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ARTICULO CIENTÍFICO

LOS EFECTOS NOCIVOS DEL TABACO Y DERIVADOS CON


NICOTINA SOBRE LA SALUD ORAL

Autoras:
Diana Lincango
Denia Moro
ÍNDICE
1. HIPÓTESIS
2. ABSTRACT
a. OBJECTIVES
b. METHODS
c. RESULTS
i. About the kind of nicotine product and the result of each of them
ii. Mechanism how they affect to oral health
d. REFERENCES
1.HIPÓTESIS:
Los efectos nocivos sobre la salud bucodental del tabaco, los cigarrillos electrónicos y otros
productos derivados del tabaco.
Palabras clave smoking AND dental care, hemos acotado la búsqueda a los últimos 7 años
(2015-2022) y hemos filtrado entre 901 resultados.
A raíz de las lecturas ampliamos el estudio e incluimos los cigarrillos electrónicos,
vapeadores, cachimbas, cigarros tipo puros, canabis, etc

Estudios elegidos para comprobar el impacto de estos productos sobre la salud bucodental.

“Oral and periodontal implications of tobacco and nicotine products”


https://pubmed.ncbi.nlm.nih.gov/34463989/
“Personalized periodontal treatment for the tobacco- and alcohol-using patient”
https://pubmed.ncbi.nlm.nih.gov/30198132/
“ Electronic cigarette use promotes a unique periodontal microbiome”
https://pubmed.ncbi.nlm.nih.gov/35189698/
“ The effects of vaping electronic cigarettes on periodontitis”
https://pubmed.ncbi.nlm.nih.gov/32003453/

2. ABSTRACT:

Tobacco use contributes to more morbidity and mortality globally than any other behavioral
risk factor.
Electronic cigarettes have become prevalent as an alternative to conventional cigarette
smoking, particularly in youth, also increasingly used to help reduce or cease smoking
traditional cigarettes. Electronic cigarette aerosols contain unique chemicals which alter the
oral microbiome.
The use of various forms of tobacco is one of the most important preventable risk factors for
the incidence and progression of periodontal disease.

A. OBJECTIVES:
We have two objectives, first of all we try to demonstrate the risk of tobacco and e-cigs,
cannabis, non-smoking tobacco and similar products in oral health and their consequences,
and to check if the consequences are different depending on the kind of product.
Also we try to find which of the ingredients of them are the ones that are worse for oral
health.

B. METHODS:
We chose four different author articles that studied different patients (different ethnicity, age,
country, etc) to check our theory and find if tobacco and their derived products have effects
on our oral health and which are them.
● ART.1 “Oral and periodontal implications of tobacco and nicotine products”

A group of 705 individuals (21 to 92 years-old) who were among volunteer participants in the
ongoing Baltimore Longitudinal Study of Aging were examined clinically to assess their
periodontal status and tooth loss. A structured interview was used to assess the participants'
smoking behaviors with regard to cigarettes, cigar, and pipe smoking status. For a given
tobacco product, current smokers were defined as individuals who at the time of examination
continued to smoke daily. Former heavy smokers were defined as individuals who have
smoked daily for 10 or more years and who had quit smoking. Non-smokers included
individuals with a previous history of smoking for less than 10 years or no history of smoking
● ART. 2. Oral and periodontal implications of tobacco and nicotine products”

1. TOBACCO. To talk about the effects of the tobacco the article made reference to a
lot of studies, older and newer and tell us that they demonstrated strong associations
between cigarette smoking and gingival disease,diminished epithelial attachment and
alveolar bone height,and tooth loss.These studies generally also noted greater levels
of plaque and calculus accumulation among smokers,leading to some academic
debate at the time over whether smoking and periodontal disease associations
reflected merely poor oral hygiene practices among smokers or a causal contribution
of the tobacco exposure itself. Also said more recent investigations support a causal
role, with large representative patient-based and population-based studies confirming
a strong, consistent association of smoking with worse periodontal status including
independently of dental plaque levels and other plausible confounders, such as age,
sex, and socioeconomic position. Furthermore, distinct microbial patterns between
the plaque biofilm of tobacco smokers and nonsmokers have been characterized,
suggesting a more pathogenic profile. The gingival vascular response to plaque
bacteria is impeded in tobacco smokers via mechanisms still under study but which
may include suppressed angiogenesis or vasoactive smoke constituents.Finally,
tobacco smoking appears to diminish the reparative capacity of periodontal cells,
including fibroblasts, osteoblasts and cementoblasts, reducing the ability to form new
tissue and potentially impeding responsiveness to periodontal therapy. Whereas
whole tobacco smoke is clearly damaging to oral cells and tissues, deciphering which
of the many components of tobacco smoke are most responsible for these effects is
challenging. A recent review of the in vitro evidence concluded that nicotine, the
highly addictive chemical, was alone unlikely to be cytotoxic to oral tissues at
physiologic levels.

