Wound definition
 Classification of wounds
 Healing
 Types of wound healing
 Phases of wound healing
 Healing of fracture
o Immediate effect of fracture
o Sequence of fracture healing

 Factors affecting wound healing
 Some important procedures of healing in
dentistry
o Healing after biopsy
o Healing of gingivectomy
o Healing of extraction wound
o Immediate reaction following extraction
 Complication of extraction wound

o Healing after Replantation.
o Healing after Implants.
 Complication of wound healing
 References

WOUND
 A wound is a break in the integrity of the skin or
tissues often which may be associated with
disruption of the structure and function.
(SRB 4th edition)
 A cut or break in the continuity of any tissue,
caused by injury or operation.
(Baillière’s 23rd Ed)

CLASSIFICATION OF WOUNDS
Rank and Wakefield classification
a) Tidy wounds
b) Untidy wounds

Classification based on type of wound
i. Clean incised wound
ii. Lacerated wound
iii. Bruising and contusion
iv. Haematoma
v. Puncture wound
vi. Abrasion
vii. Crush injury

viii. Injuries to bone and joint (maybe open or
closed)
ix. Injuries to nerve (either clean cut or crush)
x. Injuries to arteries and veins
xi. Injuries to internal organ

Classification based on thickness of wound
a) Superficial wound
b) Partial thickness
c) Full thickness
d) Deep wounds
e) Complicated wounds
f) Penetrating wound

Superficial
Partial thickness
Full thickness
Deep wound

HEALING
• Healing is the body’s response to injury in an
attempt to restore normal structure and
function.

The process of healing involves 2 distinct
processes:
A. REGENERATION
B. REPAIR

 Regeneration: Is when healing takes place by
proliferation of parenchymal cells and usually
results in complete restoration of the original
tissues.
 The goal of all surgical procedures should be
regeneration which returns the tissues to their
normal microstructure and function.

 Repair: It is a healing outcome in which tissues
do not return to their normal architecture and
function.
 Repair typically results in the formation of scar
tissue.

TYPES OF WOUND HEALING
 Healing by first intention (wounds with
opposed edges)
 Healing by secondary intention (wounds with
separated edges)

I) HEALING BY PRIMARY INTENTION

HEALING OF A WOUND WHICH HAS :
1. Clean & uninfected ;
2. Surgically incised ;
3. Without much loss of cells and tissue; and
4. Edges of wound are approximated by surgical
sutures.

THE SEQUENCE OF EVENTS IN
PRIMARY UNION:-
1. Initial hemorrhage
 Immediately after injury ,the
space between approximated
surfaces of incised wound is
filled with blood which then
clots and seals the wound
against dehydration and
infection.

2. Acute inflammatory response
 This occurs within 24hrs with appearance of
polymorph from the margins of incisions by 3rd
day polymorphs are replaced by macrophages.

3. Epithelial changes
 The basal cells of epidermis from both the cut
margins start proliferating and migrating towards
incisional space in the form of epithelial spurs.
 A well approximated wound is covered by a layer
of epithelium in 48hrs.
 By 5th day a multilayered new epidermis is
formed which is differentiated into superficial &
deeper layers .

4. Organisation
 By 3rd day ,fibroblasts also invade the wound
area.
 By 5th day ,new collegen fibrils start forming
which dominate till healing is completed .
 In 4 weeks the scar tissue with scanty cellular &
vascular elements , a few inflammatory cells &
epithilialised surface is formed .

5. Suture tracks
 Each suture track is a separate wound and incites
the same phenomena as in healing of the primary
wound i.e. filling the space with heamorrage
,some inflammatory cell reaction ,epithelial cell
proliferation along the suture track from both
margins ,fibroblastic proliferation of young
collegen.

 When suturs are removed around 7th day ,much of
epithelialised suture track is avulsed and the
remaining epithelial tissue in the track is
observed.

