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J D Beck

Publications and source records attributed to J D Beck.

At least 55 records · Page 3Linked to original sources
PubMed2000

Periodontal medicine: emerging concepts in pregnancy outcomes.

The term periodontal medicine encompasses the study of the contribution of periodontal infections on several systemic conditions such as atherosclerosis, myocardial infarction, stroke, diabetes, and premature delivery. The early reports of a linkage between periodontitis and systemic conditions are gaining further support from additional epidemiological studies. The evidence continues to suggest that maternal periodontitis may bean important risk factor or risk indicator for pregnancies culminating in preterm low birth-weight deliveries. Potential mechanisms by which infectious challenge of periodontal origin and systemic inflammation may serve as a potential modifier of parturition are discussed. Furthermore, preliminary data are presented, supporting a hypothetical model in which periodontal pathogens disseminate systemically within the mother and gain access to the foetal compartment. Several aspects of this hypothetical model remain to be elucidated. Only the clarification of the mechanisms of pathogenesis of both periodontitis and premature deliveries will ultimately allow for accurate diagnoses and successful therapies. The concept of diagnosing and treating a periodontal patient to minimise the deleterious effects of this chronic infectious and inflammatory condition on systemic conditions represents both an unprecedented challenge and opportunity to our profession.

Female↗
PubMed1999

The concept of "risk" and the emerging discipline of periodontal medicine.

Dental clinicians intuitively weigh patient risks for developing disease and use that information for making treatment decisions and recommendations. Periodontitis, for instance, is one oral disease with documented risk factors including smoking, specific plaque bacteria and diabetes mellitus. While this link between systemic disease and periodontitis was thought to be unidirectional, mounting evidence in the last decade suggests that the relationship may be bi-directional. Cross sectional and case control studies indicate that periodontitis may confer two and seven-fold elevations in risk for cardiovascular disease and premature low birth weight respectively. While these early studies indicate potential associations between oral and systemic health, they support the central hypothesis that periodontitis triggers both local and systemic host inflammatory responses. Consequently, a new discipline, periodontal medicine, has emerged in dentistry which seeks to further define these interrelationships through scientific inquiry. Ultimately, this new knowledge may prove useful in intervention strategies to reduce patient risks and prevent systemic disease outcomes. This manuscript clarifies the concept of risk, traces the emergence of periodontal medicine and serves as a resource for the oral health professional in assessing and utilizing the current evidence on periodontal-systemic disease connections.

Bacteria, Anaerobic↗
PubMed1999

Rapid isolation of chromosomal breakpoints from patients with t(4;11) acute lymphoblastic leukemia: implications for basic and clinical research.

Chromosomal translocations t(4;11)(q21;q23) are associated with a group of acute lymphoblastic leukemias with very poor prognosis. From the complete sequences of the breakpoint cluster regions of the human MLL and AF-4 translocation partner genes, a novel set of 66 oligonucleotides that facilitates the rapid identification of translocation breakpoints by PCR analysis of genomic DNA was designed. For each breakpoint, a pair of optimally snited primers can be assigned, which improves the monitoring of the disease during treatment. Comparison of the breakpoints with the corresponding parental sequences also contributes to our better understanding of the illegitimate recombination events leading to these translocations.

Alu Elements↗
PubMed1999

[Disorders of endocrine function after brain tumor therapy in childhood].

BACKGROUND: Advances in the therapy of malignant brain tumors in children have led to a significant improvement in survival rates over the last few decades. As a result, the recognition and treatment of late effects have become more important. In addition to secondary tumors and deficiencies in cognitive and intellectual skills, the resulting endocrine disturbances play an important role. METHOD: Own data and literature review. RESULTS: Deviations from the normal growth hormone secretion are usually recognized first and are most common, and have already been observed after conventional whole brain irradiation with 18 Gy. With some delay, other hypothalamo-pituitary deficiencies may occur, including panhypopituitarism. Puberty may come too early or too late or may not appear at all. Girls in particular, frequently experience an early and rapid pubertal development after brain tumor therapy, which may lead to further reduction in height due to an accelerated bone maturation. Functional disturbances of the thyroid and adrenal glands due to hypothalamic or pituitary deficiency are less common, and usually seen only after a radiation dose of over 40 Gy. CONCLUSION: Survivors of childhood brain tumors must be considered as long-term survivors, in whom the first therapy-induced long-term side effects appear almost immediately after the end of therapy. Maximum quality of life for the individual patient can only be achieved by long-term care and close cooperation of specialists in the different medical disciplines involved.

