Non-smoking Periodontitis Patients Research Articles

Glutathione S-transferase M1, T1, and P1 polymorphisms and periodontitis in a Caucasian population: a case-control study

BackgroundGlutathione S-transferases (GSTs) play important roles in protecting cells against oxidative stress and toxic chemicals. This study aimed to investigate the distribution of GSTM1, GSTT1, and GSTP1 variants and their roles in periodontitis susceptibility in a Caucasian population.MethodsWe analyzed 406 participants, including 204 healthy controls and 203 periodontitis patients. A multiplex polymerase chain reaction (PCR) approach was used to analyze GSTM1 and GSTT1 loci. GSTP1 variants were detected by PCR-haplotyping method in a subgroup of participants (N = 350). Chi-square or Fisher´s exact tests were used to compare genotypic and allelic differences. The Bonferroni method was applied to correct for multiple comparisons (pcorr).ResultsThe GSTM1 genotype distribution did not differ significantly between controls and periodontitis patients (p = 0.44). Additionally, the wild/null genotypes of GSTT1, Ile105Val and Ala114Val frequencies of GSTP1 were not significantly different between the two groups after correction for multiple comparisons (p = 0.05, p = 0.55, p = 0.02, pcorr>0.05, respectively). The GSTM1 and GSTP1 Ile105Val gene variants were similarly distributed between non-smokers and smokers in both groups (p = 0.38, p = 0.20, and p = 0.14, p = 0.35, respectively). However, the wild genotype of the GSTT1 and Ala114Ala variant of the GSTP1 genes were present more frequently in non-smoking periodontitis patients than in non-smoking controls (p = 0.03, pcorr>0.05, and p = 0.009, pcorr>0.05, respectively) although their frequencies did not differ between smoking periodontitis patients and smoking controls (p = 0.23, p = 0.68, respectively).ConclusionsThis study in a Czech Caucasian population did not confirm a highly significant association between GST gene variants and susceptibility to periodontitis, as previously reported by Arshad and colleagues in Pakistanis. However, a weak relationship between GSTT1 and GSTP1 rs1138272 polymorphisms and periodontitis in non-smokers was observed.

Decreased GCF DEL-1 and increased GCF neutrophils with increasing probing pocket depth.

Developmental endothelial locus-1 (DEL-1) plays a role in regulating neutrophil migration within the periodontium. The objective of this study was to evaluate the levels of DEL-1 in saliva and gingival crevicular fluid (GCF), as well as the number of neutrophils in patients with periodontitis. Forty systemically healthy, non-smoking periodontitis patients participated in this study. Clinical periodontal parameters, including the plaque index, probing pocket depth (PPD), clinical attachment level, bleeding on probing, modified sulcular bleeding index, and marginal bone level, were measured. Levels of DEL-1, interleukin (IL)-1β, IL-6, and IL-8 in unstimulated saliva samples, as well as DEL-1 in the GCF of 3 teeth from each participant, were assessed. Neutrophil counts in oral rinse and GCF samples were recorded. Spearman correlation coefficients were used to examine the correlation between protein levels, clinical parameters, and neutrophil quantities. Participants were divided into 2 age groups (those under 50 years and those 50 years or older) in order to investigate potential age-related differences. DEL-1 levels in the GCF showed a negative relationship with PPD (sum). Neutrophils in oral rinse samples were positively correlated with PPD, IL-8, and IL-1β levels. Neutrophils in GCF exhibited a positive correlation with PPD (sum). Salivary DEL-1 levels showed correlations with IL-8 and IL-1β, but not with the clinical parameters of periodontitis. The negative relationship observed between PPD and GCF DEL-1 levels is consistent with the proposed protective role of DEL-1.

Effects of smoking on the salivary and GCF levels of IL-17 and IL-35 in periodontitis.

