healing in periodontics

1. WOUND HEALING
AND HEALINGAFTER
PERIODONTAL
PROCEDURES
GUIDED BY:
Dr Tanvi Mehta
PRESENTED BY: DR.
Rutu Dabhi
PG II YEAR

2. CONTENTS
1. INTRODUCTION
2. REGENERATION &
REPAIR
3. GROWTH FACTORS IN
WOUND HEALING
4. WOUND HEALING
5. FACTORS INFLUENCING
WOUND HEALING
1. HEALING OF ORAL WOUNDS
2. WOUND HEALING FOLLOWING
VARIOUS PERIODONTAL
THERAPIES
3. COMPLICATIONS
4. USE OF LASERS IN WOUND
HEALING
5. CONCLUSION
6. REFERENCES
PART – I PART – II

3. INTRODUCTION
Awound/Injury is
Healing is a cell
a disruption of
the anatomic WOUND response to injury in
structure and HEALIN an attempt to restore
function in any G the normal structure
body part. and function.
3/45

4. Wound healing may either take place by:
 Primary Intention
 Secondary Intention
 Tertiary Intention
4/45

5. REGENERATION
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 original
tissues.
Growth from the same type of tissue that has been destroyed or
from its precursors.
Periodontal tissues are limited in their regenerative capacity.

6. REGENER
- ATION
REPAIR
 PROCESS OF HEALING
 At times, both the processes take place simultaneously

7. Manifested by:
Mitotic activity in the epithelium of
the gingiva and connective tissue of PDL
Bone remodelling
Continuous deposition of cementum
•Most gingival and periodontal diseases are
chronic
inflammatory process and, as such are, healing lesions
Regenration related to periodontal tissue

8. 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
Phase of inflammation
Phase of clearance
Phase of ingrowth of
granulation tissue
a. Amgiogenesis
b. fibrogenesis

9. Essential molecules for regeneration

12. I. THE INFLAMMATORY PHASE
It can be broken down further into :
a) Haemostasis – Clot formation
b)Early inflammation - Chtzd by production of PMNs
c) Late inflammation - Presence of macrophages
Primary contributors to haemostasis include:
Vasoconstriction
PlateletAggregation
Fibrin Deposition

15. Recruitment of PMNs (Early inflammatory phase)
recruitment of macrophages (Late inflammatory phase
First infiltrating cells to enter the wound site, peaking at 24 to 48 hours
migration is stimulated by - ↑ vascular permeability, Local PG release, presense of
chemotactic substances complement factors, IL-1, TNF-α, TGF β, platelet factor4 or
bacterial products.
following activation - scavenge necrotic debris, foreign material, and bacteria
undergo apoptosis once they have completed their tasks - engulfed & degraded by
macrophages.

17. Key role in transition from inflammation to granulation
tissue formation

18. ECM–growth factor interactions and production ofMMPs in wound

19. MATRIX METALLOPROTEINASES IN WOUNDHEAlING

20.  Proliferative phase of wound healing & roughly spans days 4 through 12.
 It is during this phase that tissue continuity is re-established
 The initial fibrin–fibronectin matrix is heavily populated by inflammatory cells,
whereas FIBROBLASTS & ENDOTHELIAL CELLS will predominate as healing
progresses.
 Cytokines continue to be a part of the process as its release contributes to:
THE PROLIFERATIVE PHASE

21. Suprabasal keratinocytes are the first migratory cellssliding over the basal
keratinocytes.
Re-epithelialization

22.  Integrins play a crucial role in the fibrin clot removal
 The two activators, tissue-type plasminogen activator and urokinase-type
plasminogen activator along with its receptor, are upregulated in the
migrating keratinocytes.
 Creation of a migrating path for keratinocytes : achieved by the
dissolution of the fibrin barrier by the enzyme plasmin.
 Migrating keratinocytes express:
 MMP-1 degrades native collagens and aids cell migration by destroying
collagens I and III.
 MMP-9 can cleave the collagen in basal lamina (type IV) and the collagen
that forms the anchoring fibrils (type VII)
 MMP10 is also expressed in wounds and is thought to have a wide spectrumof
substrate specificity for collagen

23. • As the basal keratinocytes at the wound margin are exposed to the
new provisional matrix, the phenotype of the cells is changed from
stationary to migratory.
• In this process, keratinocytes detach themselves from the basement
membrane, migrate laterally into the wound bed and finally regenerate
the basement membrane.
• The components of the basement membrane zone such as Type IV
and VII collagens, laminin-1 and heparan sulfate proteoglycan are
missing underneath migrating keratinocytes.
• Laminin-5, however, appears to be always deposited against the
wound bed matrix by keratinocytes during migration