Brain↗
PubMed1999

Dental infections and atherosclerosis.

In most countries, coronary heart disease is one of the leading causes of morbidity and death. This report reviews the current evidence indicating that oral conditions (specifically periodontitis) may be a risk factor for atherosclerosis and its clinical manifestations and provides new preliminary data. This review is done in the context of the research indicating that inflammation plays a central role in atherogenesis and that there is a substantial systemic microbial and inflammatory burden associated with periodontal disease. Our review concentrates on 5 longitudinal studies that show oral conditions being associated with the onset of coronary heart disease while controlling for a variety of established coronary heart disease risk factors. In addition to published evidence, preliminary findings from our Dental Atherosclerosis Risk in Communities study also indicate that periodontal disease is associated with carotid intimal-medial wall thickness, a measure of subclinical atherosclerosis, adjusting for factors known to be associated with both conditions.

Arteriosclerosis↗
PubMed1999

Effects of puberty on bone age maturation in a girl after medulloblastoma therapy.

BACKGROUND: Craniospinal radiotherapy for malignant brain tumors can result in a variety of neuroendocrine disturbances, among which are the development of growth hormone deficiency and early puberty, which can markedly reduce adult height. METHODS: The authors report the case of a girl who received craniospinal radiotherapy for a medulloblastoma at the age of 3.4 years. At 9.1 years, growth hormone therapy was started, and spontaneous onset of puberty (Tanner stage B2) occurred at age 10.3 years. Interval until menarche was short, at only 0.9 years. RESULTS: Although chronologic age at appearance of Tanner stages was within the normal range, the patient showed a rapid acceleration in skeletal maturation, resulting in adult short stature. CONCLUSION: Bone age seems to be a more precise parameter for biologic maturation in some patients after craniospinal irradiation than is clinical assessment of pubertal stages. Thus, if progression of bone age and decreasing final height predictions are noted, puberty should be stopped with gonadotropin-releasing hormone analogs, even if pubertal development seems to be adequate for chronologic age, because this increases the remaining time for growth hormone treatment.

Age Determination by Skeleton↗
PubMed1999

Etiologic models for incident periodontal attachment loss in older adults.

Etiologic factors for incident periodontal attachment loss (ALOSS) have not been conclusively identified. The purpose of this study was to develop etiologic models for ALOSS in older adults. Data on 697 older blacks and whites were obtained from 5 sequential examinations over 7 years in the Piedmont 65+ dental study, a complex random sample of older adults in North Carolina. Multivariable Poisson regression models were fit for average number of ALOSS events per person or site month at risk. In models for whites, molar sites, sites with adjacent caries, sites in persons who had: Porphyromonas gingivalis (P.g.) at least 2% of total microbial count (TMC), never had a dental checkup, more depression symptoms, fewer than 12 years of education, higher BANA score, or smoked, had significantly higher rates of ALOSS. In a separate model for blacks, interproximal and molar sites, sites in blacks who had: P.g. at least 2% of TMC, higher BANA score, never had a dental checkup, lower socioeconomic status (SES), or smoked, had significantly higher rates of ALOSS. These results confirm a multifactorial etiology for ALOSS in older adults and indicate that interventions aimed at infection, smoking, and preventive dental care utilization, may be most useful.

Black or African American↗
PubMed1999

Periodontitis-atherosclerosis syndrome: an expanded model of pathogenesis.

The early reports of a linkage between periodontitis and atherosclerosis have garnered further support by additional data generated by several investigative teams in many different countries. The evidence continues to suggest that periodontitis may be an important risk factor or risk indicator for cardiovascular pathology for some individuals. The term periodontitis-atherosclerosis syndrome (PAS) is proposed as a new diagnostic term to describe this condition in these individuals. Current evidence, albeit preliminary in nature, which describes a cluster of clinical signs and symptoms that are associated with this condition, is presented. It is clear that this syndrome will require considerable study and refinement before a definitive diagnosis and treatment plan can be formulated. Potential mechanisms by which systemic inflammation and infectious challenge of periodontal origin may serve as a potential modifier of cardiovascular disease are discussed in the context of a detailed working model of pathogenesis. This hypothetical model embraces many cellular and molecular components of atherogenesis and thromboembolic diseases from the perspective of periodontitis pathogenesis. Many aspects of the hypothetical model remain unproved; however, it is our opinion that only through the clarification of the mechanisms of pathogenesis can we ultimately construct a knowledge framework for accurate diagnoses and successful therapies. The concept of diagnosing and treating a periodontal patient to minimize the deleterious effects of this chronic infectious and inflammatory condition on the cardiovascular system represents an unprecedented challenge to our profession.

