Influence of cigarette smoking on vascular reaction during experimental gingivitis

The influence of cigarette smoking on the vascular reaction during plaque induced gingivitis was studied in humans for 28 days. Sixteen healthy dental students, 8 smokers and 8 non-smokers, aged 19-42 yr, volunteered for the experiment. A numerical method was used for the evaluation of the vascular reaction. With the aid of stereophotographs changes in the number of gingival vessels were followed during the experiment. It was found that the number of vessels identified increased over time during the experiment in both smokers and non-smokers. However, in spite of the fact that the plaque accumulation rate was equal, the vascular reaction was less pronounced in smokers. At the end of the experiment after 28 days the intensity of the vascular reaction in smokers was only 50% of that observed in non-smokers. The difference was statistically significant at the P-level of 0.05. One week after termination of the experiment and reinstitution of oral hygiene the number of gingival vessels equaled the pre-experimental values in both groups. The results indicate that the vascular reaction associated with plaque induced gingivitis is suppressed in smokers.     

The influence of cigarette smoking on the development of experimental gingivitis

The aim of this investigation was to study the influence of cigarette smoking on the development of gingivitis. Experimental gingivitis was induced in the mandibular anterior region by abstention from oral hygiene for 28 days. The study group consisted of 20 healthy dental students, 10 of whom were regular smokers. The clinical parameters studied were gingival bleeding on probing (60 g), gingival redness and gingival exudate. The results showed that the plaque formation rate was similar in both groups. However, smokers displayed a less pronounced gingival inflammatory reaction as compared with non-smokers. Concerning gingival bleeding and gingival redness, the reaction in smokers was significantly less elevated from d 14 through d 28 and concerning the amount of gingival exudate it was significantly less elevated from d 21 through d 28. The differences between groups tended to increase with time. These results suggest that the inflammatory gingival response to accumulating plaque may be suppressed under the influence of cigarette smoking.     

Effect of cigarette smoking on the transition dynamics in experimental gingivitis

This paper reports the findings of an experimental gingivitis study conducted in smokers and non-smokers. 33 volunteers were examined and underwent prophylaxis during a period of 4 weeks. 28 subjects who showed a plaque index less than 0.20 on all prophylaxis occasions were permitted to continue in the study. Subjects then had their gingival status recorded, had their teeth polished and were requested to abstain from all oral hygiene measures for the following 21 days. After 5 days, 10 days and 21 days, plaque and gingival status were recorded using the criteria of the plaque index and gingival index. After the examination on day 21, the teeth were polished and oral hygiene was re-instituted. Following 2 weeks of supervised oral hygiene, recordings of plaque and gingival status were performed. At the initial examination, there was no difference between the clinical assessment of plaque and gingival status in smokers and non-smokers. Similar amounts of plaque accumulated in the 2 groups during the period of no oral hygiene, but smokers exhibited less gingival inflammation assessed clinically than non-smokers. This difference occurred as a result of an apparently lowered incidence rate and a markedly higher recovery rate in smokers compared to non-smokers. These findings may indicate that smokers for reasons yet unknown have a reduced capacity to mount and maintain an effective defense reaction to a given plaque challenge.     

Evaluation of 2 methods to assess gingival bleeding in smokers and non-smokers in natural and experimental gingivitis

Abstract. The purpose of the present study was to compare the bleeding tendency as elicited by probing the marginal gingiva (BOMP) and probing to the bottom of the pocket (BOPP) in smokers and non-smokers in natural gingivitis and during experimental gingivitis, 11 smokers (sm) and 14 non-smokers (nsm) were recruited. When they had less than 20% approximal bleeding sites, they entered a 14-day trial period of experimental gingivitis'. Subjects returned 30 days later, after resuming normal oral hygiene procedures, for a final gingival assessment. A split-mouth design was chosen using 2 contra-lateral quadrants for each index (being either BOMP or BOPP). A consistently higher bleeding score of approximately 10% was observed by probing to the bottom of the pocket. At day 14 with both indices, a significant difference between smokers and non-smokers was detected (BOMP: sm=15%, nsm = 30%; BOPP: sm = 27%, nsm=44%). The increment between gingival health and experimental gingivitis was significantly higher in non-smokers than in smokers but comparable for both indices (BOMP: sm=8%, nsm = 23%; BOPP: sm=9%, nsm=26%). Probing to the bottom of the pocket results in significantly more bleeding in gingival health and gingivitis as compared to probing of the marginal gingiva. This shows that evaluation of the gingival condition with BOMP, the method of choice with respect to gingivitis, can be used as a parameter for inflammation when comparing smokers and nonsmokers. The suppressed inflammatory response to plaque accumulation, as observed in smokers, indicates that they should be identified as a separate group when they participate as panellists in (experimentally induced) gingivitis     

