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H.K.Ajeya Ranganathan
G D C R I , Bangalore.
*

Periodontitis is one of the most common oral diseases and is
characterised by gingival inflammation and alveolar bone
resorption

*

Periodontitis is a multifactorial and cumulative condition,
initiated and propagated by bacteria and host factors

*

There are two forms of periodontitis; chronic and aggressive
Periodontitis

* Both differ from each other not only in clinical findings but also
age of onset and rate of progression.
*
*Factors playing role in Periodontitis are
 LOCAL FACTORS

like calculus, food impaction and microbial plaque

which includes

Aggrobacter actinomycetemcomitans, Bacteroides
forsuthus & Prevotella intermedia , Fusobacterium nucleatum ,
Bacteroides melaninogenicus

ENVIRONMENTAL FACTORS
Cigarette smoking, beedi,
Smokeless tobacco usage like beeda, pan masala, pan chewing, Gutka

SYSTEMIC FACTORS
*

Environmental factors are not found in oral cavity always
but are acting as and when habits are cultivated

* Environmental factors include
* SMOKING
* Pan chewing
* Smokeless tobacco consumption and
* Poor dental awareness
* Acetone

Aluminium
Ammonia

Arsenic
Benzene
Butane

Cadmium
Carbon monoxide
Carbon dioxide
Chloroform

Cyanide
DDT/Dieldrin
Ethanol
Formaldehyde
Hydrogen cyanide
Lead

Methanol
Nicotine
Tar
Vinyl Chloride

* 1. Filter made of 95% cellulose acetate.
* 2. Tipping paper to cover the filter.
* 3. Rolling paper to cover the tobacco.
* 4. Tobacco blend.
Rolling paper

Tobacco blend

Cigarette filter

Cigarette but

• Holds tobacco blend
• Controls the rate of
burning and production
of ash

• It provides taste and
flavour
• It may vary from region
to region

• It is the biodegradable
part of cigarette made
of cellulose acetate.
• It filters the main
stream of smoke from
tobacco blend to the
mouth piece

• It holds the burnt ash
and remnants of
tobacco
• It is 30% of the length
of a cigarette
* Gingivitis:
smokers develop less inflammatory response than non smoking
counterparts which shows that occurrence of gingivitis is
comparatively low in smokers than in non-smokers

* Periodontitis
Smokers are more prone to periodontitis than non smokers since
smoking plays an important role in destruction of periodontium , loss
of attachment and sub-gingival plaque accumulation.
Serum

Osteoprotegerin
levels increased
initially followed
by
decreased
gradually

M-CSF, OPG , PGE2
are decreased

Saliva

OPG levels
decreased and
sRANKL levels
increased

OPG/sRANKL ratio
is reduced
* Increased destruction of periodontia by smoking would lead to the
breakdown balance between microbial colonies and host immune
response and causes changes in the contents of sub-gingival
plaque

*

This would lead to increased virulence and changes the host
response to the bacterial challenge which in turn lead to
increased periodontal destruction
Increased
levels of
T.forsythia ,
T.denticola,
P.gingivalis

Increased
tissue
destruction

Increased
colonization
of bacteria in
sub gingival
plaque

Impaired
mechanical
prophylaxis
Increased
levels of TNFα
and matrix
metalloprotien
8

Decreased
levels of
neutrophils
and PGE2

Impaired
neutrophil
activity

Increased
risk of
tissue
destruction
Decrased GCF
production
Decreased blood
flow
Decreased
Microvasculature

Added
vasoconstriction

Decreased
Inflammatory
response
Slow recovery
from Local
anaesthasia

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Effects of tobacco on periodontal health

  • 1. H.K.Ajeya Ranganathan G D C R I , Bangalore.
  • 2. * Periodontitis is one of the most common oral diseases and is characterised by gingival inflammation and alveolar bone resorption * Periodontitis is a multifactorial and cumulative condition, initiated and propagated by bacteria and host factors * There are two forms of periodontitis; chronic and aggressive Periodontitis * Both differ from each other not only in clinical findings but also age of onset and rate of progression.
  • 3. * *Factors playing role in Periodontitis are  LOCAL FACTORS like calculus, food impaction and microbial plaque which includes Aggrobacter actinomycetemcomitans, Bacteroides forsuthus & Prevotella intermedia , Fusobacterium nucleatum , Bacteroides melaninogenicus ENVIRONMENTAL FACTORS Cigarette smoking, beedi, Smokeless tobacco usage like beeda, pan masala, pan chewing, Gutka SYSTEMIC FACTORS
  • 4. * Environmental factors are not found in oral cavity always but are acting as and when habits are cultivated * Environmental factors include * SMOKING * Pan chewing * Smokeless tobacco consumption and * Poor dental awareness
  • 5. * Acetone Aluminium Ammonia Arsenic Benzene Butane Cadmium Carbon monoxide Carbon dioxide Chloroform Cyanide DDT/Dieldrin Ethanol Formaldehyde Hydrogen cyanide Lead Methanol Nicotine Tar Vinyl Chloride * 1. Filter made of 95% cellulose acetate. * 2. Tipping paper to cover the filter. * 3. Rolling paper to cover the tobacco. * 4. Tobacco blend.
  • 6. Rolling paper Tobacco blend Cigarette filter Cigarette but • Holds tobacco blend • Controls the rate of burning and production of ash • It provides taste and flavour • It may vary from region to region • It is the biodegradable part of cigarette made of cellulose acetate. • It filters the main stream of smoke from tobacco blend to the mouth piece • It holds the burnt ash and remnants of tobacco • It is 30% of the length of a cigarette
  • 7. * Gingivitis: smokers develop less inflammatory response than non smoking counterparts which shows that occurrence of gingivitis is comparatively low in smokers than in non-smokers * Periodontitis Smokers are more prone to periodontitis than non smokers since smoking plays an important role in destruction of periodontium , loss of attachment and sub-gingival plaque accumulation.
  • 8. Serum Osteoprotegerin levels increased initially followed by decreased gradually M-CSF, OPG , PGE2 are decreased Saliva OPG levels decreased and sRANKL levels increased OPG/sRANKL ratio is reduced
  • 9. * Increased destruction of periodontia by smoking would lead to the breakdown balance between microbial colonies and host immune response and causes changes in the contents of sub-gingival plaque * This would lead to increased virulence and changes the host response to the bacterial challenge which in turn lead to increased periodontal destruction
  • 11. Increased levels of TNFα and matrix metalloprotien 8 Decreased levels of neutrophils and PGE2 Impaired neutrophil activity Increased risk of tissue destruction