 However, some times suture track gets infected
(stitch abscess), or
 Epithelial cells may persist in the track
(implantation or epidermal cysts).
 Thus, the scar formed in a sutured wound is neat
due to close apposition of the margins of the
wound .

II)HEALING BY SECONDARY
INTENTION

Healing of a wound having the following
characteristics :
 Open with a large tissue defect, at times
infected ;
 Have extensive loss of cells and tissue ; and
 The wound is not approximated by surgical
sutures.

 The basic events in secondary union are
similar to primary union but differ in having a
larger tissue defect which has to be bridged.
 In this process healing takes place from the
base-upwards as well as from the margins-
inwards.
 The healing by second intention is slow and
result in a large, at times ugly, scar as
compared to rapid healing and neat scar of
primary union.

The sequence of events in secondary union are:-
1. Initial haemorrhage:-
As a result of injury, the wound space is filled
with blood and fibrin clot which dries.

2. Inflammatory phase:-
There is an initial acute inflammatory response
followed by appearance of macrophages which
clear off the debris similar to the primary
union.
PMNs

3. Epithelial changes:-
 As in primary healing, the epidermal cells from
both the margins of wound proliferate and
migrate into the wound in the form of epithelial
spurs till they meet in the middle and re-
epithelialise the gap completely.
 The proliferating epithelial cells do not cover
the surface fully until granulation tissue from
base has started filling the wound space.

 In this way , pre-existing
viable connective tissue
is separated from
necrotic material and clot
on the surface, forming
scab which is cast off.
 In time the regenerated
epidermis becomes
stratified and keratinised
.

4. Granulation tissue:-
 The main bulk of secondary healing is by
granulations.
 Granulation tissue is formed by proliferation of
fibroblasts and neovascularisation from the
adjoining viable elements.
 The newly formed granulation tissue is deep red,
granular & very fragile.

 With time, the scar on maturation becomes pale and
white due to increase in collagen and decrease in
vascularity.
 The specialised structures of skin Iike hair follicles
and sweat glands are not replaced unless their viable
residues remain which may regenerate.

5. Wound contraction:-
 Contraction of wound is an important feature of
secondary healing, not seen in primary healing.
 Due to the action of myofibroblasts present in
granulation tissue, the wound contracts to one-
third to one-fourth of its original size.

 Wound contraction
occurs at a time when
active granulation tissue
is being formed.

6. Presence of infection:-
 Bacterial contamination of an open wound delays
the process of healing due to release of bacterial
toxins that provoke:
 necrosis,
 suppuration and
 thrombosis.
 Surgical removal of dead and necrosed tissue,
debridement, helps in preventing the bacterial
infection of open wounds.

DIFFERENCE BETWEEN 1˚ & 2˚
UNION OF WOUND
FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FREQUENT FREQUENT

PHASES OF WOUND HEALING
For soft tissue wound healing:
1. Inflammatory phase: It can be broken down
into further
a) Clot formation
b) Early inflammation
c) Late inflammation
2.Proliferative phase
3.Maturation phase

INFLAMMATORY PHASE
a) Clot formation:
- Begins with three events:
i. Blood vessel contraction initiated by
platelet degranulation of serotonin, which
acts on endothelial cell and increases the
permeability of the vessel, allowing a
protein rich exudate to enter the wound site
ii. A platelet plug formation
iii. Activation of extrinsic and intrinsic clotting
mechanism

 These events stabilize hemostasis, begins
production of chemoattractants and initiate the
process of wound decontamination.
 This result in formation of a coagulum.

b) Early inflammation:
 Characterized by production of
polymorphonuclear neutrophils (PMNs)
 Begin to enter the wound site within 6 hours of
clot stabilization.
 The number of PMNs increases steadily,
peaking at about 24 to 48 hours after the
injury.

 Three key steps mark PMN migration into the
wound site:
a) Pavementing
b) Emigration
c) Migration
 Main role of PMNs is wound decontamination
by phagocytosis of bacteria.
 The number of PMNs drop rapidly after the
third day.

c) Late inflammation:
 Presence of macrophages.
 Reaches peak concentration by approximately
third or fourth day.
 They have longer life than PMNs and remain
in wound till healing is completed.

