infamattion in dentistry (dept of public health dentistry ) part 2

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Good morning

Continuations of

INFLAMMATION

&

CHEMICALMEDIATIORS

(DENTAL ASPECT )

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Dr. Sharanprakash R S1st year MDS NPDCH, Visnagar.

INTRODUCTION - History

General features of inflammation

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CLASSIFICATION OF INFLAMMATION

CHEMICAL MEDIATORS OF INFLAMMATION

DENTAL ASPECTS OF INFLAMMATION

DENTAL ABSCESS

CONCLUSION

REFERENCE

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 4

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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

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INFLAMMATION OF PULP & PERIAPICAL TISSUE

DEEP DENTAL

CARIES

TOOTH

FRACTURE

CRACKED TOOTH

SYNDROME

CHEMICAL

CHANGES

THERMAL

CHANGES8

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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 10

HISTOLOGIC FEATURES OF PULPITIS

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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

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UNTREATED PULPITIS

• Inflammation of periodontal ligament around root apex..

Changes localised around root

apex…..since richly vascular Resorption of bone –

ABSCESS FORMATION

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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

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MICRO-

ABSCESS

Rise in pressure with inflammatory

exudate

Local tissue hypoxia

Localised destruction

….breakdown of leucocytes ,

bacteria & tissue

ABSCESS FORMATIONPERIAPICAL

ABSCESS16

Disintegrating PMNLs

Viable leukocytes , lymphocytes , bacterial colonies

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

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( DENTO-ALVEOLAR ABSCESS / ALVEOLAR ABSCESS )

Tender on

percussion

Will feel slightly

extruded from socket

Fever & regional

lymphadenitis18

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ACUTE

PERIAPICAL

ABSCESS

CHRONIC FORM

Takes the path of

least resistance in

tissuesSINUS

FISTULA / PARULIS / GUM BOIL

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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

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• 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

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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

References……..

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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

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THANK YOU