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PubMed1999

Association of a vitamin D receptor gene polymorphism with localized early-onset periodontal diseases.

BACKGROUND: Early-onset periodontal diseases (EOP) are caused by interactions between host factors, specific microbial pathogens, and environmental factors. It is, therefore, of interest to investigate the nature of host factors as they may provide useful risk markers and reveal important information regarding the disease pathogenesis. Genetic polymorphisms in the vitamin D receptor (VDR) gene are associated with parameters of bone homeostasis and with diseases in which bone loss is a cardinal sign, in particular osteoporosis. Rapidly progressive bone loss is one feature of EOP. We, therefore, sought to determine whether EOP is associated with a polymorphism in the VDR gene. METHODS: A restriction fragment length polymorphism (RFLP) for Taq I in exon nine of the VDR gene was analyzed by PCR, followed by restriction digestion with Taq I and gel electrophoresis. We analyzed the genotypes of 69 EOP patients, including 20 patients with unequivocal evidence of localized disease (L-EOP), and 72 controls with no history of EOP. RESULTS: The genotype distribution in the L-EOP patient group was 7 (35%), 5 (25%) and 8 (40%) and in the control group 31 (43.1%), 36 (50.0%) and 5 (6.9%) for TT, Tt and tt respectively (where t and T represent the alleles with and without the Taq I RFLP respectively). Chi2 analysis indicated that the distribution of the genotypes between these two groups was highly significantly different (P = 0.001). Allele frequencies were 47.5% and 52.5% for T and t in the L-EOP group; 68.1% and 31.9% in the control group, showing a significant association between the prevalence of the less frequent allele (t) and L-EOP (P = 0.017). There was no significant difference in the genotype distribution or the allele frequencies between the control samples and the larger EOP patient group (n = 69) which included patients with generalized and localized disease. CONCLUSIONS: These data indicate that carriage of the less frequent allele of the Taq I RFLP (t) in the VDR gene significantly increases the risk of developing L-EOP. However, VDR genotype may not affect the incidence of all cases of EOP. These findings contribute to our understanding of the genetic basis for periodontal disease and may help define sub-groups of this disease which share common pathogenic factors.

Adolescent↗
PubMed2005

Strengthening the prevention of periodontal disease: the WHO approach.

BACKGROUND: The aim of this paper is to provide an overview of the burden of periodontal disease in adult populations worldwide, to emphasize the essential risk factors common to periodontal disease and chronic diseases, to outline important new strategies for effective prevention of periodontal disease, and to inform about the role of the World Health Organization (WHO) in developing a national capacity for the prevention of disease. METHODS: Information about periodontal health status as measured by the Community Periodontal Index system is stored in the WHO Global Oral Health Data Bank. Updated information concerning WHO standard age groups was used to describe the prevalence rates of signs of periodontal disease, i.e., gingival bleeding, periodontal pocketing, and loss of attachment. RESULTS: Gingival bleeding is highly prevalent among adult populations in all regions of the world; advanced disease with deep periodontal pockets (> or =6 mm) affects approximately 10% to 15% of adults worldwide. The available evidence shows that important risk factors for periodontal disease relate to poor oral hygiene, tobacco use, excessive alcohol consumption, stress, and diabetes mellitus. Integrated preventive strategies based on the common risk factors approach are recommended for public health practice. CONCLUSIONS: The vast majority of countries need to establish a surveillance system for measuring progress in the control of periodontal disease and promotion of oral health. WHO has designed approaches for the integration of oral disease prevention within the prevention of non-communicable chronic diseases, and global strategies are currently being implemented in all regions of the world.

Adult↗
PubMed2000

Periodontal disease and coronary heart disease risk.

