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Wound healing [including healing after periodontal therapy]
Wound healing [including healing after periodontal therapy]
2. Regeneration & repair
3. Healing by primary and secondary intension
4. Molecular biology of wound healing
5. Factors influencing/ complications of wound healing
6. Healing of oral wounds
7. Role of saliva and GCF in wound healing
8. Wound healing following various periodontal therapies
9. Use of lasers in wound healing
A wound/Injury is
a disruption of
function in any
Healing on the other
hand is a cell response
to injury in an attempt
to restore the normal
structure and function.
Periodontal wound healing
A more complex situation presents itself when a
mucoperiosteal ﬂap is apposed to an instrumented root surface
deprived of its periodontal attachment.
In this case, the wound margins are not two opposing vascular
gingival margins but comprise the rigid nonvascular
mineralized tooth surface, on the one hand, and the connective
tissue and epithelium of the gingival ﬂap, on the other hand.
Process of healing
It involves 2 distinct processes :
At times, both the processes take place
Natural renewal of a structure, produced by growth &
differentiation of new cells and intercellular substances to
form new tissues or parts which function the same as
Growth from the same type of tissue that has been destroyed
or from its precursors.
Periodontal tissues are limited in their regenerative
Regeneration related to periodontal tissues
Mitotic activity in the epithelium of the gingiva and connective tissue
Continuous deposition of cementum
Most gingival and periodontal diseases are chronic inflammatory
process and, as such are, healing lesions.
Repair- “healing by scar”
Replacement of one tissue with another tissue,
such as fibrous connective tissue, which may not function the
same as the tissue replaced.
Two processes are involved in the repair:
1. Granulation tissue formation
2. Contraction of wounds
Granulation tissue formation
Each granule histologically corresponds to proliferation of new
small blood vessels which are slightly lifted on the surface by a
thin covering of fibroblasts and young collagen
Phase of clearance
Phase of ingrowth
necessary to sustain newly formed granulation tissue
proliferation of endothelial cells from the margins of the severed
Emigration and proliferation of the fibroblasts at the site of injury
Deposition of these cells which in turn increases collagen synthesis
As the maturation proceeds: there is an increase in the collagen, and a
decrease in the fibroblasts and blood vessels .
This leads to the formation of scar know as CICATRISATION.
It starts after 2-3 days and the process is completed by the 14th day.
Wound is reduced by 80% of its original size which helps in rapid
healing since lesser surface area of the injured tissue has to be
Repair related to periodontal tissues
Simply restores the continuity of the diseased marginal
gingiva and re-establishes a normal gingival sulcus at the
same level on the roots as the base of the pre-existing
Arrests bone destruction but does not result in gain of
gingival attachment or bone height.
wound strength- extracellular matrix
The wound is strengthened by proliferation of fibroblast and myofibroblast
which get structural support from the extracellular matrix
ECM has five main components:
2. adhesive glycoprotein
fibronectin - plasma/ tissue type
tenascin or cytotactin
3. basement membrane
4. elastic fibres
Healing by first intention
This is defined as healing of a wound which has the following
Clean and uninfected
Without much loss of cells and tissue
Edges of wound are approximated by surgical suture
Primary union involves the following sequence of events:
Acute inflammatory response- within 24 hours
Epithelial changes- completes by 48 hours
Organization of fibroblasts- starts around 3rd day
Wound maturation- starts after 1 week and completes
around 4 weeks
The incised wound as well as suture
track on either side are filled with
blood clot and there is inflammatory
response from the margins
spurs of epidermal cells migrate along the
incised margin on either side as well as round the
suture track, formation of granulation tissue also
begins from below.
removal of sutures at around 7th day
result in scar tissue at the sites of
incision and suture track
Healing by secondary intention
This is defined as-
Open wound with a large tissue defect, at times infected
Extensive loss of cells and tissues
Not approximated by sutures, but is left open
Secondary union consists of the following events :
Granulation tissue formation
A. The open wound is filled with blood clot and there is inflammatory response at
the junction of viable tissue
B. Epithelial spurs from the margins of wound meet in the middle to cover the gap
and separate the underlying viable tissue from necrotic tissue at the surface forming
C. After contraction of the wound ,a scar smaller than the original wound is left
A B C
Molecular biology of wound healing
1. The ﬁbrin clot and inﬂammatory cells
The important functions of the clot are:
plugs the cut blood vessels and also serves to protect the
denuded tissues temporarily.
reservoir of growth factors and cytokines that are released by the
degranulation of activated platelets and serving as a provisional
matrix for cell migration and might be providing the start signals
for wound repair.