Arteriosclerosis↗
PubMed1999

Plausibility of periodontal disease estimates from NHANES III.

OBJECTIVES: This study investigated possible reasons for observed discrepancies in prevalence estimates and measures of association for periodontal disease between phases (1988-91 and 1991-94) of the third National Health and Nutrition Examination Survey (NHANES III). METHODS: NHANES III data on CD-ROM were obtained from the National Center for Health Statistics. Accompanying documentation states that each phase and combined phases constitute national probability samples of the US population. Weighted estimates of prevalence (percent of persons affected) and extent (percent of sites affected) for previously reported thresholds of gingival bleeding (GB), attachment loss (AL), and probing pocket depth (PD) were generated using data from all 15,511 persons aged 13-90 years who received periodontal examinations. Odds ratios for associations between four selected risk indicators and both PD and AL were compared between phases. RESULTS: Phase 2 estimates of GB and PD were as much as 56 percent lower than phase 1 estimates and both were different from combined-phase estimates. However, AL prevalence was consistent between phases. Prevalence differences between phases could be explained in part by examiner variations. Odds ratios for PD differed between phases by as much as one-third, although the direction and precision of associations were not affected, and differences were reduced after controlling for examiner. CONCLUSIONS: Combined-phase estimates of GB and PD prevalence and extent differ from previously published estimates derived from Phase 1, apparently because estimates in at least one phase of the NHANES III study are biased. However, associations with selected risk indicators were fairly consistent between phases.

Adolescent↗
PubMed1999

A comparison of increment and incidence density analyses in evaluating the anticaries effects of two dentifrices.

This study aimed to determine whether incidence density (ID) calculations of caries incidence rates would provide a more sensitive means of detecting caries-preventive effects than would traditional techniques. A secondary analysis was conducted using data from a 1981 study in which three dentifrices were compared in a double-blind randomized clinical trial. Subjects were examined at baseline and 1, 2 and 3 years after baseline. Three-year DMFS increments were calculated for 1,754 subjects attending the baseline and 3-year examinations. Caries ID rates then were calculated for 2, 661 subjects who had at least two examinations, using each surface's net increment (-1, 0 or +1) as the numerator and the surface's time at risk as the denominator. Despite theoretical advantages, the ID method did not alter the conclusions drawn using DMFS increments, apparently because (a) subjects lost to follow-up were similar to those completing the study, and (b) loss to follow-up was similar among treatment groups.

Adolescent↗
PubMed1999

Association between extent of periodontal attachment loss and self-reported history of heart attack: an analysis of NHANES III data.

Coronary heart disease is responsible for one of every five deaths in the United States. Recent epidemiological studies have shown an association between periodontal disease and coronary heart disease. The purpose of this cross-sectional study was to verify this association using data from the third National Health and Nutrition Examination Survey (NHANES III). Data for 5564 people 40 years of age and older who had complete periodontal assessments and information on heart attack were evaluated. The outcome was the self-reported history of heart attack (yes vs. no). The main independent variable was the percent of periodontal sites per person with attachment loss of 3 mm or greater (categorized as 0%, > 0-33%, > 33-67%, and > 67%). Periodontal attachment loss was measured at two sites per tooth in randomly assigned half-mouths, one upper and one lower quadrant. The covariables included sociodemographic variables and established risk factors for cardiovascular disease. Relative to the 0% category, the unadjusted odds of heart attack increased with each higher category of attachment loss-2.2 (95% confidence interval = 1.3-3.8), 5.5 (3.4-9.1), and 9.8 (4.5-21.0), respectively. Adjustment for age, sex, race, poverty, smoking, diabetes, high blood pressure, body mass index, and serum cholesterol decreased these odds to 1.4 (0.8-2.5), 2.3 (1.2-4.4), and 3.8 (1.5-9.7), respectively. This study supports findings from previous studies of an association between periodontal disease and coronary heart disease.

Adult↗
PubMed1998

Detection of hyperdiploid karyotypes (>50 chromosomes) in childhood acute lymphoblastic leukemia (ALL) using fluorescence in situ hybridization (FISH).

