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PubMed1984

A longitudinal study of untreated periodontal disease.

1016 textile workers were examined during a baseline study in 1969/70. A follow-up examination in 1979/80 identified 82 subjects who had not been treated for periodontal disease in the intervening period. There were 39 male and 43 female subjects; the average age at the initial examination was 27.0 years. There was an average tooth loss of 2.5 (SEM 0.6) teeth per subject over the 10-year period. While periodontal disease was significantly related to oral hygiene at the outset, neither factor was significantly related to the degree of tooth loss. A detailed analysis of the dynamics of the periodontal condition was undertaken. The subsequent results are presented in the form of transition matrices and clearly illustrate both the progression of periodontal disease and the degree of tooth loss associated with each level of periodontal disease at the initial examination. The main findings are as follows. (a) Overall 6% of teeth initially free of periodontal disease (P.I.O.) were lost compared to 14% with destructive periodontal disease (P.I.6). (b) Progression of periodontal disease was slow for teeth initially free of periodontal disease and with mild gingivitis (P.I.0 and P.I.1) for all age groups. However severe gingivitis (P.I.2), resulted in more rapid deterioration of the supporting tissues in subjects over 35 years old at the final examination; 35% of such teeth changed to destructive periodontal disease (P.I.6) compared to 17% of corresponding teeth for the under 35-year age group. In contrast, a poorer prognosis was found for the teeth with destructive periodontal disease (P.I.6) in the younger age group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2006

Periodontal disease and adverse pregnancy outcomes: a systematic review.

BACKGROUND: Recent studies suggest that periodontal disease, as a source of subclinical and persistent infection, may induce systemic inflammatory responses that increase the risk of adverse pregnancy outcomes. OBJECTIVES: To examine the existing evidence on the relationship between periodontal disease and adverse pregnancy outcomes. SEARCH STRATEGY: Published studies identified via searches of the MEDLINE, EMBASE, CINAHL, and Current Contents full-text databases. SELECTION CRITERIA: We identified and selected observational studies (i.e. case-control, cross-sectional, and cohort) and nonrandomised controlled studies or randomised controlled trials that examined periodontal disease as a risk factor for adverse pregnancy outcomes. DATA COLLECTION AND ANALYSIS: Odds ratios (OR) or risk ratios (RR) were extracted or calculated from the studies' data. We calculated pooled effect size for two clinical controlled trials but not for the observational studies due to the heterogeneity in definitions for periodontal disease and adverse pregnancy outcomes across studies. MAIN RESULTS: Twenty-five studies (13 case-control, 9 cohort, and 3 controlled trials) were identified. The studies focused on preterm low birthweight, low birthweight, preterm birth, birthweight by gestational age, miscarriage or pregnancy loss, and pre-eclampsia. Of the chosen studies, 18 suggested an association between periodontal disease and increased risk of adverse pregnancy outcome (ORs ranging from 1.10 to 20.0) and 7 found no evidence of an association (ORs ranging from 0.78 to 2.54). Three clinical trial studies suggest that oral prophylaxis and periodontal treatment can lead to a 57% reduction in preterm low birthweight (pooled RR 0.43; 95% CI 0.24-0.78) and a 50% reduction in preterm births (RR 0.5; 95% CI 0.20-1.30). AUTHOR'S CONCLUSIONS: Periodontal disease may be associated with an increased risk of adverse pregnancy outcome. However, more methodologically rigorous studies are needed for confirmation.

Abortion, Spontaneous↗
PubMed2001

Periodontal disease and risk of subsequent cardiovascular disease in U.S. male physicians.

