[Free gingival graft for treatment of periodontal disease ---use of periodontal materials (1) (author's transl)].
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Adult↗
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Results for “PERIODONTAL DISEASE”
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Periodontal disease and mortality in type 2 diabetes.
OBJECTIVE: Periodontal disease may contribute to the increased mortality associated with diabetes. RESEARCH DESIGN AND METHODS: In a prospective longitudinal study of 628 subjects aged > or =35 years, we examined the effect of periodontal disease on overall and cardiovascular disease mortality in Pima Indians with type 2 diabetes. Periodontal abnormality was classified as no or mild, moderate, and severe, based on panoramic radiographs and clinical dental examinations. RESULTS: During a median follow-up of 11 years (range 0.3-16), 204 subjects died. The age- and sex-adjusted death rates for all natural causes expressed as the number of deaths per 1,000 person-years of follow-up were 3.7 (95% CI 0.7-6.6) for no or mild periodontal disease, 19.6 (10.7-28.5) for moderate periodontal disease, and 28.4 (22.3-34.6) for severe periodontal disease. Periodontal disease predicted deaths from ischemic heart disease (IHD) (P trend = 0.04) and diabetic nephropathy (P trend < 0.01). Death rates from other causes were not associated with periodontal disease. After adjustment for age, sex, duration of diabetes, HbA1c, macroalbuminuria, BMI, serum cholesterol concentration, hypertension, electrocardiographic abnormalities, and current smoking in a proportional hazards model, subjects with severe periodontal disease had 3.2 times the risk (95% CI 1.1-9.3) of cardiorenal mortality (IHD and diabetic nephropathy combined) compared with the reference group (no or mild periodontal disease and moderate periodontal disease combined). CONCLUSIONS: Periodontal disease is a strong predictor of mortality from IHD and diabetic nephropathy in Pima Indians with type 2 diabetes. The effect of periodontal disease is in addition to the effects of traditional risk factors for these diseases.
Adolescent↗
[Periodontal disease--an additional risk factor for cardiovascular diseases?].
In 1989, a case-control study was published, linking between coronary heart disease and periodontal disease in the studied population. Since then, a number of additional studies, focused the attention to the possible role of dental infections in the pathogenesis of atherosclerosis. Some of these newer cohort studies, are prospective in nature, measuring incidence of the two diseases in large patient populations. The present article reviews these studies, and the proposed mechanisms which might explain the relationships between these two systemically distinct diseases.
Arteriosclerosis↗
Defensin-induced adaptive immunity in mice and its potential in preventing periodontal disease.
The severity of periodontal disease is dependent on a combination of host, microbial agent and environmental factors. One strong correlate related to periodontal disease pathogenesis is the immune status of the host. Here we show that human neutrophil peptide (HNP) defensins or human beta-defensins (HBD), co-administered intranasally with the antigen ovalbumin (OVA), induce unique immune responses that if used with microbial antigens may have the potential to hinder the pathogenesis of periodontal disease. C57BL/6 mice were immunized intranasally with phosphate buffered saline (PBS) containing 1 micro g HNP-1, HNP-2, HBD1 or HBD2 with and without 50 microg OVA. At 21 days, isotypes and subclasses of OVA-specific antibodies were determined in saliva, serum, nasal wash, bronchoalveolar lavage fluid, and fecal extracts. OVA-stimulated splenic lymphoid cell cultures from immunized mice were assessed for interferon (IFN)-gamma, Interleukin (IL)-4 and IL-10. In comparison with mice immunized with only OVA, HNP-1 and HBD2 induced significantly higher (P < 0.05) OVA-specific serum IgG, lower, but not significant, serum IgM and significantly lower (P < 0.05) IFN-gamma. In contrast, HNP-2 induced low OVA-specific serum IgG and higher, but not significant, serum IgM. HBD1 induced significantly higher (P < 0.05) OVA-specific serum IgG, higher, but not significant, serum IgM, and significantly higher (P < 0.05) IL-10. The elevated serum IgG subclasses contained IgG1 and IgG2b.
Adjuvants, Immunologic↗
Validation of self-reported periodontal disease: a systematic review.
