Smoking swings of gingival crevicular fluid secretion.

OBJECTIVE: Smoking is detrimental to gingival and periodontal health. It has been reported to produce changes in gingival crevicular fluid (GCF) flow, but the cumulative effects of smoking on GCF have not been studied till date. The present study was designed to discover and evaluate transitional dynamics, if any, in GCF flow just immediately before and after smoking.
MATERIALS AND METHODS: The study comprised age- and gender-matched 20 male subjects. Half of the study population was constituted by non-smokers who comprised the control group and the remaining half of the study population was chronic smokers constituting the test group. The GCF samples were collected using the micropipettes before smoking, immediately after, and 10 min after smoking for the test group and during similar timings for the control group. RESULTS AND
CONCLUSION: The study reveals an overall low GCF volume in smokers than in non-smokers. More interestingly, a transitional decrease immediately after smoking is followed by a marked increase in GCF volume 10 min after smoking.

INTRODUCTION

Smoking is detrimental to periodontal tissues. The association between smoking and periodontal disease has consistently demonstrated negative effects and greater probabilities of established periodontal disease among smokers in comparison with non-smokers.[1] As we get closer to the effects, it has been established that smoking is a significant risk factor in the initiation and progression of periodontal diseases.

Subjects who smoke cigarettes have a greater risk of exhibiting more extensive and more severe alveolar bone loss.[2] Smokers tend to have greater numbers of deeper periodontal pockets and mean probing pocket depth.[3] Several clinical and epidemiological studies indicate that cigarette smoking has harmful effects on the response to a variety of non-surgical[4] and surgical procedures including modified Widman flap surgery,[5] guided tissue regeneration,[6] dental implants,[7] and supportive periodontal treatment.[8] Also, Smoking affects neutrophils and macrophages, which are important as gingival immunocompetent cells.[9]

The mechanism through which smoking deleteriously affects the periodontium remains somewhat obscure although several possibilities have been described. Both locally and systemically induced effects on the periodontium have been described. Smoking tends to mask gingival inflammation[1011] by causing constriction of the blood vessels[12] of the gingiva. Paradoxically, smokers seem to have less gingival bleeding than non-smokers with comparable supragingival plaque.[13] However, there is scarce information about impact of smoking on the gingival crevicular fluid (GCF) flow.

GCF is a transudate as well as an inflammatory exudate. At its very beginning, in a perfectly sound and histologically normal gingival, the crevicular fluid seems to contain a low concentration of protein which could represent interstitial liquid generated locally by an osmotic gradient. But as a result of increased permeability of gingival venules following inflammation, it may progress to a classical inflammatory exudate containing higher amount of total proteins.[1415]

The amount of gingival fluid is greater when inflammation is present and is sometimes proportional to the severity of the inflammation.[12] Gingival fluid production is increased by mastication of coarse foods, tooth brushing, gingival massage, ovulation, hormonal contraceptives, and smoking.[13]

GCF volume is a well-known marker of gingival health and has been used in many studies.[16] Smoking induces hyperemic response on gingival tissues, affecting their vascular dynamics, but the cumulative effects of smoking in on GCF have not been studied.

Hence, the present study was designed to discover and evaluate transitional dynamics, if any, in GCF flow just immediately after smoking.

MATERIALS AND METHODS

The study sample included age-matched 20 subjects. Their age range was 23–27 years and all the subjects selected were males. After ethical committee clearance was obtained, all the subjects who volunteered in the study were provided with the information and a written consent was obtained for the said research. The study group included both smokers and non-smokers.

Test group

Smokers who claimed to have smoked at least 6–7 cigarettes for the past 3 years at the minimum constituted the test group for the study. This group was studied at:

T0 : (baseline) value of GCF volume before smoking

Ti : Value of GCF volume immediately after smoking

T10 : Value of GCF volume 10 minutes after smoking.

Control group

Non-smokers were defined as people who had never smoked and constituted the control group for the study.

To ensure complete standardization; clinical examinations, group allocation, sampling site selection, and sample collection were performed by one examiner. The sampling site was predetermined to be the disto-palatal region of right maxillary second premolar. The timing and duration for collection of each day GCF sample was standardized for a period of 5 min between 10 a.m. and 11 a.m.