OBJECTIVES: We sought to prospectively assess whether self-reported periodontal disease is associated with subsequent risk of cardiovascular disease in a large population of male physicians. BACKGROUND: Periodontal disease, the result of a complex interplay of bacterial infection and chronic inflammation, has been suggested to be a predictor of cardiovascular disease. METHODS: Physicians' Health Study I was a randomized, double-blind, placebo-controlled trial of aspirin and beta-carotene in 22,071 U.S. male physicians. A total of 22,037 physicians provided self-reports of presence or absence of periodontal disease at study entry and were included in this analysis. RESULTS: A total of 2,653 physicians reported a personal history of periodontal disease at baseline. During an average of 12.3 years of follow-up, there were 797 nonfatal myocardial infarctions, 631 nonfatal strokes and 614 cardiovascular deaths. Thus, for each end point, the study had >90% power to detect a clinically important increased risk of 50%. In Cox proportional hazards regression analysis adjusted for age and treatment assignment, physicians who reported periodontal disease at baseline had slightly elevated, but statistically nonsignificant, relative risks (RR) of nonfatal myocardial infarction, (RR, 1.12; 95% confidence interval [CI], 0.92 to 1.36), nonfatal stroke (RR, 1.10; CI, 0.88 to 1.37) and cardiovascular death (RR, 1.20; CI, 0.97 to 1.49). Relative risk for a combined end point of all important cardiovascular events (first occurrence of nonfatal myocardial infarction, nonfatal stroke or cardiovascular death) was 1.13 (CI, 0.99 to 1.28). After adjustment for other cardiovascular risk factors, RRs were all attenuated and nonsignificant. CONCLUSIONS: These prospective data suggest that self-reported periodontal disease is not an independent predictor of subsequent cardiovascular disease in middle-aged to elderly men.

Adult↗
PubMed1989

Non-proteolytic activation of latent human neutrophil collagenase and its role in matrix destruction in periodontal diseases.

Collagenases are known to be associated with tissue destruction in chronic inflammatory diseases such as periodontal diseases and rheumatoid arthritis. Collagenases are secreted by circulating inflammatory cells (polymorphonuclear leukocytes and monocytes), resident mesenchymal cells and epithelial cells in latent forms, which can be activated by proteases and compounds reacting with protein thiol groups. We have studied here the effects of oxygen-derived free radicals (ODFR) on latent human neutrophil collagenase. Also, in order to elucidate the cellular sources of collagenases, the ability of human gingival crevicular fluid (GCF) collagenases both from adult periodontitis (AP) and localized juvenile periodontitis (LJP) patients to degrade soluble interstitial collagen types I and II was studied. ODFR generated by the xanthine oxidase/hypoxanthine system in the presence of trace amounts of iron and EDTA activated latent neutrophil collagenase to an equal extent as the known activators phenylmercuric chloride and gold thioglucose. ODFR activation was inhibited by desferoxamine and mannitol as well as by superoxide dismutase and catalase. Clear differences in the susceptibility of collagen types I and II to AP and LJP GCF collagenases were observed. AP GCF collagenase degraded type I and II collagens at equal rates, resembling the substrate-specificity of human neutrophil collagenase. LJP GCF collagenase degraded type I collagen considerably faster than type II collagen, which was only negligibly degraded. This corresponds to the substrate specificity of fibroblast collagenase. Zymographic evaluation of gelatinolytic proteases showed the presence of 90 and 68 kD gelatinases in both AP and LJP GCF. Non-proteolytic means apparently provide a potent activation pathway of neutrophil collagenase in vivo and the hydroxyl radical was identified to be one of the potent activating oxidants.(ABSTRACT TRUNCATED AT 250 WORDS)

Body Fluids↗
PubMed2004

Advances in periodontal disease markers.

A computer-assisted medline search was conducted to find the relevant articles concerning the periodontal disease markers in gingival crevicular fluid (GCF) and saliva published during the 10-year period from 1993 to July 2003. This review suggests that certain diagnostic uses of saliva and GCF show promise. Although both fluids have been used to evaluate the risk for an individual to develop periodontal disease and to monitor of the host response to periodontal therapy, GCF has the chance of being closely approximated to the periodontal tissues where periodontal disease begins. The enzymes contributed to extracellular matrix (ECM) molecules and non-ECM molecules degradation and markers for polymorphonuclear leukocytes (PMN) activity and influx into the gingival tissue seem to provide valuable information regarding the periodontal disease diagnosis and prognosis. There is also an increasing evidence implicating reactive oxygen species and nitric oxide pathway in the pathogenesis of periodontal diseases. Although promising results have been achieved with the assays evaluating the markers in assessment of periodontal disease status, up to now, none of these tests are used routinely. Further, one commercially available genetic test has been reported to have the potential to be used to predict the periodontal disease, but there are controversial reports on this genetic susceptibility test.

Biomarkers↗
PubMed1975

Early periodontal disease in the Syrian hamster.

An investigation into periodontal disease in the Syrian Golden hamster was conducted over a period of six months. With the periodontitis-producing Diet 2000 only mild destruction of the periodontium was observed. The interproximal area between M1 and M2 may be a better area for analysis of early periodontal disease in the Syrian Golden hamster, as it more nearly approaches the human situation than does the mesial surface of M1. On the whole the hamster may not be a good model species for studying periodontal disease on morphological grounds, despite its excellence in terms of bacteriology and ease and cheapness of animal maintenance. Other animal models are discussed.

