bluuebunny/crossref_metadata_2025_split huggingface dataset:
Periodontal Disease and Mortality From All Causes in the VA Dental Longitudinal Study
Authors: Garcia Raul I. , Krall Elizabeth A. , Vokonas Pantel S. 
Published: October 2010

AbstractThe role that oral conditions may play as risk factors or indicators for various medical outcomes, including mortality, is not well understood. We have examined the relationship of periodontal disease to mortality from all causes in the VA Dental Longitudinal Study and Normative Aging Study, a prospective cohort study of the determinants of disease in aging men. Subjects were screened for entry into the closed‐panel cohort in the mid‐1960s, based on good medical health. They are not VA patients. We have used proportional hazards regression models to assess the relationship of periodontal health status at baseline to all‐cause mortality over a 25+‐year follow‐up period. A total of 804 dentate subjects who were alive and medically healthy through their first follow‐up exam were used in the analysis; of these, 166 died during subsequent follow‐up through December 1996. Survival was calculated in years from baseline exam to death or censoring (most recent study examination date). To define periodontal health status at baseline, we separately used radiographic alveolar bone loss (ABL) (person‐level scores of mean whole‐mouth % ABL, measured with a Schei ruler using full‐mouth series of periapical films) and periodontal clinical probing depths. Covariates included age at baseline, and assessments at baseline of smoking and alcohol use, education, body mass index, serum cholesterol, white blood cell count, blood pressure, family history of heart disease, and number of teeth present. We found that periodontal status at baseline was a significant and independent predictor of mortality in this cohort, while controlling for other recognized predictors in multivariate models. For each 20% increment in mean whole‐mouth ABL, the subject's risk of death increased by 51% (RR = 1.51; 95%o CI = 1.11 – 2.04). The increase in risk attributable to periodontal status was found to be similar in magnitude to, and independent of, that attributable to cigarette smoking in this cohort. While the increased risk due to smoking was 1.52‐fold (95% CI = 1.06 – 2.19), being in the population quintile with highest ABL scores (i.e., worst periodontal status) was associated with a 1.85‐fold increase in risk (95% CI = 1.25 – 2.74) using multivariate analyses. The hypothesis that chronic oral infections, as in periodontitis, may have important systemic sequelae merits further investigation in prospective controlled studies. Ann Periodontol 1998;3:339–349.
Early‐Onset Periodontitis Associated With Down's Syndrome–A Clinical Interventional Study
Authors: Cichon P. , Crawford L. , Grimm W‐D 
Published: October 2010

AbstractIndividuals with Down's syndrome (DS) have an increased prevalence of periodontal disease compared with otherwise normal, age‐matched control groups and other mentally handicapped patients of similar age distribution. The exaggerated immune‐inflammatory response of the tissues cannot be explained by poor oral hygiene alone and might be the result of an impaired cell‐mediated and humoral immunity and a deficient phagocytic system. As far as the progression and severity of destruction, the oral manifestations of DS patients are consistent with the juvenile periodontitis (JP) disease pattern. The purpose of the present study was 1) to assess the periodontal clinical and microbiological status of 10 DS patients aged 20 to 31 years (mean: 26.3 years) relative to that of 11 patients with cerebral palsy (CP) aged 23 to 53 years (mean: 36 years) without defective immunological functions, and 2) to determine the effect of supragingival plaque control and oral hygiene instruction in these patient groups. Subsequent to the initial examination and a professional tooth cleaning program, clinical and microbiological parameters were monitored over a period of 12 weeks. The clinical examination included the recording of plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL). Subgingival plaque samples were always obtained from the same pocket with the highest disease activity (deepest bleeding site at baseline examination) in each subject for a morphotype analysis by dark‐field microscopy and for identification and quantitation of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Eikenella corrodens, Bacteroides forsythus, Fusobacterium nucleatum, Treponema denticola, and Campylobacter rectus by DNA probes. The results of the baseline examinations demonstrated that DS patients and patients with cerebral palsy had inflamed gingiva associated with a high amount of plaque. The mean probing depth and percentage of sites with probing depth ≥ 4 mm corresponded to age and poor oral hygiene in CP patients. Deep pockets in DS patients demonstrated a high prevalence of periodontal disease compared with agematched children with mental retardation and non‐handicapped patients. Regarding the young age of onset, the severe destruction of periodontal tissues and pathogenesis of periodontitis in DS patients are consistent with the juvenile periodontitis disease pattern. The missing clinical benefit and alteration of the subgingival flora following supragingival plaque control in DS patients underlined the alteration in the immunological response. Ann Periodontol 1998;3:370–380.
Alterations of Neutrophil Oxidative Burst by In Vitro Smoke Exposure: Implications for Oral and Systemic Diseases
Authors: Ryder Mark I. , Fujitaki Ron , Johnson Greg , Hyun William 
Published: October 2010

