bluuebunny/crossref_metadata_2025_split huggingface dataset:
The East London Study of Maternal Chronic Periodontal Disease and Preterm Low Birth Weight Infants: Study Design and Prevalence Data
Authors: Davenport Elizabeth S. , Williams Catherine E.C.S. , Sterne Jonathan A.C. , Sivapathasundram Vythilingam , Fearne Janice M. , Curtis Michael A. 
Published: October 2010

AbstractThe influence of subject‐based and environmental factors on the balance between the subgingival microbial challenge and the host response in periodontal diseases illustrates the intimate link between oral and systemic health. From this stems the hypothesis that the persistent Gram‐negative challenge and associated inflammatory sequelae in periodontal disease may have consequences extending beyond the periodontal tissues themselves. This paper addresses the design of a case‐control study to examine the relationship between preterm low birth weight (PLBW) and maternal periodontal disease. We present preliminary data on the prevalence of these 2 conditions in a group of mothers at the Royal Hospitals Trust, London, U.K. Cases are defined as mothers delivering an infant weighing less than 2,500g before 37 weeks' gestation and controls as mothers delivering an infant of more than 2,500g after 38 weeks. We estimated that a study involving 800 mothers (1:3 case:control) should have sufficient power to detect an association with a minimum odds ratio of 3 at the 5% significance level. Demographic details of 177 subjects demonstrated that they were representative of the local population, and the prevalence of PLBW was within the expected range. However, the extent and severity of periodontal disease were higher than predicted and may have reflected elevations in gingival inflammation associated with pregnancy. The final outcome of the study should help determine the need for further interventionist studies to demonstrate a causal relationship between periodontal disease and PLBW, as well as provide information on the prevalence of periodontal diseases in this study population. Ann Periodontol 1998;3:213–221.
Potential Pathogenic Mechanisms of Periodontitis‐Associated Pregnancy Complications
Authors: Offenbacher S. , Jared H.L. , O'Reilly P.G. , Wells S.R. , Salvi G.E. , Lawrence H.P. , Socransky S.S. , Beck J.D. 
Published: October 2010

AbstractDuring normal pregnancy, maternal hormones and locally acting cytokines play a key role in regulating the onset of labor, cervical ripening, uterine contraction, and delivery. Maternal infections during pregnancy have been demonstrated to perturb this normal cytokine and hormone‐regulated gestation, sometimes resulting in preterm labor, preterm premature rupture of membranes, and preterm low birth weight (PLBW), i.e., < 2,500 g and < 37 weeks of gestation. Our research focus has been to determine whether periodontal infections can provide sufficient challenge to the mother to trigger PLBW. New experiments from 48 case‐control subjects have measured gingival crevicular fluid (GCF) levels of PGE2 and IL‐1β to determine whether mediator levels were related to current pregnancy outcome. In addition, the levels of 4 periodontal pathogens were measured by using microbe‐specific DNA probes. Results indicate that GCF–PGE2 levels are significantly higher in PLBW mothers, as compared with normal birth weight (NBW) controls (131.4 ± 21.8 vs. 62.6 ± 10.3 [mean ± SE ng/mL], respectively, at P = 0.02). Furthermore, within primiparous PLBW mothers, there was a significant inverse association between birth weight (as well as gestational age) and GCF–PGE2 levels at P = 0.023. These data suggest a dose‐response relationship for increasing GCF–PGE2 as a marker of current periodontal disease activity and decreasing birth weight. Microbial data indicate that 4 organisms associated with mature plaque and progressing periodontitis—Bacteroides forsythus, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Treponema denticola—were detected at higher levels in PLBW mothers, as compared to NBW controls. These data suggest that biochemical measures of maternal periodontal status and oral microbiol burden are associated with current PLBW. Ann Periodontol 1998;3:233—250.
Associations Between Oral Conditions and Respiratory Disease in a National Sample Survey Population
Authors: Scannapieco F.A. , Papandonatos G.D. , Dunford R.G. 
Published: October 2010

