in addition to the known harmful effects caused to the human body , the oral cavity is directly affected by the smoking habit .
several studies have demonstrated that tobacco is , per se , a risk factor in the etiology of periodontal disease , with a local and systemic effect9,28 .
a positive association between cigarette smoking and acute necrotizing ulcerative gingivitis ( anug ) was first reported over 4 decades ago23 .
recent studies have confirmed a greater prevalence of attachment loss2,25 , recession2 , severe destructive periodontal disease9,12 and less favorable response to nonsurgical2,25 or surgical2 periodontal treatment in smokers , as compared to non - smokers .
additionally , it seems difficult to discern the effect caused by tobacco from that provoked by bacterial infection15 . in this
regard , recent knowledge on plaque formation is controversial as for the possibility that smoking may interfere with the natural occurrence of plaque accumulation on dental surfaces . regarding periodontal blood supply , several studies related to plaque - induced gingivitis , showed a reduction of clinical signs10,11 , with a smaller propensity for gingival bleeding7,8,10 , owing to vascular changes caused by smoking7 .
clinical and epidemiological studies also reported that most refractory periodontal condition cases occur in smokers and that there is a dose - dependant relation , in which , the greater the quantity of cigarettes smoked a day and the duration of the smoking habit , the greater the periodontal bone loss9 .
therefore , the purpose of this study was to compare periodontal clinical parameters of probing depth ( pd ) , clinical attachment level ( cal ) , gingival index ( gi ) , gingival bleeding index ( gbi ) , plaque index ( pi ) and gingival recession ( gr ) between smoking and non - smoking groups and correlate these parameters between groups .
the sample was composed of 55 subjects , being 29 smokers ( 55.2% females and 44.8% males ) and 26 non - smokers ( 65.4% females and 34.6% males ) .
the participants were recruited from private practices in the city of cascavel , pr , brazil .
the patients attended a lecture on periodontal disease , tobacco as a risk factor on the oral cavity and were given information on the research project .
the study design and informed consent form were approved by the ethics in research committee of the dental school of bauru , university of so paulo ( process number 019/2002/fob ) .
the criteria for sample screening were : 1 ) non - smokers and smokers between 30 and 50 years of age ; 2 ) smokers of approximately 1 pack or more of cigarettes / day ; 3 ) absence of systemic or acute periodontal alterations ; 4 ) no periodontal treatment in the previous 6 months ; 5 ) no antibiotic therapy within the previous 8 months ; 6 ) at least one region with periodontal pocket of 5 mm or more , in a posterior tooth .
patients were given no instruction on hygiene and oral physiotherapy , and no procedure of basic preparation was carried out , not to interfere with clinical data collection .
the following clinical parameters were evaluated : probing depth ( pd ) , clinical attachment level ( cal ) , gingival index ( gi - le19 ) , gingival bleeding index ( gbi - ainamo and bay3 ) , plaque index ( pi - silness and le27 ) and gingival recession ( gr ) .
the measurements were performed with a michigan ( hu - friedy pc15 usa ) millimeter manual periodontal probe , in six sites of each tooth ( distobuccal surface , center of vestibular surface , mesiobuccal surface , distolingual surface , center of lingual surface and mesiolingual surface ) . in order to minimize the variability of the examination , during assessment of pi27 , mesial ( m ) and distal ( d ) measurements were made only in the buccal surface because the palatal / lingual surfaces were indirectly seen with a buccal mirror , according to the technique proposed by silness and le 27 .
all clinical periodontal parameters ( pd , cal , gi , gbi , pi and gr ) were analyzed statistically by regions ( ps = postero - superior ; as = antero - superior ; pi= postero - inferior ; ai = antero - inferior ) . multiple regression analysis was performed for comparison between smokers ( n=26 ) and non - smokers ( n=29 ) , using age and gender as the control variables and adopting a 5% significance level .
a sample size of 26 patients is capable of proving a difference of 1.7 times the standard deviation , for a significance level of 5% and a statistical power of 80%.calculations were performed using the spss statistical software version 13.0 ( spss inc , chicago , il , usa ) .
for all situations evaluated , there was a trend towards greater pd ( figure 1 ) and cal ( figure 2 ) means for the smoking group .
gi means ( figure 3 ) were greater in the non - smoking group , with statistical significance in all regions ( p<0.05 ) .
although there were no statistically significant differences between smoking and non - smoking groups , there was an overall trend towards greater gbi means , almost always , for non - smokers ( figure 4 ) .
regarding pi means between smokers and non - smokers ( figure 5 ) , greater plaque accumulation was observed for the smoking group . in relation to gr
, there was no constancy of greater values for smokers or non - smokers and , in none of the situations there were statistically significant differences ( figure 6 ) . comparing the group of smokers , as for the number of missing teeth ( table 1 ) , taking into account posterior / anterior and superior / inferior regions , the differences were not significant statistically , though there was a tendency for greater upper tooth loss in smokers and greater lower tooth loss in non - smokers . regarding the variables analyzed between the groups of smokers and non - smokers , table 2 shows a mean age of 40 years old , a greater participation of females and a mean of 24.5 cigarettes smoked a day .