Oral hygiene compliance and gingivitis expression in cigarette smokers

The compliance with an oral hygiene intervention program and its effect on oral cleanliness and gingivitis was studied in smokers and non-smokers. The study group represented patients with regular dental attendance. It comprised 68 patients 21-60 yr of age, including 28 habitual smokers. The program included toothbrushing with an electric toothbrush for 12 months. Oral cleanliness was evaluated according to a percentage plaque index and gingivitis according to the percentage of bleeding sites. The compliance with the oral hygiene program was very high among smokers and non-smokers. Plaque index at baseline was very similar in smokers and non-smokers and remained so during the course of the investigation. Following the introduction of the oral hygiene program, plaque index decreased in both groups, and there were no statistically significant differences between the two groups. In spite of the similarity in plaque index, gingival bleeding was significantly lower in smokers than non-smokers. The results suggest that smokers and non-smokers do not differ with respect to habitual oral hygiene or compliance with hygiene programs. In smokers, however, the clinical gingivitis expression in response to plaque is suppressed.     

Oral hygiene compliance and gingivitis expression in cigarette smokers

Abstract – The compliance with an oral hygiene intervention program and its effect on oral cleanliness and gingivitis was studied in smokers and non-smokers. The study group represented patients with regular dental attendance. It comprised 68 patients 21-60 yr of age, including 28 habitual smokers. The program included toothbrushing with an electric toothbrush for 12 months. Oral cleanliness was evaluated according to a percentage plaque index and gingivitis according to the percentage of bleeding sites. The compliance with the oral hygiene program was very high among smokers and non-smokers. Plaque index at baseline was very similar in smokers and non-smokers and remained so during the course of the investigation. Following the introduction of the oral hygiene program, plaque index decreased in both groups, and there were no statistically significant differences between the two groups. In spite of the similarity in plaque index, gingival bleeding was significantly lower in smokers than non-smokers. The results suggest that smokers and non-smokers do not differ with respect to habitual oral hygiene or compliance with hygiene programs. In smokers, however, the clinical gingivitis expression in response to plaque is suppressed.     

Effect of smoking on gingival crevicular fluid cytokine profile during experimental gingivitis

BACKGROUND: Cigarette smoking is a significant risk factor in the pathogenesis of periodontal disease, able to influence both the subgingival microbiota and host responses. AIM: The aim of the present study was to determine the influence of smoking on the amount of IL-1beta, IL-4 and IL-8 in gingival crevicular fluid (GCF) during experimental gingivitis in humans. MATERIAL AND METHODS: Twenty-two healthy subjects, 10 smokers and 12 non-smokers, participated in the study. After professional cleaning, they performed optimal hygiene to reach perfect clinical gingival health. Oral hygiene measures were ceased for a period of 10 days. Clinical indices, including plaque index (PI), gingival index (GI), probing pocket depth (PPD) and bleeding on probing (BOP), were assessed 2 days before (day -2), at the beginning (day 0) and at the end of the experimental gingivitis period (day 10). At the same time, GCF was collected from 12 sites in each patient, by means of durapore filter membranes. Total amounts of IL-1beta, IL-4 and IL-8 were determined by enzyme-linked immunoadsorbent assay. RESULTS: Clinical data revealed that both smokers and non-smokers showed an increase in PI, GI and BOP scores during the experiment. Although no differences were noted with regard to PI at day 10, the GI and BOP were significantly less pronounced in smokers than non-smokers (p < 0.005). Non-smokers showed higher total amounts of IL-4 but lower amounts of IL-8 than smokers, throughout the experiment. Total amounts of IL-1beta and IL-8 increased significantly during plaque accumulation in both groups. IL-4 remained stable for the smoker group and decreased for the non-smoker group. CONCLUSIONS: The present results indicate that smoking interferes with cytokine production. When performing studies regarding the pathogenesis of periodontitis, the smoking status of the participants needs to be taken into consideration.     