Periodontitis progression is associated with a host response in which anti-inflammatory and pro-inflammatory cytokine networks play a key role. Smoking is involved in the production of various mediators. The study aims to evaluate the levels of IL-17 and IL-35 in saliva and gingival crevicular fluid (GCF), to investigate the effects of smoking on these cytokines in smoker and non-smoker periodontitis patients. 19 smokers with periodontitis, 20 non-smokers with periodontitis, and 18 periodontally healthy subjects were included in the study. Periodontal clinical indexes were recorded and the levels of IL-17 and IL-35 in saliva and GCF were analyzed. No significant difference was detected among the groups in terms of salivary IL-17 and IL-35 levels. GCF IL-17 and IL-35 concentration levels in the non-smoker periodontitis group were significantly lower than the others (p < 0.05). Total levels of GCF IL-17 were significantly higher in both periodontitis groups than the control group; and total levels of GCF IL-35 were significantly higher in non-smoker periodontitis group than the others (p < 0.05). A positive correlation was detected between the salivary IL-17 and IL-35 levels (r = 0.884), GCF IL-17 and IL-35 concentrations (r = 0.854), and total GCF IL-17 and IL-35 (r = 0.973) levels (p < 0.01). The present study revealed a positive correlation between the IL-35 and IL-17 levels both in saliva and GCF. IL-17 and IL-35 can be considered as one of the cytokines that play a role in periodontal health and periodontitis; and smoking may be among the factors that affect the levels of these cytokines in GCF and saliva.

Clinical and Biochemical Effects of Smoking on Non-Surgical Periodontal Treatment in Grade III Stage C Periodontitis Patients

Objective: The purpose of this study was to evaluate the effect of smoking on clinical parameters and the serum and saliva levels of RANKL, OPG, and IL-34 in periodontitis stage III grade C (III-C) patients after non-surgical periodontal treatment (NSPT).&#x0D; Methods: A total of 60 subjects, 40 periodontitis-III-C patients (20 smokers and 20 non-smokers) and 20 non-smoker periodontally healthy individuals, were included. All clinical periodontal parameters were recorded, and unstimulated saliva and serum samples were collected from all patients at baseline, but at 1 and 3 months only from periodontitis patients (N=40). Saliva and serum levels of RANKL, OPG, and IL-34 were analyzed by ELISA.&#x0D; Results: At baseline only whole mouth probing depth (PD) and percent of sites with PD&gt;5mm were higher in smokers than non-smoker periodontitis patients (p

GCF Levels of Osteoclastogenesis-Related Cytokines in Periodontitis in Relation to Smoking During Non-Surgical Periodontal Therapy

Objective: Interleukins (IL) -1β, -34, receptor activator of nuclear factor-kB ligand (RANKL), and osteoprotegerin (OPG) play a crucial role in osteoclastogenesis and bone resorption through modulating inflammatory processes and osteoclastogenesis. Smoking is the major risk factor in the initiation and progression of the periodontitis, and adversely affects the outcomes of non-surgical periodontal therapy. To date, there is no study investigating both gingival crevicular fluid (GCF) IL-1β, IL-34, RANKL, and OPG levels before and after non-surgical periodontal therapy in smoking and non-smoking patients with periodontitis stage 3, grade B and C. The aim of current research was to examine the GCF levels of some osteoclastogenesis-related cytokines in periodontitis in relation to smoking before and after periodontal therapy. Methods: At baseline, full-mouth periodontal status together with GCF samples were collected from 116 individuals, including 60 periodontitis patients (30 smokers and 30 nonsmokers) and 56 periodontally healthy controls (28 smokers and 28 nonsmokers). Non-surgical periodontal therapy, consisting of instruction for daily plaque control and scaling and root planing (SRP), was performed. GCF sampling and full-mouth periodontal measurements were repeated 6 weeks after completion of SRP. The GCF levels of biomarkers were measured by enzyme-linked immunosorbent assay. Results: The periodontitis groups exhibited significant improvement in clinical parameters. At baseline, the GCF IL-1β levels in periodontitis groups were significantly higher than periodontally healthy controls (p&amp;lt;0.05) and it was significantly decreased in periodontitis groups after non-surgical periodontal therapy. At baseline, the GCF IL-34 levels in periodontitis groups were significantly higher than periodontal healthy controls(p&amp;lt;0.05) and the GCF IL-34 level was significantly decreased in non-smoking periodontitis patients. At baseline and after periodontal therapy, the GCF RANKL levels were similar in all groups. The GCF OPG level was significantly lowest in non-smoking periodontitis patients at baseline and the GCF OPG level was significantly increased in smoking and non-smoking periodontitis patients after non-surgical periodontal therapy. Conclusion: In the periodontal inflammation process, GCF IL-34 level followed a similar pathway to GCF IL-1β, suggesting that IL-34 may be a marker in the pathogenesis of periodontal disease. The significant decrease in GCF IL-34 and a significant increase in GCF OPG level in the non-smoker periodontitis group after periodontal therapy suggest the negative effect of smoking on the response to periodontal therapy. More comprehensive studies are needed by increasing the number of samples included in the study groups in order to better understand the pathogenesis of periodontitis.