 Are more bioactive then PMNs – secrete a
vast array of cytokines – leads to initiation of
proliferative phase of wound healing.
 Major functions of macrophages:
 Wound decontamination through
phagocytosis and digestion of
microorganisms and tissue debris.
 Ingestion and processing of antigens for
presentation to T lymphocytes
 Regulation of wound healing

PROLIFERATIVE PHASE
 Characterized by formation of granulation
tissue in the wound.
 2 key cell types are present in this phase:
a) fibroblasts
b) endothelial cells

 Granulation tissue:
It is a fragile structure composed of an
extracellular matrix of fibrin, fibronectin,
glycosaminoglycans, proliferating endothelial
cells, new capillaries, and fibroblasts mixed
with inflammatory macrophages and
lymphocytes.

 Epithelial cells are active during this phase and
are responsible for initial wound closure.
 GTR(guided tissue regeneration) procedures are
based on control of the epithelial cell growth rate
during this phase.

a) Fibroblasts: Fibroplasia
 They migrate into the wound site on the 3rd
day after injury and achieve their peak
numbers by approximately 7th day.
 This action is stimulated by combination of
cytokines produced initially by platelets
and subsequently by macrophages and
lymphocytes.

 As the number of macrophages declines and
fibroblasts population increases the wound
transforms from granulomatous tissue to
granulation tissue.
 Fibroblasts produces collagen (first detected
in the wound about the third day of injury) .

 Fibroblasts produce type III collagen initially
and as the wound matures type I collagen is
formed.
 As wound healing progresses, the collagen
fibers become organized by cross-linking.
 A focused type of fibroblast known as a
myofibroblast plays a significant role in wound
contraction, particularly in incisional-type
wounds.

 Myofibroblasts align themselves parallel with
the wound surface and then contract, drawing
the wound edges together.
 These cells are eliminated by apoptosis after
wound closure.

b)Endothelial cells: Angiogenesis
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.

Epithelium:
 The first step is formation of an epithelial seal on
the surface of the fibrin clot. It begins at the edge
of the wound, where the basal and suprabasal
prickle cells rapidly undergo mitosis.
 Migration stops as a result of contact inhibition of
the epithelial cells from the opposing wound edge.
 In wounds healing by primary intention, formation
of an epithelial seal typically takes 21 to 28 hours
after reapproximation of the wound margins.

MATURATION PHASE
 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.

 Scar strength is:
 3% in 1 week
 20% in 3 weeks
 80% in 12 weeks

:Growth Factors and Cytokines Affecting Various Steps in
Wound Healing
Monocyte chemotaxis PDGF, FGF, TGF-ß
Fibroblast migration PDGF, EGF, FGF, TGF-ß, TNF,
IL-1
Fibroblast proliferation PDGF, EGF, FGF, TNF
Angiogenesis VEGF, Ang, FGF
Collagen synthesis TGF-ß, PDGF
Collagenase secretion PDGF, EGF, FGF, TNF, TGF-ß
inhibits
PDGF- platelet-derived growth factor
FGF- fibroblast growth factor
TGF- transforming growth factor
EGF- epidermal growth factor
IL- interleukin
TNF- tumor necrosis factor
VEGF- vascular endothelial growth factor

HEALING OF FRACTURE
 Fractures of jaws are common injuries & many
ranges from minor alveolar process fracture to
destructive injuries of the maxillofacial region.

IMMEDIATE EFFECT OF FRACTURE
 When fracture of a bone occurs,the Haversian
vessels of bone are torn at the fracture site, as are
the vessels of the periosteum & the marrow
cavity that happen to cross the fracture line.
 The resulting tissue damage evokes acute
inflammation in the soft tissue adjacent to the
fracture line, specially in the periosteal region,
marrow spaces , & the Haversian canals.

