inflammation & healing & dental implications

1

INFLAMMATION

AND HEALING

Dr. Rupali PG – CODS , Davangere

& DENTAL IMPLICATIONS

2

INTRODUCTION - History General features of inflammation

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

WOUND HEALING

Introduction

Regeneration & Repair

Healing by primary intention & secondary intention

Healing in oral tissues - Extraction socket Re-implanted tooth Alveolar bone Newer concepts in healing

Factors affecting 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 ROBINSINFLAMMATION 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

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”

JULIUS CONHEIM-1st used microscope to observe inflamed blood vessels & cells

6

SIGNS OF INFLAMMATIONGIVEN BY CELSUS

• REDNESS

• SWELLING

• HEAT

• PAIN

Rubor

Tumor

Dolor

Calor

• LOSS OF FUNCTION FUNCTIO LAESA

BY VIRCHOW

7

CLASSIFICATION

ACUTE INFLAMMATION

CHRONIC

INFLAMMATION

8

ACUTE INFLAMMATION

An acute condition is one with a rapid onset and/or a short course

INFECTIONS :Bacterial / viral /

parasitic & microbial toxins

Trauma : Blunt / penetrating

Physical / chemical agents

eg thermal injury

Foreign body eg sutures / splinters

Immune reactions / hypersensitivity

reactions

9

ACUTE INFLAMMATION

Alteration in vascular calibre/HEMO-DYNAMIC

change

Structural changes in micro-

vasculature

Emigration of leukocytes &

accumulation in focus of injury

10

ACUTE INFLAMMATION

VASCULAR CHANGES HEMODYNAMIC CHANGES /

Change in vascular flow & calibre

CHANGE IN VASCULAR PERMEABILITY

11

ACUTE INFLAMMATION

HEMODYNAMIC CHANGES / Change in vascular flow & calibre

Begin earlyDevelop at varying rates…..severity…

Transient vasoconstriction

Vasodilation

Increased permeability of microvasculature

Stasis

Emigration of leukocytes

12

TRANSIENT VASOCONSTRICTION

Arterioles 3-5 sec. in mild injury………5 minutes ; severe injury

13

PERSISTENT PROGRESSIVE VASODILATION

• 1st involves arteriole ………then other capillary bed• seen in 1st 30 min.• Results in Incr. blood vol. in microvascular bed

• By mediators - Nitric oxide (NO) - Histamine

Heat

Redness

14

INCREASED PERMEABILITY OF MICROVASULATURE

• 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

STASIS

16

LEUCOCYTIC MIGRATION & EMIGRATION

Stasis is followed by peripheral orientation of leucocytes along vascular endothelium

LEUCOCYTIC MIGRATION

Movement of leucocytes in extracellular space through gaps b/w endothelium.

EMIGRATION

17

CELLULAR EVENTS

18

CELLS OF INFLAMMATION

19

Neutrophils Macrophages

20

CELLULAR EVENTS

Deliver leukocytes to site of injury

To perform their ‘FUNCTION’

ACTIVATE

Ingest offending bacteria

Kill bacteria & other microbes

Get rid of necrotic tissue & foreign substance

21

CELLULAR EVENTS

DELIVERY OF LEUKOCYTES TO SITE OF INJURY

• Margination • Rolling• Adhesion

IN THE LUMEN

CHEMOTAXIS

PHAGOCYTOSIS

FUNCTION

22

CELLULAR EVENTS • Margination • rolling• Adhesion

IN THE LUMEN

MARGINATION

23

• Margination • Rolling• Adhesion

IN THE LUMEN

CELLULAR EVENTS

ROLLING

Leukocytes now tumble along the endothelium

Have a TRANSIENT adhesion with endothelium

24

• Migration • Rolling• Adhesion

IN THE LUMEN

CELLULAR EVENTS

ADHESION

25

TRANS- MIGRATION

CELLULAR EVENTS

‘ TRANS ‘ across

PSEUDOPODIA

SQUEEZE THROUGH INTER-ENDOTHELIAL JUNCTION

LIE B/W ENDOTH. CELLS & BASEMENT MEMBRANE

‘across’ the endothelial wall..