2. SMOKELESS (SPIT) TOBACCO.


Smokeless tobacco its a variety of noncombustible tobacco products that are held in
the mouth or chewed, This includes areca nut products, such as betel quid (paan),
gutka, and mainpuri in South and Southeast Asia, where the consumption of these
and similar products has been strongly associated with oral cancer.These smokeless
products contain high levels of tobacco-specific nitrosamines, believed to be highly
carcinogenic, in contrast to low-nitrosamine snus products consumed in Sweden,
which most existing epidemiologic studies have not associated with oral cancer.In the
United States, oral moist snuff is the predominant form of smokeless tobacco used,
more often among younger men in rural communities. In 2017, the United States
Food and Drug Administration estimated that a product standard to mandate low
nitrosamine content in US smokeless tobacco products would prevent 12 700 cases
of oral cancer over 20 years

● CIGARS AND PIPES. A longitudinal evaluation of the Baltimore Longitudinal Study of


Aging found that cigar and/or pipe users had more missing teeth and more sites with
severe loss of attachment and advanced recession compared with nonsmokers.
Another longitudinal study evaluated tooth loss risk and alveolar bone loss in cigar
and pipe smokers.These authors reported that cigar and pipe users were at a higher
risk of tooth loss than nonsmokers were and that more calculus and interdental bone
loss were observed in cigar and pipe users than in nonsmokers.An earlier
cross-sectional analysis of this same male veteran population in the United States
had reported greater accumulation of plaque and calculus in cigar/pipe smokers than
in nonsmokers after adjusting for age.However, when compared with cigarette
smokers, cigar/pipe users had lower accumulations of plaque and calculus and less
alveolar bone loss.These studies were limited to older, male, predominantly white
populations and often grouped cigar and pipe users together
● HOOKAH.One study found higher plaque index, increased bleeding on probing, and
more sites with attachment loss and probing depth greater than 3 mm in hookah
users compared with nonsmokers, with no difference in these parameters between
hookah users and cigarette smokers.Another evaluation similarly identified greater
marginal bone loss and more missing teeth among hookah users than among
nonsmokers and reported comparable periodontal status between hookah and
cigarette smokers.In a third study, increased periodontal bone loss and greater
prevalence of vertical bone defects were found in hookah users than in nonsmokers
● CANNABIS. A limited number of epidemiologic studies have evaluated the
association between cannabis use and periodontitis. Using data from the Dunedin
Multidisciplinary Health and Development Study birth cohort in New Zealand,
cannabis use measured between ages 18 and 26 years was associated with greater
odds of experiencing 3 mm or more clinical attachment loss between ages 26 and 32
years, including after controlling for tobacco use and other sociodemographic and
behavioral risk factors.Following this same cohort to age 38 years confirmed the
positive association between cannabis use and declining periodontal health. Using
data the from Aboriginal Birth Cohort study in Australia, investigators examined the
prevalence of periodontitis among young adults (mean age 18 years). Almost all
cannabis users also used tobacco, precluding an assessment of cannabis-only use
on periodontal outcomes; however, among tobacco users, co-use with cannabis was
associated with a higher prevalence of periodontal disease. In contrast, a
cross-sectional study evaluating the presence of periodontal disease in Chilean
adolescents did not identify an association between cannabis use and clinical
attachment loss.

● Art 3 :
We investigated the effects of e-cig use on the composition of the human subgingival plaque
(SGP) microbial community of 84 subjects over a 6-month interval, integrating microbiome
data with clinical measures and SGP cytokine concentrations. All subjects presented with at
least mild periodontitis and did not receive prophylactic cleaning during the study period,
providing an opportunity to compare alterations of a dysbiotic subgingival microbial
community due to habit and monitor disease progression. We compared conventional
cigarette smokers (CS; n = 27), e-cig-only users (ES; n = 28), and nonsmokers (NS; n = 29)
to assess the degree to which the e-cig subgingival microbiome resembles those of
conventional smokers and nonsmokers. Our data suggest that e-cig use promotes a stable
periodontal microbiome that is between those of the conventional cigarette smoker and
nonsmoker and has unique features that may impact host oral health in a manner different
than conventional cigarette use. ()

Art 4:
The study included a total of 57 individuals who were divided into three groups: T-cig
smokers (Group I, n = 19), E-cig vapers (Group II, n = 19) and former smokers (Group III, n
= 19). Full-mouth clinical periodontal parameters were recorded and gingival crevicular fluid
(GCF) samples were collected.

