Seminar of inflammation in dentistry with view of public health dentistry

1. 1
Good
mornin

2. Continuations of
INFLAMMATION
&
CHEMICALMEDIATIORS
(DENTAL ASPECT )
2
Dr. Sharanprakash R S
1st year MDS
NPDCH, Visnagar.

3. INTRODUCTION - History
General features of inflammation
3
CLASSIFICATION OF INFLAMMATION
CHEMICAL MEDIATORS OF INFLAMMATION
DENTAL ASPECTS OF INFLAMMATION
DENTAL ABSCESS
CONCLUSION
REFERENCE

4. 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

5. 5
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

6. 6

7. 7

8. INFLAMMATION OF PULP & PERIAPICAL TISSUE
DEEP DENTAL
CARIES
TOOTH
FRACTURE
CRACKED TOOTH
SYNDROME
CHEMICAL
CHANGES
THERMAL
CHANGES
8

9. 9
Involves enamel
Progresses to
dentin
Invade pulp

10. 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

11. HISTOLOGIC FEATURES OF PULPITIS
11
 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

12. UNTREATED PULPITIS
ACUTE CHRONIC
PULPITIS
UNTREATE
D
APICAL
PERIODONTITIS
PERIAPICAL
ABSCESS
PERIAPICAL
GRANULOMA
12

13. UNTREATED PULPITIS
• Inflammation of periodontal ligament around root apex..
Changes localised around root
apex…..since richly vascular Resorption of bone –
ABSCESS FORMATION
13

14. 14
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 inflammation
Eg Tubercular
abscess

15. ABSCESS FORMATION / SUPPURATION
Acute bacterial inf. + intense neutrophillic infiltrate
TISSUE
NECROSIS
Cavity is formed called an
ABSCESS
Contain purulent exudate called as
PUS
15

16. MICRO-
ABSCESS
Rise in pressure with inflammatory
exudate
Local tissue hypoxia
Localised destruction
….breakdown of leucocytes ,
bacteria & tissue
ABSCESS FORMATIONPERIAPICAL
ABSCESS
16

17. Disintegrating
PMNLs
Viable leukocytes ,
lymphocytes , bacterial
colonies
Dil. Blood vessels in
adj. PDL and
marrow spaces +
serous exudate
17

18. ( DENTO-ALVEOLAR ABSCESS / ALVEOLAR ABSCESS )
Tender on
percussion
Will feel slightly
extruded from socket
Fever & regional
lymphadenitis
18

19. 19
ACUTE
PERIAPICAL
ABSCESS
CHRONIC FORM
Takes the path of
least resistance in
tissues
SINUS
FISTULA / PARULIS
/ GUM BOIL

20. 20
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

21. 21
• 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 gingivaGingival recession
CLINICAL FEATUARES

22. 22
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.

23. 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

24. References……..
24
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

25. 25
THANK
YOU