Oral microbiota in smokers and non-smokers in natural and experimentally-induced gingivitis

Abstract. The present study primarily aimed at investigating the oral microbiota in smokers and non-smokers with established gingivitis and monitoring its composition during experimental gingivitis. Secondly, it aimed at examining whether the composition of the microbiota is associated with different levels of gingival inflammation during this experimental gingivitis trial. For this purpose, 25 non-dental university students with gingivitis were recruited. 11 subjects were smokers and 14 were non-smokers. After achieving gingival health, they entered a 14-day experimental gingivitis trial. Plaque and bleeding were assessed before entering into the study (intake), at day 0. day 5 and at day 14 of the experiment. Microbiological samples from mucosal sites and dental plaque (taken at intake, day 0, and day 14) were analysed for the presence of Actinomyces species. Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros. Porphyromonas gingivalis, Prevotella intermedia and Streptococcus species. At day 14 of the experimental period, the level of plaque formation was not different between smokers and nonsmokers, but bleeding scores were lower in smokers than in non-smokers (15% and 30%) respectively, p= 0.01). The change from natural gingivitis to a state of gingival health and a subsequent change from gingival health to experimentally induced gingivitis was accompanied by quantitative alterations in the cultivable microbiota in both groups. Changes were most prominent in the transition from gingival health to experimental gingivitis and were found in dental plaque for Actinomyces species, C. rectus, F. nucleatum, and P. intermedia. Within the group of non-smokers, a distinction was made between subjects with a‘weak’or 'strong’inflammatory response. No relationship with a single bacterial species could be established which would likely explain the differences in levels of inflammation. It is concluded that differences in response to experimental gingivitis are not caused by major differences in the composition of the oral microbiota.     

Microcirculatory dynamics in experimental human gingivitis

Abstract The purpose of this study was to determine the changes that occur in the gingival microcirculation during the development of experimental gingivitis in humans. There have been no studies published to date combining videomicroscopy and laser Doppler flowmetry to study vascular dynamics in experimental gingivitis. Alterations occurring in the microcirculation of the marginal gingiva in 10 (18–30-year-old), healthy male humans when they suspended oral hygiene procedures in a proscribed area for 12–16 days were monitored. A partial mouth, experimental gingivitis model was employed. Gingival health was evaluated before and after the experimental period by assessing gingival and plaque indices and gingival crevicular fluid volume. Gingival vascular monitoring included measurement of red blood cell velocity in individual gingival microvessels via video-microscopy and measurement of regional gingival blood flow using laser doppler flowmetry. The number of vessels visible in a given microscopic field in a given subject and the number of vessels exhibiting flow were also determined from the videotapes. Systemic cardiovascular and respiratory parameters were monitored to ensure that gingival vascular changes were not secondary to systemic changes. Gingivitis developed in all subjects; significant increases (Student t-test, P < 0.05) were seen in plaque index, gingival index, bleeding on probing and crevicular fluid volume. No change in superficial capillary blood velocity and a significant decrease in gingival regional blood flow were seen with gingivitis. A significant increase in the number of vessels visible in microscopic fields and a decrease in the % of vessels exhibiting flow were observed. Gingival microcirculation exhibited a dramatic, dynamic change in response to the development and progression of gingivitis.     

Bleeding on probing in smokers and non-smokers in a steady state plaque environment

An altered gingival inflammatory response to supragingival plaque in smokers had been claimed by several authors. Relatively limited information exists with regard to the consistency of naturally occurring plaque and bleeding upon probing within the oral cavity under usual oral hygiene measures. The aims of the present study were to describe the distribution of tooth surfaces covered by supragingival plaque and gingival units bleeding upon probing in a steady state environment of no dental intervention. In addition relative consistency of plaque and bleeding was investigated. 65 volunteers, 14 women and 51 men in the age range of 19 to 30 years, participated. 33 volunteers were heavy smokers and 32 non-smokers. Clinical examinations revealed mild, plaque-induced gingivitis with no overt destructive periodontitis. Within a 6-month period. presence and amount of plaque, calculus and gingival bleeding was site-specifically assessed four times, i.e., every 8 weeks. Well-defined, symmetric and consistent patterns of plaque and calculus distribution within the oral cavity were observed, which were rather identical in smokers and non-smokers. Smokers had evenly more plaque in all regions of the oral cavity. In contrast, there was no obvious pattern of bleeding upon probing. Consistency of observations was considerably lower than for plaque scores. This was particularly true for smokers, where the association between bleeding scores was generally smaller than in non-smokers. A large portion of the variation of gingival bleeding may be due to presently unknown factors other than plaque and calculus with considerable consequences for preventive programmes.     

