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Specific fibronectin fragments as markers of periodontal disease status.

BACKGROUND: The diagnosis of progressing periodontal disease typically relies on retrospective methods that detect changes in the amount of periodontal breakdown. Fibronectin (FN) fragments are found in vivo in association with periodontal disease, and specific FN fragments compromise periodontal ligament cell functions in vitro. The overall goal of this cross-sectional study was to determine whether specific FN fragments are present in gingival crevicular fluid (GCF) and can be used as markers for periodontal disease status. The eventual goal is to test these FN fragments in a longitudinal study as potential markers of disease activity. METHODS: GCF was collected from 94 subjects with untreated periodontitis from clinically healthy, mild/moderate periodontitis, and severe periodontitis sites. Sites were defined on the basis of clinical criteria, including gingival bleeding index, probing depth, and clinical attachment level. Western immunoblotting was used to detect FN fragments in GCF using antibodies to specific FN domains, including the collagen/gelatin-, central cell-, and carboxyl terminal heparin-binding domains, plus the CS-1 site on the alternatively spliced V region and the EIIIA region. FN fragments identified by immunoblotting and analyzed by NIH image software were scored based on pixel intensity and an ordinal grade scale. RESULTS: We identified several fragments highly associated with severe periodontitis sites, including 40-kDa, 120-kDa, and 68-kDa fragments. CONCLUSIONS: This study demonstrates that specific FN fragments are markers for periodontal disease status and supports the role of FN fragments as potential components in the pathogenesis of periodontal disease.

Adult↗

The accuracy of individual self-reported items to determine periodontal disease history.

The objective of this study was to evaluate the validity of self-reported periodontal disease and symptoms to predict periodontal disease history in a German population. We analysed data from 246 patients who answered a self-administered questionnaire on self-perceived periodontal disease and self-reported symptoms of periodontal disease. Actual periodontal status was assessed from panoramic radiographs and periodontal disease was defined as > or = 3 teeth with radiographic alveolar bone loss (ABL) > 5 mm (prevalence 39%). Sensitivity (SN) and specificity (SP) of self-reported items for diagnosis of periodontal disease history were calculated. The diagnostic accuracy of any individual item was generally low. For example, self-perceived periodontal disease had SN of 49% and SP of 67%. All self-reported items had low sensitivity, while self-reported professionally diagnosed bone loss, tooth loss caused by periodontal disease and mobility had SP > 90%. In conclusion, we did not identify a single individual question that can assess periodontal disease from self-reporting with satisfactory validity. Future studies will evaluate whether multivariate prediction rules using information from several self-reported variables are a valid means to ascertain periodontal disease history.

Adult↗

A multifaceted molecule, nitric oxide in oral and periodontal diseases.

Nitric oxide (NO) is a molecule with multiple effects on different tissues. NO takes important roles in vasodilatation, bacterial challenge and cytokine stimulation, regulation of mineralized tissue function, neurotransmission, and platelet aggregation, etc. However, under pathological conditions, NO has damaging effects. NO is synthesized by NO synthases (NOS) and inducible isoform of NOS (iNOS) is closely related to the pathophysiological characteristics of inflammatory diseases such as periodontal diseases. The expression of iNOS has been investigated in salivary gland-related diseases, temporomandibular joint disorders and oral cancer as well. The beneficial and damaging effects of NO in diseases related with periodontal, dental and maxillofacial area are discussed in this review. The biological pathways involved with NO and NO inhibitors may be good drug targets to have a role in the future management of patients with diseases in orofacial region.

Arginase↗

[The association between periodontal diseases and coronary artery diseases--a literature review].

The relation between periodontal disease and atherosclerotic cardiovascular disease was reported the first time at the end of the Eighties. Screening of the English written reported research papers revealed an increased risk of coronary artery disease and Cerebrovascular disease, in patients suffering from chronic periodontal infection. The same relation was found in patient who underwent multiple tooth extraction as a result of chronic advanced periodontal disease. These observations stress the importance of maintaining good oral hygiene and the prevention of chronic periodontal disease. The precise mode of influence, pathophysiology is still obscured, possible mechanisms were suggested. An indirect risk, by raising infection markers, such as fibrinogen and c-reactive protein. Other possibilities are by direct influence on Atherosclerotic plaque formation or another common cardiovascular risk factor such as smoking which influence both cardiovascular and periodontal diseases.

