1. The document discusses inflammation, its classification as acute or chronic, the vascular and cellular events of acute inflammation, and the various chemical mediators involved. 2. Chronic inflammation is characterized by infiltration of mononuclear cells like macrophages and lymphocytes. Macrophages persist long-term in chronic inflammation and cause tissue destruction through the release of enzymes and cytokines. 3. Healing occurs through proliferation and replacement of damaged tissues with connective tissue in chronic inflammation.

1. INFLAMMATION HEALING AND
REPAIR
1
& DENTAL
IMPLICATIONS
Dr. SAUMYA PAUL
Pg 1st yr
Dept . Of Paedodontics

2. INTRODUCTION - History
General features of inflammation
2
Classification of inflammation
ACUTE INFLAMMATION – Stimuli
Vascular Events & Cellular Events Morphology of acute
inflammation
CHEMICAL MEDIATORS OF INFLAMMATION
CHRONIC INFLAMMATION – causes
features
DENTAL ASPECTS OF INFLAMMATION
DENTAL ABSCESS

3. 3
WOUND HEALING
Introduction
Regeneration & Repair
Healing by primary intention & secondary
intention Factors affecting healing
Healing in oral tissues - Extraction socket
Re-implanted tooth Alveolar bone
Newer concepts in healing

4. INTRODUCTION
"A localised protective response elicited by
injury or destruction of tissues , which
serves to destroy , dilute or wall off both
infective agent and injured tissue.
According to ROBINS
INFLAMMATION is a complex reaction to
injurious agent such as microbes and damaged
, necrotic cells that consist of vascular
responses , migration , and activation of
leukocytes and systemic reaction
4

5. HISTORICAL HIGHLIGHTS
Egyptian Papyrus , 3000 BC CELSUS , Roman Writer
- 1 AD - CARDINAL SIGNS
JOHN HUNTER , 1793 –
“ Inflammation is not a disease
but a salutary effect on host” blood vessels & cells 5
JULIUS CONHEIM-1st used
microscope to observe inflamed

6. GIVEN BY CELSUS
• REDNESS
• SWELLING
• HEA
T
• PAIN
Rubor
Tumor
Calor
Dolor
• LOSS OF FUNCTION function
laesa
BY VIRCHOW
6

7. CLASSIFICATION
ACUTE
INFLAMMATION
CHRONIC
INFLAMMATION
7

8. ACUTE INFLAMMATION
INFECTIONS :
Bacterial / viral /
parasitic & microbial
toxins
An acute condition is one with a rapid onset and/or a short course
Physical / chemical
agents
ex. thermal injury
Trauma :
Blunt / penetrating Foreign body eg
sutures / splinters
Immune reactions /
hypersensitivity
reactions
8

9. ACUTE INFLAMMATION
Alteration in
vascular calibre/
HEMO-DYNAMIC
change
Structural changes
in micro-
vasculature
Emigration of
leukocytes &
accumulation in
focus of injury
9

10. ACUTE INFLAMMATION
HEMODYNAMIC CHANGES /
Change in vascular flow
CHANGE IN VASCULAR
PERMEABILITY
10

11. ACUTE INFLAMMATION
HEMODYNAMIC CHANGES / Change in vascular flow & calibre
Transient vasoconstriction
Vasodilation
Increased permeability of
microvasculature
Stasis
Emigration of leukocytes
11

12. TRANSIENT VASOCONSTRICTION
 Arterioles
 3-5 sec. in mild injury
 5 min in severe injury
12

13. PERSISTENT PROGRESSIVE VASODILATION
• 1st involves arteriole , then other capillary bed
• seen in 1st 30 min.
• Results in Incr. blood vol. in microvascular bed -
redness and warmth
• By mediators
- Nitric oxide (NO)
- Histamine 13

14. INCREASED PERMEABILITY OF
MICROVASULATURE
14
• Contraction of endothelial cells - Histamine
• Retraction of endothelial cells – cytokine IL – 1 , TNF
• Direct injury to endothelial cells
• Endothelial injury mediated by leukocytes
• Leakage from new blood vessels

15. STASIS
Increased vascular permeability leads
to loss of fluid from microvasculature
Concentration of red cells in small
vessels
Slower blood flow
S
T
A
S
I
S 15

16. LEUCOCYTIC MIGRATION & EMIGRATION
Stasis is followed by peripheral
orientation of leucocytes along vascular
endothelium
Movement of leucocytes in
extracellular space through gaps b/w
endothelium.
16