24. • After the epithelium has been disrupted by tissue injury, re-
epithelialization must occur as rapidly as possible in order to re- establish
Tissue Integrity.
• Keratinocytes start moving into the defect about 24 hours after the injury.
• The keratinocytes use receptors on their surface, known as Integrins to
bind to laminin in the basal lamina.
• Mobilization of cells: achived by 2 distinct processes
• Migration: locomotion of epithelial cells
• Mitosis: mitotic growth of cells
A)-REEPTHELIALIZATION

25. FIG : Keratinocytes express a number of integrin receptors (a2b1 to a6b4) and
extracellular matrix proteins (LM5: laminin-5; TN: tenascin-C; FN ED-A:
fibronectin isoform EIIIA) while they migrate through wound provisional
matrix.FC: fibrin clot; CT: connective tissue; E: epithelium. +++ refers to the
strong immunoreaction at this stage of healing.

27. β3 - inhibits the growth of primary human keratinocytes β1- stimulate
keratinocyte motility by switching the cells from the differentiating to
regenerative phenotype and by inducing their production of fibronectin
& laminin-5

28. • Basal and suprabasal cells from both the cut margins undergoes
dedifferentiation and acquire potential for amoeboid movement
• Start proliferating and migrating towards the incisional
space in the form of epithelial spurs.
• The movement of monolayer or sheets of cells during this
migration is termed “streaming”
• Pattern: caterpillar track, frog leap phenomemon, sliding
model
FIrst keratinocytes to migrate are highly phagocytic

29. • migration and proliferation of epithelial cells -Begins within 24 hours and
Well approximated wound is covered by a layer of epithelium in 48
hours.
• For excised wound time depends upon its surface area
• Cell migratory rate: 0.5-1mm/day
• Contact from opposing edges: Epithelial seal
• Once seal is established- mitosis and definitive layers of stratified
squamous epithelium forms.

30.  connective tissue repair by:
1. Activation of FIBROBLASTS
2. Formation of GRANULATION TISSUE
3. ANGIOGENESIS
4. CONTRACTION of the wound by
Myofibroblasts.
HEALING OF CONNECTIVE TISSUE

31.  Wound repair involves phenotypic change of fibroblasts from quiescent -
proliferating cell - to migratory - 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 majorcomponents.
 Consequently, quiescent fibroblasts express collagen receptors α1β1 and
α2β1 and the major fibronectin receptor α5β1 integrin which they use for
adhesion to the matrix.
1.ACTIVATION OF FIBROBLASTS

32. Fibrin –
fibrinogen
matrix
FibroblAsts
will require
Fibronectin
in the ECM
Cell
membrane
bound
integrins,to
be bound to
Factors
stimulating
migration –
PDGF,TGF-B,
EGF
Fibroblasts
Will migrate
Growth
Factors
Macrophage
s
Migrating cells
develop
lamellopodia
Extend until
2nd site is
detected in
the matrix.
Cell
migrates,
using the
new site as
an anchor
Fibroblasts secrete several
proteolytic enzymes : MMP-1,
MMP-2, MMP-3
unde
r the influence of TGF-β
To facilitate
migration
through such
debris
Cell
migration
may be
impeded by
residual
debris

33. Prominent cell type by 3 to 5
days in clean, noninfected
wounds
Initial wound matrix
is provisional -
composed of fibrin,
GAG & hyaluronic
acid
Cell division &
proliferation
Concomitantly, collagens
types I and III are
deposited onto the
fibronectin and GAG
scaffold in a
disorganized array.
Proteoglycan
concentration
increases with
time in a manner
paralleling
collagen

34.  Synthesis is stimulated by TGF-β, PDGF & EGF
 Collagen deposition ↑ the strength of the wound providing
moreresistance to traumatic injury
 Cells involved in inflammation, angiogenesis, and
connective tissue construction attach to, grow and
differentiate on the collagenmatrix.
 Type III collagen predominates initially : 30%
 Accelerated type III collagen synthesis is correlated with
fibronectin secretion after injury
 Collagen synthesis continues at a maximal rate for 2 to 4
weeks andsubsequently begins to slow.
 COLLAGEN production starts by the 3rd post-wounding day

35.  PROTEOGLYCANS binds to proteins and alter their orientationin a
manner that influences their activity.
• Dermatan Sulfate - orients collagen molecules in a manner thatfacilitates
fibril formation
• Hyaluronan - contributes to tissues viscoelastic properties andacts as a
potent modulator of cellular migration .
• Elastin, an another component of wound matrix that provides elasticity to
normal skin is not synthesized in response to injury and is the reason for
increased stiffness and decreased elasticity ofscar as compared with normal
dermis.