in addition to bacterial plaque , other factors can modify the host response , predisposing the individual to a higher risk of periodontal disease . among the factors considered as fundamental in the host resistance - bacterial aggression interrelation ,
hereditary predisposition , age , systemic conditions , stress , drugs and tobacco may be cited .
nowadays , it is known that the action of tobacco in the periodontium might predispose the individual to various periodontal diseases7,11,13,14,16 and not only to anug23 .
however , the large number of studies in this field is justified by the fact that the effects of cigarette smoking on the periodontal status have not been completely elucidated .
the age range of the study subjects was delimited in order to exclude those either too young or too old .
this approach was important for the sample as an effort to minimize aspects related to overage , which might influence the periodontal conditions .
on the other hand , the effects of smoking ( time of action ) might be less expressive in younger individuals , so they were also excluded , establishing a mean age of 40 years old ( table 2 ) .
however , in many of them , the examinations are carried out by different professionals and data are obtained only from some sites of the mouth , such as the use of cpitn4,12 .
it is noteworthy that all records of the study were accomplished by a single examiner , previously calibrated by the kappa test , which is important for an accurate standardization , especially in the examinations where the subjectivity load is critical .
the results of the present study , in which clinical parameters were considered , showed an evident negative influence of tobacco , particularly for pd ( figure 1 ) and cal ( figure 2 ) .
there was a tendency of greater pd and cal means in all regions analyzed in smokers , in relation to non - smokers .
it should be highlighted that , in a previous study2 , the prevalence of greater pds occurred for smokers of cigarettes , cigars or pipe , alike .
stoltenberg , et al.28 ( 1993 ) found 5 times more periodontal pockets = 3.5 mm in smokers , in the proximal surfaces of all upper teeth , with no qualitative differences in the microbiota of smokers and non - smokers .
a smaller pd reduction in all regions after nonsurgical periodontal therapy and a greater difference for the antero - superior region was observed by preber and bergstrm24 ( 1985 ) . as for maintenance therapy , jansson and hagstrm15(2002 ) , found greater pd in subjects who interrupted the treatment , independently of the smoking habit .
when the tobacco variable was considered , the authors demonstrated that smokers with no periodontal support therapy had higher risk of periodontitis progression .
the results obtained by haffajee and socransky14 ( 2001 ) were similar to those of this study .
the authors examined the clinical characteristics of periodontal disease and standards of insertion loss among usual smokers , occasional smokers and those who had never smoked , in 6 sites per tooth , in all teeth , excluding the third molars .
the study showed that this parameter was more significant in usual smokers than in the other 2 groups , particularly , in the palatal upper sites and in antero - inferior teeth . according to the authors , these greater attachment losses observed in these sites suggested the possibility of a local effect of cigarette . in the present investigation ,
the dose - reaction relation may have influenced the results of this variable as well because the study subjects smoked 24.5 cigarettes / day on the average ( table 2 ) . in this context
, martinez - canut , et al.20 ( 1995 ) also related the cigarette dose - reaction to cal , showing a direct relation of greater insertion loss with the increase in the number of cigarettes consumed .
although it was not within the scope of this study , another less favorable parameter in smokers is the insertion gain , following periodontal therapy . ah ,
et al.1 ( 1994 ) evaluated the effect of tobacco on clinical response to surgical and non - surgical periodontal therapy between smokers and non - smokers .
there are some evidences that tobacco may be associated with less expressive signs and symptoms in periodontal inflammation , such as gingival bleeding , erythema and edema , indicating a suppressive influence in inflammatory response7,8,10,11,13,17 . in this study ,
the comparative analysis of gi ( figure 3 ) , between smokers and non - smokers , with a mean age of 40 years , showed that in all analyzed situations , there were greater values for non - smokers , which reflects a greater clinical inflammatory exuberance , in this group .
these greater means in non - smokers may be related to the nicotine 's vasoconstrictor effect .
several articles are consistent with this work , revealing that the clinical signs of inflammation are less evident in smokers7,11,14,17,21 .
other researches reported that the dose - dependent reaction would attenuate the clinical signs , proportionally to tobacco consumption20 . on the other hand , some works did not demonstrate a relation with the gingival conditions , in subjects with gingival health6 or presented with periodontal disease7 .
some more ancient works , correlated the gi , not considering the oral hygiene standards , showing a greater inflammation evidence in smokers21,23,26 . in this context ,
5(1987 ) presented the effects of cigarette on blood flow , causing a significant increase and not a decrease in gingival blood circulation , concluding that the theory that smoking would damage the gingival blood flow might not be true in smokers .
however , this result might be related to the reduced age of the subjects participating in the experiment ( 19 to 25 years old ) .