17. 17

18. 18

19. CELLULAR EVENTS
Deliver leukocytes to site
of injury
To perform their function
Ingest offending
bacteria
Kill bacteria &
other microbes
Get rid of necrotic
tissue & foreign
substance 20

20. CELLULAR EVENTS
• Margination
• Rolling
• Adhesion
IN THE LUMEN
TRANS-
MIGRATION
EMIGRATION
CHEMOTAXIS
• Migration into
interstitial tissue
CHEMOTAXIS
PHAGOCYTOSIS
20

21. CELLULAR EVENTS • Margination
• rolling
• Adhesion
IN THE LUMEN
21

22. • Margination
• Rolling
• Adhesion
IN THE LUMEN
CELLULAR EVENTS
Leukocytes now tumble along the endothelium
Have a TRANSIENT adhesion with endothelium
22

23. • Migration
IN THE LUMEN
• Rolling
• Adhesion
CELLULAR EVENTS
23

24. TRANS- MIGRATION
CELLULAR EVENTS
PSEUDOPODIA
SQUEEZE THROUGH INTER-ENDOTHELIAL
JUNCTION
LIE B/W ENDOTH. CELLS & BASEMENT
MEMBRANE
24
“Across” the endothelial wall

25. EMIGRATION
CELLULAR EVENTS
EXTRA-VASCULAR
SPLACE
Leukocytes lodged b/w BASEMENT MEMBRANE
& ENDOTHELIUM
Release COLLAGENASES and cause local defect
in membrane.
25

26. EMIGRATION
CELLULAR EVENTS
EXTRA-VASCULAR
SPLACE
26

27. CHEMOTAXIS
CELLULAR EVENTS
Along chemical gradient
27
The chemotatctic factor mediated
transmigration of leucocytes after
crossing several barriers reach
the interstitial tissues , known as
CHEMOTAXIS

28. EXOGENOUS
SUBSTANCES
ENDOGENOUS
SUBSTANCES
Bacterial Products :
a)Peptides – N – formyl
methionine terminal amino
acid
b)Lipids
a) Leukotriene -B4
b) PF-4
c) Components of
complement system
d) Cytokine :
IL – 1, 5 , 6
e) Monocyte
chemoattractant
protein
f) Chemotactic factor
for CD-4 + T cells
g) Eotaxin chemotactic
factor for
eosinophils
CELLULAR EVENTS
28

29. PHAGOCYTOSIS
Process of engulfment of solid
particulate material by the cell
(cell eating)
2 phagocytic cells are :-
PMN’S
MICROPHAGES

30. CELLULAR EVENTS
PHAGOCYTOSIS
E DEGRADATION / KILLING STAGE
RECOGNITION AND ATTACHMENT OF
PARTICLE
ENGULFMENT WITH FORMATION OF
PHAGOCYTIC VESICLE
DEGRANULATION STAGE / KILLING &
31

31. CELLULAR EVENTS
RECOGNITION AND ATTACHMENT OF PARTICLE
1
CHEMO-TACTIC AGENTS
 Ig G
 C3b
Opsonin
 Lectins
 MANNOSE
RECEPTOR
 SCAVENGER
RECEPTOR
32

32. ENGULFMENT WITH FORMATION
OF PHAGOCYTIC VESICLE
2
CELLULAR EVENTS
32

33. DEGRANULATION STAGE
3
CELLULAR EVENTS
Preformed granule stored products of PMNs are released into
phagolysosome
Mononuclear phagocyte also secrete enzymes eg
•IL-2 , 6-TNF
•Arachidonic acid metabolites (Prostaglandin , leukotriene , platelet activating factor
•Oxygen metabolites
33

34. KILLING & DEGRADATION STAGE
4
CELLULAR EVENTS
OXYGEN – DEPENDENT
BACTERICIDAL
MECHANISM
OXYGEN–INDEPENDENT
MECHANISM
34

35. KILLING & DEGRADATION STAGE
 Production of reactive oxygen metabolites
 NADPH oxidase
ESSENTIAL ENZYME
H2O2
35

36.  AZUROPHILLIC GRANULES contain
MPO – DEPENDENT KILLING
H202 HOCl + H2O
MPO – INDEPENDENT KILLING
MPO
MORE POTENT
ANTIBACTERIAL
AGENT
H2O2  Performs
the action
 weaker
36
Hypohalous
acid

37. CELLULAR EVENTS
They include:
 Lysosomal hydrolases
 Permeability increasing factors
 Defensins
 Cationic proteins
37
Some agents do not require oxygen for bacterial activity

38. VARIOUS TERMS USED IN INFLAMMATION
EXUDATION:-the escape of
fluid, protein and blood
cells from the vascular
system into the interstitial
tissue or body cavitie is
known as exudation.
An exudate is an inflammatory
extravascular fluid that has a
high protein concentration much
cellular debris and a specific
gravity of > 1.020.
Its an ultra filtrate of blood
plasma and results from
hydrostatic imbalance across
the vascular endothelium.
Transudate :- is a fluid with
low protein content most of
which is albumin and a
specific gravity of < 1.012.