Longitudinal association between plaque and gingival bleeding in smokers and non-smokers

BACKGROUND/AIMS: Whereas accumulation of dentogingival plaque inevitably leads to inflammatory reactions in the adjacent gingival tissue, there is limited information with regard to factors influencing naturally occurring fluctuation between gingival health and disease. The major aims of the present study were to investigate site-specific associations between plaque and gingivitis as well as transition dynamics of naturally occurring gingivitis in smoking and non-smoking young adults. METHODS: 65 systemically healthy young adults, 19 to 30 years old, participated. 33 volunteers smoked at least 20 cigarettes per day, whereas 32 subjects were non-smokers. Clinical periodontal conditions were assessed four times within a time period of 6 months. An ecological approach in data analysis as well as site-specific analyses considering the correlated structure of data were performed. RESULTS: At the outset and after 6 months, smokers had significantly more supragingival plaque than non-smokers. At the final examination, bleeding upon probing as well as calculus were more prevalent in smokers. A site-by-site analysis revealed that smokers tended to have a weaker association between supragingival plaque and bleeding on probing than non-smokers (median Mantel-Haenszel's common odds ratio 1.91 vs. 2.89, p=0.07). Multiple logistic regression analyses adjusted for periodontal probing depth, plaque and calculus identified smoking status to significantly increase the risk for the first transition of non-bleeding to bleeding upon probing by 86% (p<0.01). In contrast, recovery of bleeding sites was positively influenced by female gender, but not smoking. CONCLUSIONS: In multivariate analyses adjusted for probing depth, plaque and calculus, smokers appeared to be at higher risk for the transition from non-bleeding to bleeding on probing. Weaker associations between plaque and naturally occurring gingivitis in smokers may have important consequences for preventive strategies for gingivitis.     

Multivariate multilevel models for repeated measures in the study of smoking effects on the association between plaque and gingival bleeding

Multivariate multilevel modeling was applied to analyze repeated measures data on the influence of heavy smoking on the association between the amount of supragingival plaque and gingival bleeding on probing (BOP) in a steady-state plaque environment. Data acquired in 65 systemically healthy young adults with mild plaque-induced gingivitis were analyzed. 33 heavy smokers consumed at least 20 cigarettes per day while 32 were non-smokers. Periodontal examinations at the outset consisted of periodontal probing depth, clinical attachment level, BOP, plaque index, and presence of calculus at 6 sites of every tooth present. They were repeated 3 times every 8 weeks. A multivariate 4-level variance component model revealed that the odds of BOP was twice as high in smokers. In addition, females had a lower likelihood for BOP but, with increasing bleeding scores during the course of the study, this effect attenuated. Low biserial correlations for BOP at the site level of between 0.11 and 0.2 were found. At the tooth level, correlations were moderate (0.2–0.5), and highest at the subject level (0.8–0.9). Variations at subject and tooth levels were very large at the outset but notably attenuated in the course of the study. Plaque consistently influenced the tendency for BOP with an odds ratio of about 1.7–1.8 for each increase in score in both smokers and non-smokers. The present study did not reveal evidence for attenuation of the plaque/gingival bleeding relationship in heavy smokers.     

Quantitative evaluation of the vasculature and fibronectin localization in gingival connective tissue of smokers and non-smokers

BACKGROUND: It has been shown that tobacco is a significant risk factor for periodontal disease. The reason for decreased gingival bleeding in smokers is not known. The aim of the present study was to demonstrate the localization of fibronectin in the extracellular matrix of the inflamed gingiva of smokers and non-smokers and to evaluate the chronic effect of smoking on the gingival microvessel number (NVES) and vascular surface density (VSD). METHODS: Seventy-four (74) adult patients with periodontitis were included in this investigation. Of these patients, 38 were smokers and 36 were non-smokers. Probing depths (PD), papillary bleeding index (PBI) of both groups, and the smoking habits of the smokers were recorded. Biopsy specimens obtained during periodontal surgery were prepared to evaluate fibronectin distribution and to quantitate the vasculature. RESULTS: The mean VSD values of smokers and non-smokers were 6.721 +/- 1.845 and 5.721 +/- 3.118 (mean +/- SD), and the mean NVES of smokers and non-smokers was 31.582 +/- 11.810 and 30.145 +/- 15.442, respectively. The difference between the mean PD and PBI values of the 2 groups was not statistically significant. The location of the biopsy specimen, whether in the anterior or posterior area of the mouth, did not lead to any statistically significant differences between the groups. In addition, the number of years smoked and the tobacco brand used did not result in statistically significant differences. The most intense staining of fibronectin was observed beneath the epithelium around the blood vessels of the uppermost region of the connective tissue, showing a fibrillar and diffuse distribution; however, there was no significant difference between smokers and non-smokers. CONCLUSION: The results of the present study indicate that smoking does not affect the vascular surface density, number of vessels per mm2 stroma, or fibronectin distribution in subepithelial gingival connective tissue.     