AbstractRespiratory infectious diseases such as bacterial pneumonia and bronchitis are common and costly, especially in institutionalized and elderly inpatients. Respiratory infection is thought to rely in part on the aspiration of oropharyngeal flora into the lower respiratory tract and failure of host defense mechanisms to eliminate the contaminating bacteria, which then multiply to cause infection. It has been suggested that dental plaque may act as a reservoir of respiratory pathogens, especially in patients with periodontal disease. However, the impact of poor oral health on oral respiratory pathogen colonization and lung infection is uncertain, especially in ambulatory, non‐institutionalized populations. To begin to assess potential associations between respiratory diseases and oral health, data from the National Health and Nutrition Examination Survey I (NHANES I) were analyzed. This database contains information on the general health status of 23,808 individuals. Of these, 386 individuals reported a suspected respiratory condition that was further assessed by a physician. These subjects were categorized as having a confirmed chronic respiratory disease (chronic bronchitis or emphysema) or an acute respiratory disease (influenza, pneumonia, acute bronchitis). They were compared to those not having a respiratory disease. Initial non‐parametric analysis noted that individuals with a confirmed chronic respiratory disease (n = 41) had significantly greater oral hygiene index scores than subjects without respiratory disease (n = 193; P = 0.0441). Logistic regression analysis of data from these subjects, which considered age, race, gender, smoking status, and simplified oral hygiene index (OHI), suggested that subjects having the median OHI value were 1.3 times more likely to have a chronic respiratory disease relative to those with an OHI of 0. Similarly, subjects with the maximum OHI value were 4.5 times more likely to have a chronic respiratory disease than those with an OHI of 0. No evidence was found to support an association between poor oral health with acute respiratory diseases. Also, no association was noted between the periodontal index and any respiratory disease. These results suggest OHI to have a residual effect on chronic respiratory disease of both practical and statistical significance. Ann Periodontol 1998;3:251–256.
Anaerobic Bacteremia and Fungemia in Patients Undergoing Endodontic Therapy: An Overview
Authors: Debelian Gilberto Jirair , Olsen Ingar , Tronstad Leif 
Published: October 2010

AbstractOral focal infection, a concept neglected for several decades, is a subject of controversy. Recent progress in classification and identification of oral microorganisms has renewed interest in focal infection. The aim of this study was to use phenotypic and genetic methods to trace microorganisms released into the bloodstream during and after endodontic treatment back to their presumed source—the root canal. Microbiological samples were taken from the root canals of 26 patients with asymptomatic apical periodontitis of single‐rooted teeth. The blood of the patients was drawn during and 10 minutes after endodontic therapy. Microorganisms in blood were collected after anaerobic lysis filtration and cultured anaerobically on blood agar plates. The phenotypic methods used for characterization and tracing of microorganisms in blood and root canals were: biochemical and antimicrobial susceptibility tests, SDS‐PAGE of whole‐cell soluble proteins, and gas chromatography of cellular fatty acids. Phenotypic data were verified by DNA restriction patterns and corresponding ribotypes of the root canal and blood isolates by using a computer‐assisted system for gel analysis. All root canals contained anaerobic bacteria. The frequency of bacteremia varied from 31% to 54%. The microorganisms from the root canal and blood presented identical phenotypic and genetic characteristics within the patients examined. These characteristics differed between patients. The present study demonstrated that endodontic treatment can be the cause of anaerobic bacteremia and fungemia. The phenotypic and genetic methods used appeared valuable for tracing microorganisms in the blood back to their origin. Ann Periodontol 1998;3:281–287.
Epidemiological and Clinical Aspects of Periodontal Diseases in Diabetics
Authors: Soskolne W. Aubrey 
Published: October 2010