 The Haversian canals of bone contain only a
singal vessel.
 When the flow of blood in this vessel is
interrupted by tearing at the fracture site, the bone
cells or osteocytes of the Haversian system
supplied by this vessel die.
 The blood clot play an imp. role in healing of the
fracture through the replacement by granulation
tissue & its subsequent replacement by bone .

SEQUENCE OF FRACTURE HEALING
1) primary union of fracture :
It occurs in a few special situations when the
ends of fracture are approximated as is done by
application of compression clamps.
In these cases , bony union takes place with
formation of medullary callus without
periosteal callus formation.

2) Secondary union of fracture :
It is the more common process of fracture
healing .
It is described under the following headings:
i) Procallus formation
ii) Osseous callus formation
iii) Remodelling

1.PROCALLUS FORMATION
1) Heamatoma –
 Forms due to bleeding from torn blood vessel,
filling the area surrounding the fracture .
 Loose meshwork is formed by blood & fibrin
clot which acts as framework for subsequent
granulation tissue formation .

2) Local inflammatory response –
 It occurs at the site of injury with exudation of
fibrin ,polymorphs & macrophages .
 The macrophages clear away the fibrin ,red blood
cells ,inflammatory exudate & debris .
 Fragments of necrosed bone are scavenged by
macrophages and osteoclasts.

3) Ingrowth of granulation tissue –
It begins with neo-vascularisation and
proliferation of mesenchymal cells from
periosteum & endosteum .
A soft tissue callus is formed which joins the
ends of fractured bone without much strength .

4) Callus composed of woven bone & cartilage-
 ‘Callus’ is a latin word means “over growth of
hard skin”.
 Starts within the first few days.
 The cells of inner layer of the periosteum have
osteogenic potential and lay down collagen as
well as osteoid matrix in the granulation tissue.
 The osteoid undergoes calcification and is called
woven bone callus.

 As much wide zone over the cortex on either side
of fractured ends is covered by the woven bone
callus and united to bridge the gap between the
ends, giving spindle-shaped or fusiform
appearance to the union.
 At times callus is composed of woven bone as
well as cartilage, temporarily immobilization the
bone ends.
 The stage is called procallus formation.

2.OSSEOUS CALLUS FORMATION
 The procallus acts as scaffolding on which
osseous callus composed of lamellar bone is
formed .
 The woven bone is cleared away by incoming
osteoclasts and the calcified cartilage
disintegrates.
 In their place , newly-formed blood vessels and
osteoblasts invade ,laying down osteoid which is
formed by developing Haversian system .

3.REMODELLING
 Remodelling means transformation of hard callus
to compact bone.
 May take a few years.
 Completed when the fractured bone has been
restored to its original form or shape or when it
can withstand the imposed stresses placed on it.

HARD TISSUE HEALING
 The inflammatory and proliferative phases are
similar to those for soft tissue.
 The maturation phase differs markedly from
that for soft tissues because of the tissue
involved.

 Bone formation is categorized into two types:
a) Matrix vesicle – based process
b) Osteoid secretion

A) MATRIX VESICLE – BASED PROCESS
 Woven bone formation occurs by this process.
 In this process 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.

B) OSTEOID SECRETION
 Lamellar bone formation occurs by this process.
 Osteoblasts secrete an organic matrix composed
of longitudinally arranged collagen matrix fibrils.
 Mineralization occurs by mineral deposition
directly along the collagen fibrils.