C. RESULTS:
a. About the kind of nicotine product and the result of each of them
● TOBACCO. Smoking is associated with worse outcomes following nonsurgical
debridement, open surgical debridement,bone grafts,guided tissue regeneration, and
periodontal plastic surgery. Smoking is similarly a risk factor for dental implant failure
● SMOKELESS (SPIT) TOBACCO.Oral health conditions associated with use of moist
snuff or chewing tobacco are oral mucosal lesions, including hyperkeratotic or
erythroplakic lesions, are commonly found even among young users. Gingival
recession and periodontal attachment loss have been reported near the areas where
smokeless tobacco is held in the mouth, as well as dental erosion and gingival
recession
● CIGARS AND PIPES. More severe periodontal disease was observed among cigar
smokers compared with nonsmokers, but small sample sizes precluded a detectable
difference between cigar and cigarette users. More recently, cigar-product users and
pipe users were both at higher odds of self-reporting gum disease diagnosis and
treatment than non–tobacco users were. To our knowledge, no studies have
examined possible differences in oral health effects by type of cigar, such as
premium cigars versus cigarettes or cigarette-like small cigars.
● HOOKAH. Often perceived as less harmful than cigarette smoking,hookah smoke
contains levels of volatile organic compounds, ultrafine particles, nicotine, and carbon
monoxide matching or exceeding cigarette smoke.
● CANNABIS. Even when this analysis was restricted only to tobacco never-users, the
odds of severe periodontitis were approximately double among frequent cannabis
users.The potential connections between cannabis use and other oral health
conditions are less well studied
● T-CIGS AND VAPING E-CIGS: They have the same unfavorable effects on the
markers of oxidative stress and inflammatory cytokines.

b. Mechanism how they affect to oral health


The second study demonstrated that in smokers higher levels of periodontal
pathogens in shallow, clinically healthy periodontal pockets and on oral mucous
membranes.
In addition, significant differences in the microbiota during the initial stages of plaque
formation have been found between smokers and non-smokers, as well as a higher
recovery rate of pathogens around healthy peri-implant tissues in smokers. Other
differences in smoking versus non-smoking periodontal patients include an increased
recovery rate of super infecting microorganisms such as Escherichia coli and
Candida. We can explain how common tobacco and similar products damage as a
response of oral microflora because it’s altered by acute exposures to high
concentrations of tobacco constituents during smoking or use of a smokeless
tobacco and by chronic exposures to chemicals that remain in the tissues, saliva,
crevicular fluid, or bloodstream in lower concentrations after tobacco use

D. REFERENCES:

● ART 1:
Chaffee BW, Couch ET, Vora MV, Holliday RS. Oral and periodontal implications of tobacco
and nicotine products. Periodontol 2000. 2021 Oct;87(1):241-253. doi: 10.1111/prd.12395.
PMID: 34463989; PMCID: PMC8444622.

● ART 2:
Ryder MI, Couch ET, Chaffee BW. Personalized periodontal treatment for the tobacco- and
alcohol-using patient. Periodontol 2000. 2018 Oct;78(1):30-46. doi: 10.1111/prd.12229.
PMID: 30198132; PMCID: PMC6132065.

● ART3:
Thomas SC, Xu F, Pushalkar S, Lin Z, Thakor N, Vardhan M, Flaminio Z,
Khodadadi-Jamayran A, Vasconcelos R, Akapo A, Queiroz E, Bederoff M, Janal MN, Guo Y,
Aguallo D, Gordon T, Corby PM, Kamer AR, Li X, Saxena D. Electronic Cigarette Use
Promotes a Unique Periodontal Microbiome. mBio. 2022 Feb 22;13(1):e0007522. doi:
10.1128/mbio.00075-22. Epub 2022 Feb 22. PMID: 35189698; PMCID: PMC8903898.

● ART4:
Karaaslan F, Dikilitaş A, Yiğit U. The effects of vaping electronic cigarettes on periodontitis.
Aust Dent J. 2020 Jun;65(2):143-149. doi: 10.1111/adj.12747. Epub 2020 Feb 11. PMID:
32003453.

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