The influence of gingival stimulation on recovery from human experimental gingivitis

The present study concerns an investigation carried out to determine the effects of gingival stimulation on the resolution of a human experimental gingivitis. 10 young male dental students participated in the experiment. Following the baseline examination (day 0), the participants were instructed to abstain from all oral hygiene procedures during a 21-day period. Heavy plaque accumulation and gingivitis developed during the 21-day induction period. On the evening of the 21st day, active oral hygiene measures were reinstitued, for an 8-day period, using 2 different methods. For the left side of the maxillary arch, a hygiene procedure including gingival stimulation was prescribed. On the other hand, for the right side, a hygiene method without gingival stimulation was instituted. On both sides of the upper arch, the gingival condition was assessed by means of the gingival index, and soft deposits were assessed by the plaque index (selected teeth: 13, 14, 15, 23, 24, 25). Measurements were performed on days 0, 21, 22, 23, 24, 25, 26, 27, 28, 29. On day 29, ideal oral hygiene conditions and gingival health were re-established on both sides. However, a statistical analysis of the data collected during the recovery period revealed that gingival index scores were temporarily, but significantly, higher on the side where mechanical stimulation was performed, although plaque deposits there decreased more rapidly. Thus the present work supports the idea that gingival stimulation does not in any way improve recovery from experimental gingivitis.     

Parotid salivary S-IgA antibodies during experimental gingivitis in smokers and non-smokers

Persons who smoke display a less pronounced increase of gingival bleeding in the experimental gingivitis model as compared with non-smokers. The aim of the present study was to investigate whether this could partly be explained by differences in levels of parotid total secretory IgA (S-IgA) or parotid S-IgA reactive with selected oral microorganisms. Parotid saliva samples were obtained from 11 smoking and 14 non-smoking volunteers, at baseline, after 5 and 14 days of full mouth experimental gingivitis. Output levels of total S-IgA and of specific S-IgA reactive with cell extracts from Actinobacillus actinomycetemcomitans, Actinomyces naeslundii, Campylobacter rectus, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Peptostreptococcus micros, Streptococcus gordonii and Streptococcus mutans were determined in the samples by means of ELISA. Smokers and non-smokers were found to have similar output levels (microg/min) of total S-IgA, and the values did not significantly change during the experimental gingivitis trial. Parotid salivary outputs (units/min) of the bacteria-specific S-IgA at baseline and at days 5 and 14, were not different between smokers and non-smokers; no changes were observed during the experimental gingivitis trial. The present observations indicate that total S-IgA and bacteria-specific S-IgA in saliva are not main factors that can explain the less pronounced increase of gingival bleeding in the experimental gingivitis model in smokers as compared with non-smokers.     

Effect of non-surgical treatment on gingival bleeding in smokers and non-smokers

According to previous findings, gingival bleeding seems to be reduced under the influence of cigarette smoking. The present study deals with the effect of non-surgical therapy on gingival bleeding in smokers and non-smokers. The underlying hypothesis was that the therapeutic effect in terms of reduction of gingival bleeding might differ in smokers and non-smokers. Twenty patients with moderate to severe periodontitis, 10 smokers and 10 non-smokers, took part in the study. Gingival bleeding was assessed by probing under a standardized pressure (60 g), and measurements were performed before and 1 month after the completion of active treatment. The active treatment included debridement of supra- and sub-gingival deposits by means of hand instrumentation. The treatment caused a reduction in plaque index and gingival bleeding both in smokers and in non-smokers. The plaque reduction was significantly greater in smokers. Nevertheless, the reduction in gingival bleeding was significantly less pronounced than that attained in non-smokers. The findings suggest that the gingival bleeding response to treatment is reduced in smokers. It would seem that in response to a given amount of plaque reduction the changes in gingival bleeding will be less apparent under the influence of smoking.     