Arteriosclerosis↗

Risk indicators for tooth loss due to periodontal disease.

BACKGROUND: Several risk indicators for periodontal disease severity have been identified. The association of these factors with tooth loss for periodontal reasons was investigated in this cross-sectional comparative study. METHODS: All extractions performed in 21 general dental practice clinics (25% of such clinics in Kuwait) over a 30-day period were recorded. Documented information included patient age and gender, medical history findings, dental maintenance history, toothbrushing frequency, types and numbers of extracted teeth, and the reason for the extraction. Reasons were divided into periodontal disease versus other reasons in univariate and binary logistic regression analyses. RESULTS: A total of 1,775 patients had 3,694 teeth extracted. More teeth per patient were lost due to periodontal disease than for other reasons (2.8 +/- 0.2 versus 1.8 +/- 0.1; P <0.001). Factors significantly associated with tooth loss due to periodontal reasons in logistic regression analysis were age >35 years (odds ratio [OR] 3.45; 95% confidence interval [CI] 2.79 to 4.26), male gender (OR 1.42; 95% CI 1.17 to 1.73), never having periodontal maintenance (OR 1.48; 95% CI 1.23 to 1.78), never using a toothbrush (OR 1.81; 95% CI 1.49 to 2.20), current or past smoking (OR 1.56; 95% CI 1.28 to 1.91), anterior tooth type (OR 3.23; 95% CI 2.57 to 4.05), and the presence of either of the following medical conditions: diabetes mellitus (OR 2.64; 95% CI 2.19 to 3.18), hypertension (OR 1.73; 95% CI 1.41 to 2.13), or rheumatoid arthritis (OR 4.19; 95% CI 2.17 to 8.11). CONCLUSION: Tooth loss due to periodontal disease is associated with the risk indicators of age, male gender, smoking, lack of professional maintenance, inadequate oral hygiene, diabetes mellitus, hypertension, rheumatoid arthritis, and anterior tooth type.

Adolescent↗

Aspartat aminotransferase--a marker of periodontal disease activity.

Active and inactive periodontal pockets exist in periodontal disease and the progression of periodontitis is episodic and cyclical. Current diagnostic tests do not distinguish between active and inactive lesions. Objective assessment of disease activity could significantly affect periodontal therapy. Aspartat aminotransferase (AST) activity in gingival crevicular fluid is a potential quantitative marker of periodontal disease activity. Thirty-six patients with periodontitis, twenty with adult periodontitis and sixteen with rapidly progressive periodontitis were evaluated clinically prior to treatment and AST activity in periodontal pockets was determined prior to and after initial therapy. Clinical measures included plaque index, gingival inflammation degree and attachment loss. The results show that AST levels do not correlate with clinical indices and that they decrease after treatment. AST is a possible novel biochemical marker of periodontal disease activity independent of commonly used clinical measures. It could also be useful for early monitoring of treatment success.

Adult↗

Potassium channel-blockers as therapeutic agents to interfere with bone resorption of periodontal disease.

