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Smoking is generally accepted as a major environmental risk factor for

periodontal diseases. Majority of previous investigations have examined the

association between periodontitis and active smoking.11 In most investigations,

smoking status was examined exclusively via a self administered questionnaire, the

validity of which is often questioned because of it’s under estimation. 123 Self report

measures, such as number of cigarettes smoked, hours per day exposure to

environmental smokes, are likely to be imprecise indicators of intake of tobacco

smoke owing to variations in environmental smoke, proximity to other smokers, room

ventilation and other environmental characteristics, as well as individual differences

in sensitivity to and / or concern about adverse effects of ETS.123

Markers of exposure to cigarette smoke include carbon monoxide

(carboxyhemoglobin), thiocyanate ion, nicotine, and cotinine, a primary metabolite of

nicotine.74 A general consensus is that cotinine, has the prerequisites of specificity,

retention time in the body, and detectable concentration levels that make it the analyte

of choice for quantifying tobacco smoke exposure.76 At present, cotinine is generally

regarded as the best marker for monitoring tobacco exposure in either actively or

passively exposed individuals. Moreover, cotinine has a much longer half-life of 18–

20 hours, making it more appropriate for use as an exposure marker. To study the

long term effects of smoking, cotinine levels may represent an alternative measure to

complement, confirm, or better quantify self reported.3. However few studies have

demonstrated an association between cotinine level in body fluids and periodontitis.123

Hence in our study cotinine levels were assessed.


Cotinine can be measured in a variety of body fluids, including blood, saliva,

urine, breast milk, and crevicular mucus. Noninvasive samples of urine and saliva are

of particular importance in field settings. Saliva and blood cotinine levels are highly

correlated, with saliva to blood ratio of 1.1 – 1.4.7 Therefore, saliva and blood cotinine

levels can be used interchangeably. Another investigation by Bernert et al.9 reported

that the serum levels of cotinine were more closely correlated with un-stimulated (>

by 4%) than stimulated saliva (> by 41%). Hence un-stimulated salivary cotinine

levels were assessed in the current study.

Cotinine has been measured in the biologic matrices by various methods like

chromatography, colorimetry, raido-immuno assay and enzyme linked immune assay.

The enzyme linked immunosorbant assay with monoclonal antibodies has been

proven useful in detecting cotinine in saliva. The NicAlert™ strip is a device that

contains cotinine specific monoclonal antibodies and is an immunochromatographic

strip based on the principle of ELISA.82 It is designed to provide a semiquantitative

estimate and can be evaluated conveniently by non specialists based solely on visual

inspection. Studies by Fiona Cooke et al.83 have shown that NicAlert™ cotinine test

strips are a valid alternative to the more expensive and time consuming gas

chromatographic test when testing saliva to verify smoking status. NCTS detects

exposure to nicotine from all sources. They have a specificity of 95% and a

sensitivity of 93%, a positive predictive value of 95% and a negative predictive value

of 93%.

In the present study, eighty patients with chronic periodontitis participated.

The mean age was (Table:1). Subjects were divided into smokers and non-smokers

and salivary cotinine level assessment was done by an immuno-chromaotgraphic

assay. Smokers have been shown to have significantly higher amounts of cotinine in

saliva (Table:8). In the present investigation the inclusion of non-smokers would

elucidate the possible influence of tobacco smoking on the prevalence and severity of

periodontitis. The periodontal parameters recorded were Gingival index, Gingival

bleeding index, Plaque index, probing pocket depth and clinical attachment level and

gingival recession.

On evaluation of gingivitis and bleeding on probing, in smokers versus non-

smokers, most investigations have found that smokers had less bleeding on

provocation than non-smokers.127 Our study shows that the mean gingival index was

higher in smokers than in non-smokers, and the difference was found to be

statistically significant (Table:2). These findings are consistent with the data of

Newbrun et al.127 The mean gingival bleeding index was significanlt higher in non-

smokers when compared to smokers (Table:4). These findings were consistent with

that of Neubrun et al.127 Decreased gingival bleeding in smokers has been explained as

being due to nicotine, which causes vasoconstriction of peripheral blood vessels such

as in forearm, skin, and hands.106, 16 Lang et al.128 demonstrated that the absence of

bleeding on probing was an indicator of periodontal stability. However, the lack of

bleeding on probing in smokers with advanced periodontal disease represents a false

negative predictor, thus making the presently accepted clinical significance of

bleeding on probing of uncertain value in smokers.16

One of the variables commonly associated with prevalence and severity of

periodontitis is plaque. The present study has shown that there was no statistically


significant difference in plaque index between smokers and non smokers (Table:3).