Self-report is an efficient and accepted means of assessing many population characteristics, risk factors, and diseases, but has rarely been used for periodontal disease (chronic periodontitis). The availability of valid self-reported measures of periodontal disease would facilitate epidemiologic studies on a much larger scale, allow for integration of new studies of periodontal disease within large ongoing studies, and facilitate lower-cost population surveillance of periodontitis. Several studies have been conducted to validate self-reported measures for periodontal disease, but results have been inconsistent. In this report, we conducted a systematic review of the validation studies. We reviewed the 16 studies that assessed the validity of self-reported periodontal and gingivitis measures against clinical gold standards. Seven of the studies included self-reported measures specific to gingivitis, four included measures only for periodontitis, and five included both gingivitis and periodontal measures. Three of the studies used a self-assessment method where they provided the patient with a detailed manual for performing a self-exam. The remaining 13 studies asked participants to self-report symptoms, presence of periodontal disease itself, or their recollection of a dental health professional diagnosing them or providing treatment for periodontal disease. The review indicates that some measures showed promise, but results varied across populations and self-reported measures. One example of a good measure is, "Has any dentist/hygienist told you that you have deep pockets?", which had a sensitivity of 55%, a specificity of 90%, positive predictive value of 77%, and negative predictive value of 75% against clinical pocket depth. Higher validity could be potentially obtained by the use of combinations of several self-reported questions and other predictors of periodontal disease.
Adolescent↗
Current status of systemic antibiotic usage in destructive periodontal disease.
The recognition that periodontal diseases are primarily caused by specific microorganisms has led researchers to explore the possibility that antibiotics may enhance the effect of mechanical debridement procedures such as scaling and surgery. For some selected periodontal diseases, this has proven to be true. This paper will review systemically-administered antibiotics and the clinical studies and case reports supporting their use. In periodontal therapy, the tetracyclines are the most commonly-used antibiotics in the United States. Tetracycline hydrochloride, minocycline, and doxycycline have been shown to inhibit in vitro most putative periodontal pathogens. Several studies support the use of tetracyclines in the treatment of localized juvenile periodontitis. Penicillins such as amoxicillin are effective in vitro against most periodontal pathogens but have limited efficacy due to the presence of beta-lactamases in gingival fluid. Amoxicillin/clavulanate potassium (Au) has proven effective in treating adult refractory periodontitis characterized by a Gram-positive flora. Metronidazole is an effective adjunct in adult periodontitis associated with high numbers of "black-pigmented Bacteroides" ad spirochetes. A combination of metronidazole and amoxicillin produces a synergistic effect against A. actinomycetemcomitans and has been shown to be effective at eliminating this organism. Clindamycin is an effective adjunct in the treatment of adult refractory periodontitis associated with a predominantly Gram-negative flora. The use of macrolides, quinolones, and combinations of antibiotics is discussed. Clinical studies do not support the use of systemically-administered antibiotics in routine adult periodontitis. Clinical studies do, however, support the use of antibiotics in the treatment of specific periodontal diseases.
Anti-Bacterial Agents↗
Periodontal disease and adverse pregnancy outcomes.
Periodontal disease is a common infectious disease in women of reproductive age. The disease is often not diagnosed and in studies of over 10 000 women has been associated with preterm birth, small for gestational age newborns, and preeclampsia. It has been shown in a smaller number of women that treatment of periodontal disease may reduce the rate of preterm birth. The pregnancy complications of periodontal disease may be due to lipopolysaccharide from the periodontal pockets inciting prostaglandin pathways controlling parturition. Three large randomized controlled trials of treatment of periodontal disease are underway and may provide confirmation of the importance of periodontal disease in causing complications of pregnancy.
Abortion, Spontaneous↗
Expression of suppressors of cytokine signaling in diseased periodontal tissues: a stop signal for disease progression?
BACKGROUND AND OBJECTIVE: Inflammatory cytokines are thought to trigger periodontal tissue destruction. In addition to being regulated by anti-inflammatory mediators, their activity is under the control of suppressors of cytokine signaling (SOCS), which down-regulate the signal transduction as part of an inhibitory feedback loop. We therefore investigated the expression of SOCS-1, -2 and -3, and the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-10, in different forms of human periodontal diseases. MATERIAL AND METHODS: Quantitative polymerase chain reaction (RealTime-PCR) was performed with mRNA from gingival biopsies of control subjects and from that of patients with chronic gingivitis and chronic periodontitis. RESULTS: Our results show that patients with chronic gingivitis and chronic periodontitis exhibit significantly higher SOCS-1, -2 and -3, TNF-alpha and interleukin-10 mRNA expression when compared with healthy controls. The data also demonstrate that SOCS-1 and -3 mRNA expression was higher in tissue from patients with chronic gingivitis than chronic periodontitis, while the levels of SOCS-2, TNF-alpha and interleukin-10 mRNA were similar in these groups. CONCLUSION: The increased expression of SOCS-1, -2 and -3 mRNA in diseased periodontal tissues is believed to be involved in the down-regulation of inflammatory cytokine and Toll-like receptor signaling, and therefore in the attenuation of both the inflammatory reaction and disease severity. Furthermore, it is possible that variation in the levels of SOCS mRNA expressed in different forms of periodontal diseases may determine the stable or progressive nature of the lesions.