CONTEXT: Research has suggested a relationship between periodontal disease and coronary heart disease (CHD), but data on the association between these 2 common conditions are inconclusive due to the possibility of confounding. OBJECTIVE: To evaluate the risk of CHD in persons with periodontitis, gingivitis, or no periodontal disease. DESIGN: Prospective cohort study. SETTING: The First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study, conducted in 1982-1984, 1986, 1987, and 1992. PARTICIPANTS: A total of 8032 dentate adults aged 25 to 74 years with no reported history of cardiovascular disease, including 1859 individuals with periodontitis, 2421 with gingivitis, and 3752 with healthy periodontal tissues. MAIN OUTCOME MEASURE: First occurrence of death from CHD or hospitalization due to CHD, or revascularization procedures, obtained from death certificates and medical records, by baseline periodontal status. RESULTS: During follow-up, 1265 individuals had at least 1 CHD event, including CHD fatality (n = 468) or at least 1 hospitalization with a diagnosis of CHD (n = 1022), including coronary revascularization procedures (n = 155). After adjustment for known cardiovascular risk factors, gingivitis was not associated with CHD (hazard ratio, 1.05; 95% confidence interval, 0.88-1.26), while periodontitis was associated with a nonsignificant increased risk for CHD event (hazard ratio, 1. 14; 95% confidence interval, 0.96-1.36). CONCLUSION: This study did not find convincing evidence of a causal association between periodontal disease and CHD risk. JAMA. 2000;284:1406-1410.

Adult↗
PubMed2003

Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review.

BACKGROUND: Recent studies implicate exposure to systemic conditions involving chronic inflammation, including chronic periodontitis, in the etiology of atherosclerosis. RATIONALE: A systematic review of the literature was conducted to assess the association between chronic inflammatory periodontal disease and atherosclerosis. FOCUSED QUESTION: Does periodontal disease influence the initiation/progression of atherosclerosis and, therefore, cardiovascular disease (CVD), stroke, and peripheral vascular disease (PVD)? SEARCH PROTOCOL: MEDLINE, pre-MEDLINE, MEDLINE Daily Update, and the Cochrane Controlled Trials Register were searched to identify human studies that related variables associated with atherosclerosis to periodontal disease. Searches were made for papers published from 1966 through March 2002. INCLUSION CRITERIA: Published randomized controlled clinical trials (RCTs), longitudinal, cohort, and case-control studies were included. Study participants included those with atherosclerosis, myocardial infarction (MI), stroke, or PVD. Oral conditions included periodontal disease. EXCLUSION CRITERIA: Only studies on humans were included. DATA COLLECTION AND ANALYSIS: Because the studies used different oral assessment measures, it was not possible to perform a meta-analysis of the data reported. Weighted mean differences, relative risks, or odds ratios were compared for cohort studies. MAIN RESULTS: 1. Of the initial 1,526 studies identified, 31 (including 8 case-control and 18 cross-sectional reports) were included in the analysis. Taken together, most of the literature supports a modest association between periodontal disease and atherosclerosis. However, data reported in several studies do not show this association. 2. The absence of a standard definition and measures for periodontal disease complicates interpretation of results, as do potential confounding risk factors common to both conditions. REVIEWERS' CONCLUSIONS: 1. Periodontal disease may be modestly associated with atherosclerosis, MI, and CVD. 2. Additional large-scale longitudinal epidemiologic and intervention studies are necessary to validate this association and to determine causality.

Arteriosclerosis↗
PubMed1992

Significance of epidemiologic research in the understanding of periodontal disease.

This review describes the development of periodontal index systems which during the last 50 yr have made it possible to gradually expand our understanding of the etiology and pathogenesis of periodontal diseases. Modern epidemiologic research on the prevalence and severity of periodontal diseases is based on a substantial amount of scientific data collected since the early 1940's. The work of a number of innovative researchers has eventually resulted in the clarification of one unsolved problem after the other. At the same time new ideas have been developed for the inclusion of public health aspects in the epidemiologic analyses. The assessment of periodontal treatment needs has become an issue of great importance in many countries of the world and has initiated a discussion and studies on the role of the possibilities for self-assessment of treatment needs. A completely new area of interest has developed when recent epidemiologic surveys demonstrated a substantial increase in the numbers of elderly people together with a substantial increase in the number of teeth per elderly person.