39. EDEMA :-denotes an excess of
fluid in the interstitial tissue or
serous cavities it can be either a
exudate or transudate.
PUS:- a purulent exudate is an
inflammatory exudate rich in
leukocytes and parenchymal cell
debris

40. MORPHOLOGY OF ACUTE INFLAMMATION
40

41. MORPHOLOGY OF ACUTE INFLAMMATION
40

42. SYSTEMIC EFFECTS OF ACUTE INFLAMMATION
FEVER LEUCOCYTOSIS
LYMPHANGITIS -
LYMPHADENITIS
Rigors chills Malaise
, anorexia
Increased pulse
rate
42

43.  filters the extravascular fluids
 in inflammation…. lymph flow is inc. and helps drain the edema fluid
from extravascular space
LYMPHATICS
LYMPHANGITIS
DRAINING LYMPH NODES
LYMPHADENITIS
43

44. ͚ MEDIATOR ‘ :One that reconciles differences b/w disputants
CHEMICAL MEDIATORS :chemical substances that mediate the
process of inflammation.
44

45. CHEMICAL MEDIATORS OF INFLAMMATION
 Present
45
in plasma in
precursor form
 Must be activated to
acquire biologic properties
 Pr. In intracellular granules
 Major cellular sources
Platelets Neutrophil
Monocyte / macrophage

46. CHEMICAL MEDIATORS OF INFLAMMATION
VASO – ACTIVE AMINES
HISTAMINE
Sources:
1) Mast cells in CT adjacent to
Blood vessels
2) Blood basophils
3) Platelets
STIMULI : Injury
Immune reactions
Fragments of complement -
C3a , C5a
Neuropeptides
eg substance P
Cytokines IL – 1 , 8
SEROTONIN
46
 SOURCE : 1) Platelets
2) Enterochromaffin cells
 STIMULI : Platelet aggregation after
contact with collagen ,
thrombin

47. Dilation of arterioles
Permeability of
vasculature
47

48. CHEMICAL MEDIATORS OF INFLAMMATION
ARACHIDONIC ACID METABOLITES
A fatty acid with 2 main sources :
 Directly through diet
 Through conversion of essential fatty acid
Arachidonic acid ARACHIDONIC
ACID METABOLITES
Cyclo – oxy- genase pathway
Lipo – oxy- genase Pathway
CYCLO – OXY- GENASE
PATHWAY
 Prostaglandin -
PGD2 ,
E2 , F2
 Thromboxane A2
 Prostacyclin
LIPO – OXY – GENASE
PATHWAY
48
 5 – HETE
 Leukotrienes

49. CHEMICAL MEDIATORS OF INFLAMMATION
LYSOSOMAL COMPONENTS
PRIMARY SECONDARY
 MPO
 ACID
HYDROLASES
 NEUTRAL
PROTEASES
 LACTOFERRIN
 LYSOZYME
Alk. Phosph
Collagenase
• ACID PROTEASE
• COLLAGENASE
• ELASTASE
• PLASMINOGEN ACTIVATOR 48

50. CHEMICAL MEDIATORS OF INFLAMMATION
CYTOKININS
49
• proteins produced mainly by- activated lymphocytes & macrophages , also
from endothelium, epithelium & connective tissue cells.
TNF and IL - 1
• major cytokines that mediate inflammation.
• Produced mainly by activated macrophages
STIMULI :
• Immune reactions,
• physical injury & variety of inflammatory stimuli.
• endotoxins & other microbial products

51. CHEMICAL MEDIATORS OF INFLAMMATION
NITROUS OXIDE
 mediates in vascular dilation
Released by activated neutrophils and macrophages
Superoxide , hydrogen peroxide , hydroxl ion
ACTION : Endothelial cell damage- inc. vascular permeability
Damage to cells and tissue matrix by activating protease and inactivating anti-
protease
6 OXYGEN METABOLITES
59