The impact of smoking on periodontitis patients’ GCF/serum cytokine profile both before and after periodontal therapy: a meta-analysis

BackgroundSmoking is an established modifying factor for the host immune response of periodontitis patients. However, its exact influence remains unclear. We aimed to compare the cytokine profile of periodontitis patients with and without smoking habits both before and after periodontal therapy to preliminarily explore its influence on the host immune response to periodontitis.MethodsThe protocol of the present meta-analysis was registered in the International Prospective Register of Systematic Reviews (PROSPERO) under the code CRD42021255656. Meta-analysis was performed for each cytokine if at least three studies were included. We synthesized the evidence to compare the cytokine profile of periodontitis with and without smoking both in gingival cervical fluid (GCF) and serum to explore the impact of smoking on periodontitis both locally and systemically. Moreover, we also compared the cytokine profile of the two groups of patients after periodontal therapy to explore the effect of smoking on the outcome of periodontal therapy.ResultsFifteen studies were included in this meta-analysis. We found that there was no significant difference between the two groups of patients in the baseline cytokine profile. However, after periodontal therapy, smoking periodontitis patients showed significantly higher IL-1β levels in their GCF than nonsmoking patients.DiscussionThere was no significant difference between smoking and nonsmoking periodontitis patients in the baseline cytokine profile. However, after periodontal therapy, smoking periodontitis patients showed significantly higher IL-1β levels in their GCF than nonsmoking patients, which indicates that smoking may impair the response of periodontitis to periodontal treatment.

Randomized Clinical Trial of a Topical Botanical Patch for the Adjunctive Management of Periodontitis.

This randomized, controlled clinical trial aimed to evaluate the clinical, adjunctive effects of an approved botanical barrier device or patch on probing parameters in patients with periodontitis. Eighty patients with periodontitis were recruited for this single-blinded trial. Patient demographic data, including gender, age, self-reported smoking status, and history of diabetes or cardiovascular disease, were collected. At baseline, all patients received a full-mouth probing examination followed by scaling and root planing (SRP). Thereafter, patients were randomized to receive either adjunctive botanical patch applications (i.e. at 2-4 treatment sites with baseline pocket depth PD ≥6 mm) or no additional therapy (SRP alone, control). Patients applied botanical patch devices per randomization to treatment sites three times on day 0 and once daily on days 1-6. Study devices were spontaneously shed or removed by the patient at 2-2.5 h after each application. Patients were recalled for probing reexaminations at 1, 2 and 3 months. Statistical analyses focused on intergroup differences in probing parameters and included ANOVA for baseline measures and ANCOVA controlling for baseline measures at 1, 2 and 3 months in the overall population and in subpopulations (e.g. smokers vs nonsmokers). Randomized patient groups were balanced with respect to baseline periodontal status (mean and extent PD) but not smoking, with statistically significantly more smokers clustering in the control group (p = 0.002). For the overall population and the non-smoking subpopulation, statistically significantly improved PD and clinical attachment levels (CAL) were observed with adjunctive botanical patch therapy vs control at 1 and 2 months (p < 0.05) but not 3 months (p = 0.08 for PD). For smokers, no statistically significant intergroup differences in PD or CAL were detected with botanical patch treatment. The data from this trial indicate short-term improvements in probing parameters with the botanical patch device when used adjunctively with SRP, especially with non-smoking periodontitis patients.