Adult↗
[Relationship between periodontal disease and histamine. I. Histamine contents in whole saliva and gingival fluid from patients with periodontal disease (author's transl)].
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Gingival Crevicular Fluid↗
[Microbiological and serological investigation of periodontal disease activity].
If disease activity in periodontal disease can be determined, the therapeutic measures of periodontitis may become diverse and different from patient to patient. The purpose of the present study was to evaluate the usefulness of microbiological and serological examination of periodontopathic bacteria in detecting destructive periodontal disease activity. One hundred and forty-eight sites in 52 subjects with moderate to severe periodontitis were studied clinically. Clinical parameters included plaque index, gingival index, probing depth, bleeding on probing and percent bone loss as measured radiographically. Subgingival plaque of whole sites was investigated microbiologically by means of indirect fluorescent-antibody technique with rabbit antibodies against Actinomyces viscosus, Actinobacillus actinomycetemcomitans (2 serotypes), Eikenella corrodens, Fusobacterium nucleatum, Bacteroides gingivalis and Bacteroides intermedius. The levels of serum IgG antibody to these organisms were determined by enzyme-linked immunosorbent assay with whole cell preparations. Thirty-two of 52 subjects were instructed in oral hygiene and received several sessions of scaling and root planing. The clinical, bacteriological and serological assessments were also performed after periodontal therapy. Active disease site was defined as the site of which clinical status did not be improved even after periodontal treatment. B. gingivalis, B. intermedius and A. viscosus were detected in 80% of periodontal lesions, and the proportion of B. gingivalis was the highest among six bacterial species tested. A. actinomycetemcomitans, E. corrodens and F. nucleatum were found only occasionally and in low numbers. The proportion of B. gingivalis was higher in severely inflamed sites than in clinically healthy sites. B. gingivalis and B. intermedius are rarely found in treated periodontitis sites, while the proportion of A. viscosus was slightly increased after treatment. Sera of the pre-treatment patients demonstrated significantly higher antibody levels to B. gingivalis and significantly lower levels to A. viscosus than those of healthy persons. Antibody levels reactive with other four species in the patients did not significantly differ from the levels in healthy persons. After periodontal therapy, antibody levels to B. gingivalis, B. intermedius and A. actinomycetemcomitans (serotype a) significantly decreased and the levels to A. viscosus increased to a slight degree. B. gingivalis was found more frequently in disease-active sites than in disease-inactive sites. The proportions of other bacterial species in disease-active sites did not differ from those in disease-inactive sites. The results of the present investigation suggest that monitoring B. gingivalis in subgingival plaque and serum IgG antibody titer against this organism may aid in the description and adequate treatment of the periodontal disease.
Bacteroides↗
The role of IL-6 in the pathogenesis of periodontal disease.
The mechanisms underlying periodontal disease involve complex interactions between bacterial products, host cells and locally produced, biologically active factors. The umbrella term cytokine has been used to include a variety of such factors, including the interleukin family. The role of one cytokine, IL-1 beta, in periodontal disease pathogenesis has been widely reported. More recent studies have focused on a potential role for IL-6 in driving the destructive processes. Most of these reports have suggested a pro-inflammatory role for IL-6 alongside IL-1 and TNF-alpha. This manuscript reviews the biological functions of IL-6, specifically related to tissue destruction at the periodontal site. We would suggest that the activity of IL-6 in periodontal disease differs from IL-1 and TNF-alpha, and may, in part, play a protective role.
Extracellular Matrix↗
New technologies for the diagnosis of periodontal disease.
Historically the initial onset of periodontal disease in an individual was considered slow but continuously progressive over time. It was inferred that an individual would experience progressive destruction of the attachment structures until edentulous. However, several studies in the early 1970s contested the traditional concept of continuous disease progression. These studies suggested that periodontal disease progressed by recurrent acute episodes. In specific individuals, the loss of attachment was faster than the concept of slowly progressing disease. There were also sites in patients that progressed slower (or not at all) than anticipated on the basis of radiographic and clinical history of previous disease progression. These findings clearly indicated the need to explore the nature of periodontal disease progression and to institute a major effort into innovative methods to diagnose periodontal diseases. Dentists and researchers could more effectively prevent and treat periodontal disease and relate pertinent research findings to specific disease initiation and progression.
