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Periodontitis is an inflammatory disease casued by the action of microorganisms present in the

dentogingival biofilm and leading to the destruction of the periodontal tissue. One of the main risk
factors for the development of periodontitis is smoking.

Smoking is a habit very prevalent Around the world. around 1300 million people smoke today.
This corresponds to 47.5% of men and 10.3% of women. As a consequenceTobacco is responsible
for 1 in 10 deaths of adults (5 million deaths each year) and it is believed that by 2020 the figure
will reach 10 million per year

Periodontitis is a multifactorial disease and smoking constitutes one of the environmental factors
that most influences the susceptibility of the individual to the development of the disease (3

v Smoking not only increases the risk of developing periodontitis, but also significantly affects the
response to both surgical and non-surgical periodontal therapy5,6.

The National Health and Nutrition Examination Survey (NHANES) III has provided data for the
epidemiological study on smoking and periodontitis. the sample of the study were almost 12,329
adult Americans. It has been observed that tobacco was responsible for periodontitis in half of the
cases and that smokers were four times more likely to have the disease

Cross-sectional studies (3; 7-10), cases and controls (11), cohorts (12) and, more recently,
longitudinal ones (13-15) have linked smoking with a higher prevalence of clinical signs of disease

Tobacco is considered a specificity factor when, after the elimination of the habit, a favorable
periodontal effect occurs. The temporality relationship has been evidenced in longitudinal studies
where, in the sequence of exposure to the causative agent, there is a greater progression of the
disease (13-15) and a response to inadequate treatment Biological Gradient it has been found that
the higher the number of cigarettes consumed per day or packages per year, the greater the risk of
developing the disease (7; 8).Biological Plausibilitythe current knowledge of a biopathogenic
process whereby tobacco intervenes in the periodontium can give a biological explanation to the
association. This process will be

To verify that tobacco is a cause of periodontitis, it would be necessary to make prospective

randomized controlled studies and studies with a rigorous experimental design. However, these
studies would involve subjecting individuals to exposure to a risk factor, and that would be
ethically unacceptable.

INTERVENCIÓN DEL TABACO A NIVEL DE LA MICROFLORA

smokers have a higher probability of infection with pathogenic bacteria (Porphyromona gingivals,
Tanerella forsythensis, Prevotella intermedia, Peptostreptococcus micros, Fusobacterium
nucleatum, Campylobacter rectus) (23; 25) and higher prevalence of exogenous flora (Escherichia
coli, Candida albicans) (24). These results may be a consequence of a decrease in the oxygen
pressure in the bag (local effect of tobacco smoke), which favors anaerobic growth

INTERVENTION OF TOBACCO IN THE RESPONSE OF THE GUEST

It has been observed that smokers have a decreased inflammatory response There is less bleeding
to the probe and less gum blush

Immune System One of the mechanisms by which tobacco can intervene in the pathogenesis of
periodontal disease is changing the body's defense capacity in 1977, Kenney et al have observed
that the neutrophils of smokers had a lower capacity of phagocytosis and a lower viability.
phagocytosis but also other functions of polymorphonuclear agents, such as chemotaxis,
production of the protease inhibitor, the generation of superoxide and hydrogen peroxide, and
the expression of adhesion molecules, I have as a consequence poor defensive activity and
increased tissue destruction

Cigarette smoke is a complex mixture of about 4,000 components with cytotoxic, mutagenic and
carcinogenic properties, nicotine being the most studied, due to its relationship with the addiction
of patients9.Passive or active inhalation causes a dissolution of combustion products in the oral
epithelium and airway. These combustion products can be divided into gaseous and particulate,
being the latter type of particle the one that concentrates the highest toxicity Cigarette smoke as
such directly damages oral epithelial cells inducing chemokine production and release of
inflammatory mediators

CICATRIZATION AND RESPONSE TO TREATMENT

90% of refractory periodontitis were found in smokers (38).

A great inability to heal and regenerate tissues in smokers has been observed: less reduction in the
depth of the bag and less insertion gain The response to treatment can be explained by the
intervention of tobacco at the microflora level and the response of the host, as discussed above.

In summary, the role of tobacco in the pathogenesis of periodontal disease still has several points
to clarify. However, for what has been searched in the literature, it can be concluded that tobacco
potentiates periodontal disease through its intervention in what are considered the key points of
the pathogenesis paradigm of periodontal disease

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Studies whose methodology has used Doppler laser flowmetry have concluded that after the
consumption of cigarettes the blood flow has been modified by 25%, but that after 5 minutes it is
restored to normal levels. Other studies by Morozumi et al. They have detected that patients who
stop smoking at 4 to 8 weeks progressively increase blood flow, which could be related to the gum
can recover their state, at least during the study period15.

Smoking produces a masking effect of the clinical signs of inflammation, which influences the
detection of the disease and subsequent referral to specialist2