52. MEDIATORS BRINGING ABOUT ROLLING& ADHESION
SELECTINS
INTEGRINS
IMMUNOGLOBULIN
SUPERFAMILY
ADHESION
MOLECULES
52
• P – Selectins
• E – Selectins
• L – Selectins
• ICAM – 1
• VCAM - 1

53. CHEMICAL MEDIATORS OF INFLAMMATION
KININ SYSTEM
CLOTTING SYSTEM
COMPLEMENT
SYSTEM
53

54. FACTOR XII
FACTOR XIIa
FIBRINOLYTIC
SYSTEM
CLOTTING
SYSTEM
KININ SYSTEM
PLASMIN FIBRIN BRADYKININ
COMPLEMENT SYSTEM
C3a , C5a
54

55. FATE OF ACUTE INFLAMMATION
ACUTE
INFLAMMATION
RESOLUTION
HEALING BY
SCARRING
PROGRESSION TO
SUPPURATION
PROGRESSION TO
CHRONIC
INFLAMMATION
55

56. CHRONIC INFLAMMATION
Inflammation of prolonged duration (weeks to months) in which
are proceeding
inflammation , tissue destruction and
simultaneously.
attempts at repair
CAUSES
Following acute inflammation
Begin insidiously as a low – grade inflammation
 Persistent inf. By micro-organisms : tubercle bacilli ,
 Prolonged exposure to toxic agents
 Auto - immunity
56

57. FEATURES OF CHRONIC INFLAMMATION :
CHRONIC
INFLAMMATION
Tissue
destruction
Healing by Proliferation &
connective tissue replacement
of damaged tissue
57
Infiltration with mononuclear cells
-macrophages , lymphocytes and
plasma cells

58. INFILTRATION WITH MONO-NUCLEAR CELLS
58

59. • Incr. lysosomal enzymes
• Greater ability to
ACTIVATION OF MACROPHAGE
Cytokine
Endotoxin ,
fibronectin
chemical
mediators
phagocytose 59

60. MACROPHAGE
IN ACUTE
INFLAMMATION
* Irritant eliminated
– macrophage
disappears
IN CHRONIC INFLAMMATION
Persistent macrophage accumulation by
following mechanisms :
1. )Recruitment from circulation –
Chemotactic stimuli include :
a)C5a
b)Platelet derived growth factor
c)Transforming growth factor
2.) Local proliferation of macrophages
3.) Immobilization of macrophages
MACROPHAGE
59

61. TISSUE DESTRUCTION OR NECROSIS
• ACTIVATED
MACROPHAGES
Elastase
Protease
Collagenase
Reactive oxygen radical
Cytokine IL-1,8
69

62. PROLIFERATION
NEW BLOOD
VESSELS
62
FIBROBLAST
Helps in healing of damaged tissue

63. INFLAMMATION OF PULP & PERIAPICAL TISSUE
DEEP DENTAL
CARIES
TOOTH
FRACTURE
CRACKED TOOTH
SYNDROME
CHEMICAL
CHANGES
THERMAL
CHANGES
63

64. 64
Involves enamel
Progresses to
dentin
Invade pulp

65. REACTIONS OF PULP TO BACTERIAL INVASION
ᶲVascular changes take place inside
blood vessels.
ᶲPMNLs reach the area of inflammation
ANATOMICAL FEATURES OF
PULP THAT TEND
TO ALTER THE RESPONSE
Enclosure of pulp in rigid calcified walls -
PREVENTS EXCESSIVE SWELLING thus more painful.
Pressure leads to decr. Blood supply and ischemia
– does not get corrected since collateral circulation
cannot develop through tiny apical foramina 65

66. HISTOLOGIC FEATURES OF PULPITIS
ACUTE CHRONIC
•Through quiescence of
acute pulpitis
•Begin as chronic d/s
from onset
MONONUCLEAR CELLS
PREDOMINATE - chiefly
plasma cells &
lymphocytes.
Fibroblastic activity is
evident
collagen fibres seen
in bundles
66
• Continued vascular dilation
• Accumulation of oedemal
fluid in connective tissue
• Pavementing Of PMNLs
along endothelial wall

67. UNTREATED PULPITIS
ACUTE CHRONIC
PULPITIS
UNTREATED
APICAL
PERIODONTITIS
PERIAPICAL ABSCESS PERIAPICAL
GRANULOMA
67

68. UNTREATED PULPITIS
• Inflammation of periodontal ligament around root apex..
Changes localized around the
root- periapical radioluscency
Abscess Formation
68
Bone resorption