2. Re-epithelialization of wounds
keratinocytes start moving into the defect about 24 hours after the
The keratinocytes use receptors on their surface, known as integrins
to bind to laminin in the basal lamina.
Integrins are a family of cell adhesion receptors that mediate cell
surface interactions with extracellular matrix and in some cases
with other cells
At this edge, the cells will have to dissolve the hemidesmosome
attachment, downregulate the expression of α6β4, and upregulate
integrin receptors α5β1, αVβ6 and αVβ5 that are suitable for adhesion
to provisional matrix components.
epidermal growth factor
transforming growth factor-α
heparin-binding epidermal growth factor and
keratinocyte growth factor are involved in stimulating the
proliferation of the epithelial cells here.
3. Matrix degradation and the wound-cleaning
creation of a migrating path for keratinocytes is achieved by
the dissolution of the ﬁbrin barrier by the enzyme plasmin
that is derived from the activation of plasminogen in the clot.
The two activators, tissue-type plasminogen activator and
urokinase-type plasminogen activator along with its receptor,
are upregulated in the migrating keratinocytes
MMP-1 degrades native collagens and aids cell migration by
destroying collagens I and III.
MMP-9 (also known as gelatinase B) can cleave the collagen in basal
lamina (type IV) and the collagen that forms the anchoring ﬁbrils
MMP10 (also known as stromelysin-2) is also expressed in wounds
and is thought to have a wide spectrum of substrate speciﬁcity for
Connective tissue repair by:
Activation of ﬁbroblasts by platele granules
Angiogenesis by VEGF and b-FGF
Formation of Granulation tissue by TGF, PDGF, FGF and EGF
contraction of the wound by myofibroblasts.
Wound repair involves phenotypic change of fibroblasts from
quiescent to proliferating cells, and subsequently to migratory, and
then to stationary matrix producing and contractile cells.
In the connective tissue, fibroblasts are surrounded by a matrix
that contains collagen and cellular fibronectin as the major
components. Consequently, quiescent fibroblasts express collagen
receptors α1β1 and α2β1 and the major fibronectin receptor α5β1
integrin which they use for adhesion to the matrix
Healing of oral wounds
Oral wounds heals faster and with less scarring
than extra oral wounds
It is mainly due to:
factors in saliva
specific microflora of the oral cavity
resemblance of fetal fibroblast with gingival
Role of saliva & GCF in oral wound healing
Physico-chemical factors favoring healing are:
calcium and magnesium ions
Saliva has an efficient capacity to reduce redox activity
caused by transitional metal ions and inhibit the
production of free radicals that may be beneficial for the
Lubrication of oral mucosa is beneficial for
Advantages of moist environment:
Prevention of tissue dehydration and cell death
incremental breakdown of fibrin and tissue debris
Presence of growth factor – produced by saliva
Healing following scaling & root planing
Numerous polymorphonuclear leucocytes can be seen between
residual epithelial cells & crevicular surface in about 2 hrs
There is dilation of blood vessels, oedema & necrosis in the
lateral wall of the pocket
24 hrs after scaling a widespread infiltration of inflammatory
cells and migration of keratinocytes have been observed, in
all areas of the remaining epithelium& in 2 days the entire
pocket is epithlialized.
In 4-5 days a new epithelial attachment may appear at bottom of
Depending on the severity of inflammation & the depth of
the gingival crevice, complete epithelial healing occurs in 1-2
connective tissue repair by Immature collagen fibers occur within
healing occurs with the formation of a long thin junctional
epithelium with no connective tissue attachment.
Healing following curettage
A blood clot forms between the root surface & the lateral wall
of the pocket, soon after the curettage
Large number of polymorphonuclear leucocytes after the procedure
rapid proliferation of granulation tissue
Epithelisation of the inner surface of the lateral wall is completed
in 2-7 days
The junctional epithelium is also formed in about 5 days
Healing after surgical gingivectomy
Initial response- formation of a protective surface clot
Clot is then replaced by granulation tissue
By 24 hours there is an increase in new connective tissue cells,
mainly angioblasts just beneath the surface layer of inflammation and
By the 3rd day numerous young fibroblasts are located in
the area which start granulation tissue formation.
The highly vascular granulation tissue grows coronally,
creating a new free gingival margin and sulcus
Capillaries derived from the blood vessels of the
periodontal ligament migrate in to the granulation tissue
and within 2 weeks they connect with gingiva vessels
After 5-14 days: surface epitheliazation is complete
During first 4 weeks: keratinization is less than it was
Complete epithelial repair takes 1 month.
