Download smoking and periodontal disease

‘SMOKING AND PERIODONTAL DISEASE’
Dr Xavier Calvo- Medical Advisor Dentaid
Introduction
Smoking is a habit that is extremely damaging to health and that continues to be
widespread throughout society. It is currently the leading preventable cause of
premature death in the world, and it is estimated that in 2020 it will be directly
related to some 10 million annual deaths, mainly in developing countries (1).
According to the most recent INE (Spanish National Institute of Statistics) 2011-12
survey data, approximately 1 in every 3 adults in Spain is a regular smoker.
The mechanism of action of tobacco smoke and its components can be seen both at
the local and at the systemic level in the human body. At the local level, the mouth is
the gateway for tobacco smoke to enter our bodies, and therefore is a direct irritant
on oral mucosa. Nicotine also has direct effects on the gums. At the systemic level,
tobacco alters the innate and adaptive defense mechanisms and interferes with
multiple cellular processes.
Smoking is associated with a long list of systemic diseases and disorders, several of
which have an impact on oral health, including, most importantly, periodontal
disease and oral cancer. And, tobacco in all of its different forms and uses is, along
with alcohol consumption and certain nutritional deficiencies, the leading cause of
oral cancer (2). Other disorders that can be caused by smoking include delayed oral
wound healing, whether lesions are caused by accidents or periodontal surgery and
tooth extraction (3), bad breath, from of the odour of tobacco itself and slight changes
in the bacterial microbiota in the oral cavity (4).
Nevertheless, the most commonly occurring smoking-related oral is periodontal
disease. Now we will discuss the relationship between smoking and periodontal
disease.
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Smoking and periodontal disease
Etiopathogenic mechanisms of tobacco
Tobacco has an impact on defense mechanisms mainly affecting neutrophils and
inflammatory cell activation, by increasing levels of C-reactive protein, fibrinogen,
interleukin-6 and haptoglobin.
Neutrophils are white blood cells that belong to the body's first line of immune
defense and are essential for managing the commencement of any infection invading
the body. Therefore, neutrophils are essential in the periodontal pocket for holding off
the continuous aggression of biofilm when it settles and matures. In this regard,
smoking greatly affects the proper function of the neutrophils by reducing
chemotaxis, and altering their migration and phagocytosis. In fact, in aggressive
periodontal disease a similar problem is observed with an altered neutrophil function,
whether acquired or genetic. An altered phagocytic activity may lead to a deficiency in
the elimination of pathogens from the oral cavity (5).
Also, B- and T-lymphocytes, when exposed to tobacco smoke, show reduced
capacity for proliferation and production of antibodies or immunoglobulin G (IgG),
particularly IgG2 against some periodontal pathogens. One explanation could be the
increase in systemic oxidative stress that is produced by smoking.
Regarding the effect on cytokines, there is no real conclusive evidence, although
overall there seems to be a decrease in cytokines in the gingival crevicular fluid of
smokers compared to non-smokers. However, the opposite occurs for serum levels,
and the effect on TH2 lymphocytes would increase in relation to periodontal disease
progression.
With respect to collagen synthesis and the insertion and proliferation of fibroblasts,
in vitro studies, where nicotine levels tend to be very elevated, indicate that these
functions are impaired. However, on a clinical level, and with vastly lower nicotine
plasma concentrations, it is difficult to extrapolate these results. Furthermore,
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Smoking and periodontal disease
smoking greatly increases the release of collagenase-type tissue-degrading enzymes,
and at the same time reduces their inhibition, both in serum and in gingival crevicular
fluid.
Another key aspect is the increase in reactive oxygen species or free radicals that are
observed in smokers. Thus, an imbalance would occur between the levels of oxidants
and antioxidants, in favour of the former, and an increase would be observed in the
proinflammatory processes such as periodontal destruction.
The relationship between smoking and certain genetic susceptibility traits, such as
interleukin 1A and 1B polymorphism, also seems to be important. The probability of
having periodontal disease would increase by between 3 and 5 times in smokers
who test positive for these polymorphisms.
Smoking and periodontal disease
Smoking is the leading environmental risk factor and the second most important
modifiable factor, following plaque control, for periodontal disease development (6).
