Infamattion in dentistry (dept of public health dentistry )

1

Good morning

INFLAMMATION

&

CHEMICALMEDIATIORS

2

Dr. Sharanprakash R S1st year MDS NPDCH, Visnagar.

INTRODUCTION - History

General features of inflammation

3

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

4

CONCLUSION

REFERENCE

INTRODUCTION

,, and. Hence in the importance of inflammation is that it can

sometimes be, and is thus the cause of tissue injury in many

disorders.

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

Without inflammation

, infections would go

unchecked

Wounds would

never heal

Injured tissues might

remain permanent

decaying lesions

In practice of medicine

inappropriately triggered

or poorly controlled

Imagine suppose

inflammation is not present

HISTORICAL HIGHLIGHTS

Egyptian Papyrus , 3000 BC CELSUS , Roman Writer

- 1 AD - CARDINAL SIGNS

JOHN HUNTER , 1793 –

“ Inflammation is not a disease

but a constructive effect on host”

JULIUS CONHEIM-1st used

microscope to observe inflamed

blood vessels & cells 6

7

GIVEN BY CELSUS

• REDNESS

• SWELLING

• HEAT

• PAIN

Rubor

Tumor

Dolor

Calor

• LOSS OF FUNCTION FUNCTIO LAESA

BY VIRCHOW

8

English Greek/Latin Caused By

Redness Rubor Hyperaemia

Warmth Calor Hyperaemia

Swelling Tumor Increased permeability

Pain Dolor Low pH

Loss of function Functio laesa Pain, swelling

CLASSIFICATION

9

ACUTE INFLAMMATION

CHRONIC INFLAMMATION

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

10

ACUTE INFLAMMATION

11

CHANGES

CELLULAR EVENTS

ACUTE INFLAMMATION

HEMODYNAMIC

CHANGES / Change in

vascular flow & calibre

CHANGE IN VASCULAR

PERMEABILITY

12

Transient vasoconstriction

Vasodilation

Increased permeability of microvasculature

Stasis

Emigration of leukocytes13

HEMODYNAMIC CHANGES / Change in vascular flow

& caliber

TRANSIENT VASOCONSTRICTION

Arterioles

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

injury

14

PERSISTENT PROGRESSIVE

VASODILATION

• 1st involves arteriole ………then other capillary

bed

• seen in 1st 30 min.

• Results in, increase blood vol. in microvascular

bed, which is responsible for redness and warmth

at site

15

16

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

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

S17

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.

18

19

CHANGE IN VASCULAR PERMEABILITY

In initial due to vasodilation and hydrostatic pressure the fluid is seen its called transudate

Transudate is a

fluid with low

protein content

(most of which is

albumin), little or

no cellular

material, and low

specific gravity

Exudate The

escape of fluid,

proteins, and blood

cells from the

vascular system

into the interstitial

tissue or body

cavities is known

as exudation

Edema denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate

20

21

CELLULAR EVENTSDeliver leukocytes to site of

injury

To perform their

‘FUNCTION’

Ingest offending bacteria

Kill bacteria & other microbes

Get rid of necrotic tissue & foreign

substance

22

23

CELLULAR EVENTS

1) DELIVERY OF LEUKOCYTES TO SITE OF

INJURY

2) PHAGOCYTOSIS

CELLULAR EVENTS

• Margination

• Rolling

• Adhesion

IN THE LUMENEMIGRATION

•Eigration into interstitial tissue

CHEMOTAXIS

24

1 )

CELLULAR EVENTS • MARGINATION

• rolling

• Adhesion

IN THE LUMEN

25

• Margination

•Rolling• Adhesion

IN THE LUMEN

CELLULAR EVENTS

Leukocytes now tumble along the endothelium

Have a TRANSIENT adhesion with endothelium

26

• Migration

• Rolling

•Adhesion

IN THE LUMEN

CELLULAR EVENTS

27

CELLULAR EVENTS

PSEUDOPODIA

SQUEEZE THROUGH INTER-

ENDOTHELIAL

JUNCTION

LIE B/W ENDOTH. CELLS &

BASEMENT MEMBRANE 28

‘across’ the endothelial

wall..

EMIGRATION

EMIGRATION

CELLULAR EVENTS

EXTRA-

VASCULAR

SPLACE

29

CHEMOTAXIS

CELLULAR EVENTS

Along chemical gradient

30

After exiting the circulation,

leukocytes emigrate in

tissues toward the site of

injury by a process called

chemotaxis

EXOGENOUS

SUBSTANCES

ENDOGENOUS

SUBSTANCES

Bacterial Products :

a) Peptides – N – formyl

methionine terminal

amino acid

b) Lipids

a) LTB-4 (Lukotriene B-4)

b) PF-4 (platelet factor-4)

c) Components of

complement system

d) Cytokine :

IL – 1, 5 , 6

e) Monocyte

chemoattractant

protein

f) Chemotactic factor for

CD-4 cells

g) Eotaxin chemotactic

factor for eosinophils

CELLULAR EVENTS

31

At the end of cellular events that

leukocytes migrate toward the

inflammatory stimulus in the direction

of the gradient of locally produced

chemo attractants.