Epidemiologic Methods↗
PubMed2000

Polymorphisms in the IL-1A gene are correlated with levels of interleukin-1alpha protein in gingival crevicular fluid of teeth with severe periodontal disease.

Interleukin-1 (IL-1) is a potent stimulator of bone resorption and is strongly implicated in the destruction due to bystander damage seen in periodontal disease. Recent studies suggest that polymorphisms of the (IL-1) gene complex may be significant risk factors for a number of chronic inflammatory diseases. The severity of periodontal disease has been positively associated with carriage of allele 2 at position -889 of the IL-1A gene in conjunction with allele 2 of the IL-1B gene at position +3953. In this study, we tested the hypothesis that allele 2 of the IL-1A gene at position -889 might act to elevate levels of IL-1alpha protein in patients with periodontal disease. Since levels of IL-1alpha protein are low in healthy individuals, we used a group of patients with severe periodontal disease to investigate if levels of IL-1alpha protein in gingival crevicular fluid can be correlated to patient genotype. IL-1alpha levels were measured by enzyme immunoassay in 46 patients with severe periodontal disease. These patients were genotyped by PCR and allele-specific restriction digests. The carriage rate for allele 2 in the diseased population was 68%. Overall, the carriage of allele 2 was associated with almost a four-fold increase in IL-1alpha protein levels. Differences were most pronounced in non-smokers, while heavy smokers showed reduced levels of IL-1alpha protein regardless of genotype. These results suggest a mechanism whereby this genetic polymorphism acts to modulate IL-1alpha protein production and may influence the pathogenesis of periodontal disease by affecting the extent of IL-1-associated bystander damage.

Adult↗
PubMed2006

[Application of dietary supplement to periodontal disease and osteoporosis].

It is known that there is a relationship between various systemic diseases, life style and periodontal disease. In such a situation, it is becoming clear a relationship between the systemic bone density and the mandibular bone, alveolar bone density and clinical periodontal parameters. And it is also cleared that to lower common risk factors related to these conditions might be useful to prevent osteoporosis and periodontal disease. As it is reported that medical treatment such as hormone replacement therapy (HRT) is effective not only preventing lowering skeletal bone density but also maintaining mandibular and alveolar bones, it is also considered that continuing supplementation of some nutritions such as calcium and isoflavone is also expected to have preventive effects.

Calcium↗
PubMed1994

The role of proteolytic enzymes in the development of pulmonary emphysema and periodontal disease.

Pulmonary emphysema and periodontal disease are each characterized by the uncontrolled proteolysis of connective tissue proteins by proteinases derived from human neutrophils. Although these diseases would not appear to be related in terms of the initial insult to individual tissues, the ultimate result in each disease is the accumulation and degranulation of neutrophils at inflammatory sites, apparently as a result of frustrated phagocytosis and specific activation of these phagocytic cells. This result is easily recognized in the case of emphysema, where there is clear evidence that the primary cause of the disease is the accumulation of foreign materials in the lung (e.g., smoke condensate), followed by the recruitment of neutrophils to the organ and the release of oxidative and hydrolytic enzymes. In periodontitis, however, the problem begins with the accumulation of plaque at the base of the teeth, followed by the growth of opportunistic anaerobic bacteria below the gum line. These parasitic microbes, which are resistant to killing by both monocytes and granulocytes, secrete proteinases that can activate the kallikrein-kinin pathway, degrade clotting factors, and release the potent neutrophil chemotactic factor, C5a, from complement. It is under such conditions that neutrophils are recruited to infected sites within the periodontium. After the neutrophil-recruitment stage, the two diseases become similar in that degranulation of neutrophils occurs during attempted phagocytosis of either cigarette smoke components (emphysema) or bacteria (periodontitis), followed by inactivation of tissue proteinase inhibitors and degradation of connective tissue proteins, the ultimate result being the destruction of the alveolus or gingiva, respectively.

Animals↗
PubMed1999

Relationship of stress, distress and inadequate coping behaviors to periodontal disease.