Alveolar Bone Loss↗
Relevance of local Th2-type cytokine mRNA expression in immunocompetent infiltrates in inflamed gingival tissue to periodontal diseases.
It has been suggested that the types of inflammatory round cell infiltrates and the divergence in the cytokine production profile by macrophages and helper T cells regulate the course of infectious or inflammatory diseases, including periodontitis and gingivitis. We examined the expression of IL-1alpha, IL-1beta, IL-2, IL-4, IL-5, IL-6 and tumour necrosis factor-alpha (TNF-alpha) mRNA in the inflamed gingiva by in situ hybridization. The results of single-cell analysis were used as data sets for statistical analyses. The density of cells expressing IL-1alpha, IL-4 and IL-5 mRNA was higher in periodontitis than in gingivitis. IL-2 mRNA-expressing cells were almost absent in gingivitis specimens. Principal component analysis disclosed three factors explaining 84.8% of the variance: one accounting for 40.5% of the variance and mainly regulated by IL-1alpha, IL-1beta, IL-6 and TNF-alpha, and two others, explaining 29.9% and 14.4% of the variance, describing the relationship between the types of cytokines derived from macrophages or Th2 type. These results suggest that the cytokines produced by inflammatory cells infiltrating in the gingival tissue are influential on the progression of gingivitis, an acute and reversible inflammatory condition, to chronic and destructive periodontitis. Thus, periodontal disease progression may be regulated by the local cytokine network, and the bias in this network towards a Th2-type cytokine dominance could be an exacerbating factor.
Adult↗
Factors for progression of periodontal diseases.
Progression factors for periodontal diseases have been suggested by in vitro study of peripheral blood and gingival cells; however, those factors are not established in vivo. This investigation assessed biopsies of three groups of gingival tissues: those adjacent to a 1) < or =3 mm (normal), 2) 4-6 mm, and 3) >6 mm gingival sulcus, to determine changes in the gingival microenvironment coincident to the progression of periodontal disease. Superoxide dismutase (SOD) and catalase activity, and IL-12 and bcl-2 levels, were decreased at >6 mm; total protein and IL-6 concentrations were increased adjacent to >6 mm, as compared to < or =3 and 4-6 mm, sites. Apoptotic cells were evident only within gingiva adjacent to >6 mm sites. These data suggest that IL-12 is an important factor in the shift from a TH1 to TH2 cell profile and that a favorable gingival microenvironment for hyperinflammation may develop coincident to progression of periodontal diseases due to decreased bcl-2 and increased IL-6 concentrations within gingiva. These changes in the gingival microenvironment could impair apoptosis and promote enhanced release of reactive oxygen species (ROS) by phagocytes; decreased catalase and SOD activity could promote accumulation of ROS and result in additional tissue destruction.
Analysis of Variance↗
Prevaccination with SRL172 (heat-killed Mycobacterium vaccae) inhibits experimental periodontal disease in Wistar rats.
Periodontal disease is a bacterial dental plaque-induced destructive inflammatory condition of the tooth-supporting tissues, which is thought to be mediated by T lymphocytes secreting T helper 2 (Th2) cytokines, resulting in recruitment of high numbers of antibody-producing B lymphocytes/plasma cells as well as polymorphonuclear leucocytes (PMN) secreting tissue-destructive components, such at matrix metalloproteinases and reactive oxygen metabolites into the gingival connective tissues. One treatment strategy may be to down-regulate the Th2 response to those dental plaque microorganisms which induce the destructive inflammatory response. In this study we have examined the effects of a potent down-regulator of Th2 responses on ligature-induced periodontal disease in an experimental rat model. A single s.c. injection into Wistar rats of 0.1 or 1 mg of SRL172, a preparation of heat-killed Mycobacterium vaccae (NCTC 11659), 13 days before application of the ligature, significantly reduced the subsequent destruction of the tooth-supporting tissues, as measured by loss of periodontal attachment fibres (P < 0.001) and bone (P < 0.002). This protective effect occurred not only on the experimental (ligatured) side but also on the control unligatured side. SRL172 has undergone extensive toxicological studies and safety assessments in humans, and it is suggested that it may provide a safe and novel therapeutic approach to periodontal disease.