UNLABELLED: Inflammatory lesions of periodontal disease contain all the cellular components, including abundant activated/memory T- and B-cells, necessary to control immunological interactive networks and to accelerate bone resorption by RANKL-dependent and -independent mechanisms. Blockade of RANKL function has been shown to ameliorate periodontal bone resorption and other osteopenic disorders without affecting inflammation. Development of therapies aimed at decreasing the expression of RANKL and pro-inflammatory cytokines by T-cells constitutes a promising strategy to ameliorate not only bone resorption, but also inflammation. Several reports have demonstrated that the potassium channels Kv1.3 and IKCa1, through the use of selective blockers, play important roles in T-cell-mediated events, including T-cell proliferation and the production of pro-inflammatory cytokines. More recently, a potassium channel-blocker for Kv1.3 has been shown to down-regulate bone resorption by decreasing the ratio of RANKL-to-OPG expression by memory-activated T-cells. In this article, we first summarize the mechanisms by which chronically activated/memory T-cells, in concert with B-cells and macrophages, trigger inflammatory bone resorption. Then, we describe the main structural and functional characteristics of potassium channels Kv1.3 and IKCa1 in some of the cells implicated in periodontal disease progression. Finally, this review elucidates some recent advances in the use of potassium channel-blockers of Kv1.3 and IKCa1 to ameliorate the clinical signs or side-effects of several immunological disorders and to decrease inflammatory bone resorption in periodontal disease. ABBREVIATIONS: AICD, activation-induced cell death; APC, antigen-presenting cells; B(K), large conductance; CRAC, calcium release-activated calcium channels; DC, dendritic cell; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IFN-gamma, interferon-gamma; IP(3), inositol (1,4,5)-triphosphate; (K)ir, inward rectifier; JNK, c-Jun N-terminal kinase; I(K), intermediate conductance; LPS, lipopolysaccharide; L, ligand; MCSF, macrophage colony-stimulating factor; MHC, major histocompatibility complex; NFAT, nuclear factor of activated T-cells; RANK, receptor activator of nuclear factor-kappaB; T(CM), central memory T-cells; T(EM), effector memory T-cells; TNF, tumor necrosis factor; TRAIL, TNF-related apoptosis-inducing ligand; OPG, osteoprotegerin; Omp29, 29-kDa outer membrane protein; PKC, protein kinase C; PLC, phospholipase C; RT-PCR, reverse-transcriptase polymerase chain-reaction; S(K), small conductance; TCR, T-cell receptor; and (K)v, voltage-gated.

Alveolar Bone Loss↗

The potential for increase in the periodontal diseases of the aged population.

The periodontal disease trends in the nation's older adults aged 55 to 74 years are assessed using National Center for Health Statistics data spanning an approximate 12-year period. Both the 1960 to 1962 Health Examination Survey and the 1971 to 1974 Health and Nutrition Examination Survey I surveys used similar multistaged stratified probability samples. Examinations were calibrated and the collection of periodontal disease (PI), oral hygiene (OHI) and tooth loss scores were standardized. Data were collected on 1567 persons in 1960 to 1962 and 4746 persons in 1971 to 1974. The mean PI scores between the two surveys were not statistically different. However, when the periodontal diseases were divided into individuals with or without pockets, there was a significant decline in the per cent without pockets (P less than 0.001) while the per cent with pockets remained unchanged or increased. The significant reduction in OHI scores (P less than 0.02) seems to validate the decrease in gingivitis. The improvement in tooth loss was reflected by both the greater proportion of dentulous adults, and among the dentulous, a retention of more than two teeth per person by 1971 to 1974. A hypothesis is discussed regarding tooth retention and the periodontal diseases with projections for the year 2000.

Age Factors↗

Host response tests for diagnosing periodontal diseases.