Effects of smoking on the gingival crevicular fluid levels of interleukin-17A, interleukin-17E, and oxidative stress following periodontal treatment process.

How smoking affects periodontal inflammation and healing still needs to be revealed with all its mechanisms. In this study, the gingival crevicular fluid (GCF) levels of: (a) interleukin-17A (IL-17A) and interleukin-17E(IL-17E) with their ratios and (b) oxidative stress by means of total oxidative stress (TOS), total anti-oxidant capacity (TAOC), and their ratios as the oxidative stress index (OSI) were evaluated and compared for smoking and non-smoking periodontitis patients after a periodontitis management process including both the non-surgical and surgical treatments. Fifteen smoker and 15 non-smoker generalized periodontitis patients as 2 distinct groups participated in the study. Conventional clinical and radiographical examinations were utilized for the periodontitis diagnosis. The clinical data and GCF samples were collected at baseline, 4week after non-surgical periodontal treatment (NSPT), and 4weeks after surgical periodontal treatment (SPT). IL-17A, IL-17E, TOS, and TAOC were determined by ELISA and Rel Assay. Clinical parameters in both smokers and non-smokers improved following periodontal treatment (P<.001) and their clinical data were similar for all the examination times (baseline, NSPT, and SPT) (P>.05). Following the treatment phases, the IL-17A concentration decreased and the IL-17E concentration increased in both the smokers and non-smokers (P<.01). The total amount of IL-17A decreased while the total amount of IL-17E increased in smokers throughout NSPT and SPT (P<.01). Such an alteration was seen only at SPT compared to NSPT and baseline in non-smokers (P<.01). The concentration and total amount of IL-17A were higher at baseline, and the concentration and total amount of IL-17E were lower at all examination time points in non-smokers as compared to smokers (P<.01). The 17A/E ratio decreased in both groups following the treatment phases and was higher in smokers at all the examination times (P<.01). TOS were higher and TAOC were lower in smokers versus non-smokers at all the time points, but the differences were significant only for TOS levels (P<.01). Throughout the treatment phases, the concentration and total amount of TOS decreased in smokers(P<.01) and only the total amount of TOS decreased in non-smokers (P<.01). The concentration and total amounts of TAOC increased throughout the treatments in both smokers and non-smokers without significant changes (P>.05). The baseline OSI was higher in smokers, and it decreased only in smokers following the treatment phases (P<.01). Smoking and periodontal inflammation were found to alter IL-17A, IL-17E, and oxidant/anti-oxidant statuses in periodontitis patients. The intra-group assessments in smokers demonstrated more apparent alterations in the oxidant/anti-oxidant statuses and IL-17A and IL-17E levels after periodontitis management.

Evaluation of apoptosis and hypoxia-related factors in gingival tissues of smoker and non-smoker periodontitis patients.