Actinomyces↗
PubMed2001

The effect of alcohol consumption on periodontal disease.

BACKGROUND: Alcohol consumption, like smoking, may be related to periodontal disease independently of oral hygiene status. This study assessed the relationship between alcohol consumption and severity of periodontal disease. METHODS: A cross-sectional study of 1,371 subjects ages 25 to 74 in the Erie County, NY population was performed. Alcohol intake was assessed by means of previously validated self-reported questionnaires. Outcome variables were gingival bleeding, clinical attachment loss, alveolar bone loss, and presence of subgingival microorganisms. RESULTS: Logistic regression analyses adjusting for age, gender, race, education, income, smoking, diabetes mellitus, dental plaque, and presence of any of 8 subgingival microorganisms showed that those consuming > or =5 drinks/week had an odds ratio (OR) of 1.65 (95% CI: 1.22 to 2.23) of having higher gingival bleeding, and OR of 1.36 (95% CI: 1.02 to 1.80) of having more severe clinical attachment loss compared to those consuming <5 drinks/week. Those consuming > or =10 drinks/week had an odds ratio (OR) of 1.62 (95% CI: 1.12 to 2.33) of having higher gingival bleeding and OR of 1.44 (95% CI: 1.04 to 2.00) of having more severe clinical attachment loss compared to those consuming <10 drinks/week. Alcohol consumption was not significantly related to alveolar bone loss nor to any of the subgingival microorganisms. CONCLUSIONS: The results suggest that alcohol consumption is associated with moderately increased severity of periodontal disease. Longitudinal studies are needed to determine whether alcohol is a true risk factor for periodontal disease.

Adult↗
PubMed2004

Evidence for local production of antibodies to auto and non-self antigens in periodontal disease.

UNLABELLED: Autoimmune mechanisms may contribute to periodontal disease (PD) pathogenesis; autoantibody to collagen type 1 is produced at the periodontal site and local levels are found to be higher than in serum. OBJECTIVES: To find any evidence of autoimmune destruction in diseased periodontal tissues in patients with periodontitis. The study examines the relationship of antibodies to a self antigen collagen Type 1 and antigens from two periodontal pathogens namely Porphyromonas gingivalis (Pg), Actinobacillus actinomycetemcomitans (Aa) and a non-oral bacterium Bacteroides fragilis (Bf) in disease sites and in serum. MATERIALS AND METHODS: Granulomatous tissues from periodontally diseased sites and serum samples were obtained from 13 patients (15 sites) undergoing surgical therapy. Tissues were homogenized at 4 degrees C on Tris saline buffer [1 g (5 ml)-1], homogenate was centrifuged and the resultant supernatants were used in assays. Antibody to collagen and Aa, Pg and Bf in tissue eluates and serum were determined by competitive enzyme linked immunosorbant assay (ELISA) and conventional ELISA respectively using an alkaline phosphatase/p-nitrophenyl phosphate enzyme-substrate system. Sera from age and sex matched healthy subjects and pooled human serum were used as controls. Antibody (Ab) levels in tissues and serum were standardized by concomitant albumin assay. RESULTS: Level of antibodies to collagen type 1 in tissue was significantly higher than in serum (P = 0.0001). Antibody levels in tissue to Pg were significantly higher than in serum (P = 0.0271). Ab levels to both Aa and Bf in tissues and serum were not significantly different from each other. CONCLUSIONS: These findings confirm the process of the local production of antibodies to autoantigen namely collagen type-1 and to bacterial antigens in the granulomatous tissues housed within the periodontal lesions in patients with periodontitis.

Adult↗
PubMed1984

Long-term maintenance of patients treated for advanced periodontal disease.