Extensive data collected over the past decade demonstrate clearly that disease-active and disease-inactive periodontal pockets exist, disease progression is infrequent and episodic, and most progression occurs in a small proportion of highly susceptible individuals. Furthermore, traditionally used diagnostic procedures do not identify susceptible individuals nor distinguish between disease-active and disease-inactive periodontal sites. New diagnostic tests based on host response factors that will aid in resolving these problems appear to be possible. Sources of material for use in such tests include gingival crevicular fluid (GCF), blood cells, and blood serum. Of these, components in GCF are most promising, at least in the immediate future. Although more than 40 GCF components have been studied, efforts that attempt to relate the presence and amount of a given component to an independent measure of active disease are very few in number. As a consequence, we do not yet know the potential for most GCF components as the basis of diagnostic tests. Those components that have been documented to associate with active disease as measured by attachment loss of 2 mm or greater include alkaline phosphatase, beta-glucuronidase, prostaglandin-E2, aspartate aminotransferase, and IgG4 antibody subclass. Even in these cases, the data base is small and additional clinical studies are needed to document claims. At the present time, tests based on beta-glucuronidase, nonspecific neutral proteases, and aspartate aminotransferase are being commercialized. One test has received FDA approval. Tests based on blood cells have limited application for patients with adult periodontitis, but are useful for patients with early-onset forms of periodontitis. An abnormality in the leukocyte adherence molecules on the surfaces of neutrophils is diagnostic for generalized prepubertal periodontitis, and defects in chemotactic receptor numbers and in a surface molecule designated as GP110 are found on the neutrophils of most but not all localized juvenile periodontitis patients. Recent data indicate that enhanced unstimulated or stimulated release of PGE2 and Interleukin-1 by peripheral blood monocytes may be an indicator of susceptibility to severe periodontitis. Assessment of the humoral immune response as reflected by serum antibodies to antigens of periodontopathic bacteria shows little promise as the basis for tests diagnostic of site-specific disease activity. However, the capacity of an individual to mount an IgG2 subclass response to carbohydrate antigens may have potential as an indicator of disease susceptibility.

Gingival Crevicular Fluid↗

The relative importance of plaque and occlusion in periodontal disease.

A series of studies has investigated interactions between periodontal trauma and marginal periodontitis in relation to the initiation, progression and treatment of periodontal disease. Lesions of trauma in the periodontal ligament do not initiate the loss of connective tissue attachment characteristic of marginal periodontitis. Studies conducted in squirrel monkeys and beagle dogs in which jiggling forces were superimposed upon an established marginal periodontitis reported increased loss of alveolar bone, but the accelerated loss of attachment which occurred in the dog model did not occur in the monkey model. In order to clarify the relative importance of inflammation and tooth mobility in the treatment of advanced periodontal disease, periodontal responses were evaluated after removing combinations of traumatic and inflammatory components. Elimination of trauma in the presence of existing marginal inflammation did not reduce tooth mobility or increase bone volume. Osseous regeneration and decreased tooth mobility occurred after resolving both components; however, similar findings occurred after resolving inflammation in the presence of continued tooth mobility. After resolution of inflammation, remaining tooth mobility does not result in increased loss of connective tissue attachment. On a clinical level for periodontal disease treatment, the findings place decreased emphasis upon management of tooth mobility and increased emphasis upon resolution of marginal inflammation.

Animals↗

The diagnosis, progression, prognostic indication and classification of periodontal disease: a review (Part 3).

Periodontal disease may be largely divided into gingivitis and periodontitis depending on the extent of tissue involved. It is not inevitable that all sites or patients exhibiting gingivitis will progress to periodontitis although it is rare for the latter to arise de novo. Although periodontal diseases frequently occur in the systemically healthy individual, systemic disease often modifies the response of these tissues and may offer an early chance to diagnose any underlying general health problems. A detailed full mouth periodontal examination must constitute part of the dental examination and can prove a valuable health screening measure as part of general health care.

Adult↗

[The relationship between smoking and periodontal diseases].

The oral hygiene, periodontal status and smoking habits of 432 males were surveyed in order to study the relationship between smoking and periodontal disease. The results showed that there was no difference between smokers and non-smokers on oral hygiene and gingivitis. The percentage of smokers with periodontitis was higher than that of non-smokers. The prevalence of periodontitis in heavy smokers was higher than that of light and middle smokers and non-smokers. It was indicated that smoking may be one of the risk factors in the development of periodontal disease.

Adult↗

[Morphological study of periodontal tissues in the initial stage of periodontal disease. Part 1. Application of a morphological measurement and a system for evaluating the periodontal status].