AbstractAlterations of neutrophil functions by tobacco products may play a central role in the pathogenesis of periodontal diseases and several smoking‐related systemic diseases. In the present study, we examined the in vitro effects of cigarette smoke on neutrophils at times and concentrations that may be encountered during smoke exposure. We measured the level of smoke exposure in the in vitro system by measuring the levels of nicotine and comparing these to levels in the oral cavity in smokers before and after smoking. We examined both the unstimulated and stimulated release of 2 oxidative burst products: Superoxide (O2−) and hydrogen peroxide (H2O2). Salivary washings were collected from 7 smokers (> 1 pack/day) before smoking a cigarette. Immediately after they smoked a cigarette, a second set of washings was collected. In vitro exposure to smoke involved incubating aliquots of neutrophils in phosphate‐buffered saline for 1 to 5 minutes. Nicotine and cotinine levels were quantitated using gas chromatography, with detection by electron impact mass spectrometry. Peripheral neutrophils were isolated from medically healthy non‐smoking volunteers via a doubledensity gradient technique and incubated in vitro with whole cigarette smoke for 0 to 5 minutes. Phorbol myristate acetate (PMA; 10−7 M) was used to stimulate half of the cell aliquots. Superoxide generation was assessed through the Superoxide dismutase (SOD) inhibitable reduction of ferricytochrome c. H2O2 production was assessed through the H2O2‐dependent breakdown of dichlorofluorescin diacetate to its fiuorophore and measured by flow cytometry. There was a marked elevation in salivary nicotine concentration from before smoking (mean: 80.8 ng) to after smoking (mean: 1,685 ng/mL). In the in vitro smoke box system, there was a time‐related elevation in nicotine from 1 to 5 minutes (50→136 ng/mL). In PMA‐stimulated cells exposed to smoke, there was a time‐related inhibition of both Superoxide and H2O2 production. However, in unstimulated cells exposed to smoke, there was a time‐related increase in the release of Superoxide and H2O2. A novel finding in unstimulated cells exposed to smoke was that there appeared to be 2 distinct populations of cells—one of “high” H2O2 producers and one of “low” H2O2 producers. The proportion of high H2O2 producers increased relative to smoke exposure. The relative production of H2O2 in the unstimulated high producers was comparable to PMA‐stimulated cells at 5 minutes. This release of Superoxide and H2O2 in unstimulated cells exposed to smoke may alter the pathogenic processes both in periodontal diseases and other systemic diseases. Ann Periodontol 1998;3:76–87.
Cigarette Smoking and Periodontal Diseases: Etiology and Management of Disease
Authors: Tonetti Maurizio S. 
Published: October 2010

AbstractCigarette smoking has long been suspected to be associated with a variety of oral conditions including periodontal diseases. Experimental evidence accumulated over the last 2 decades has indicated that cigarette smoking is probably a true risk factor for periodontitis. This environmental exposure has been associated with 2‐ to 3‐fold increases in the odds of developing clinically detectable periodontitis. Smokers have both increased prevalence and more severe extent of periodontal disease, as well as higher prevalence of tooth loss and edentulism, compared to non‐smokers. The greater severity of periodontal destruction may be partly accounted for by the reported increases in the rate of periodontal disease progression. The noxious effect of smoking has been shown to be dose dependent and to be particularly marked in younger individuals; in these subjects, up to 51% of the observed risk of periodontitis was associated with smoking. Much of the literature has also indicated that smokers affected with periodontitis respond less favorably to both non‐surgical, surgical, and regenerative periodontal treatments. The success rate of dental implants has also been shown to be compromised in smokers. Furthermore, longterm studies have pointed out that smoking was associated with recurrence of periodontitis during periodontal maintenance; the effect appeared to be dose dependent, with heavy smokers (> 10 cigarettes I day) presenting with higher levels of disease progression. The indication that previous smokers have lower levels of risk for periodontitis compared to current smokers is considered to be the strongest available evidence that smoking cessation will result in improved periodontal health and that smoking cessation counseling should be an integral part of periodontal therapy and prevention. So far, however, no randomized controlled clinical trial establishing the effect of smoking cessation and/or reduction on the periodontal outcomes has been reported. Given the present state of uncertainty about the periodontal benefits, but in light of the established general health gains for the patient that could be derived from a smoking cessation program, practitioners are incorporating smoking cessation counseling as an integral part of periodontal therapy. Furthermore, smoking status represents a key parameter to assess the periodontal risk of an individual subject and therefore to make evidence‐based clinical decisions. Ann Periodontol 1998;3:88–101.
Actinobacillus actinomycetemcomitans in Human Periodontal Disease: Prevalence in Patient Groups and Distribution of Biotypes and Serotypes Within Families
Authors: Zambon Joseph J. , Christersson Lars A. , Slots Jørgen 
Published: October 2010