AbstractThe association between diabetes mellitus and periodontal disease has long been discussed, with conflicting conclusions. On the one hand, numerous reports indicate a high prevalence of periodontal disease in diabetics compared to healthy controls, while others fail to show such a relationship. Clarification of this dilemma has been occurring as the diagnostic criteria for periodontal disease destruction improve and the number and size of the populations surveyed grow. This review is based on a selective review of the literature from the present decade. To date, based mainly on an extensive study of the Pima Indians who have an extremely high incidence of non–insulin‐dependent diabetes mellitus (NIDDM), it seems to be clear that patients with NIDDM have a higher prevalence and severity of periodontal disease destruction than non‐diabetics in the same population. However, it must be borne in mind that these data are for a special population. Studies on patients with insulin‐dependent diabetes mellitus (IDDM) indicate results similar to those found in studies on NIDDM. There is an increase in prevalence and severity of periodontitis compared to controls. For both IDDM and NIDDM, there does not appear to be any correlation between the prevalence or the severity of periodontal disease and the duration of diabetes. Well‐controlled diabetic patients as measured by blood glycated hemoglobin levels have less severe periodontal disease than poorly controlled diabetics. The principles of treatment of periodontitis in diabetics are the same as those for non‐diabetic patients and are consistent with our approach to all high‐risk patients who have already developed periodontal disease. The major efforts should be directed at the prevention of periodontitis in patients at risk of developing diabetes. Another important clinical question relates to the influence of periodontal disease on the control of the diabetic state. Here again the literature is unclear; however, a recent development suggests that effective control of periodontal infection in patients with diabetes reduces the level of advanced glycosylation end products in the serum. If future studies can confirm this effect, then periodontal infection control must be considered an integral part of diabetic control. Ann Periodontol 1998;3:3–12.
Effect of Aging on Functional Changes of Periodontal Tissue Cells
Authors: Abiko Yoshimitsu , Shimizu Noriyoshi , Yamaguchi Masaru , Suzuki Hiroshi , Takiguchi Hisashi 
Published: October 2010

AbstractAlthough the severity of periodontal disease is known to be affected by age, functional changes of periodontal tissue cells during the aging process are not well characterized. It is important to define how cellular aging affects the progression of periodontal diseases associated with the aging process. In vitro aging of human gingival fibroblast (HGF) and periodontal ligament fibroblast (HPLF) cells was prepared by sequential subcultivations (5 to 6 passages as young, 18 to 20 passages as old). GFs were also prepared from gingiva of Down's syndrome patients and 60‐week‐old rats. Fetal rat calvarial osteoblasts were prepared by sequential digestion with collagenase. HGF and HPLF cells were treated with lipopolysaccharide (LPS) and cyclic tension force, respectively. Amounts of PGE2, interleukin (IL)‐1β, IL‐6, and plasminogen activator (PA) in conditioned media were measured. Total RNA was extracted, and mRNA expression was analyzed by reverse transcription Polymerase chain reaction (RT‐PCR). LPS‐stimulated PGE2, IL‐1β, IL‐6, and PA production was increased in “old” HGF compared to younger cells. According to RT‐PCR analysis, gene expression of COX‐2, IL‐1β, IL‐6, and tissue type (t) PA was higher in old cells than in young cells. Cyclic tension force to HPLF also stimulated phenotypic and gene expression of IL‐1β, PGE2 (COX‐2 gene) and tPA. These findings suggest that aging in both HGF and HPLF may be an important factor in the severity of periodontal disease through higher production of inflammatory mediators in response to both LPS and mechanical stress. In addition, oxygen radical‐treated fibronectin (FN) as substratum diminished bone nodule formation by osteoblasts when compared with intact FN. This finding suggests that FN plays an important role in osteoblast activity and that FN damaged by oxygen radicals during the aging process may be related to less bone formation. Ann Periodontol 1998;3:350–369.
Periodontal Disease and Diabetes Mellitus: A Two‐Way Relationship
Authors: Grossi Sara G. , Genco Robert J. 
Published: October 2010

AbstractSevere periodontal disease often coexists with severe diabetes mellitus. Diabetes is a risk factor for severe periodontal disease. A model is presented whereby severe periodontal disease increases the severity of diabetes mellitus and complicates metabolic control. We propose that an infection‐mediated upregulation cycle of cytokine synthesis and secretion by chronic stimulus from lipopolysaccharide (LPS) and products of periodontopathic organisms may amplify the magnitude of the advanced glycation end product (AGE)‐mediated cytokine response operative in diabetes mellitus. In this model, the combination of these 2 pathways, infection and AGE‐mediated cytokine upregulation, helps explain the increase in tissue destruction seen in diabetic periodontitis, and how periodontal infection may complicate the severity of diabetes and the degree of metabolic control, resulting in a 2‐way relationship between diabetes mellitus and periodontal disease/infection. This proposed dual pathway of tissue destruction suggests that control of chronic periodontal infection is essential for achieving long‐term control of diabetes mellitus. Evidence is presented to support the hypothesis that elimination of periodontal infection by using systemic antibiotics improves metabolic control of diabetes, defined by reduction in glycated hemoglobin or reduction in insulin requirements. Ann Periodontol 1998;3:51–61.
New Concepts Regarding the Pathogenesis of Periodontal Disease in HIV Infection
Authors: Lamster Ira B. , Grbic John T. , Mitchell‐Lewis Dennis A. , Begg Melissa D. , Mitchell Aaron 
Published: October 2010