The aim of the present investigation was to evaluate the periodontal conditions of a group of patients who, following active treatment of extremely advanced periodontal disease, had been maintained for 14 years in a well-supervised maintenance care program. The present sample included 61 subjects out of an initial group of 75 individuals who in 1969 were referred to and treated by the authors. Following an initial examination, the patients were given detailed instructions in proper plaque control measures and were subjected to scaling and root planning and surgical elimination of pathologically deepened pockets. After the termination of the active treatment phase, the patients were placed in a maintenance care program including recall appointments every 3-6 months. At the initial examination, immediately after the completion of the active treatment phase and then once a year, all patients were examined regarding oral hygiene, gingival conditions, probing depths and clinical attachment levels. In addition, the interproximal alveolar bone height was determined from full mouth radiographs obtained before active treatment, at the completion of active therapy and 1, 3, 5, 8, 10, 12 and 14 years after treatment. The results from the repeated examinations demonstrated that treatment of advanced forms of periodontal disease resulted in clinically healthy periodontal conditions and that this state of "periodontal health" could be maintained in most patients and sites over a period of 14 years. It was also demonstrated that the treatment and maintenance programs described were equally effective in young and older patients. The individual mean values describing probing depths, attachment levels, and bone heights did not vary significantly over the 14 years of observation. A more detailed analysis of the data revealed, however, that a small number of sites in a few patients lost a substantial amount of attachment. This attachment loss occurred at different time intervals during the course of the maintenance period. Thus, 43 surfaces in 15 different patients were exposed to recurrent periodontal disease of a significant magnitude. This recurrent inflammatory periodontal disease caused the loss of 16 teeth in 7 different patients during the maintenance period. The data reported question the validity of using individual mean values to describe alterations of the periodontal conditions during maintenance following active periodontal therapy.

Adult↗
PubMedDate not supplied

Periodontal diseases and awareness among patients.

Awareness of periodontal problems and how they interpret this and their timely intervention affects periodontal health. Many people neither recognize the symptoms of periodontal disease nor do they associate existing symptoms with the disease. Hence one should ensure that the routes of science transfer are open so that the appropriate knowledge regarding the prevention and control of periodontal diseases are available to the public.

Attitude to Health↗
PubMed1985

Orthodontic extrusion of single-rooted teeth affected with advanced periodontal disease.

Orthodontic extrusion of teeth with advanced periodontal disease was evaluated in beagle dogs. Surgical destruction of one third to one half of the attachment apparatus and the inducement of chronic periodontal disease was accomplished on the hemisected mesial roots of the mandibular premolars. The roots on one side of the mandible were extruded toward a cemented stainless steel bridge by means of elastics providing 20 to 25 gm of force. The force was examined daily. When extruded teeth came into contact with the bridge, they were ligated in place for 21 days of stabilization. Clinical results showed that control teeth maintained their position and signs of advanced periodontitis. Extruded teeth had shallower pocket depths, less gingival inflammation, and no bleeding on probing. Radiographic evaluation showed no demonstrable changes in the control teeth. Early in the extrusion process, the teeth appeared to be avulsed, with more than three fourths of the root coronal to the alveolar crest. After stabilization, approximately 2 mm of new bone was seen coronal to the original alveolar crest, and the periapical areas had filled in as well. This bone formation was verified histologically. The extruded teeth had an intact attachment apparatus with all components in the same relative position on the teeth as in the controls. However, a shallower sulcus and less gingival inflammation were noted in the extruded teeth. There were statistically significant findings of a wider periodontal ligament space, greater cementum width, and increased bone height in the crestal areas of extruded teeth. Extruded teeth also had less cementum width and greater new bone formation at the apex.(ABSTRACT TRUNCATED AT 250 WORDS)

Alveolar Process↗
PubMed2005

Diabetes and periodontal disease: a case-control study.

BACKGROUND: Periodontitis is often associated with diabetes and might be considered one of the chronic complications of diabetes mellitus, both in Type 1 (T1DM) and Type 2 (T2DM). This case-control study was designed to evaluate the possible association between non-insulin-dependent diabetes (T2DM) and clinical and microbiological periodontal disease among adult Sardinians. METHODS: A total of 212 individuals participated in this study: 71 T2DM patients aged 61.0 +/- 11.0 years and 141 non-diabetic controls in good general health aged 59.1 +/- 9.2 years. All subjects were given a clinical periodontal examination for probing depth, attachment level, presence of calculus, bleeding on probing, and assessment of plaque. Subgingival plaque samples were obtained, and P. gingivalis, P. intermedia, and T. forsythensis were identified using multiplex polymerase chain reaction. RESULTS: T2DM patients showed a significantly lower number of teeth present (P = 0.002); a significant increase in number of probing depths >4 mm, and percent of pocket depths >4 mm (P = 0.04 and P = 0.05, respectively); periodontitis (P = 0.046); bleeding on probing (P = 0.02); and plaque index (P = 0.01). A significant association with diabetes was detected for plaque (X2= 4.46; P <0.05) and bleeding on probing (X2= 3.60; P <0.05). Concerning bacteria prevalence, a positive association was detected for P. gingivalis (X2= 2.80; P <0.05) and T. forsythensis (X2= 3.87; P <0.05). Presence of plaque was positively associated with case status (odds ratio [OR] = 1.3; 95% confidence interval [CI]: 1.2, 3.6) and with prevalence of P. gingivalis and T. forsythensis (OR = 1.2, 95% CI: 1.3, 2.2; and 1.2, 95% CI: 1.2, 1.8, respectively). CONCLUSION: Patients with T2DM undoubtedly have a susceptibility for more severe periodontal disease.