Smoking causes pathological changes in all tissues, including gingiva and alveolar bone. The aim of present study was to evaluate apoptotic tissue alterations and tissue destruction in smoker and non-smoker periodontitis patients and healthy individuals. Gingival biopsy samples from 15 systemically and orally healthy individuals (Group 1), 15 systemically healthy periodontitis patients (Group 2), 15 systemically and orally healthy smokers (Group 3), and 15 systemically healthy smoker periodontitis patients (Group 4) were enrolled in the present study. Clinical periodontal measurements as plaque index (PI), gingival index (GI), and clinical attachment levels (CAL) were recorded, and gingival biopsies were obtained. Biopsy samples were fixed in formalin solution and embedded in paraffin. Fibroblast and inflammatory cell counts were determined via histomorphometrically. Hypoxia-inducible factor alpha (HIF-1α), vascular endothelial growth factor(VEGF), tissue inhibitor of matrix metalloproteinase-1(TIMP-1), matrix metalloproteinases-8(MMP-8) expressions, Bax, Bcl-2, and caspase-3 expressions were evaluated via immunohistochemistry. Demographic data of the study groups were similar. Smoking levels of the smokers were also similar. The highest fibroblast cell counts were observed in healthy controls and the counts were similar in other groups. The highest inflammatory cell counts were found in smoker periodontitis group, and the lowest counts were found in healthy control groups. The differences were statistically significant. HIF-1α and Bax expressions were elevated and Bcl-2 decreased in smoker periodontitis patients compared with healthy individuals. However, there were no differences in VEGF, MMP-8, and TIMP-1 expressions. Within limits of present study, it can be suggested that both smoking and periodontitis caused similar decrease in fibroblast counts while causing a dramatic increase in inflammatory cell counts. Increased apoptosis and hypoxia also accompanied to the increased inflammation.

Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti‐citrullinated peptide antibody titres

Anti-citrullinated protein antibody (ACPA) responses may precede clinical onset of rheumatoid arthritis. Porphyromonas gingivalis peptidylarginine deiminase can citrullinate proteins possibly inducing autoimmunity in susceptible individuals. To determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. Serum and plaque samples were collected from 39 periodontitis patients before and after non-surgical periodontal treatment, and from 36 healthy subjects. Carriage of P. gingivalis was determined by PCR of plaque DNA. ACPA was determined by anti-cyclic citrullinated peptide (CCP) enzyme-linked immunosorbent assay (ELISA). Anti-P. gingivalis titres were determined by ELISA. Untreated periodontitis patients had higher anti-CCP antibody titres than healthy controls [three patients (8%) greater than manufacturer suggested assay diagnostic threshold (5 Assay Units/AU) versus none (0%); mean ± SEM: 1.37 ± 0.23 versus 0.40 ± 0.10 AU, p < 0.0001]. Periodontitis patients who smoked demonstrated lower anti-P. gingivalis (15956 ± 4385 versus 2512 ± 1290 Units/ml, p < 0.05), but similar anti-CCP than non-smoking periodontitis patients (smokers: 1.31 ± 0.35; non-smokers: 1.41 ± 0.32 AU). Healthy smokers demonstrated elevated anti-CCP titres (0.75 ± 0.19 AU), at levels between healthy non-smokers (0.15 ± 0.05 AU) and non-smoker periodontitis patients. Six months after periodontal treatment, there were significant reductions in anti-CCP (non-smokers p < 0.05) and anti-P. gingivalis (all participants p < 0.01). In subjects with periodontitis, P. gingivalis infection may be responsible for inducing autoimmune responses that characterize rheumatoid arthritis.

Peripheral blood monocyte responses in periodontitis

Periodontitis results from the interaction of bacteria on the tooth surfaces and the host immune response. Although periodontal pathogens are essential for the initiation and progression of the disease, the tissue damage in periodontitis is primarily mediated by the host immune response. Differences in the susceptibility to the disease and in the clinal outcome of the therapy seem to be less dependent on genetics but more on lifestyle factors, like smoking, overweight, stress and nutrition. It has been shown that these lifestyle factors may modulate the immune response and therefore influence the initiation and progression of the disease. To study the host immune response, whole blood cell cultures (WBCC) stimulated with lipopolysaccharide (LPS) have been widely used and they specifically reflect the behaviour of monocytes. It has been shown that peripheral blood monocytes in LPS-stimulated WBCC from non-smoking periodontitis patients display a T-helper 2 (Th2)-promoting phenotype in comparison with controls. After periodontal therapy, this phenotype reversed and was comparable with controls. However, in smoking but treated patients, the Th2-promoting phenotype of monocytes still remained. Therefore, the aberrant phenotype of monocytes in the peripheral blood from periodontitis patients is likely to be a systemic response to exogenous and endogenous danger molecules released or induced by the periodontal infection or by smoking. It can be concluded that periodontal therapy in non-smoking periodontitis patients has beneficial health effects and that smoking cessation should be an integral part of the therapy as well for general health reasons as for the clinical outcome.