 In this stage alkaline phosphatase plays an
important role in mineralization.
 Several growth factors identified as a key
components in the production of osseous tissue
are:
a. TGF- ß
b. PDGF
c. FGF
d. IGF

FACTORS AFFECTING WOUND
HEALING:
1) Local factors:
i. Infection
ii. Presence of necrotic tissue and foreign
body
iii. Poor blood supply
iv. Venous or lymph stasis
v. Tissue tension

vi. Hematoma
vii. Large defect or poor apposition
viii. Recurrent trauma
ix. X-ray irradiated area
x. Site of wound, eg.wound over the joints and
back has poor healing
xi. Underlying diseases like osteomyelitis and
malignancy

2) General factors:
i. Age, obesity,smoking
ii. Malnutrition, zinc, copper
iii. Vitamin deficiency (vit C, vit A)
iv. Anemia
v. Malignancy
vi. Jaundice
vii. Diabetes
viii. HIV and immunosupressive diseases
ix. Steroids and cytotoxic drugs

SOME IMPORTANT HEALING
PROCEDURES IN DENTISTRY

HEALING AFTER BIOPSY
 The healing of biopsy wound of oral cavity is
identical with the healing of a similar wound in
any other part of the body.
 Thus healing here may be classified into primary
& secondary healing (same as that of skin).

 Primary healing occurs when the edges of wound
can be brought into apposition, often by
SUTURING.
 Secondary healing occurs when the edges of the
wound cann’t be apposed; like in big wounds
(e.g. removal of a lesion of palate or a large
lesion at alveolar ridge etc.)

HEALING OF GINGIVECTOMY WOUND:
 Gingiveoplasty, simillar to the gingivectomy ,is
surgical reshaping of the gingiva to produce the
physiologic gingival contour.
 Numerous techniques are in use for the removal
of the tissue, and different type of post operative
packing materials are available to control
bleeding, maintain tissue position, relive pain,
and keep fresh wound free from debris.

Early healing phase:-
 There is some evidence which shows healing
may be slightly facilitated by dressing.
 Two days after the gingivectomy the surface of
the tissue is covered by a grayish blood clot,
and beneath this clot there is histologic
evidence of delicate connective tissue
proliferation.
 After the four days of operation, the deeper
portion of the blood clot demonstrates
considerable organization.

 while superficial portion exhibits dense number
of Polymorphonuclear leukocytes entrapped in
fibrin meshwork
 There is proliferation of young cappilaries and
fibroblast into the base of the blood clot.
 The epithelium has extended over a portion of the
wound below the necrotic surface layer of the
clot, but above the proliferating and organizing
connective tissue.

Late healing phase:-
 After 8-10 days clinically wound has a red
granular apperance and bleeds readily.
 Epithiliazation is complete with in 10-14 days
after gingivectomy.
 Healing of the interproximal tissue is lag behind
to the adjacent labial or buccal surfaces.

 The surface epithelium grows downward along the
surface of the cementum within a month after
gingivectomy.
 Healing of the gingivectomy wound is basically
simillar to the wound present elsewhere in the body,
but is somewhat modified by the special anatomy of
the involved region.
 Healing varies considerably depending upon the
local condition and the systemic status of the
individual.

HEALING OF EXTRACTION WOUND
After removal of teeth:-
 Formation of blood clot filling the socket.
 Organisation of the clot.
 Epithelialization of the surface of the wound.
 Formation of woven bone in the connective
tissue filling the socket.
 Replacement of woven bone by trabecular
bone and remodeling of the alveolus.

IMMEDIATE REACTION FOLLOWING
EXTRACTION
 After the removal of tooth ,the blood filling the
socket coagulates, red blood cells being
entrapped in the fibrin meshwork , and the ends
of the torn blood vessel in the periodontal
ligament become sealed off .
 Within the first 24-48 hrs after the extraction , a
variety of phenomena occur which consist
principally of alterations in vascular bed.

 The surface of blood clot is covered by thick
layer of fibrin .
 It is important to recognize that collaps of
unsupported gingival tissue into the fresh
extraction wound is of great aid in maintaining
the clot in position.

FIRST WEEK WOUND
 Within the first week after tooth extraction,
proliferation of fibroblasts from connective tissue
cells in the remnants of periodontal ligament is
evident,& these fibroblast have begun to grow
into the clot around the entire periphery.
 This clot forms an actual scaffold upon which
cells associated with the healing process may
migrate.