36. • New connective tissue begins to form approx. 2–4
days afterwounding.
• Begins with the formation of the epithelial seal.
• According to Gillman (1955)
• In shallow wound: onset of fibrogenesis occurs
after migration of the epithelial cells
• Deep excised wound: first granulation tissue is
built up from the base and then epithelial
migration occurs on this new C.T.
1.GRANULATION TISSUE FORMATION

37. Fibroblasts + RBCs matrix + patent single cell lined capillaries
surrounded by fibroblasts & inflm cells
•Fluid rich, source of growth factors & Defensins

38. During the formation of granulation tissue, macrophages, fibroblasts and new blood
vessels grow into the wound space in a coordinated manner
•On the granulation tissue frame work
•Migration & proliferation of fibroblasts
•Deposition of ECM by fibroblast
•Driven by PDGF, FGF-2,TGF-β : Inflammatory cells &
: Activated endothelial

39. During the formation of granulation tissue, macrophages,
fibroblasts and new blood vessels grow into the wound
space in a coordinated manner
•On the granulation tissue frame work
•Migration & proliferation of fibroblasts
•Deposition of ECM by fibroblast
•Driven by PDGF, FGF-2,TGF-β : Inflammatory cells &

40.  Angiogenesis or Neovascularisation is a fundamental process to
healing and becomes active from 2nd day after wounding.
 Angiogenesis process
• stimulation by chemical signals or hypoxia
• endothelial cell proliferation
• directional migration of endothelial cells
• organisation and differentiation to form capillary tubes
 Functions of new formed blood vessels
• supply of oxygen and nutrients
• transport of degradation products
• cell settlement
3.ANGIOGENESIS

43. MAYOFIBROBLAST • Modified fibroblasts - described by Gabbiani et al
(1971) •
• Appear 4 to 6 days after injury & seen in the wound during the later 2 to
3 weeks.
• Move along fibronectin linked to fibrin in the provisional ECM in order
to reach the wound edges & form connections to the ECM and attach to
each other & to the wound edges
• As the actin in myofibroblasts contracts, the wound edges are pulled
together and fibroblasts lay down collagen to reinforce the contracted
wound.
• Reduces wound size by 40-80%
• After contraction –apoptosis →New normal CT fibroblasts emerge

44. 4. CONTRACTION
Phase includes: • Collagen Remodeling • Blood Vessel
Apoptosis
About 14 days post operatively wound is filled with fibers
that run in all direction and remodeling begins • Decrease
in fibroblasts • Decrease in vascularity
Remodeling consist of 2 distinct processes (Homes,1959) •
Resorption & change in orientation of the first deposited
fibers
Enlarging or increasing the numbers of oriented fibers

45. Phase includes: • Collagen Remodeling • Blood Vessel
Apoptosis About 14 days post operatively wound is
filled with fibers that run in all direction and
remodeling begins • Decrease in fibroblasts • Decrease
in vascularity Remodeling consist of 2 distinct
processes (Homes,1959) • Resorption & change in
orientation of the first deposited fibers • Enlarging or
increasing the numbers of oriented fibers

46. TYPE III COLLAGEN, which is prevalent during
proliferation, is gradually degraded and the stronger
TYPE I COLLAGEN is laid down.
Originally disorganized collagen fibers are rearranged,
cross linked, and aligned along tension lines, the
tensile strength of the wound increases
After tissue remodeling is finished redundant blood
vessels undergo apoptosis.

47. FACTORS INFLUENCING HEALING LOCAL FACTORS •
Oxygenation
Infection
Foreign Body
Venous Insufficiency
Exposure To UV Light Facilitates Healing
Exposure To Ionizing Radiation

48. SYSTEMIC FACTORS • Age and gender • Sex hormones • Stress •
Diseases: diabetes, keloids, fibrosis.hereditary healing
disorders.Jaundice. • Obesity • Alcoholism • Smoking • Medications:
glucocorticoid steroids, NSAIDS, chemotherapeutic drugs. •
Immunocompromised conditions: cancer, radiation therapy, AIDS •
Nutrition

51. HEALING OF ORAL WOUNDS Oral wounds heal
faster and with less scarring than extra oral wounds
It is mainly due to:
FACTO
R
MECHANI
SM
Saliva Moisture, ionic strength, ions – Mg
& Ca Growth factors(EGF,VEGF,
TGFΒ,FGF,IGF)
Bacteria Stimulation of macrophage influx,
Direct stimulative action on keratinocyte and
fibroblast
Phenotype
ofcells
Fetal like fibroblasts with unique
response, Specialized epithelium &
Connective tissue

52. HEALING AFTER PERIODONTAL
PROCEDURES

53. Numerous polymorphonuclear leucocytes can be seen b/w residualepithelial cells &
crevicular surface