Oxidative Stress in Periodontitis

Periodontitis is one of the most common oral infections induced by bacteria and bacterial products of dental plaque. Cigarette smoking is considered to be a risk factor for periodontitis. However, the exact mechanism by which smoking exerts its deleterious effects on periodontium remains unclear. Therefore the present study was planned to evaluate the relationship between cigarette smoking and periodontal damage in terms of the levels of free radicals and antioxidants. A total of 75 subjects were included in the study. Out of these, 25 were healthy controls, 25 were nonsmoker periodontitis patients and 25 were smoker periodontitis patients. All subjects were screened for serum lipid peroxide, nitric oxide and antioxidants such as superoxide dismutase, glutathione peroxidase along with total antioxidant capacity. A significant increase in serum lipid peroxide and nitric oxide with a corresponding decrease in serum superoxide dismutase, glutathione peroxidase and total antioxidant capacity was observed in both groups of periodontitis patients. Further, it was noticed that the oxidant levels were significantly higher and antioxidants were significantly lower in smoker patients than non-smoker patients. Thus, smoking plays a pivotal role in enhancing oxidative burden in periodontitis.

Smoking influences salivary histamine levels in periodontal disease

Histamine, a potent vasoactive amine, is increased in saliva of periodontitis patients. The present study aimed to further investigate the diagnostic potential of histamine for periodontal disease and assessed smoking, a major risk factor of periodontitis, as a possible influencing factor. Salivary and serum samples of 106 participants (60 periodontitis patients, 46 controls) were collected. Salivary histamine was determined by a commercially available ELISA kit, and serum C-reactive protein was measured by a routine laboratory test. Cigarettes per day and packyears were assessed as smoking exposure parameters. Statistically significantly increased levels of salivary histamine and serum C-reactive protein were detected between the patient and control group (P = 0.022 and P = 0.001). Salivary histamine levels were significantly higher in smoking compared with non-smoking patients (P < 0.001), and salivary histamine as well as serum C-reactive protein correlated significantly positively with smoking exposure parameters (P < 0.05). Smoking, an established and common risk factor of periodontitis, was assessed as a possible influencing factor for salivary histamine. Most interestingly, salivary histamine differed highly significantly between smoking and non-smoking periodontitis patients. Our results suggest a possible involvement of histamine in tobacco-exacerbated periodontal disease, but do not suggest salivary histamine as a reliable diagnostic marker for periodontitis.

Plasma antibody levels in periodontitis patients and controls

A major aspect of the adaptive host response in periodontitis is the production of antibodies. Several risk and susceptibility factors for periodontitis, including smoking, age and composition of the subgingival microflora, have also been suggested to influence antibody production. The present study was conducted to investigate plasma levels of immunoglobulin (Ig) G, A and M antibodies in periodontitis patients of Caucasian European heritage in relation to disease severity, smoking, diagnosis and prevalence of periodontopathogens. In this study, 29 patients with severe periodontitis, 51 with moderate periodontitis and 55 controls without periodontal destruction were enrolled. From the total of 80 patients, 18 were diagnosed with aggressive periodontitis and 62 with chronic periodontitis. Total IgG, IgA and IgM as well as IgG isotypes were analyzed in plasma samples. Levels of total IgG, IgA and IgM were not different between patients and controls; however, in periodontitis, higher levels of IgG1 and IgG2 were observed. Smoking appeared to be significantly and inversely related to antibody levels in periodontitis, in particular for total IgG and IgG2. The absence of an elevated total IgG and IgG2 in smoking patients was irrespective of severity, prevalence of periodontal pathogens and diagnosis. The elevation of total IgG and IgG1 and IgG2 in non-smoker periodontitis patients was observed in patients with moderate periodontitis and even greater in patients with severe periodontitis, but was independent whether patients were infected with Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis and independent of diagnosis. Clinically, it was observed that patients who smoked had more periodontal bone loss; the current findings on antibody levels may be one of several mechanisms related to more extensive periodontal breakdown in smoker patients. The current study shows that non-smoker periodontitis patients have higher levels of total IgG and IgG2 than smoker periodontitis patients.