69. PYOGENIC ABSCESS PYAEMIC ABSCESS COLD
69
ABSCESS
• Commonest type
• mostly found in soft
tissues
• eg periapical abscess
• occurs due to
circulating bacterial
emboli in blood
Abscess without signs
of inflammation
Eg Tubercular abscess

70. ABSCESS FORMATION / SUPPURATION
Acute bacterial inf. + intense neutrophillic infiltrate
TISSUE NECROSIS
Cavity is formed called an ABSCESS
Contain purulent exudate called as PUS
70

71. Rise in pressure with inflammatory
exudate MICRO- ABSCESS
Local tissue hypoxia
Localised destruction , breakdown of
leucocytes , bacteria & tissue
ABSCESS FORMATION
PERIAPICAL ABSCESS
71

72. Disintegrating
PMNLs
Viable leukocytes ,
lymphocytes , bacterial
colonies
Dil. Blood vessels in
adj. PDL and marrow
spaces + serous
exudate
72

73. ( DENTO-ALVEOLAR ABSCESS / ALVEOLAR ABSCESS )
Tender on percussion
Will feel slightly away
from socket
Fever & regional
lymphadenitis
73

74. ACUTE PERIAPICAL
ABSCESS
CHRONIC FORM
Takes the path of
least resistance in
tissues
SINUS
FISTULA / PARULIS
/ GUM BOIL
74

75. Clinical application of inflammation
Gingival inflammation
PHOENIX ABSCESS (Sinus formation)
Pyogenic granuloma
Periapical granuloma Periapical/radicular
cyst
Periapical/radicular cyst

76. 76

77. WOUND : Anatomic or functional interruption in continuity of a
tissue that is accompanied by cellular damage and death
MAY BE INFLICTED BY :
INTRODUCTION
Physical injury Chemical injury
directed towards
Biologic injury
the injured
Series
tissue of body to
of co-ordinated processes restoring
as near normal as possible is termed as WOUND
HEALING
77

78. GOAL
a.) to restore continuity b/w wound edges
b.) To re-establish tissue function
REGENERATION
REPAIR
Biologic process by which
both structure and
function of disrupted or lost
tissue is completely restored.
Biologic process whereby
continuity of disrupted or
lost tissue is regained by
new tissue which
does not restore
structure & function 78

79. REGENERATION
• Healing by proliferation of
parenchymal cells,
• results in complete restoration of the
original tissues
Cell growth
Cell
differentiation
Cell-matrix
interaction
79
GROWTH FACTORS
1. Epidermal
2. Fibroblast
3. Platelet derived
4. Endothelial
5. Transforming

80. REPAIR
Healing by conn. Tissue Fibrosis and scarring
Phase of inflammation
Phase of clearance
Phase of growth of granulation tissue
80

81. TYPES OF WOUND HEALING
PRIMARY SECONDARY TERTIARY
80

82. HEALING BY PRIMARY INTENTION / FIRST
INTENTION
82
Conditions:
• Clean and uninfected wounds
• Surgically incised
• Edges are Approximated
• Without much loss of tissue

83. Initial Hemorrhage:
Acute inflammatory
Response: Epithelial changes:
Organization :
HEALING BY PRIMARY INTENTION
/ FIRST INTENTION
83

84. Initial hemorrhage
INJURY SEVERES VASCULATURE
Leads to extravasation of
plasma
, platelets , erythrocytes and
leukocytes
Initiates coagulation
cascade that produces
blood clot
84

85. INFLAMMATORY RESPONSE
Begins within 24 hrs with
appearance of polymorphs from
margin of incision
From 3rd day Polymorphs replaced
with macrophages
85

86. Basal cells from both cut margins start proliferating
and migrating towards incisional space in form of
epithelial SPURS
A well approximated wound is covered by layer of
epithelium in 48 hrs
By 5th day a multilayered new epidermis is formed.
86
PROLIFERATIVE PHASE – involves epithelial changes

87. Organisation starts by 3rd day
5th day : new collagen fibrils start forming
which dominate till healing is complete
In 4 weeks Scar tissue formed
• Scanty cellular and vascular elements
• few inflammatory cells
87
REMODELLING PHASE – involves ORGANISATION

88. CONDITIONS:
Open wound with a large tissue defect
Having extensive loss of cells and tissue
Wound is not approximated by sutures
HEALING BY SECONDARY INTENTION
88