as for gbi ( figure 4 ) , although no statistically significant differences were found , there was a general trend to more bleeding sites in the non - smoker group , and , as observed for the gi , the clinical aspects seem to be masked by tobacco .
goultschin , et al.12 ( 1990 ) compared individuals with mean age similar to that of the population of this study , showing that smokers had smaller gbi means than non - smokers .
the authors attributed this finding to a reduction in the gingival flow , caused by nicotine .
another essential aspect in this clinical analysis is the bacterial plaque accumulation ( figure 5 ) .
it is important to highlight that the study subjects were given no instruction on oral hygiene along the research , not to bias data collection .
however , in all analyzed situations , there was a general trend for greater pi means for smokers . when comparing pi and gi in smokers , no inflammatory characteristics
this fact may be related to nicotine 's vasoconstrictor effect , causing a decrease in the blood flow and masking the local inflammation .
the findings of this study are in agreement with those of ah1 , while other authors have found similar plaque scores4,7,10,11,17,28 , a hypothesis that smokers may be less motivated to keep a high - quality oral hygiene6,10 or did not show a significant difference in plaque accumulation8,9,18,21,26 when the groups were matched by oral hygiene .
other studies9,18 showed that there was no significant difference in the pi means , for smoking and non - smoking individuals , with the same oral hygiene level .
bergstrm , et al.9 ( 1991 ) suggested a direct influence of tobacco on periodontal health , independently of plaque infection .
it is noteworthy that the qualitative difference in bacterial plaque has also been addressed in the present study .
some authors do not show this association13,16,17 , while others confirm the difference in microbiological quality6,22 .
this difference in the prevalence of anaerobic species would also explain the greater periodontal destruction severity in smokers than in non - smokers14 . while assessing gingival recessions between smokers and non - smokers ( figure 6 ) , it was not possible to detect significant differences for any of the analyses .
evidently , it can not be stated categorically , based on the results of the present study , that tobaccoism does not interfere with gingival recession ; however , the multiple factors involved in the etiology of gingival recessions , which were not addressed in this study , should be considered .
in this regard , albandar , et al.2 ( 2000 ) found greater prevalence of recessions , with =3 mm gingival , in smokers of cigarette , pipe and cigars , as compared to non - smokers .
another goal of this study was to compare the number of missing teeth by area ( anterior and posterior ) and arch ( upper and lower ) in the smoking and non - smoking groups ( table 1 ) . in this aspect , it was not possible to establish a significant condition for any of the situations .
nevertheless , there was a tendency for a greater upper tooth loss in smokers and a greater lower tooth loss in non - smokers .
a previous epidemiological study4 examined the periodontal condition and the smoking habits of 1,093 individuals in the 35 - 75-year - old age range , concluding that smoking is a significant risk factor for dental loss .
the same condition has reported in relation to types of tobacco by albandar , et al.2 ( 2000 ) , who suggested that smokers of cigarette , cigar or pipe present a greater prevalence of periodontal problems and greater dental loss than non - smokers .
all aspects discussed hereby are of paramount importance in the prevalence of tobacco as a periodontal risk factor . in general ,
various other subjects must be considered and further research should be carried out in order to elucidate the divergences existing on the interrelation tobacco - periodontal disease .
based on the methodology employed and considering its limitations , it may be concluded that : 1 . tobaccoism may aggravate the probing depth ( pd ) , the clinical attachment level ( cal ) and the plaque index ( pi ) ; 2 .
the gingival indexes ( gi ) and gingival bleeding ( gbi ) might suffer interference fromtobaccoism and be masked ; 3 .
gingival recessions ( gr ) alone are not clearly associated with tobaccoism ; 4 . in smokers
 given that tobacco smoking habit is a risk factor for periodontal diseases , the aim of this study was to compare clinical periodontal aspects between smokers and non - smokers . 
 the clinical status were assessed in 55 patients , 29 smokers and 26 non - smokers , aged 30 to 50 years , with mean age of 40 . 
 the clinical parameters used were : probing depth ( pd ) , plaque index ( pi ) , gingival index ( gi ) , clinical attachment level ( cal ) , gingival recession ( gr ) and gingival bleeding index ( gbi ) for arches ( upper and lower ) and teeth ( anterior and posterior ) . 
 tooth loss was also evaluated in both groups . 
 multiple regression analysis showed : tendency of greater probing depth and clinical attachment level means for smokers ; greater amount of plaque in smokers in all regions ; greater gingival index means for non - smokers with clinical significance ( p<0.05 ) in all regions . 
 although , without statistical significance , the analysis showed greater gingival bleeding index means almost always for non - smokers ; similar gingival recession means in both groups and tendency of upper tooth loss in smokers and lower tooth loss in non - smokers . 
 the findings of this study showed that clinical periodontal parameters may be different in smokers when compared to non - smokers and that masking of some periodontal signs can be a result of nicotine 's vasoconstrictor effect . 
INTRODUCTION
MATERIAL AND METHODS
RESULTS
DISCUSSION
CONCLUSIONS