AbstractPeriodontal manifestations of human immunodeficiency virus (HPV) infection were first described in 1987. Initially, the lesions receiving attention were HW‐associated gingivitis (now known as linear gingival erythema [LGE]) and HTV‐associated periodontitis (now known as necrotizing ulcerative periodontitis [NUP]). The true prevalence of LGE was difficult to determine due to variable diagnostic criteria. Recently, LGE has been associated with intraoral Candida infection. The prevalence of NUP is low (≤ 5%), and this lesion is associated with pronounced immunosuppression. Current focus on the periodontal manifestations of HIV infection centers on rapid progression of chronic adult periodontitis in HIV+ patients. Attempts to identify the pathogenesis of the increased progression of periodontitis have not proven successful. For example, analysis of subgingival plaque for the presence of bacterial pathogens has failed to detect differences between HIV+ and HIV− patients. Recently our laboratory has identified alterations in the host response in the gingival crevice of HIV+ patients. Comparing HIV+ and HIV− injecting drug users (IDU), levels of the proinfiammatory cytokine interleukin‐1 β (IL‐1β) in gingival crevicular fluid (GCF) were slightly elevated at sites with a probing depth of 1 to 3 mm. At deeper sites (≥ 4 mm), total IL‐1β in GCF was significantly greater in HIV+ individuals. Using the lysosomal acid glycohydrolase β‐glucuronidase (βG) as a measure of the influx of polymorphonuclear leukocytes (PMN) into the gingival crevice, our data indicated a significant correlation of total βG in GCF and probing depth in the HIV–IDU (r = 76; P = .02). This result was similar to what we have observed in other studies. In contrast, for HIV+ subjects, total βG was not associated with probing depth (r = .20; NS). These data suggest that HIV+ patients have altered regulation of PMN recruitment into the gingival crevice. We have begun to investigate the conditions under which subgingival Candida may contribute to periodontal lesions in HIV+ individuals. Candida from subgingival sites has been cultured in HIV+ individuals. Subgingival Candida was distinct from Candida isolated from tongue and buccal mucosal surfaces (as indicated by genomic fingerprinting). We hypothesize the absence of adequate priming of PMN by HIV+ patients. This may be due to a reduced Th1 lymphocyte response. The inability of HIV+ individuals to adequately prime PMN may allow Candida to colonize the subgingival environment. In that milieu, it may act directly or in concert with subgingival bacterial pathogens, or as a cofactor (by inducing production of proinflammatory cytokines) to increase the occurrence of periodontal attachment loss. Ann Periodontol 1998;3:62–75.
Fibroblast Cytotoxicity Associated With Plasma Cells and Lymphocytes in Chronic Periodontitis Lesions in Rats
Authors: Garant Philias R. , Paik Ki‐Suk , Cho Moon‐Il 
Published: October 2010

Interdental periodontitis lesions in rats 20 to 27 months of age were found to contain large aggregations of plasma cells and lymphocytes. Fibroblasts in areas of dense immunocyte infiltration appeared damaged. The close juxtaposition of both plasma cells and lymphocytes to the altered fibroblasts suggests that a cytotoxic effect of immunocyte origin might be a significant element in connective tissue alteration in advanced periodontitis lesions in older rats.At the ultrastructural level, the damaged fibroblasts exhibited alteration of the nucleus, loss of cytoplasmic content including microfilaments and microtubules, swelling and degeneration of mitochondria and Golgi vesicles and cisternae. Dilation of the rough endoplasmic reticulum, including the perinuclear cisterna, along with vesiculation of the cytoplasmic membranes, suggests osmotic dysfunction in various cellular organelles.
Clinical and Microbiological Evaluation of Therapy for Juvenile Periodontitis
Authors: Kornman Kenneth S. , Robertson Paul B. 
Published: October 2010