Impact of increased occlusal contact, interleukin-1 genotype, and periodontitis severity on gingival crevicular fluid IL-1beta levels.

The study of occlusal therapy in humans with periodontitis is problematic due to potential irreversible bone loss in control subjects. The hypothesis of this pilot investigation was that increased interocclusal contact initiated by short-term occlusal splint disuse would increase tooth mobility and the bone-resorptive cytokine interleukin (IL)-1beta in gingival crevicular fluid (GCF), comparable to IL-1-positive genotype and increased periodontitis severity. Nineteen non-smoking chronic periodontitis patients using nocturnal occlusal splints and undergoing periodontal maintenance in a private practice were evaluated at five time points: 24 hours after continuous splint use; 1, 2, and 3 days after no occlusal splint use; and 14 days after resumption of customary nighttime splint use. Subjects were evaluated to confirm that the plaque index and gingival index were < or = 1.0, and to categorize past periodontitis (moderate or severe) and IL-1 genotype (1A +4845 plus IL-1B +3954). Test sites on two anterior teeth vulnerable to occlusal trauma were sampled for mobility, GCF IL-1beta, and IL-1 receptor antagonist (ra). Tooth mobility remained low during the 3-day period when patients were not wearing their occlusal appliance. GCF IL-1beta decreased after not wearing the appliances (P = 0.016), especially at 48 hours. At this time, genotype-positive subjects had higher levels of GCF IL-1beta/IL-1ra than genotype-negative subjects (P = 0.045), and patients who had experienced severe periodontitis had higher IL-1beta levels than moderate periodontitis subjects (P = 0.004). These findings suggest that short-term discontinuation of occlusal splint therapy in non-smoking periodontitis patients undergoing periodontal maintenance does not result in potential signs of early occlusal trauma (increasing mobility or GCF IL-1beta). Longer-term studies may be needed to determine appropriate therapy applications for periodontitis-susceptible patients with definable occlusal discrepancies and/or parafunction.

Effect of Cigarette Smoking on Oral Elastase Activity in Adult Periodontitis Patients

We have previously reported that elastase activity in oral fluids is significantly increased in most adult periodontitis patients. In some patients, however, elastase levels remain low despite the presence of deep periodontal pockets. In this study we explored whether or not smoking is related to the unexpected low elastase values in these patients. We determined what proportion of the periodontitis patients that showed low oral elastase values were smokers. Paraffin-stimulated saliva or oral rinse samples (3 ml of water, 30 second rinse) were assayed for elastase activity by incubating with 1 mM succinyl-alanyl-alanyl-valine-p-nitroanilide for 20 hours at 37 degrees C, and the color formation read with a spectrophotometer. Neutrophil numbers were analyzed by staining the cells in the oral rinse smear samples. In 2 patient groups, one in Helsinki, Finland (n = 46) and the other in Vancouver, British Columbia (n = 25), 63% and 83%, respectively, of the adult periodontitis patients who had one or more pockets > or =6 mm and had low oral elastase values (increase of optical density <0.5) were smokers. Non-smoking periodontitis patients had elevated neutrophil numbers compared to healthy subjects, while the smoking patients showed no significant change. Next we analyzed elastase levels in stimulated whole saliva in a group of smokers (n = 300) and those who had quit smoking (n = 102). Smokers had significantly lower oral elastase levels than former smokers in both advanced and moderate periodontitis groups. In this subject group, 56% of all smokers with periodontitis (at least one pocket > or =6 mm) had oral elastase values less than 0.5 U while only 31% of those patients who had quit smoking had low values. Cigarette smoking leads to lowered elastase and neutrophil levels in the oral cavity. The oral neutrophil elastase assay, therefore, cannot be used to measure the periodontal status of smokers.