Adult↗
PubMed2003

[Classification of periodontal diseases].

During the past centuries the basic understanding of periodontal disease and the concepts of etiopathogenesis have evolved and substantially changed. The changes in paradigm has always been followed by the conceptual changes in the classification of periodontal disease. The earliest entirely descriptive classifications were based on the clinical signs and symptoms of periodontal disease. These were followed by a classification system based on the classical pathology paradigm established by Orban and Gottlieb. This was replaced by the next classification reflecting the infection/host response paradigm during the late '60s started with the pioneering works by Loe and coworkers. It is because many data indicated that the host response (determined by genetics, immunology and behavioral factors) was at least as important in the clinical manifestation of periodontal destruction than the bacterial biofilm this classification had been also updated. The AAP published its latest official classification system in 1999. Nevertheless this new system is far from perfect and should evolve as soon as enough data are collected by periodontal research to answer many controversy still existing to day.

Atrophy↗
PubMed1989

Periodontal diseases in the U.S. in 1981: prevalence, severity, extent, and role in tooth mortality.

Prevalence, severity, and extent of periodontal diseases as well as the role of periodontal diseases in tooth mortality are described for persons 19 years and older in the U.S. in 1981. The data were collected with a household probability sample of non-institutionalized persons living in the contiguous 48 states. Plaque and calculus scores were collected for six index teeth. All permanent teeth present and capable of being assessed were scored for gingivitis; pocket depths were measured on the mesial of each tooth with a periodontal probe. Examinations were conducted by trained dentists calibrated on specific criteria. Only 15% of persons in the U.S. in 1981 were free from any sign of periodontal diseases. Periodontitis (pockets greater than or equal to 4 mm) affected approximately 36% of the population. Advanced periodontitis (pockets greater than or equal to 6 mm) was present in 8% of the population and was usually found on only one or two teeth when present. End-stage periodontal destruction requiring extraction of teeth was found in only 4% of all persons while less than 20% of all missing teeth were listed as missing due to periodontal disease.

Adult↗
PubMed2006

Periodontal disease and diabetes. A two-way street.

BACKGROUND: The association between diabetes and inflammatory periodontal diseases has been studied extensively for more than 50 years. The author reviews the bidirectional relationships between diabetes and periodontal diseases. CONCLUSIONS: A large evidence base suggests that diabetes is associated with an increased prevalence, extent and severity of gingivitis and periodontitis. Furthermore, numerous mechanisms have been elucidated to explain the impact of diabetes on the periodontium. While inflammation plays an obvious role in periodontal diseases, evidence in the medical literature also supports the role of inflammation as a major component in the pathogenesis of diabetes and diabetic complications. Research suggests that, as an infectious process with a prominent inflammatory component, periodontal disease can adversely affect the metabolic control of diabetes. Conversely, treatment of periodontal disease and reduction of oral inflammation may have a positive effect on the diabetic condition, although evidence for this remains somewhat equivocal. CLINICAL IMPLICATIONS: Patients with diabetes who have periodontal disease have two chronic conditions, each of which may affect the other, and both of which require frequent professional evaluations, in-depth patient education and consistent educational reinforcement by health care providers.

Blood Glucose↗
PubMed1991

Epidemiology and prevention of periodontal disease in individuals with diabetes.