ALL patients with a hyperdiploid karyotype of more than 50 chromosomes (high hyperdiploidy) carry a better prognosis in contrast to patients presenting with other cytogenetic features, and an appropriate less intensive therapy protocol should be developed for these patients. For this reason it is desirable to have a quick screening method identifying those with this type of hyperdiploidy. We therefore studied the bone marrow and/or blood cells of 278 children with ALL using double target fluorescence in situ hybridization (FISH) on interphase. A combination of DNA probes (repetitive, centromere specific) was applied detecting chromosomes which are most frequently overrepresented in patients with hyperdiploidy (>50), at chromosomes 6, 10, 17 and 18. All patients showing hybridization signals differing from the normal signal distribution of two spots for each tested chromosome were analyzed cytogenetically as well. 102 children (102/278; 36.7%) were found to have a clone with aberrant FISH results. In 80 patients (80/278, 28.8%) the cytogenetic analysis detected a hyperdiploid karyotype >50 chromosomes, whereas the remaining patients (n=12) could be related to other ploidy subgroups, ie hyperdiploidy with 47-50 chromosomes, haploidy, triploidy/tetraploidy. Comparison of the FISH results with the measurements of the DNA content showed good agreement for 88.8% (208/234) of the investigated patients. The detected rate of 28.8% patients with a high hyperdiploid karyotype in our investigated cohort is comparable to the frequency of other studies. Only one patient was not identified as having a hyperdiploid karyotype with our combination of DNA probes. Our results indicate that FISH is a feasible and quick screening method for the detection of hyperdiploid karyotypes (>50 chromosomes) and other ploidy subgroups.

Aneuploidy↗
PubMed1998

Risk revisited.

As our knowledge of dental caries and periodontal diseases has increased, our perspective has changed from viewing these diseases as ubiquitous to one which sees a variety of risk profiles in a population. Now, from a perspective of assigning risk, caries and periodontitis can be thought to be more like some of our common medical conditions, i.e., certain people or subgroups of the population are at higher risk than others and that prevention and intervention involve a combination of personal behaviors and professional practices. Research into risk assessment, however, is often hampered by confusing and ambiguous use of terminology. This commentary proposes some specific definitions for terms used in risk assessment in dentistry. These terms include risk factor, risk indicator, demographic risk factor, risk predictor (risk marker), prognostic factor, risk model, and prediction model.

Causality↗
PubMed1998

Inflammatory mediators of the terminal dentition in adult and early onset periodontitis.

Based upon the prosthodontic literature, subjects who are at the transition stage between natural dentition and edentulism are called "terminal dentition" (TD) cases. The aim of the present cross-sectional investigation was to characterize the local and systemic inflammatory responses in 2 groups of patients with terminal dentition periodontitis. Eight severe adult periodontitis terminal dentition (AP-TD) subjects and 8 early onset periodontitis terminal dentition (EOP-TD) subjects were entered into the study. Our purpose was to measure an extended battery of cytokines in the gingival crevicular fluid (GCF) and in lipopolysaccharide (LPS)-stimulated monocytic culture supernatants as well as gingival mononuclear cell messenger RNA (mRNA) transcripts determined from biopsy samples. Within the GCF there were 3 tiers (levels) of mediators based upon approximate 10-fold differences in concentration. The highest tier included prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta) and interleukin-2 (IL-2), the intermediate tier included tumor necrosis factor alpha (TNF alpha) and interferon gamma (IFN-gamma) and at the lowest concentration level were interleukin-4 (IL-4) and interleukin-6 (IL-6). Thus, the GCF analysis clearly indicated that in both AP-TD and EOP-TD groups the monocytic, i.e. IL-1 beta and PGE2 and Th1, i.e. IL-2 and IFN-gamma, inflammatory mediator levels quantitatively dominated over the Th2 mediators, i.e. IL-4 and IL-6. LPS-stimulated monocytic release of IL-1 beta, PGE2 and TNF alpha was significantly elevated in both AP-TD and EOP-TD groups compared to those of a control group of 21 subjects with moderate to advanced adult periodontitis. The cytokine mRNA expression of isolated gingival mononuclear cells showed that in both the AP-TD and the EOP-TD groups Th1 and Th2 cytokines were expressed, with low levels of IL-4 and IL-12. In conclusion, our data suggest that this cross-sectional TD periodontitis model may reflect progressive periodontal disease associated with tooth loss. Furthermore, although Th1 cytokine levels in the GCF dominate over the Th2 response, monocytic activation provides the main source of proinflammatory mediators. In addition, LPS-stimulated peripheral blood monocytes demonstrate an upregulated inflammatory mediator secretion in the terminal dentition.

Adult↗
PubMed1998

Prevalence of HIV-associated periodontitis and chronic periodontitis in a southeastern US study group.