26

EMIGRATION

CELLULAR EVENTS

EXTRA-VASCULAR SPLACE

Leukocytes lodged b/w BASEMENT MEMBRANE & ENDOTHELIUM

Release COLLAGENASES ….cause local defect in membrane

27

EMIGRATION

CELLULAR EVENTS

DIAPEDESIS

EXTRA-VASCULAR SPLACE

28

CHEMOTAXIS

CELLULAR EVENTS

Along chemical gradient

29

CHEMO-ATTRACTANTS

EXOGENOUS SUBSTANCES

ENDOGENOUS SUBSTANCES

Bacterial Products :a) Peptides – N – formyl

methionine terminal amino acid

b) Lipids

a) LTB-4b) PF-4c) Components of

complement systemd) Cytokine : IL – 1, 5 , 6e) Monocyte chemoattractant proteinf) Chemotactic factor

for CD-4 cellsg) Eotaxin chemotactic

factor for eosinophils

CELLULAR EVENTS

30

6 to 24 hours 24 to 48 hours

CELLULAR EVENTS

In chemotaxis…..

31

CELLULAR EVENTS

PHAGOCYTOSIS

RECOGNITION AND ATTACHMENT OF PARTICLE

ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE

DEGRANULATION STAGE

KILLING & DEGRADATION STAGE

32

CELLULAR EVENTS

RECOGNITION AND ATTACHMENT OF PARTICLE 1

CHEMO-TACTIC AGENTS

‘ OPSONINS ‘

Ig G

C3b Opsonin

Lectins

MANNOSE RECEPTOR

SCAVENGER RECEPTOR

33

ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE2

CELLULAR EVENTS

Fig 10.6 harsh mohan pg 101

PHAGO-LYSO-SOME

34

DEGRANULATION STAGE3

CELLULAR EVENTS

Mononuclear phagocyte also secrete enzymes eg • IL-2 , 6-TNF• Arachidonic acid metabolites (Prostaglandin , leukotriene , platelet activating

factor• Oxygen metabolites

Preformed granule stored products of PMNs are released into phagolysosome

35

KILLING & DEGRADATION STAGE4

CELLULAR EVENTS

OXYGEN – DEPENDENT BACTERICIDALMECHANISM

OXYGEN–INDEPENDENT MECHANISM

36

KILLING & DEGRADATION STAGE

OXYGEN – DEPENDENT MECHANISM

Production of reactive oxygen metabolites

NADPH oxidase ESSENTIAL ENZYME

H2O2

37

MYELO - PEROXIDASES AZUROPHILLIC GRANULES contain

MPO – DEPENDENT KILLING MPO – INDEPENDENT KILLING

H202 HOCl + H2O

MORE POTENT ANTIBACTERIAL AGENT

MPO

H2O2 Performs the action

weaker

38

OXYGEN – INDEPENDENT MECHANISM

CELLULAR EVENTS

Followed by :

Lysosomal hydrolases

Permeability increasing factors

Defensins

Cationic proteins

39

MORPHOLOGY OF ACUTE INFLAMMATION

40

MORPHOLOGY OF ACUTE INFLAMMATION

ACUTE

INFLAMMATION

PSEUDO-

MEMBRANE

BACTERIAL

INF. OF

BLOOD

CELLULITIS

ULCER

ABSCESS

41

SYSTEMIC EFFECTS OF ACUTE INFLAMMATION

FEVER LEUCOCYTOSISLYMPHANGITIS - LYMPHADENITISRigors chills

Malaise , anorexiaIncreased pulse rate

42

LYMPHATICS IN INFLAMMATION 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

CHEMICAL MEDIATORS OF INFLAMMATION‘ MEDIATOR ‘ : one that reconciles differences b/w disputants

CHEMICAL MEDIATORS : chemical substances that mediate the process of inflammation………..