Complete repair of the C.T. takes about 7 weeks
Flow of GCF is initially increased after gingivectomy and
diminishes as healing progresses.
Healing following electrosurgical gingivectomy
There appears to be little difference in the results obtained after
shallow gingival resection with electrosurgery and that with
when used for deep resection close to bone, electrosurgery can
produce gingival recession, bone necrosis and sequestration, loss of
bone height, furcation exposure, and tooth mobility, which do not
occur with the use of periodontal knives.
Healing following depigmentation of gingiva
Healing after surgical depigmentation:
After surgery it was found necessary to cover the exposed lamina propria
with periodontal packs for 7 to 10 days.
After 6 weeks the attached gingiva regenerated by only a delicate scar
present. The newly formed gingiva was clinically non-pigmented.
Healing following cryosurgical depigmentation:
At 2nd to 3rd day: superficial necrosis becomes apparent and a whitish
slough could be separated from the underlying tissue, leaving a clean
In 1-2 weeks: normal gingiva
In 3-4 weeks: keratinization completed.
No postoperative pain, hemorrhage, infection or scarring seen in patients.
Healing following depigmentation by laser:
During lasing gingiva gets covered with a yellowish layer, that could
be easily removed by a wet gauze.
After 1-2 weeks: completion of re-epithelization.
At 4th week: gingiva is similar to normal untreated gingiva i.e.,
lacking melanin pigmentation completely
Healing following flap surgery
Immediately response- clot formation
At edge of flap numerous capillaries are seen
1-3days after surgery space between flap & tooth surface & bone
appears reduced & the epithelial cells along border of the flap start
By 1 week after surgery
epithelial cells have migrated & established an attachment to root
surface by means of hemidesmosomes.
The blood clot is replaced by granulation tissue proliferating from
the gingival connective tissue, alveolar bone and periodontal ligament
By 2nd week collagen fibers begins to appear. Collagen fibers gets
arranged parallel to root surface rather than at right angles. The
attachment between soft tissue & tooth surface is weak
By end of one month following surgery the epithelial attachment is
well formed & the gingival crevice is also well epithealised
There is beginning functional arrangement of supracrestal fibres.
In cases where Mucoperiosteal flap…
superficial bone necrosis have been observed during first 3 days
Osteoclastic Resorption occurs in that area which reaches its peak at
Osteoblastic Remodelling occurs subsequently
Loss of alveolar bone height by about 1 mm may be expected after
Healing following osseous resection
Elevation of Mucoperiosteal Flap results in
temporary loss of nutrient supply to the bone
In addition, surgical resection of bone also
contributes to necrosis of the alveolar crest & osteoclastic resorption
of the bone takes place initially
The initial loss in bone height is compensated to some extent by the
osteoblastic repair and remodelling.
Thus final loss in bone height is clinically insignificant
Osteoblastic activity is even seen after 1 yr. post-operatively
Healing after implant placement
The interface area consists of bone, marrow tissue, and a hematoma
mixed with bone fragments from the drilling process.
In the early phase of healing, woven bone is formed by osteoblasts at
the surfaces of trabecular and endosteal cortical bone surrounding the
In the late phases of healing, lamellar bone replaces woven bone in a
process of creeping substitution.
Stages of healing of implants
a. Woven Bone Formation: When bone matrix is exposed to extra-cellular
fluid, non-collagenous proteins & growth factors are set free & initiate
Woven bone formation dominates the first4-6 weeks
b. Lamellar Bone Formation: From 2nd month post-operatively the
microscopic structure of bone changes to lamellar bone
c. Bone Remodelling: It begins around 3rd month post-operatively.
Initially rapid remodeling occurs which slows down & continues
for rest of the life
Thus complete healing probably takes longer than 3 to 6 months.
Use of lasers in wound healing
Lasers employing low-level energy have been claimed to produce
a positive effect on the biological and bio-chemical processes of
Dermatologic investigations have demonstrated more rapid
epithelialization, enhanced neovascularization, and increased
production of collagen by fibroblasts in vivo
Ultimately, accelerated wound healing, reduced pain and enhanced
Current scientific evidence points to the presence of:
1. cells originating from the periodontal ligament,
2. wound stability,
3. space provision
4. primary intention healing, as fundamental biologic and clinical
factors that must be met to obtain periodontal regeneration.
Wound healing is achieved by a series of coordinated efforts by
inflammatory cells, keratinocytes, fibroblasts and endothelial
cells responding to a complex array of signals.
Future research will have to be directed towards understanding
in more detail the molecular mechanisms of differential gene
expression in healing wounds.
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wound healing, periodontology 2000, vol. 24, 2000, 127–152.
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