BACKGROUND: The association of stress, distress, and coping behaviors with periodontal disease was assessed. METHODS: A cross-sectional study of 1,426 subjects between the ages of 25 and 74 years in Erie County, New York, was carried out to assess these relationships. Subjects were asked to complete a set of 5 psychosocial questionnaires which measure psychological traits and attitudes including discrete life events and their impact; chronic stress or daily strains; distress; coping styles and strategies; and hassles and uplifts. Clinical assessment of supragingival plaque, gingival bleeding, subgingival calculus, probing depth, clinical attachment level (CAL) and radiographic alveolar crestal height (ACH) was performed, and 8 putative bacterial pathogens from the subgingival flora measured. RESULTS: Reliability of subjects' responses and internal consistencies of all the subscales on the instruments used were high, with Cronbach's alpha ranging from 0.88 for financial strain to 0.99 for job strain, uplifts, and hassles. Logistic regression analysis indicated that, of all the daily strains investigated, only financial strain was significantly associated with greater attachment and alveolar bone loss (odds ratio, OR = 1.70, 95% CI = 1.09 to 2.65 and OR = 1.68, 95% CI = 1.20 to 2.37, respectively) after adjusting for age, gender, and cigarette smoking. When coping behaviors were evaluated, it was found that those with more financial strain who were high emotion-focused copers (a form of inadequate coping) had a higher risk of having more severe attachment loss (OR = 2.24, 95% CI = 1.15 to 4.38) and alveolar bone loss (OR = 1.91, 95% CI = 1.15 to 3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. Similar results were found among the low problem-focused copers for AL (OR = 2.21, 95% CI = 1.11 to 4.38) and ACH (OR = 2.12, 95% CI = 1.28 to 3.51). However, subjects with high levels of financial strain who reported high levels of problem-based coping (considered adequate or good coping) had no more periodontal disease than those with low levels of financial strain, suggesting that the effects of stress on periodontal disease can be moderated by adequate coping behaviors. CONCLUSIONS: We find that psychosocial measures of stress associated with financial strain and distress manifest as depression, are significant risk indicators for more severe periodontal disease in adults in an age-adjusted model in which gender (male), smoking, diabetes mellitus, B. forsythus, and P. gingivalis are also significant risk indicators. Of considerable interest is the fact that adequate coping behaviors as evidenced by high levels of problem-based coping, may reduce the stress-associated risk. Further studies also are needed to help establish the time course of stress, distress, and inadequate coping with respect to the onset and progression of periodontal disease, and the mechanisms that explain this association.

Adaptation, Psychological↗
PubMed1990

Measurement of interleukin-1 alpha and -1 beta in gingival crevicular fluid: implications for the pathogenesis of periodontal disease.

Samples of gingival crevicular fluid (GCF) were harvested from sites manifesting features characteristic of active disease including inflammation, periodontal attachment loss, and radiographic signs of alveolar bone destruction in untreated patients with advanced periodontitis. The presence and concentrations of interleukin-1 alpha (IL-1 alpha) and interleukin-1 beta (IL-1 beta) were measured using ELISAs specific for these cytokine molecules. IL-1 alpha and/or IL-1 beta were identified in the GCF of 15 of 15 patients having untreated periodontitis. Ninety percent (71 of 79) of the sites tested contained measureable amounts of IL-1, with IL-1 beta as the more frequently occurring form. IL-1 alpha levels ranged from 0.23 nM to 13.9 nM in the GCFs. IL-1 beta levels were between 0.04 nM and 5.28 nM. Marked reductions of total IL-1 levels were observed following effective treatment. Both forms of IL-1 messenger RNA (mRNA) were detected in 17 of 17 gingival tissue samples from 6 patients. These results demonstrate that IL-1 is produced and released locally in periodontal disease at concentrations sufficient to mediate tissue inflammation and bone resorption. IL-1 may serve as a marker of periodontal tissue destruction.

Adult↗
PubMed2004

Association between serum concentrations of 25-hydroxyvitamin D3 and periodontal disease in the US population.