44

CHEMICAL MEDIATORS OF INFLAMMATION

Present in plasma in precursor form

Must be activated to acquire biologic properties

Pr. In intracellular granules

Major cellular sources Platelets Neutrophil Monocyte / macrophage

45


CELL DERIVED MEDIATORS

VASO – ACTIVE AMINES

HISTAMINE

SOURCE : 1) Mast cells in C.T 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

SOURCE : 1) Platelets 2) Enterochromaffin cells

STIMULI : Platelet aggregation after contact with collagen , thrombin

46

ROLE IN INFLAMMATION

Dilation of arterioles

Permeability of vasculature

47


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

5 – HETE

Leukotrienes

48


LYSOSOMAL COMPONENTS

PRIMARY SECONDARY

MPO

ACID HYDROLASES

NEUTRAL PROTEASES

LACTOFERRIN

LYSOZYME Alk. Phosph Collagenase

• ACID PROTEASE

• COLLAGENASE

• ELASTASE

• PLASMINOGEN ACTIVATOR

49


CYTOKINES

• 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

50

NITROUS OXIDE


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

mediates in vascular dilation

51

MEDIATORS BRINGING ABOUT ROLLING & ADHESION

SELECTINS

INTEGRINS

IMMUNOGLOBULIN SUPERFAMILY

ADHESION MOLECULES

• P – Selectins• E – Selectins• L – Selectins

• ICAM – 1• VCAM - 1

52


PLASMA DERIVED MEDIATORS

KININ SYSTEM

CLOTTING SYSTEM

COMPLEMENT SYSTEM

FACTOR XII

53

PLASMA DERIVED MEDIATORSFACTOR XII

FACTOR XIIa

FIBRINOLYTIC SYSTEM

CLOTTING SYSTEM KININ SYSTEM

PLASMIN FIBRIN BRADYKININ

COMPLEMENT SYSTEM

C3a , C5a

54

FATE OF ACUTE INFLAMMATION

ACUTE INFLAMMATION

RESOLUTION

HEALING BY SCARRING

PROGRESSION TO SUPPURATION

PROGRESSION TO CHRONIC

INFLAMMATION

55

CHRONIC INFLAMMATION

Inflammation of prolonged duration (weeks to months) in which inflammation , tissue destruction and attempts at repair are proceeding simultaneously.

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

FEATURES OF CHRONIC INFLAMMATION :

CHRONIC INFLAMMATI

ON

Infiltration with mononuclear cells – macrophages ,lymphocytes , & plasma cells

Tissue destruction

Healing by Proliferation & connective tissue replacement of damaged tissue

57

INFILTRATION WITH MONO-NUCLEAR CELLS

58

• Incr. lysosomal enzymes

• Greater ability to phagocytose

ACTIVATION OF MACROPHAGE

Cytokine IFN - ɤ

Endotoxin , fibronectin chemical mediators

59

MACROPHAGE

IN ACUTE INFLAMMATION

IN CHRONIC INFLAMMATION

* Irritant eliminated – macrophage disappears

Persistent macrophage accumulation by following mechanisms :

1. )Recruitment from circulation – Chemotactic stimuli include :a) C5a b) Platelet derived growth factorc) Transforming growth factor

2.) Local proliferation of macrophages

3.) Immobilization of macrophages

60

TISSUE DESTRUCTION OR NECROSIS

CENTRAL

• ACTIVATED MACROPHAGES

Elastase Protease Collagenase Reactive oxygen radical Cytokine IL-1,8

61

PROLIFERATION

NEW BLOOD VESSELS

FIBROBLAST

Helps in healing of damaged tissue

63

INFLAMMATION OF PULP & PERIAPICAL TISSUE

PULPITIS

DEEP DENTAL CARIES

TOOTH FRACTURE

CRACKED TOOTH

SYNDROME

CHEMICAL CHANGES

THERMAL CHANGES

64

Involves enamel

Progresses to dentin

Invade pulp

65

REACTIONS OF PULP TO BACTERIAL INVASION

ᶲ Vascular changes take place inside blood vessels.

ᶲ PMNLs 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 ischaemia – does not get corrected since collateral circulation cannot develop through tiny apical foramina

66

HISTOLOGIC FEATURES OF PULPITIS

PULPITIS

ACUTE CHRONIC

VASCULAR EVENTS CELLULAR

EVENTS

MONONUCLEAR CELLS PREDOMINATE - chiefly plasma cells & lymphocytes.

Fibroblastic activity is evident

collagen fibres seen in bundles

• Continued vascular dilation

• Accumulation of oedemal fluid in connective tissue

• Pavementing Of PMNLs along endothelial wall

• Through quiescence of acute pulpitis

• Begin as chronic d/s from onset

67

UNTREATED PULPITIS

ACUTE CHRONIC

PULPITIS

UNTREATED

APICAL PERIODONTITIS

PERIAPICAL ABSCESS PERIAPICAL GRANULOMA

68

UNTREATED PULPITIS

APICAL PERIODONTITIS

• Inflammation of periodontal ligament around root apex..