89. Initial Hemorrhage:
Acute inflammatory
Response: Epithelial changes:
Granulation tissue:
Wound contraction:
89

90. INFLAMMATION INGROWTH OF
GRANULATION TISSUE
CLEARANCE
• Autocatalytic
90
ANGIOGENESIS FIBROGENESIS
• Neutrophils and
monocytes enzymes

91.  MOIST ENVIRONMENT
 UNUSUAL ANATOMIC SITUATION
 COUNTLESS MICROORGANISMS
 MARKED CAPACITY FOR REGENERATION
 EASY REMODELLING OF SCAR TISSUE
fibroblasts in oral mucosa are phenotypically different from those of skin & more
closely resemble fetal fibroblasts .
90

92. HEALING OF EXTRACTION SOCKET
Consists of erythrocytes &
leucocytes in mesh of fibrin
92
STAGE 1 : coagulation
STAGE 2 : Granulation tissue
STAGE 3 : Connective
Tissue collagen & reticulo
endoth. fibres
STAGE 4 : Bone Development
Begins at 7th post op day By
40th day socket almost
completely filled with
WOVEN bone
STAGE 5 : Epithelial
Repair Begins at 4th post
op day ; completes by 24th
day
Tooth
extraction
Initial angiogenesis
Day 1 to 3 weeks
New bone
formation
3-4 weeks
Bone
growth
4-6 weeks
Bone re
organisation
6 weeks to 4
months

93. FIBROUS UNION
93
• Occurs when tooth xtn accompanied with both buccal and lingual
periosteum loss.
• RADIOGRAPHIC FEATURES : well circumscribed radiolucent area in site
of previous extraction.
May be mistaken for residual infection
• HISTOLOGIC FEATURES : dense bundles of collagen with occasional
fibrocytes and few blood vessels
• TREATMENT : Excision of wound

94. DRY SOCKET
• Most common and painful complication
• Occurs due to disintegration / loss of
blood clot
CLINICAL FEATURES :
• Foul odour
• Severe throbbing type of pain
TREATMENT
• AIM : to keep socket clean
to protect exposed bone
• Irrigation with mild warm antiseptic
Palliative socket dressing of ZOE –
iodoform gauze 94

95. HEALING OF RE-IMPLANTED TOOTH
OCLOT b/w root n ruptured PDL
O FIBROBLAST PROLIFERATION on PDL remnants on bone
side
O RECONNECTION – occurs by collagen fibres extending from
cementum to alveolar bone
O REATTACHMENT OF EPITHELIUM – by 7th day
o2-4 weeks - complete regeneration of PDL 95

96. Mainly by regeneration
1-2 weeks
96

97. RESPONSE : resorption and remodelling
CHRONIC INFECTION
RESORPTION
GRANULATION
ACUTE INFECTION
ABSCESS / CELLULITIS
Inf. In marrow - OSTEOMYELITIS
97

98. Pulp is highly specialised loose connective tissue with specific response to
surgical and traumatic injuries and bacterial insult
PREDOMINANT CELL TYPES IN PULPAL REPAIR
Fibroblasts - present uniformly throughout pulp
Undifferentiated mesenchymal cells – located paravascularly
PULPAL VASCULATURE in healing :
Within pulp -especially apically- ARTERIO-VENOUS shunts are
present
Control the tissue pressure during inflammation
When tissue pressure exceeds that of venules ,
results in decrease of blood flow
98

99. DEFENSE
RESPONSE
Aims at
neutralising or
controlling
bacterial invasion
Involves creating
barrier
against micro –
org. by
•granulation tissue
•hard tissue –
secondary dentin /
cementum
2 BASIC RESPONSE DETERMINING HEALING OF PULP
DEFENSE
RESPONSE
PULPAL WOUND
HEALING RESPONSE
Damaged pulp
tissue is
healed by replacement
with
tissue
newly differentiated
Depends upon type of progenitor cells
involved
Eg. PDL derived progenitor cells –
cementum
deposition along RC walls Patent apical
foramen - Sharpeys fibre
insertion 99

100. 99
FACTORS INFLUENCING WOUND HEALING
LOCAL FACTORS
UV X - RAY
INFECTION FOREIGN BODY MOBILITY
RADIATION

101. 100
FACTORS INFLUENCING WOUND HEALING
SYSTEMIC
FACTORS
AGE
NUTRITIONAL DEFICIENCIES
• Vitamin C , E , A
• Proteins
BLOOD DYSCRASIAS