32

CELLULAR EVENTS

33

PHAGOCYTOSIS

CELLULAR EVENTS

PHAGOCYTOSIS

RECOGNITION AND ATTACHMENT OF PARTICLE

ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE

DEGRANULATION STAGE

KILLING & DEGRADATION STAGE

34

1

2

3

4

CELLULAR EVENTS

RECOGNITION AND ATTACHMENT OF PARTICLE1

CHEMO-TACTIC

AGENTS

Ig G

C3b

Opsonin

Lectins

MANNOSE

RECEPTOR

SCAVENGE

R

RECEPTOR 35

ENGULFMENT WITH FORMATION OF PHAGOCYTIC VESICLE2

CELLULAR EVENTS

Fig 10.6 harsh mohan pg 10136

PHAGO-

LYSO-SOME

DEGRANULATION STAGE3

CELLULAR EVENTS

During this stage the

PMNs (ploymorphonuclear neutrophils)

&

Mononuclear phagocyte secrete enzymes eg

IL-2 , 6-TNF

Arachidonic acid metabolites (Prostaglandin , leukotriene ,

platelet activating factor

Oxygen metabolites

• are released into phagolysosome37

KILLING & DEGRADATION STAGE4

CELLULAR EVENTS

OXYGEN – DEPENDENT BACTERICIDAL

MECHANISM

OXYGEN–INDEPENDENT

MECHANISM

38

Phagocytes as scavenger cells

killing and digest's the micro-organism

If this mechanism fails to kill and degrade some bacteria like

TUBERCLE BACILLI

THEN

KILLING & DEGRADATION STAGE

39

Production of reactive oxygen metabolites is necessary to kill the micro

organism & Increased oxygen consumption by the phagocytic leucocytes

(respiratory brust )

2o2

NADPH

oxidase

(superoxid

e anion )

NADPH NADP + H(PLUS

ION )

2H(plus ion)

H2O2

Hydrogen peroxide

CELLULAR EVENTS

Followed by :

Lysosomal hydrolases

Permeability increasing factors

Defensing

Cationic proteins

40

41

‘ MEDIATOR ‘ : one that reunites differences b/w disputants

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

42


Present in plasma in

precursor form

Must be activated to

acquire biologic

properties

Pr. In intracellular granules

Major cellular sources

Platelets

Neutrophil

Monocyte / macrophage

43


VASO – ACTIVE AMINES

44

HISTAMINE

SOURCE : 1) Mast cells in C.T

adjacent to blood vessels

2) Blood basophils

3) Platelets

STIMULI : Injury

Immune reactions

SEROTONIN

SOURCE : 1) Platelets

2) Enterochromaffin cells

STIMULI : Platelet aggregation after

contact with collagen ,

thrombin

45

Dilation of

arterioles

Permeability

of vasculature


ARACHIDONIC ACID

METABOLITES

A fatty acid with 2 main sources :

Directly through diet

Through conversion of essential fatty acid

CYCLO – OXY- GENASE

PATHWAY

Prostaglandin -

PGD2 , E2 , F2

Thromboxane A2

Prostacyclin

LIPO – OXY – GENASE

PATHWAY

5 – HETE( hydroxy

eico-satetraenoic acid)

Leukotrienes

46

Arachidonic acid

Cyclo – oxy- genasepathway /Lipo –oxy- genase Pathwa

ARACHIDONIC ACID

METABOLITES

Chemotactic and cell adherence


LYSOSOMAL

COMPONENTS

47

Destruction of bacteria

In phagolysosome

PRIMARY

MPO(myeloperoxidase)

ACID HYDROLASES

NEUTRAL PROTEASES

SECONDARY

LACTOFERRIN

LYSOZYME

Alk. Phosph

Collagenase

• ACID PROTEASE

• COLLAGENASE

• ELASTASE

• PLASMINOGEN ACTIVATOR

Attack on Extracellular

matter


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

48

NITROUS OXIDE


Released by activated neutrophils and macrophages,such as

Superoxide , hydrogen peroxide , hydroxyl ion

ACTION : Endothelial cell damage- inc. vascular permeability

49

6 OXYGEN METABOLITES

mediates in vascular dilation


KININ

SYSTEM

CLOTTING

SYSTEM

COMPLEMENT

SYSTEM

50

51

FACTOR XII(Hageman factor)

FACTOR XIIa

Complement

system

CLOTTING

SYSTEMKININ

SYSTEM

AnaphylatoxinsFIBRIN BRADYKININ

FATE OF ACUTE INFLAMMATION

ACUTE

INFLAMMATIO

N

RESOLUTION

HEALING BY

SCARRING

PROGRESSION

TO

SUPPURATION

PROGRESSION

TO CHRONIC

INFLAMMATION

52


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 : Eg-

tubercle bacilli

Prolonged exposure to toxic agents

Auto - immunity 53

FEATURES OF CHRONIC INFLAMMATION :