OBJECTIVES: This study estimates factors associated with the prevalence of HIV-associated periodontal diseases (HIV-P) and the severity and extent of periodontitis in HIV-infected adults from North Carolina (NC). METHODS: Data are derived from a cross-sectional study of HIV-infected adults (total n = 326, dentate n = 316) treated at the University of North Carolina Hospitals. Outcomes were a diagnosis of HIV-P and measures of probing pocket depth (PPD), recession (REC), and clinical attachment level (CAL). Immunosuppression was measured by peripheral blood CD4+ cells/mm3. RESULTS: In addition to persons with HIV (non-AIDS), this study included 10 percent of the AIDS cases in North Carolina. Median age was 37 years (range = 19-67); 78 percent were male and 60 percent were black. Sixty-two percent of persons had a probing pocket depth > or = 5 mm; 46% had recession > or = 3 mm, and 66 percent had attachment level > or = 5 mm in one or more sites. Cases of HIV-P (n = 15) were rare. Persons taking HIV-antiretroviral medication were one-fifth (OR = 0.20; 95% CI = 0.07, 0.63) as likely to have HIV-P as those not taking those medications, controlling for CD4+ cell counts. CONCLUSIONS: HIV-infected persons in this study group from North Carolina exhibited severe and extensive measures of adult periodontitis. A small proportion experienced a severe form of HIV-P, which was attenuated by antiretroviral therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Periodontitis: a risk factor for coronary heart disease?

This paper evaluates the current information on the relationship between oral disease (specifically periodontitis) and atherosclerosis/coronary heart disease (CHD) to determine whether the information is sufficient to conclude that periodontitis is a risk factor for atherosclerosis/CHD. As background for this evaluation, the term "risk factor" is defined, and the 3 criteria used to establish exposures as risk factors are reviewed. In addition, epidemiologic criteria for defining an exposure as causal are presented. The available evidence then is evaluated according to the criteria for causality, which are extensions of the criteria for establishing a risk factor. This review is done in the context of the relationship between atherosclerosis/CHD and inflammation. A number of findings are briefly reviewed that link inflammation and atherosclerosis/CHD, such as: 1) prior flu-like symptoms were more common in cases of myocardial infarction than in concurrently sampled controls; 2) high levels of cytomegalovirus antibody titers were associated with elevated carotid intimal-medial wall thickness 18 years later; 3) prior infection with cytomegalovirus was a strong independent risk factor for restenosis after coronary atherectomy; 4) dental infections were more common in cases of cerebral infarction compared to community controls matched on age and sex; and 5) the gingival index was significantly correlated with fibrinogen and white cell counts in periodontal patients and controls, adjusted for age, smoking, and socioeconomic status. Three case-control studies and 5 longitudinal studies investigating the relationship between dental conditions and atherosclerosis/CHD are reviewed in terms of strength of associations, consistency of associations, specificity. of associations, time sequence between exposure and outcome, and degree of exposure and outcome. Related to the last criterion, new findings are presented which indicate that the extent of the periodontal infection, a measure reflecting microbial burden, also is related to onset of new CHD events. Our previously published model describing the potential biological mechanisms underlying the associations found is reviewed. This model places the associations into a context of an intrinsic or acquired hyperinflammatory monocyte trait that results in a more intense inflammatory response to lipopolysaccharide (LPS) challenges, such as periodontal infections. This hyperinflammatory response may promote atheroma formation and thromboembolic events. finally, new findings from ongoing animal studies are presented, indicating that high fat diets in atherosclerotic-susceptible mice induce greater inflammatory responses to Porphyromonas gingivalis challenges. We conclude that the available evidence does allow an interpretation of periodontitis being a risk factor for atherosclerosis/CHD. This conclusion, however. is made with some qualifications. While the associations found across a wide variety of subjects are remarkably consistent, for the most part they are represented by incidence odds ratios around 2.0. While this level of association would result in oral conditions contributing to a large number of CHD cases, it is possible that associations of this magnitude are due to bias in the study designs. In addition, some studies report that periodontitis is associated with all-cause mortality and low birth weight infants. These multiple associations detract from the credibility of periodontitis as a risk factor, as specificity of association is more often related to causality. However, all-cause mortality may largely be driven by mortality from cardiovascular events: and some exposures, such as smoking. are indeed risk factors for multiple conditions. On the other hand, current findings regarding the associations between oral conditions and atherosclerosis/CHD imply that the criteria for causality may be met in the not-too-distant future.

Animals↗