INITIALLY

Changes localised around root apex…..since richly vascular

LATER – if irritant present

Resorption of bone – ABSCESS FORMATION

69

TYPES OF ABSCESS

PYOGENIC ABSCESS PYAEMIC ABSCESS COLD ABSCESS

• Commonest type

• mostly found in soft tissues

• eg periapical abscess

• occurs due to circulating bacterial emboli in blood

Abscess without signs of inflammationEg 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

SUPPURATION

71

PERIAPICAL ABSCESS

MICRO-ABSCESS

Rise in pressure with inflammatory exudate

Local tissue hypoxia

Localised destruction ….breakdown of leucocytes , bacteria & tissue

ABSCESS FORMATION PERIAPICAL ABSCESS

72

PERIAPICAL ABSCESS

Disintegrating PMNLsViable leukocytes , lymphocytes , bacterial colonies

Dil. Blood vessels in adj. PDL and marrow spaces + serous exudate

73

PERIAPICAL ABSCESS( DENTO-ALVEOLAR ABSCESS / ALVEOLAR ABSCESS )

Tender on percussion

Will feel slightly extruded from socket

Fever & regional lymphadenitis

INFLAMED PERIODONTIUM

74

ACUTE PERIAPICAL ABSCESS

CHRONIC FORM

PERIAPICAL ABSCESS

Takes the path of least resistance in tissuesSINUS

FISTULA / PARULIS / GUM

BOIL

75

WOUND HEALING

76

WOUND : Anatomic or functional interruption in continuity of a tissue that is accompanied by cellular damage and death

INTRODUCTION

MAY BE INFLICTED BY :

Physical injury Chemical injury Biologic injury

Series of co-ordinated processes directed towards restoring the injured tissue of body to as near normal as possible is termed as WOUND HEALING

77

GOAL

a.) to restore continuity b/w wound edges

b.) To re-establish tissue functionREGENERATIONREPAIR

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

REGENERATION

• Healing by proliferation of parenchymal cells,

• results in complete restoration of the original tissues

Cell growthCell differentiationCell-matrix interaction

GROWTH FACTORS1. Epidermal2. Fibroblast3. Platelet derived4. Endothelial5. Transforming

79

REPAIR

Healing by conn. Tissue Fibrosis and scarring

Phase of inflammationPhase of clearancePhase of ingrowth of granulation tissue

80

TYPES OF WOUND HEALING

PRIMARY SECONDARY TERTIARY

81

HEALING BY PRIMARY INTENTION / FIRST INTENTION

Conditions:• Clean and uninfected wounds• Surgically incised• Edges are Approximated• Without much loss of tissue

82

Initial Hemorrhage:

Acute inflammatory Response:

Epithelial changes:

Organization :

HEALING BY PRIMARY INTENTION / FIRST INTENTION

83

Initial hemorrhageINJURY SEVERES VASCULATURE

Leads to extravasation of plasma , platelets , erythrocytes and leukocytes

Initiates coagulation cascade

that produces blood clot

84

INFLAMMATORY RESPONSE

Begins within 24 hrs with appearance of polymorphs from margin of incision

From 3rd day Polymorphs replaced with macrophages

85

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.

PROLIFERATIVE PHASE – involves epithelial changes

86

Organisation starts by 3rd day

5th day : new collagen fibrils start forming which dominate till healing is complete

In 4 weeks Scar tissue formed

SCAR TISSUE

• Scanty cellular and vascular elements• few inflammatory cells

REMODELLING PHASE – involves ORGANISATION

87

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

Initial Hemorrhage:

Acute inflammatory Response:

Epithelial changes:

Granulation tissue:

Wound contraction:

89

GRANULATION TISSUE

INFLAMMATION CLEARANCE INGROWTH OF GRANULATION TISSUE

ANGIOGENESIS FIBROGENESIS

• Neutrophils and monocytes

• Autocatalytic enzymes

90

Wound Healing in Oral Mucosa

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 .