Animals↗
Periodontal disease: an overview for physicians.
Periodontitis is now seen as resulting from a complex interplay of bacterial infection and host response, often modified by behavioral factors. There has been a fundamental change in the prevailing periodontal disease model of the 1960s, which suggested that the susceptibility to periodontitis increases with age, and that all individuals are susceptible to severe periodontal disease. More recent research has changed the belief in universal susceptibility to the current view that only some 5-20% of any population suffer from severe generalized periodontitis, and that only moderate disease affects a majority of adults. One major risk factor is smoking, as there is now a clear association between smoking and periodontal disease independent of oral hygiene, age, or any other risk factor. In human periodontitis, there is no simple, direct pathogen-disease link. There are three pathogens that have a strong association with progressive periodontal disease: Actinobacillus actinomycetemcomitans, spirochetes of acute necrotizing gingivitis, and Porphyromonas gingivalis. These pathogens may be the cause of continued loss of periodontal attachment in all periodontal disease classifications despite diligent periodontal therapy. This loss of attachment, or destruction of the periodontal ligament and loss of adjacent supporting bone, is seen in adult periodontitis, as well as in early-onset periodontitis, which affects young persons who otherwise appear healthy. The three forms of early-onset periodontitis are prepubertal periodontitis, localized and generalized juvenile periodontitis, and rapidly progressive periodontitis. They are distinguished from adult periodontitis by the age of onset of the disease, the rapid rate of disease progression, manifestations of defects in host response, and the composition of the subgingival microflora. Prepubertal periodontitis is associated with attachment loss around teeth of the deciduous and/or permanent dentition, and is often associated with severe congenital defects of hematological origin, and alterations in neutrophil chemotaxis function. Periodontitis may also be associated with systemic conditions such as metabolic disorders (diabetes mellitus, female hormonal alterations), drug-induced disorders, hematologic disorders/leukemia, and immune system disorders. These systemic disorders have been documented as capable of affecting the periodontium and/or treatment of periodontal disease. In order to rationally treat and prevent periodontal disease, we need to know the etiologic agents for specific patients, and the mechanism of bacterial pathogenesis in periodontitis. In systemic diseases in which the periodontal tissues are affected as well, early detection and carefully managed therapeutics with the physician and periodontist working together may prove beneficial to the patient's general health and quality of life.
Adult↗
Treatment of HIV-associated periodontal diseases.
Three presentations of periodontal disease are associated with HIV infection: necrotising periodontal disease; forms of atypical gingivitis and exacerbated attachment loss. Necrotising disease resembling aggressive acute necrotising ulcerative gingivitis and is the most acute and painful of these. Response to treatment by debridement of lesions, irrigation with aqueous chlorhexidine solution and oral metronidazole 200 mg, tds is almost diagnostic of the condition. Affected individuals are prone to relapse. Prevention by meticulous home care and frequent hygiene recalls is advised. The forms of atypical gingivitis are classically not plaque related. This means that persistence of gingivitis in the absence of plaque is required to establish the diagnosis. There is a consensus that these diseases are related to candidiasis. Treatment with antifungals may be contraindicated due to the emergence of resistant strains of Candida spp. Exacerbated attachment loss may be the legacy of repeated episodes of necrotic disease or may be due to accelerated periodontitis. In either event the principles of treatment are to encourage and facilitate plaque removal.
HIV Infections↗
Risk assessment and management of periodontal disease.
BACKGROUND: As our understanding of periodontal diseases has increased, it has become clear that certain risk factors are associated with the diseases' incidence, severity and progression. This article focuses on the role of risk assessment and disease management in improving patient outcomes, both in the general population and in specific population groups with an increased risk of developing periodontal disease or with associated comorbidities. TYPES OF STUDIES REVIEWED: The author reviewed literature related to the efficacy of risk assessment and periodontal disease management in improving clinical outcomes. In addition, he examined studies demonstrating a link between periodontal disease and specific patient populations and other comorbidities. CONCLUSIONS: Risk assessment can help predict a patient's risk of developing periodontal disease and improve clinical decision making. In turn, patient adherence to a self-care oral health regimen is a key component to successful periodontal disease management. CLINICAL IMPLICATIONS: The clinical practice of risk assessment may reduce the need for complex periodontal therapy, improve patient outcomes and ultimately reduce oral health care costs. Patients are encouraged to become actively involved in periodontal disease management by following a daily three-step regimen of brushing, flossing and rinsing with an antimicrobial mouthrinse.
Comorbidity↗