54


Infiltration with mononuclear cells –

macrophages ,lymphocytes , & plasma

cells

Tissue

destruction

Healing by Proliferation &

connective tissue replacement

of damaged tissue

INFILTRATION WITH MONO-NUCLEAR CELLS

55

• Incr. lysosomal enzymes

• Greater ability to

phagocytose 56

ACTIVATION OF

MACROPHAGE

Cytokine

IFN - ɤ

Endotoxin ,

fibronectin

chemical

mediators

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) Platelet derived growth factor

b) Transforming growth factor

2.) Local proliferation of macrophages

3.) Immobilization of macrophages57

58

TISSUE DESTRUCTION OR NECROSIS

• ACTIVATED

MACROPHAGES Elastase

Protease

Collagenase

Reactive oxygen

radical

Cytokine IL-1,8

59

Part 2

Dental aspect

Cont……

60

INFLAMMATION OF PULP & PERIAPICAL TISSUE

DEEP DENTAL

CARIES

TOOTH

FRACTURE

CRACKED TOOTH

SYNDROME

CHEMICAL

CHANGES

THERMAL

CHANGES61

62

Involves enamel

Progresses to

dentin

Invade pulp

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 deceased blood supply and ischemia – does not

get corrected since collateral circulation cannot develop through

tiny apical foramina 63

HISTOLOGIC FEATURES OF PULPITIS

64

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

UNTREATED PULPITIS

ACUTE CHRONIC

PULPITIS

UNTREATED

APICAL

PERIODONTITIS

PERIAPICAL

ABSCESSPERIAPICAL

GRANULOMA

65

UNTREATED PULPITIS

• Inflammation of periodontal ligament around root apex..

Changes localised around root

apex…..since richly vascular Resorption of bone –

ABSCESS FORMATION

66

67

PYOGENIC

ABSCESS

PYAEMIC

ABSCESSCOLD 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

ABSCESS FORMATION / SUPPURATION

Acute bacterial inf. + intense neutrophillic infiltrate

TISSUE

NECROSIS

Cavity is formed called an

ABSCESS

Contain purulent exudate called as

PUS

68

MICRO-

ABSCESS

Rise in pressure with inflammatory

exudate

Local tissue hypoxia

Localised destruction

….breakdown of leucocytes ,

bacteria & tissue

ABSCESS FORMATIONPERIAPICAL

ABSCESS69

Disintegrating PMNLs

Viable leukocytes , lymphocytes , bacterial colonies

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

70

( DENTO-ALVEOLAR ABSCESS / ALVEOLAR ABSCESS )

Tender on

percussion

Will feel slightly

extruded from socket

Fever & regional

lymphadenitis71

72

ACUTE

PERIAPICAL

ABSCESS

CHRONIC FORM

Takes the path of

least resistance in

tissuesSINUS

FISTULA / PARULIS / GUM BOIL

73

STAGES DAYS

BLOOOD

VESSELS

JN & SULCULAR

EPITHELIUM

PREDOMIN

ANT

IMMUNE

CELLS

CLINICAL

FINDINGS

INITIAL

LEASION

2-4 Vas-Dil

Vasculitis

Infiltration of

PNMs

PNMs Gingival fluid

flow

EARLY

LEASION

4-7 Vas- proliferation Same as stage 1 &

Rete pegs,

atrophic areas

Lymphocytes Erythema

Bleeding on

probing

ESTABLISH

ED LEASION

14-21 Same as stage 2

Blood stats seen

Same as above,

but advanced

Plasma cells Changes seen

in

color,size,textu

re etc.

The sequence of events in the development of gingivitis is

analyzed in three different stages

GINGIVAL INFLAMMATION

74

• From gingival sulcus on gentle probingGingival bleeding

• Red or bluish red color(normal is coral pink)Color changes

• (Normally firm and resilient) both destructive(edematous) and

reparative(fibrotic)

Changes in consistency

• Loss of stippling and surface is either smooth and shiny or firm or nodular

Change in surface texture

• Apical shift of the position of gingiva Gingival recession

CLINICAL FEATUARES

75

Conclusion………. Destroy, dilute and wash off any injurious agent & constitutes

the repair. Without inflammation, infections would go unchecked, wounds would never heal, and injured organs may remain as permanent decaying lesions.

In our day to day lives we come across many cases starting from gingivitis to oral cancer wherein inflammation exerts a direct or an indirect effect.

So understanding inflammation helps us to know the various vascular and cellular changes, mediators involved and therefore help us to evaluate the significance of various antibiotics and anti-inflammatory drugs that we do prescribe, for controlling the same.

Thank You . . .

“I choose a lazy person to do a hard job.Because a lazy person will find an easy way to do it.”

― Bill Gates

http://www.goodreads.com/author/show/23470.Bill_Gates

References……..

77

1. Essential pathology for dental students- Harsh Mohan -3rd edn.

2. Pathologic basis of disease- Robbins & Cotran – 7th edn .

3. Shafer’s text book of oral pathology – 5th edn.

4. Newman, Takei, Klokkevold, Carranza. Carranza’s clinical

periodontology. 12th ed, 2013

78

THANK YOU

Date post:	22-Jul-2015
Category:	Health & Medicine
Upload:	npdch-visnagar
View:	36 times
Download:	2 times

Infamattion in dentistry (dept of public health dentistry )

Health & Medicine