Actinobacillus actinomycetemcomitans is a Gram‐negative oral bacterium which has been implicated in the etiology of localized juvenile periodontitis. In this study, 403 subjects from four study groups were examined for A actinomycetemcomitans in subgingival dental plaque. Samples pooled from at least six periodontal sites were included from each subject. A actinomycetemcomitans was detected in 28 of 29 localized juvenile periodontitis patients but in only 15% of the other subjects including 28 of 134 adult periodontitis patients, 24 of 142 periodontally healthy subjects and 5 of 98 insulin dependent juvenile diabetics with varying degrees of gingivitis.A actinomycetemcomitans isolates from members of five families with localized juvenile periodontitis patients were biotyped on the basis of variable fermentation of dextrin, maltose, mannitol and xylose and serotyped by indirect immunofluorescence using serotype specific rabbit antisera. Individuals within a family all harbored A actinomycetemcomitans of the same biotype and serotype. However, even in families with individuals heavily infected with A actinomycetemcomitans, some family members did not appear to be infected with the organism. The apparent poor transmissibility of A actinomycetemcomitans between individuals may, in part, explain the overall low prevalence of localized juvenile periodontitis and the familial pattern of the disease.The high prevalence of A actinomycetemcomitans in the subgingival plaque of localized juvenile periodontitis patients, compared to the much lower prevalence in other patient groups, supports the hypothesis that A actinomycetemcomitans is an etiologic agent in this periodontal disease. The reason(s) an infection with A actinomycetemcomitans may result only in a localized type of periodontal breakdown is not known; this paper presents some hypotheses which may explain this characteristic clinical feature.
Fibrin Linkage: A Precursor for New Attachment
Authors: Polson Alan M. , Proye Michel P. 
Published: October 2010

Previous studies indicated that connective tissue attachment to the root surface appeared to be dependent upon a chronologic healing sequence related to fibrin and collagen interactions. It was the purpose of the present study to try and substantiate this hypothesis by using histologic techniques designed to differentiate between fibrin and collagen during healing at the root surface interface. In four squirrel monkeys, 24 normal teeth were extracted and reimplanted after either (i) surgically denuding the coronal root surface of connective tissue fibers and cementum by root planing or, (ii) surgical denudation followed by topical application of citric acid (pH = 1; 3 minutes). Three specimens were available for histological analysis 1, 3, 7 and 21 days after reimplantation. Mallory's phosphotungstic acid hematoxylin staining technique was used to differentiate between fibrin and collagen.Epithelium migrated rapidly along the denuded, non‐acid‐treated, root surfaces, had reached the alveolar crest at 3 days, and was within the ligament space to the level of root denudation at 21 days. Epithelium did not migrate apically along denuded root surfaces treated with citric acid. At 1 and 3 days, inflammatory cells were enmeshed in a fibrin network which appeared to be attached to the root surface by arcade‐like structures. At 7 and 21 days, the region had repopulated with connective tissue cells, and collagen fibers had replaced the fibrin. It was concluded that collagen fiber attachment to the root surface was preceded by fibrin linkage, and that the linkage process occurred as an initial event in the wound healing response.
Clinical, Microbiological and Immunological Studies of a Family With a High Prevalence of Early‐Onset Periodontitis
Authors: Vandesteen G. E. , Williams B. L. , Ebersole J. L. , Altman L. C. , Page R. C. 
Published: October 2010