BACKGROUND: Periodontal disease (PD) is a common chronic inflammatory disease and an important risk factor for tooth loss. Vitamin D might affect periodontal disease risk via an effect on bone mineral density (BMD) or via immunomodulatory effects. OBJECTIVE: The objective was to evaluate whether serum 25-hydroxyvitamin D(3) [25(OH)D(3)] concentrations are associated with PD in the third National Health and Nutrition Examination Survey. DESIGN: We analyzed data on periodontal attachment loss (AL) and serum 25(OH)D(3) concentrations from 11 202 subjects aged > or =20 y. Mean AL was modeled in a multiple linear regression with quintile of serum 25(OH)D(3) concentration as an independent variable. The model was stratified by age and sex and was adjusted for age within age groups, race or ethnicity, smoking, diabetes, poverty income ratio, body mass index, estrogen use, and gingival bleeding. RESULTS: 25(OH)D(3) concentrations were significantly and inversely associated with AL in men and women aged > or =50 y. Compared with men in the highest 25(OH)D(3) quintile, those in the lowest quintile had a mean AL that was 0.39 mm (95% CI: 0.17, 0.60 mm) higher; in women, the difference in AL between the lowest and highest quintiles was 0.26 mm (0.09, 0.43 mm). In men and women younger than 50 y, there was no significant association between 25(OH)D(3) and AL. The BMD of the total femoral region was not associated with AL and did not mediate the association between 25(OH)D(3) and AL. CONCLUSIONS: Low serum 25(OH)D(3) concentrations may be associated with PD independently of BMD. Given the high prevalence of PD and vitamin D deficiency, these findings may have important public health implications.

Adult↗
PubMed1992

Oral microbiology: current concepts in the microbiology of dental caries and periodontal disease.

The microbial flora of the mouth is highly complex, containing a wide variety of bacterial species. The most common types of oral disease, dental caries and periodontal disease, are both related to dental plaque and seem to occur when the normal balance between the microorganisms and the host is disturbed in some way. Dental caries is usually associated with increased numbers of mutans streptococci and lactobacilli at the sites of disease; estimation of salivary levels of these organisms may be useful for assessing caries risk in patients and for monitoring their response to preventive measures. A large number of 'candidate pathogens' have been identified as potential aetiological agents in different types of periodontal disease, although the 'specific plaque hypothesis' may still be controversial. Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, together with the poorly understood spirochaetes, have most frequently been reported as significant periodontopathogens and a number of possible virulence factors have been described. Application of modern molecular techniques to the study of the microbiology of oral diseases should allow rapid further progress to be made and will lead, hopefully, to improved methods of diagnosis, risk assessment and treatment.

Animals↗
PubMed1990

[The reliability of different groups of sample teeth in assessing the status of periodontal disease in epidemiological studies].

The possibility of evaluating periodontal disease status in a given population by examining a limited number of sample teeth is of undoubted value in epidemiological studies. To this end, a cross-section study was performed to assess whether the dental sample proposed by Ramfjord effectively reflects the entire dentition status in terms of the main Clinical Indices of Periodontal Disease, in particular pocket depth. In addition, two randomly selected samples of six teeth were also evaluated using the same criteria. On the basis of their findings, the Authors confirm the epidemiological validity of Ramfjord's dental sample and stress that different groups of sample teeth may be efficaciously used to assess the periodontal disease status of the entire dentition in epidemiological studies.

Adult↗
PubMed1998

Models to evaluate the role of stress in periodontal disease.