These results are in consistence with the studies of Jacqueline A. James et al. 58

Bastian and Waite et al.33 have studied two groups of 10 subjects, aged 17 through 29

years, to compare the rate of plaque formation. An increase in plaque accumulation

was observed in smokers, although it was not statistically significant. Studies by Jan

Bergstrom et al.117 have shown that gingival index and plaque index did not notably

differ between smoking groups. This implies that the harmful effects of smoking on

periodontal health may not be associated with plaque accumulation and poor oral


PPD and CAL estimate the degree of periodontal destruction and, therefore are

measures of periodontal morbidity. Further, as these measures are normally found

from a large number of single measurements in the individual, they must be

considered to provide robust and reliable data.129 In the present study PPD and CAL

were found to be more in smokers than in non-smokers, in spite of the plaque scores

showing no significant differences, which is consistent with the studies (Tables:5, 6).

It has been found that smokers have significantly higher probing depths and alveolar

bone loss than do non-smokers130; these findings were independent of plaque levels,

suggesting that the effect of smoking on periodontal conditions may be direct rather

than related to plaque infection.32 It has been reported that periodontitis is more

prevalent and severe among smokers; as this group of subjects possessed more

affected sites and deeper pockets than non-smokers.86 This study also establishes a

quantitative direct association between level of smoking and severity of periodontitis.

Similar results have been reported by Gonzalez et al.3


The reasons attributed to the increased PPD and CAL in smokers is twofold.

Both bacterial flora and host take part in the pathogenesis of periodontal diseases and

since no difference has been found in the periodontal pathogens between smokers and

non-smokers,32 it would appear that the deleterious effects of tobacco on the host

occur through two mechanisms. On one hand it systemically causes alteration of the

immune response and on the other, it acts locally through release of cytotoxic

metabolites and vasoactive substances. These are produced by the combustion of

tobacco and in turn affect the fibroblasts and vascular response.88

In the present study it was found that gingival recession was more in smokers

than in non-smokers (Table:7), these results are in agreement with the study by

Martinez Canut et al.36 Gunsolley et al.131 have reported that gingival recession was

twice as severe in smokers as in non-smokers. Recession in smokers could be due to

vasoconstriction and less inflammatory response caused by nicotine.16

Our results show that categorization of subjects as smokers and non-smokers,

may not be sufficient to evaluate the role of smoking in the severity of periodontal

disease. This is because smokers represent a highly heterogeneous (as they show

variations in the types and methods of tobacco use, rate of metabolism, etc.) group of

subjects. Therefore, a quantitative and more objective method to describe such a

group would provide a better analytical tool to evaluate the association between

smoking and periodontal disease. On the other hand, biochemical markers are difficult

to under estimate and are not dependent on social pressures, recollection, or brand of

tobacco used.3


Our data provide evidence that the use of cotinine levels is an objective,

reliable and quantitative method for measuring tobacco use. It may thus provide a

better or at least, alternative system for evaluating the role of smoking in periodontal

disease. Our findings confirm the relation between smoking and periodontal disease,

and also establish a quantitative direct association between level of smoking (as

determined by salivary cotinine) and severity of periodontal disease. Similar results

have been reported by Y. M. Gonzales et al.3

The advantages of measuring salivary cotinine are that its levels remain

relatively constant in active smokers over long periods of time. The ease and

convenience of providing a saliva sample may make it more preferable in a clinical

setting than the use of other body fluids.

The findings also indicate that NCTS are a valid alternative to the more

expensive, laborious and time consuming gas chromatographic studies.83 NCTS also

have the potential for use in large population based trials, for evaluating the

effectiveness of cessation programmes, and in population prevalence studies.

Immediate and personalized, feedback from a point of care test such as NCTS

improves compliance and also improves quit rates. It also helps in reinforcing

cessation of smoking.83 The validation of reported tobacco use by NCTS may have a

significant clinical importance in cessation clinics, research settings, pulmonary and

pediatric clinics, or transplant candidate selection and also may have an impact on the

determination of insurance premiums.8

The most important limitation of the present study pertain to its cross sectional

design as all information pertaining to periodontal disease and smoking status were

collected simultaneously. A single spot evaluation of cotinine level may not reflect its

long term average, which may attenuate associations with self reported measure of

exposure to smoke.72 In addition individual metabolism, rate of absorption, time of

smoking, and smoking habits, as well as ethnic differences132, all play a role in the

estimation of tobacco exposure. Longitudinal studies, involving larger population and

evaluation of more specific markers such as anabasine and anatabine are required.

The results of this study suggest that smokers have severe periodontal disease

when compared to non-smokers. Hence, dental practitioners should try to discourage

their patients from smoking for reasons of periodontal health as well as general

preventive care (AI Ismail, BA Burt,). The long-term consequences of smoking may

include not only an increased risk of periodontitis but also a strong association with

periodontitis which is refractory to treatment. These findings also should motivate

dentists and dental hygienists pertaining to promotion of tobacco cessation in their