Eight patients (mean age 15.6 yrs) with severe molar‐incisor bone loss and pocket formation characteristic of juvenile periodontitis were entered into a clinical protocol of three sequential stages: (1) scaling and root planing (S/RP); (2) S/RP concurrent with systemic tetracycline therapy (1 gm/day for 28 days); (3) periodontal surgery concurrent with systemic tetracycline therapy. Clinical and microbiological examinations were scheduled at baseline, at 1 to 2 months after Stage I, at 1 to 2 months after completion of tetracycline therapy in Stages II and III, and during recall. A decision to progress to the next stage or to place the patient on a 3‐month recall was based solely on clinical findings (suppuration, bleeding upon probing and pocket depth) at the deepest site in each patient. Paperpoint subgingival plaque samples from representative affected sites were analyzed for percentage of total cultivable microflora composed of black‐pigmented Bacteroides species (BPB), surface translocating bacteria (STB) and Actinobacillus actinomycetemcomitans (Aa). At baseline, all sites bled to probing, seven of eight sites showed suppuration, and deepest pocket depths averaged 8.0 mm. STB were detected in one and BPB in four sites, respectively, and all sites demonstrated Aa, which constituted approximately 40% of the total cultivable flora.S/RP alone had essentially no effect on either clinical or microbiological findings, and all patients progressed to Stage II. Five went on to Stage III. S/RP with tetracycline was clinically and microbiologically more effective at sites in which Aa was predominant. Surgery was required in all sites containing high levels of both BPB and Aa. These results suggest that microbiological diagnosis may be useful in selecting and monitoring treatment for juvenile periodontitis.
Disruption of Hepatocyte Growth Factor/c-Met Signaling Enhances Pancreatic β-Cell Death and Accelerates the Onset of Diabetes
Authors: Mellado-Gil Jose , Rosa Taylor C. , Demirci Cem , Gonzalez-Pertusa Jose A. , Velazquez-Garcia Silvia , Ernst Sara , Valle Shelley , Vasavada Rupangi C. , Stewart Andrew F. , Alonso Laura C. , Garcia-Ocaña Adolfo 
Published: October 2010

OBJECTIVE
To determine the role of hepatocyte growth factor (HGF)/c-Met on β-cell survival in diabetogenic conditions in vivo and in response to cytokines in vitro.

RESEARCH DESIGN AND METHODS
We generated pancreas-specific c-Met-null (PancMet KO) mice and characterized their response to diabetes induced by multiple low-dose streptozotocin (MLDS) administration. We also analyzed the effect of HGF/c-Met signaling in vitro on cytokine-induced β-cell death in mouse and human islets, specifically examining the role of nuclear factor (NF)-κB.

RESULTS
Islets exposed in vitro to cytokines or from MLDS-treated mice displayed significantly increased HGF and c-Met levels, suggesting a potential role for HGF/c-Met in β-cell survival against diabetogenic agents. Adult PancMet KO mice displayed normal glucose and β-cell homeostasis, indicating that pancreatic c-Met loss is not detrimental for β-cell growth and function under basal conditions. However, PancMet KO mice were more susceptible to MLDS-induced diabetes. They displayed higher blood glucose levels, marked hypoinsulinemia, and reduced β-cell mass compared with wild-type littermates. PancMet KO mice showed enhanced intraislet infiltration, islet nitric oxide (NO) and chemokine production, and β-cell apoptosis. c-Met-null β-cells were more sensitive to cytokine-induced cell death in vitro, an effect mediated by NF-κB activation and NO production. Conversely, HGF treatment decreased p65/NF-κB activation and fully protected mouse and, more important, human β-cells against cytokines.

CONCLUSIONS
These results show that HGF/c-Met is critical for β-cell survival by attenuating NF-κB signaling and suggest that activation of the HGF/c-Met signaling pathway represents a novel strategy for enhancing β-cell protection.