Periodontitis is one of the most common oral diseases and is
characterised by gingival inflammation and alveolar bone
Periodontitis is a multifactorial and cumulative condition,
initiated and propagated by bacteria and host factors
There are two forms of periodontitis; chronic and aggressive
* 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
like calculus, food impaction and microbial plaque
Aggrobacter actinomycetemcomitans, Bacteroides
forsuthus & Prevotella intermedia , Fusobacterium nucleatum ,
Cigarette smoking, beedi,
Smokeless tobacco usage like beeda, pan masala, pan chewing, Gutka
Environmental factors are not found in oral cavity always
but are acting as and when habits are cultivated
* Environmental factors include
* Pan chewing
* Smokeless tobacco consumption and
* Poor dental awareness
* 1. Filter made of 95% cellulose acetate.
* 2. Tipping paper to cover the filter.
* 3. Rolling paper to cover the tobacco.
* 4. Tobacco blend.
• Holds tobacco blend
• Controls the rate of
burning and production
• It provides taste and
• It may vary from region
• It is the biodegradable
part of cigarette made
of cellulose acetate.
• It filters the main
stream of smoke from
tobacco blend to the
• It holds the burnt ash
and remnants of
• It is 30% of the length
of a cigarette
smokers develop less inflammatory response than non smoking
counterparts which shows that occurrence of gingivitis is
comparatively low in smokers than in non-smokers
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.
M-CSF, OPG , PGE2
* 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
This would lead to increased virulence and changes the host
response to the bacterial challenge which in turn lead to
increased periodontal destruction
of bacteria in
levels of TNFα