91

HEALING OF EXTRACTION SOCKETHealing Of Extraction Socket

Consists of erythrocytes & leucocytes in mesh of fibrin

STAGE 1 : coagulation

STAGE 2 : Granulation tissue

STAGE 3 : Connective Tissue collagen & reticuloendoth. fibres

STAGE 4 : Bone DevelopmentBegins at 7th post op dayBy 40th day socket almost completely filled with WOVEN bone

STAGE 5 : Epithelial RepairBegins at 4th post op day ; completes by 24th day

92

COMPLICATIONS - Healing Of Extraction Socket

FIBROUS UNION

• Occurs when tooth xtn accompanied with both buccal and lingual periosteum loss.

• RADIOGRAPHIC FEATURES : well circumscribed radiolucent area in site of previous xtn

May be mistaken for residual infection

• HISTOLOGIC FEATURES : dense bundles of collagen with occasional fibrocytes and few blood vessels

• TREATMENT : excision of wound may ……..

93

DRY SOCKET

• Most common and painful complication• Occurs due to disintegration / loss of blood

clot• CLINICAL F :

• Foul odour• Severe throbbing type of pain

‘DRY’TREATMENT

• AIM : to keep socket clean to protect exposed bone

• Irrigation with mild warm antiseptic

Palliative socket dressing of ZOE – iodoform gauze

94

HEALING OF RE-IMPLANTED TOOTH

oCLOT b/w root n ruptured PDL

oFIBROBLAST PROLIFERATION on pdl remnants on bone side

oRECONNECTION – occurs by collagen fibres extending from cementum to alveolar bone

oREATTACHMENT OF EPITHELIUM – by 7th day

o2-4 weeks - complete regeneration of pdl

Healing Of RE-IMPLANTED tooth

95

Healing Of GINGIVA

Mainly by regeneration

1-2 weeks

96

Healing Of ALVEOLAR BONE

RESPONSE : resorption and remodelling

CHRONIC INFECTIONRESORPTION

GRANULATION

ACUTE INFECTIONABSCESS / CELLULITIS

Inf. In marrow - OSTEOMYELITIS

97

Healing Of DENTIN-PULP COMPLEXPulp 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 paravascularlyPULPAL VASCULATURE in healing :Within pulp…esp apically.. ARTERIO-VENOUS shunts are present

Control the tissue pressure during inflammation

When tissue pressure exceeds that of venules , a decrease in blood flow results

98

RESPONSE OF PULP2 BASIC RESPONSE DETERMINING HEALING OF PULPPULPAL WOUND

HEALING RESPONSEDEFENSE

RESPONSE

Damaged pulp tissue is healed by replacement with newly differentiated tissue

Aims at neutralising or controlling bacterial invasion

Depends upon type of progenitor cells involved

Eg. PDL derived progenitor cells – cementum deposition along RC walls Patent apical foramen - Sharpeys fibre insertion

Involves creating barrier against micro – org. by• granulation tissue• hard tissue – secondary

dentin / cementum

NOT ABSOLUTE

RESPONSE

99

FACTORS INFLUENCING WOUND HEALINGLOCAL FACTORS

UV X - RAY

INFECTION FOREIGN BODY MOBILITY

RADIATION

100

FACTORS INFLUENCING WOUND HEALING

SYSTEMIC FACTORS

SYSTEMIC CONDITIONS

AGE NUTRITIONAL DEFICIENCIES

BLOOD DYSCRASIAS

• Vitamin C , E , A• Proteins

101

Healing – NEW CONCEPTS

Healing of chronic wound can be enhanced by one of the following methods

1. Topical application of growth factors.

2. Hyperbaric oxygen therapy.

Systemic

Local.

3. Electrical stimulation for wound healing

Direct current

Low frequency pulsed current (LFPC)

High voltage pulsed current (HVPC)

4. Topical application of cultured keratinocytes.

5. Vacuum assisted closure of the wound.

102

Conclusion……….

INFLAMMATION FORMS THE BASIS OF MOST OF THE CLINICAL COMPLAINTS…..

103

Refrences……..

1) Robbin’s & Cotron Pathological basis of diseases -7th edn.

2) Essential pathology for dental students –Harsh mohan,3rd edn.

3) Text book of oral pathology – Shafer 4th edn.

4) Textbook and colour atlas of traumatic injuries to the teeth—J.O.Andreasen, F.M.Andreasen 3rd edn.

5) Google search

104

THANK YOU

inflammation & healing & dental implications

Health & Medicine