 It is only a temporary structure and gradually
replaced by granulation tissue.
 During this period the blood clot begins to
undergo organization by the ingrowth around the
periphery of fibroblast & small capillaries from
the residual periodontal ligament.

 An extremely thick layer of leukocytes form over
the surface of the clot and the edge of the wound
continues to exhibit the epithelial proliferation.

SECOND WEEK WOUND
 During the 2nd week after extraction of tooth,the
blood clot becomes organized by fibroblast
growing into the clot on fibrinous meshwork.
 At this stage new delicate capillaries penetrate to
the centre of the clot.
 Trabeculae of osteoid can be seen extending
outward from the wall of the alveolus.

 The margin of alveolar socket exhibit prominent
osteoclastic resorption.
 Fragments of necrotic bone which may have been
fractured from the rim of the socket during
extraction,are seen in the process of resorption of
sequestration.

THIRD WEEK WOUND
 As the healing process continues into the 3rd week
,the original clot appears almost completely
organized by maturing granulation tissue.
 Young trabeculae or uncalcified bone form
around the entire periphery of the wound from the
socket wall.

 This early bone is formed by osteoblasts derived
from pluripotential cells of original PDL.
 The original cortical bone of alveolar socket
undergoes remodelling so that it no longer consist
of such dense layer.

 The crest of the alveolar bone is rounded off by
osteoclastic resorption.
 By this time the surface of wound may have
became completely epithelialised.

FOURTH WEEK WOUND
 In this stage, the wound begins the final stage of
healing in which there is continued deposition and
remodeling resorption of the bone filling the alveolar
socket.
 Early bone is poorly calcified, it is seen radiolucent
on radiograph.
 Bone formation become prominent in 6th or 8th week
after tooth extraction.

 Because of crest of alveolar bone undergoes
considerable amount of osteoclastic resorption
during the healing process and the bone filling the
socket does not extend above the alveolar crest.

HEALING OF EXTRACTION WOUND
A. Tooth just before
extraction.
B. After two weeks.
C. After one month.
D. After two month.
E. After four month
F. After six month.
G. After eight month.
H. After fourteen
months.

COMPLICATIONS IN HEALING OF
EXTRACTION WOUND
 Dry socket
 Dry socket is a temporary dental condition that
sometimes occurs after extraction of a permanent adult
tooth. A dry socket occurs when the blood clot at the site
of the tooth extraction is dislodged, exposing underlying
bone and nerves and causing increasing pain.

 Synonyms:
Alveolitis sicca dolorosa/ Alveolalgia/
Postoperative osteitis/ Localized acute alveolar
osteitis, Alveolar osteitis

 Etiology:
1. Excessive trauma.
2. Impaired blood supply ( lower jaw > Upper
jaw )
3. Oral contraceptive ( oestrogens component
causes increase in serum fibrinolytic activity)
4. Osteosclerotic disease.
5. Radiotherapy.
6. Smoking.

 Pathology:
 Destruction of the blood clot either by:
1. Proteolytic enzymes produced by bacteria.
2. Excessive local fibrinolytic activity.
 Anaerobes are likely to play a major role.
 Destruction of the clot leaves an open socket,
infected food and other debris accumulate.

 The necrotic bone lodges bacteria which
proliferate freely, Leukocytes unable to
reach them through the avascular material.
 Dead bone is gradually separated by
osteoclasts.
 Healing is by granulation tissue from the
base of the walls of the socket.

 Clinical features:
 Pain usually starts few days after extraction.
 Sometimes may be delayed for few days or
more.
 Deep – seated, severe and aching or throbbing
in character.
 Mucous membrane around the socket is red
and tender.
 No clot in the socket ( Dry ).

 When debris is washed away, whitish, dead
bone may be seen or may be felt as rough area
with a probe.
 Sometimes the socket becomes concealed by
granulation tissue growing in from the edge.
 Pain may continues for week or two and rarely
longer.