We evaluated the association of stress,distress, and coping behaviors with periodontal disease in 1,426 subjects, aged 25 to 74, in Erie County, NY, Demographic characteristics, medical and dental history, and tobacco and alcohol consumption, as well as clinical assessments of supragingival plaque, subgingival flora, gingival bleeding, calculus, probing depth, clinical attachment level (CAL), and radiographic alveolar bone loss (ABL) were obtained for each subject. Subjects also completed a set of 5 psychosocial instruments that measured life events, daily strains, hassles and uplifts, distress, and coping behaviors. Internal consistencies of all subscales on the instruments were high, with Cronbach's alpha ranging from 0.88 to 0.99. Logistic regression indicated that financial strain was significantly associated with greater attachment and alveolar bone loss (OR 1.70; 95% CI, 1.09-2.65; and 1.68; 95% CI, 1.20-2.37, respectively) after adjusting for age, gender, and smoking. When those with financial strain were stratified with respect to coping behaviors, it was found that those who exhibited high emotion-focused coping (inadequate coping) had and even higher risk of having more severe attachment loss (OR 2.24; 95% CI, 1.15-4.38) and alveolar bone loss (OR 1.91; 95% CI, 1.15-3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. After further adjusting for number of visits to the dentist, those with financial strain who were high emotion-focused copers still had higher levels of periodontal disease based on CAL (OR 2.12; 95% CI, 1.07-4.18). In contrast, subjects with high levels of financial strain who reported high levels of problem-based coping (good coping) had no more periodontal disease than those with low levels of financial strain. Salivary cortisol levels were higher in a test group exhibiting severe periodontitis, a high level of financial strain, and high emotion-focused coping, as compared to a control group consisting of those with little or no periodontal disease, low financial strain, and low levels of emotion-focused coping (11.04 +/-4.4 vs/ 8.6 +/- 4.1 nmol/L salivary cortisol, respectively). These findings suggest that psychosocial measures of stress associated with financial strain are significant risk indicators for periodontal disease in adults. Further prospective studies are needed to help establish the time course of stress, distress, and inadequate coping on the onset and progression of periodontal disease, as well as to evaluate the mechanisms by which stress exerts its effects on periodontal infections.

Adaptation, Psychological↗
PubMed1998

A murine model of accelerated periodontal disease in diabetes.

Diabetes is a risk factor for periodontal disease in humans. In hyperglycemia, glycoxidation of proteins and lipids results in the formation of advanced glycation endproducts, or AGEs. The accumulation of AGEs in the plasma and tissues, and their interaction with their cellular receptor for AGE (RAGE), has been implicated in diabetic complications. In order to establish a model with which to delineate the specific host response factors that underlie the development of periodontal disease in diabetes, male C57BL/6J mice were rendered diabetic with streptozotocin. One month after documentation of diabetes or control state, mice were inoculated with the human periodontal pathogen Porphyromonas gingivalis, strain 381 (P. gingivalis) or treated with vehicle. Infection with P. gingivalis was achieved, as demonstrated by infiltration of gingival tissue with granulocytes, presence of DNA specific for P. gingivalis as well as increased serum antibody titer to P. gingivalis. At 2 and 3 months after infection, increased alveolar bone loss was demonstrated in P. gingivalis-inoculated diabetic vs. non-diabetic mice, along with enhanced tissue-destructive capacity, as demonstrated by increased collagenolytic activity in gingival extracts. Consistent with an important role for AGE-RAGE interaction, increased AGE deposition and expression of vascular and monocyte RAGE were demonstrated in diabetic gingiva compared with non-diabetic controls. Taken together, these data indicate that we have established a murine model of enhanced periodontal disease in diabetes. This model will serve to delineate molecular mechanisms which account for the increased susceptibility of diabetic patients to periodontal disease.

Alveolar Bone Loss↗
PubMed1993

Current status of tests for periodontal disease.

The methods applied to the diagnosis of periodontal disease are changing. Historically, static clinical and radiographic parameters have formed the basis of the periodontal evaluation. As the limitations of these traditional procedures became clear, several new techniques have been proposed as diagnostic tests for periodontal disease. These tests are based on improved understanding of the pathogenesis of periodontal disease, and can be considered in three categories: assessment of physical changes in the periodontium, the bacterial infection, and the host response to the infection. Several technical questions must be addressed before these tests can be widely utilized. These specific concerns include such matters as the information available from the tests (e.g., Does the test provide a measure of disease severity or identify the site, region, or patient experiencing active disease?), the most appropriate test configurations, the statistical analysis of data from trials examining the accuracy of the tests, and selection of patients who would benefit from these procedures. Last, several important practical issues must be examined before these tests can be expected to gain widespread acceptance. These include familiarization of dental practitioners with the use of diagnostic tests and the medical laboratory, the role of regulatory agencies in determining the claims made by these tests, and the medical/dental insurance benefits provided for these services.