A typical characteristic of smoking-related periodontal disease is tooth-support
tissue destruction, with signs showing bone loss, periodontal pocket formation and
ultimately, tooth loss.
Smoking increases the risk for periodontal disease, depending on the definition of
disease, by 5 to 20 times, compared to non-smokers (7). This increase depends on the
time of tobacco smoke exposure, and the cause may be related to changes in the oral
microbiota or vascular and inflammatory phenomena, as previously explained.
Furthermore, nicotine and carbon monoxide from tobacco smoke have a negative
impact on wound healing.
Most studies also show that smokers with periodontitis respond less favourably to
periodontal treatment, whether surgical or non-surgical, and regenerative and
mucogingival surgery is not recommended in these patients.
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Smoking and periodontal disease
Long-term studies have proven that smokers have a higher probability of
experiencing periodontal disease recurrence during the periodontal maintenance
phase, while people who smoke more than 10 cigarettes per day show the most
severe disease progression (9). Some studies have even shown that second-hand
smoke can have greater periodontal effects, although this is more difficult to
determine. Smokers also are at higher risk for experiencing dental implant-related
complications, both on the short and the long term. Although, the benefits
experienced when people quit smoking are huge for periodontal health.
Disease progression has been shown to be inferior in former smokers and can even be
stopped completely. Also, both surgical and non-surgical periodontal treatment
outcomes are more satisfactory. Similarly, as gingival crevicular fluid increases from
improved microcirculation, both innate and adaptive defense processes improve and
periodontopathogenic species in the oral microbiota are shown to decrease.
Conclusion
In short, we must keep in mind that the oral cavity is particularly susceptible to the
effects of smoking and that the risk of suffering from highly disabling diseases such as
periodontitis or even deadly such as oral cancer, greatly multiplies among smokers.
Therefore, the role of healthcare professionals is crucial for encouraging smokers to
reduce their consumption or to quit smoking altogether. The entire staff in the dental
office should be involved, and collaboration with other health professionals such as
general practitioners and psychologists is very important. Helping dental patients kick
their smoking habit is one of the biggest achievements that can be made in the dental
office and is a great step toward helping patients attain optimal oral health, and
therefore overall health as well.
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Smoking and periodontal disease
References
1.
World Health Organization report on the global tobacco epidemic 2013.
2.
Johnson NW, Jayasekara P, Amarasinghe AA. Squamous cell carcinoma and precursor lesions of the oral
cavity: epidemiology and aetiology. Periodontol 2000. 2011; 57(1):19-37.
3.
Meechan JG, Macgregor ID, Rogers SN, Hobson RS, Bate JP, Dennison M. The effect of smoking on
immediate post-extraction socket filling with blood and on the incidence of painful socket. Br J Oral Maxillofac
Surg. 1988; 26(5):402-9.
4.
Cortelli JR, Barbosa MD, Westphal MA. Halitosis: a review of associated factors and therapeutic approach.
Braz Oral Res. 2008; 22 Suppl 1:44-54.
5.
Zappacosta B, Martorana GE, Papini S, Gervasoni J, Iavarone F, Fasanella S, Giardina B, De Sole P, Persichilli
S. Morpho-functional modifications of human neutrophils induced by aqueous cigarette smoke extract:
comparison with chemiluminescence activity. Luminescence. 2011; 26(5):331-5
6.
Johnson GK, Guthmiller M.Th. impact of cigarette smoking on periodontal disease and treatment.
Periodontology 2000.2007; 44: 178–194.
7.
Bergström J. Tobacco smoking and chronic destructive periodontal disease. Odontology. 2004; 92(1):1-8.
8.
Barbour SE, Nakashima K, Zhang JB, Tangada S, Hahn CL, Schenkein HA, Tew JG. Tobacco and smoking:
environmental factors that modify the host response (immune system) and have an impact on periodontal
health. Crit Rev Oral Biol Med. 1997; 8(4):437-60.
9.
Tonetti MS. Cigarette smoking and periodontal diseases: etiology and management of disease. Ann
Periodontol. 1998 Jul; 3(1):88-101.
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Smoking and periodontal disease