 Prevention:
1. Minimal trauma.
2. Squeezed the socket edge firmly after
extraction.
3. In case of dis-impaction of 3rd molars dry
socket is more common:
- Minimum stripping of the periosteum.
- Minimum damage to the bone.
- Use prophylactic antibiotic.

4. In osteosclerotic disease:
 Little damage to bone (surgical extraction).
 Prophylactic antibiotic.
5. Stop smoking for two days post extraction.

 Treatment:
 Explain to the patient and warn them.
 The aim of the treatment is to keep the open
socket clean and to protect the exposed bone:
1. Irrigate the socket by antiseptic solution.
2. Fill the socket with an obtudant dressing
containing some non irritant antiseptic.
3. Frequent use of mouth wash.

 A great variety of dry socket dressing has
been formulated:
1. Iodoform - containing preparation.
2. Zinc oxide – eugenol –commonly used
socket dressing .
( The dressing should be: Obtudant, antiseptic,
softly adhere to the socket walls and
absorbable ).

 In many cases, irrigation of the socket and
replacement of the dressing has to be repeated
every few days.

FIBROUS HEALING OF EXTRACTION
WOUND
 Fibrous healing of extraction wound is an
uncommon complication ,usually following a
difficult ,complicated or surgical extraction of a
tooth.
 It occurs most frequently when the tooth
extraction is accompanied by loss of both the
lingual and labial or buccal plates & the
periosteum.
 The lesion is generally asymptomatic & is
discovered only during radiographic examination.

RADIOGRAPHIC FEATURES
 The lesion appears as a rather well-circumscribed
radiolucent area in the site of previous extraction
wound and may be mistaken for residual cyst or
granuloma .
 There is no certain way of differentiating fibrous
healing from residual infection without surgical
exploration .
 At the time of surgery ,simply a dense mass of
fibrous connective tissue or scar tissue is found .

HISTOLOGIC FEATURES
 The area of fibrous healing consist of dense
bundle of collegen fibers with only occasional
fibrocytes & few blood vessels .
 The lesion is essentially fibrous scar tissue with
little or no evidence of ossification .
 Inflammatory cell infiltration is minimal or
absent .

TREATMENT AND PROGNOSIS
 Excision of the lesion for the purpose of
establishing a diagnosis will sometimes result in
normal healing & subsequent bony repair of the
fibrous defect.

HEALING AFTER REPLANTATION:-
 Clot forms between the root surface and ruptured
periodontal ligament.
 Proliferation of fibroblasts and endothelial cells
occur in the periodontal ligament on the alveolar
bone side.
 The recconecting of periodontal ligament is
evidenced by the extension of collagen fibres
from the cementum to the alveolar bone.

 The epithelium is reattached to the tooth end of
the first week.
 Complete regenration of the periodontal ligament
is take place within two to four weeks.

HEALING OF IMPLANTS:-
 After implant insertion a period of 10 – 12 weeks
required for healing.
 During healing, compact and cancellous bone
forms around the implant together with a variable
amount of fibrous marrow.
 Implants do not have direct contact with bone.
 A certain amount of bone marrow and soft tissue
is interposed between the bone and implants.

 The implant and the mucosal interface serve
similar functions as the dentogingival junction.
 The connective tissue of the mucosa forms
intimate contact with the implants.
 The collagen fibres of the connective tissue run
parallel to the long axis of the implant and the
epithelium is attached to the implant by means of
basal lamina and hemidesmosomes.

COMPLICATION:
1. Deficient scar formation:
a) Wound dehiscence
b) Ulceration
2. Excessive formation of the repair components:
a) Aberrations of growth: -hypertrophic scar
-keloid
b) Excessive amount of granulation tissue
formation

c) Exuberant proliferation of fibroblasts and
other connective tissue elements: Desmoids or
Aggressive fibromatoses
3. Formation of contractures

REFERENCES
 Textbook of general surgery SRB’s.
 Textbook of pathology by Harsh Mohan.
 Text book of robins and cortan basic pathology.
 Textbook of oral pathology by shafer.

Wound healing

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