The functional aberration of occlusion, based on the morphology of the alveolar process, causes chronic irritation of the periodontium in addition to the concomitant effect of other local environment factors. This investigation was designed to study the role of morphological characteristics in the periodontal disease process. The periodontal health of 22 subjects was recorded by clinical and roentgenological measurements of the loss of periodontal tissue. The criteria for this selection were no loss of or a crowding of adjoining teeth and no disharmony in occlusal contact. Morphological data were measured around the premolars and molars of lower jaws on the study models individuals, in bucco-lingual width of the alveolar bone in relationship to the width of the crown and the sagittal figure of the Spee curve etc. by using a three-dimensional analyzer. The subjects were categorized as Type II when the records indicated a ratio of the crown width/bone width of 1/1.2. Types I and III, depended on a greater and smaller ratio, respectively. Type W symbolized the alveolar process, of which the interproximal bone showed a considerable curvature mediodistally. Type F showed a flat pattern. The sagittal figure of the Spee curve was divided into four patterns: Pattern A or B, when the cusp of the canine and first premolar leveled over or on the occlusal plane; Pattern C, when the cusp of the canine leveled over and the first premolar under the occlusal plane, and Pattern D, when all cusps, canine, premolar and molar, were under the occlusal plane. The distance from the occlusal plane to the deepest point of the Spee curve was divided into four groups: Pattern a, when the distance was 0-1.0 mm, Pattern b, 1.1-2.0 mm, Pattern c, 2.1-3.0 mm and Pattern d, 3.1-4.0 mm. These results suggest that the morphological evaluation is a useful diagnostic indicators on a rational basis. The morphological characteristics might be related to the presence of periodontal disease and allowed to speculate the pathological changes in established stage, and also to the response to periodontal treatment in the initial stage of periodontal disease.

Alveolar Process↗

Prevention of periodontal diseases.

The ultimate goal of periodontal disease prevention is to maintain the dentition over a lifetime in a state of health, comfort, and function in an aesthetically pleasing presentation. This article focuses on primary and secondary periodontal disease prevention as they relate to gingivitis and periodontitis. Risk assessment, mechanical plaque control, chemical plaque control, current clinical recommendations for optimal prevention, and future preventive strategies are discussed.

Dental Plaque↗

Periodontal diseases in the child and adolescent.

BACKGROUND: Periodontal diseases are among the most frequent diseases affecting children and adolescents. These include gingivitis, localized or generalized aggressive periodontitis (a.k.a., early onset periodontitis which includes generalized or localized prepubertal periodontitis and juvenile periodontitis) and periodontal diseases associated with systemic disorders. The best approach to managing periodontal diseases is prevention, followed by early detection and treatment. METHODS: This paper reviews the current literature concerning the most common periodontal diseases affecting children: chronic gingivitis (or dental plaque-induced gingival diseases) and early onset periodontitis (or aggressive periodontitis), including prepubertal and juvenile periodontitis. In addition, systemic diseases that affect the periodontium and oral lesions commonly found in young children are addressed. The prevalence, diagnostic characteristics, microbiology, host-related factors, and therapeutic management of each of these disease entities are thoroughly discussed.

Adolescent↗

Longitudinal periodontal tissue alterations during supportive therapy. Findings from subjects with normal and high susceptibility to periodontal disease.

AIM: The aim of the study was to evaluate disease progression during supportive periodontal therapy in (i) a group of 225 subjects with "normal" (NG) and (ii) a group with high susceptibility (HSG; n= 109) to periodontal disease (based on their baseline disease status). MATERIAL AND METHODS: The following variables were recorded at the baseline examination (1 year after they received non-surgical periodontal therapy) and at the re-examination after 12 years of maintenance: number of teeth, plaque, probing pocket depth, probing attachment level, bone level in full mouth radiographs. All assessments were performed in a standardized manner and by well-trained and calibrated examiners. Supportive periodontal therapy was delivered 3-4 x per year and included repeated oral hygiene instruction and debridement. In addition, sites that bled on probing and had a PPD value of > or = 5 mm received subgingival instrumentation. RESULTS: A comparison between the findings at baseline and after 12 years revealed that in the NG, most subjects maintained their periodontal condition unchanged during the maintenance period; only a few subjects experienced tooth loss and the figures describing the mean amount of bone and attachment loss were small (0.5 mm and 0.3 mm respectively). The HSG patients experienced some tooth loss and also lost significant amounts of bone and attachment during the 12 years of SPT. Thus, in this group of subjects, the mean overall PAL loss amounted to 0.8 mm, i.e., 0.06 mm/tooth surface/year. In the NG, the overall attachment loss was significantly smaller: 0.5 mm, i.e. 0.04 mm/tooth surface/year. CONCLUSION: In subjects with a high susceptibility for periodontal disease who had been treated for this condition by non-surgical means, an SPT program including regularly repeated oral hygiene instruction and subgingival debridement, made it possible to maintain bone and attachment levels at a reasonably stable level over a 12-year period. A similar SPT provided to a group of subjects with normal susceptibility to periodontal disease, on the other hand, prevented almost entirely major tooth, bone and attachment loss.