OBJECTIVE: This article reviews the epidemiological evidence of the relationship between diabetes and periodontal disease, possible physiological mechanisms for the association, and effects of interventions on the occurrence and severity of periodontal disease among individuals with diabetes. RESEARCH DESIGN AND METHODS: A comprehensive qualitative review of published literature in the area was performed. RESULTS: Much of the research in this area was found to contain methodological problems, such as failing to specify the type of diabetes, small sample sizes, and inadequate control of covariates such as age or duration of diabetes. CONCLUSIONS: Trends indicate that periodontal disease is more prevalent and more severe among individuals with diabetes. This trend may be modified by factors such as oral hygiene, duration of diabetes, age, and degree of metabolic control of diabetes. Generally, poor oral hygiene, a long history of diabetes, greater age, and poor metabolic control are associated with more severe periodontal disease. The association of diabetes and periodontal disease may be due to numerous physiological phenomena found in diabetes, such as impaired resistance, vascular changes, altered oral microflora, and abnormal collagen metabolism. With some modifications, the same prevention and treatment procedures for periodontal disease recommended for the general population are appropriate for those with diabetes. People with diabetes who appear to be particularly susceptible to periodontal disease include those who do not maintain good oral hygiene or good metabolic control of their diabetes, those with diabetes of long duration or with other complications of diabetes, and teenagers and pregnant women.

Diabetes Complications↗
PubMed2006

Gingival crevicular fluid matrix metalloproteinase-25 and -26 levels in periodontal disease.

BACKGROUND: Tissue destruction associated with the progression of periodontal disease is caused by a cascade of host and microbial proteolytic enzymes. Host-derived matrix metalloproteinases (MMPs) play an important role in the degradation of the extracellular matrix. Leukolysin/membrane-type 6 (MT-6)/MMP-25, the latest member of the MT-MMP subgroup of the MMP family, is primarily expressed by neutrophils and involved in extracellular matrix turnover. Matrilysin-2/MMP-26 (endometase), a novel member of the matrilysin subgroup of the MMP family, can degrade the extracellular matrix, alpha1-antitrypsin, and activate pro-MMP-9. Our study aimed to examine the levels, molecular forms, and degrees of activation of MMP-25 and MMP-26 in gingival crevicular fluid (GCF) from patients with different periodontal diseases. METHODS: A total of 105 subjects, 35 with generalized aggressive periodontitis (GAgP), 29 with chronic periodontitis (CP), 20 with gingivitis, and 21 periodontally healthy subjects, were included in this study. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, presence of bleeding on probing, and plaque. GCF MMP-25 and MMP-26 levels were analyzed by computer-quantitated Western immunoblotting using specific antibodies. RESULTS: The 57-kDa soluble pro-MMP-25 and 45- to 47-kDa active form of MMP-25 were detected by Western immunoblots in CP and GAgP GCF, and lesser levels of these soluble MMP-25 immunoreactive bands were detected in gingivitis GCF. An enhanced and similar degree of MMP-25 activation was found in GAgP, CP, and gingivitis groups. There were no detectable MMP-25 immunoreactivities in the healthy subjects' GCF. GAgP and CP groups had elevated GCF MMP-26 levels and degrees of activation compared to the gingivitis and healthy groups (P <0.008). The gingivitis group had higher GCF MMP-26 levels and degree of activation compared to the healthy group (P <0.008). CONCLUSIONS: The present study demonstrated the presence of soluble or shed forms of MMP-25 and MMP-26 in GCF of patients with different periodontal diseases. Increased levels and activation of MMP-25 and MMP-26 in GCF are associated with an enhanced severity of periodontal inflammation, suggesting that these novel MMPs can participate in the progression of periodontal diseases. They may prove to be diagnostically useful and could be targets of medication in the future.

Acute Disease↗
PubMed2005

Smokeless tobacco and severe active periodontal disease, NHANES III.

Whereas smoking is a major risk factor for periodontal disease, the role of smokeless tobacco is unclear. The purpose of this US population-based study of 12,932 adults participating in the Third National Health and Nutrition Examination Survey was to evaluate the association between smokeless tobacco use and severe active periodontal disease. Univariable and multivariable logistic regression modeling quantified the associations between tobacco use and severe active periodontal disease. All adults and never-smokers who currently used smokeless tobacco were twice as likely to have severe active periodontal disease at any site [respective odds ratios (OR(Adj)) and 95% confidence intervals: OR(Adj) = 2.1; 1.2-3.7 and OR(Adj) = 2.1; 1.0-4.4] or restricted to any interproximal site [respective OR(Adj) = 2.1; 1.0-4.2 and OR(Adj) = 2.3; 0.9-6.3], simultaneously adjusted for smoking, age, race, gender, diabetes, and having a dental visit in the past year. These results indicate that smokeless tobacco may also be an important risk factor for severe active periodontal disease.

Adolescent↗