Expression of ICAM-1 and E-selectin in gingival tissues of smokers and non-smokers with periodontitis.

BACKGROUND: Tobacco smoking affects systemic concentrations of soluble intercellular adhesion molecule (ICAM)-1, but its effect on local expression of adhesion molecules in gingival tissue has not been studied previously. METHODS: E-selectin and ICAM-1 expression on small blood vessel endothelia in gingival biopsies obtained from smokers (n=17) and non-smokers (n=17) with periodontitis was examined with immunohistochemistry. Blood vessels were identified with monoclonal antibody for von Willebrand's factor. RESULTS: A significantly larger number of vessels were observed in inflamed tissues of non-smokers than smokers (P<0.05). The number and proportion of vessels expressing both ICAM-1 and E-selectin was greater in sites with inflammation compared to non-inflamed sites in both smokers and non-smokers (P<0.05). The proportion of the total number of vessels expressing ICAM-1 in non-inflamed sites was greater in non-smokers compared with smokers (P<0.05). CONCLUSIONS: These results suggest that the inflammatory response in smokers with periodontitis may not be accompanied by an equivalent increase in vascularity. Reduced ICAM-1 expression in non-inflamed areas of smokers could reflect a systemic effect of tobacco smoking on ICAM-1 independent of inflammation.     

EVALUATION OF CLINICAL PERIODONTAL CONDITIONS IN SMOKERS AND NON-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.     

Observations on the initial stages of healing following human experimental gingivitis A clinical and morphometric study

The aim of the present study was to investigate stereologically the histologic alterations occurring during gingival healing after experimental gingivitis and to compare clinical parameters with histological findings. 8 dental students volunteered for the investigation. After a prophylaxis, they performed optimal oral hygiene to reach mean plaque and gingival indices approaching zero. They then abolished all oral hygiene procedures for a period of 21 days. After this experimental gingivitis phase, they again performed optimal oral hygiene for 8 days to restore gingival health. At days 0, 1, 2, 4 and 8 after experimental gingivitis, the plaque index (PlI), the gingival index (GI) and the gingival exudate flow rate (GEFR) were assessed and their buccal gingiva was biopsied. Point counting procedures were performed at 2 different levels of magnification on light microscopic sections to estimate the volume fractions of epithelium, infiltrated and non-infiltrated connective tissue, and collagen. The relative numbers of fibroblasts, polymorphonuclear neutrophils, lymphocytes, plasma cells and macrophages were estimated by counting the number of profiles of these cells in a specific connective tissue area adjacent to the apical end of the junctional epithelium. A rapid drop in the PlI was noted with increasing time after oral hygiene, followed by a slower decrease in the GI and GEFR scores. The histological picture during the entire experiment was that of an initial gingival lesion. At day 0, no chronic inflammation of the gingiva characterized by a predominance of plasma cells was observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of local anesthetic containing adrenaline on gingival blood flow in smokers and non smokers

Abstract Recent evidence suggests that fundamental differences exist in the development of gingival and periodontal diseases in smokers versus non-smokers. In part, these differences may be attributable to smoking-induced differences in the vascular dynamics of the periodontium. This study monitored gingival blood flow when challenged by a local anesthetic-containing adrenaline in 20 smokers and 20 non-smokers using laser Doppler flowmentry (LDF). The dosage of local anesthetic used (0.5 ml lignocaine hydrochloride 2% with adrenaline 1:80.000) was calculated after establishing a dose-response curve (DRC) for 3 subjects (2 non-smokers and 1 smoker). Plain lignocaine and normal saline were used as controls. The injection of lignocaine-containing adrenaline had little effect on LDF signals when different doses were injected at frequent short intervals, indicating that tolerance to adrenaline had rapidly developed in the receptors of gingival blood vessels. Injection of local anesthetics containing adrenaline consistently resulted in a marked and significant drop (average: 46%, sd:13.5) in the LDF output signals from gingiva; smokers and non-smokers responded similarly. The significant finding of this study was that the recovery of LDF signals to baseline took considerably longer in smokers than in non-smokers. This provides further evidence that gingival blood vessels in smokers with healthy gingival conditions respond differently to those of non-smokers.