Adult↗

Higher risk of preterm birth and low birth weight in women with periodontal disease.

Pregnant women with periodontal disease (PD) may be at increased risk for having preterm low-birth-weight (PLBW) children. We investigated whether the maintenance of the mothers' periodontal health after 28 weeks' gestation reduces the risk of PLBW. Of the 639 women studied, 406 had gingivitis and received treatment before 28 weeks' gestation, and 233 had PD and were treated after delivery. Data about previous and current pregnancies and known risk factors were obtained from patients' medical records. Primary outcomes were delivery before 37 weeks' gestation or an infant with birth weight below 2500 g. The incidence of PLBW was 2.5% in periodontally healthy women, and 8.6% in women with PD (p = 0.0004, relative risk = 3.5, 95% CI, 1.7 to 7.3). Risk factors significantly associated with PLBW were previous PLBW, PD, fewer than 6 pre-natal visits, and low maternal weight gain. PD was associated with both preterm birth and low birth weight, independent of other risk factors.

Adolescent↗

Calcium and the risk for periodontal disease.

BACKGROUND: Dietary calcium has long been a candidate to modulate periodontal disease. Animal as well as human studies of calcium intake, bone mineral density, and tooth loss provide a rationale for hypothesizing that low dietary intake of calcium is a risk factor for periodontal disease. METHODS: We evaluated the role of dietary calcium intake as a contributing risk factor for periodontal disease utilizing the Third National Health and Nutrition Examination Survey (NHANES III), which is representative of the U.S. civilian non-institutionalized population. Dietary calcium intake was determined from a 24-hour dietary recall. The U.S. Department of Agriculture Nutrient Database was used as a source of nutrient composition data. Periodontal disease was measured by attachment loss. In addition, serum calcium was assessed using venous blood samples. Logistic regression analysis was used to examine the association between periodontal disease and dietary calcium intake or serum calcium levels after adjusting for covariants including age, gender, tobacco consumption, and gingival bleeding. RESULTS: The association of lower dietary calcium intake with periodontal disease was found for young males and females (20 to 39 years of age), and for older males (40 to 59 years of age). The relationship between low dietary calcium intake and increased levels of periodontal disease showed an estimated odds ratio (OR) of 1.84 (95% CI: 1.36 to 2.48) for young males, 1.99 (95% CI: 1.34 to 2.97) for young females, and 1.90 (95% CI: 1.41 to 2.55) for the older group of males. These odds ratios were adjusted for gingival bleeding and tobacco consumption. The dose response was also seen in females, where there was 54% greater risk of periodontal disease for the lowest level of dietary calcium intake (2 to 499 mg) and 27% greater risk in females who took moderate levels of dietary calcium (500 to 799 mg) as compared to those who took 800 mg or more dietary calcium per day. A statistically significant association between low total serum calcium and periodontal disease was found in younger females aged 20 to 39 with OR = 6.11 (95% CI: 2.36 to 15.84) but not for males or older females, after adjusting for tobacco use, gingival bleeding, and dietary calcium intake. CONCLUSIONS: These results suggest that low dietary intake of calcium results in more severe periodontal disease. Further studies will be needed to better define the role of calcium in periodontal disease and to determine the extent to which calcium supplementation will modulate periodontal disease and tooth loss.

Adult↗