Prior to crevicular fluid collection, all the subjects underwent full mouth indexing to calculate their mean plaque and mean gingival health score. Supragingival plaque was scored using plaque index (PI) by Silness and Loe (1964). Gingival inflammation (GI) was scored using gingival index by Loe and Silness (1963). The inclusion criteria for the subjects were set at PI≤0, GI≤0.

Crevicular fluid samples were collected using micropipettes by extra-crevicular method.[17] The micropipettes were left in situ for 5 min and then measured in microliters. (The micropipettes contaminated with saliva or blood were discarded and, in case of bubbles, deductions were done from the readings.)

Data were expressed as means and standard deviations. The statistical significance of differences between groups was tested according to nonparametric analysis of variance (ANOVA; Friedman) and Mann–Whitney U test. The null hypothesis was rejected at P<0.01. For statistical analysis, SPSS 17.0 program was used.

RESULTS

This study clearly shows a clinically significant decrease in GCF volume in smokers as compared to non-smokers and interestingly an increase in the volume of GCF 10 min post-smoking.

Table 1 shows the GCF volumes collected in four groups:

Table 1

Summary of statistics for gingival crevicular fluid (mean±SD)

C (GCF value in control group of non-smokers),

T0 (pre-smoke values of smokers),

Ti (immediate post-smoke values), and

T10 (10 min post-smoke values)

The volumetric analysis revealed a decrease in mean GCF value from 0.9 to 0.4 μl of pre-smoke values in smokers as compared to that of non-smokers [Table 1, Figures 1 and 2]. This trend continued when the mean GCF volumes were further decreased from 0.4 to 0.2 μl in pre-smoke values of smokers as compared to their immediate post-smoke values. On the contrary, the mean values increased from 0.2 to 0.7 ml in immediate post-smoke values of smokers as compared to their 10 min post-smoke values.

Figure 1

Comparison of mean values of GCF volume

Figure 2

Trend of rate in increase and decrease of GCF volume in smokers and non smokers at specified interval of time

DISCUSSION

It is known that GCF is affected by ovulation and hormonal contraceptives.[13] By selecting young male subjects even in the control group, these possible physiological and any other age- and gender-dependent inter-individual susceptibility differences are eliminated.

The association of an increased volume of GCF with an increase in the severity of inflammation is well supported by evidence from the literature.[18] This probably formed the basis for the criteria of selecting healthy males with plaque score and gingival score ≤0 for the study. This can possibly explain that the changes in the GCF volumes could be attributed to nothing, but only smoking.

The mean GCF volume was lower in smokers than in age- and gender-matched non-smokers with comparable health status. An overall lower GCF volume in this study is supported by similar results reported by Morozumi et al.[21] The lower GCF volumes were linked with diminished gingival blood flow in smokers.

An immediate effect of increase of GCF volume with cigarette smoking has also been demonstrated by McLaughlin et al.[19] Also, in the study done by Barnfather, he concluded that GCF total antioxidant capacity is higher in chronic smokers, thereby increasing local anti-radical scavenging. These data imply that compensatory mechanisms develop in smokers to protect against smoke-derived radicals.

In the study, the GCF volumes were found to be decreased further immediately after smoking as compared to the baseline values and subsequently increased transiently after 10 minutes. In another study,[20] blood flow of gingiva was measured with a laser Doppler and an increase in the gingival blood flow rate was found. Authors mentioned that normally smoking causes vasoconstriction. As a consequence, gingival blood flow increased after smoking. It is speculated that small repeated vasoconstrictive attacks due to cigarette smoking may, in the long run, contribute to gingival vascular dysfunction and periodontal disease.[21]

CONCLUSION

The typical sinusoidal pattern in smokers depicts the correlation of cyclic alternating behaviors of GCF in response to smoking. Hence, it can be concluded that a rhythmic fluctuation in vascular dynamics happens with each puff one smokes. Therefore, smokers have suppressed inflammatory and altered host antibody response to antigenic challenge, leading to significantly less favorable clinical outcome than non-smokers. Other clinical trials with a different study sample and design are required to further dictate the results.