Antibodies, Bacterial↗
PubMed2000

Actinobacillus actinomycetemcomitans in destructive periodontal disease. Three-year follow-up results.

BACKGROUND: Convincing data exist that A. actinomycetemcomitans is an etiologic agent of periodontal disease. The purpose of this longitudinal study was to evaluate A. actinomycetemcomitans as a diagnostic indicator for periodontal disease in treated and periodontally maintained patients. METHODS: Following comprehensive mechanical/surgical and supportive amoxicillin plus metronidazole therapy in 13 subjects with A. actinomycetemcomitans-associated destructive periodontal disease, we monitored subgingival A. actinomycetemcomitans at 4 individual sites in each patient up to 3 years post-therapy. The periodontal status was determined, and A. actinomycetemcomitans levels were quantitatively enumerated on TSBV agar in CFU/ml. Six patients with a persistence of subgingival A. actinomycetemcomitans at each reexamination within 3 years post-therapy were selected to be at risk for minor periodontal treatment outcomes and further recurrence of periodontal disease (test group). Seven subjects with a complete suppression of A. actinomycetemcomitans at each post-therapy visit served as controls. RESULTS: The periodontal parameters decreased from overall values of 6.39 mm (probing depth, PD) and 7.64 mm (clinical attachment level, CAL) at the outset to 3.81 mm (PD) and 5.62 mm (CAL) 2 years post-therapy (Friedman, P< or =0.05). At the 3-year reexamination, the PD/CAL scores increased to 4.03/5.78 mm. Among the 6 individuals (46%) with persistence of subgingival A. actinomycetemcomitans at the final 3-year visit (test group), periodontal status yielded increased levels of 4.45 mm (PD) and 6.60 mm (CAL). The control subjects (n = 7) revealed lower values of 3.67 mm (PD) and 5.09 mm (CAL). However, on a patient level, during the 3-year observational trial, the periodontal status of the 13 individuals was not statistically affected by subgingival infection with A. actinomycetemcomitans. CONCLUSIONS: Although in advanced periodontal disease, comprehensive mechanical and antimicrobial treatment is an appropriate regimen for sustained improvement of periodontal health, long-term control of subgingival infection with A. actinomycetemcomitans could not be achieved. In the maintenance care of destructive periodontitis, the persistence of A. actinomycetemcomitans is not a diagnostic parameter for periodontal disease.

Actinobacillus Infections↗
PubMed1998

The drug delivery and biomaterial attributes of the ATRIGEL technology in the treatment of periodontal disease.

Two new products, ATRIDOX Periodontal Treatment and ATRISORB Guided Tissue Regeneration (GTR) Barrier have been evaluated as therapies for periodontal disease. Both products are based on the unique ATRIGEL technology. The system consists of a solution of a resorbable polymer in a biocompatible carrier. On in vivo administration, the polymer undergoes a phase change from a liquid to an in situ formed implant. Being in liquid form, it initially provides the advantage of in vivo placement by simple means, such as syringes to form implants at the site of use. The system is biocompatible and has the capability of serving as a biomaterial and a drug delivery system. The bioabsorption rates of various polymers and the release rates for a wide variety of drugs ranging from simple organics to proteins and peptides are tailored to the desired indication. Release periods ranging from one week to four months have been achieved with one month being the most often desired. For these reasons the ATRIGEL system is being applied to a number of medical applications ranging from site and systemic oncology to post-operative pain control and bone regeneration using growth factors. However, its most visible application to date has been in the development of a pipeline of products for the treatment of periodontal disease, which is the focus of this paper.

Journal Article↗