Extensive clinical, laboratory and microbiological studies were performed on members of a family with an unusually high prevalence of early‐onset severe periodontitis. Clinical observations included intraoral photographs and assessment of inflammation, plaque, probing depths and bone loss. Pocket bacteria were sampled, cultivated and identified. Immunological studies included assessment in vitro of neutrophil (PMN) and monocyte (MN) Chemotaxis, assessment of PMN phagocytosis and other functions using the iodination assay, measurement of serum opsonic and chemoattractant activities and determination of levels of serum antibodies specific to various putative periodontal pathogens.The proband, a 19‐year‐old white woman, had rapidly progressive periodontitis (RP). Of her six siblings available for study, all had juvenile periodontitis (JP), and both parents had been edentulous since early adulthood. Early edentulism and recurrent infections, especially otitis media, were prevalent in the forebearers, especially on the maternal side. Two married sisters of the proband had young male children with recurrent infections. Abnormalities in leukocyte Chemotaxis were found in the proband, in two of her siblings and in both parents. The pocket flora was predominantly Gram‐negative, anaerobic rods with a high prevalence of Bacteroides species, and serum antibodies specific to Bacteroides species were detected in the sera of five of the seven patients studied. Actinobacillus actinomycetemcomitans was not found in any of the pockets studied, nor were antibodies specific to any of the three known serotypes of this bacterium detected in the serum of any of the patients. There was a relatively good correlation between the bacterial species isolated from the periodontal pockets and the antibodies found in the serum. PMN iodination and serum opsonic activity were normal in all of the patients. Thus not all JP patients have detectable Actinobacillus species in their periodontal pockets, nor do all have antibody detectable with the techniques we used specific to these bacteria in their serum. In contrast, JP patients may have Bacteroides species in their periodontal pockets and antibody specific to Bacteroides species in their serum. Although abnormal leukocyte Chemotaxis is generally common in RP and JP patients, in this family the correlation between this defect and the presence of these diseases was poor.
The Subpedicle Connective Tissue Graft
Authors: Nelson Stephen W. 
Published: October 2010

A mucogingival grafting procedure has been developed to cover denuded root surfaces. This procedure, the subpedicle connective tissue graft, is a bilaminar graft that is composed of a free connective tissue graft and an overlying pedicle graft. By overlaying grafted free connective tissue with a pedicle, the otherwise compromised section of free graft which covers a denuded root surface is supplied by plasmatic circulation from capillaries in the vascular portion of the pedicle allowing it to survive.In this report 29 teeth were treated and monitored for as long as 42 months. In the group with advanced recession of 7 to 10 mm, there was an average of 88% coverage. The subpedicle graft created a healthy, functional, and esthetic result that appeared resistant to further breakdown. The subpedicle graft is indicated when a single surgical procedure is desired that will predictably cover denuded root surfaces when there is inadequate keratinized gingiva available for a pedicle graft and where the prognosis is poor for root coverage with a free gingival graft.
Altering the Progression of Human Alveolar Bone Loss With the Non‐Steroidal Anti‐Inflammatory Drug Flurbiprofen
Authors: Williams Ray C. , Jeffcoat Marjorie K. , Howard Howell T. , Rolla Arturo , Stubbs Derek , Teoh Kok W. , Reddy Michael S. , Goldhaber Paul 
Published: October 2010

The treatment of human periodontal diseases relies on mechanical and antimicrobial suppression of the etiologic bacteria. The ability to alter the progression of Periodontitis by additionally blocking host pathways involved in the destructive process is an area of current research. Prostaglandins and other metabolites of arachidonic acid are believed to be important host mediators of the bone resorption of diseases such as Periodontitis. We have previously examined the effect of inhibitors of Prostaglandin production, non‐steroidal antiinflammatory drugs (NSAIDs), on inhibiting alveolar bone loss in beagles. The present study was designed to examine the effect of the NSAID, flurbiprofen, on slowing the radiographic loss of alveolar bone in the human.Fifty‐six individuals with radiographic evidence of alveolar bone loss were recruited for study. Forty‐four patients remained in the study for the data analysis of loss of alveolar bone. Following a 6 month baseline pretreatment period to measure the radiographic progression of bone loss, half of the patients were administered flurbiprofen, 50 mg. b.i.d., while half were administered a placebo. All patients received a subgingival scaling and pumice by a hygienist every 6 months. The rate of alveolar bone loss in a 2‐year treatment period was compared to the baseline 6 month pretreatment period within and between patient groups. Throughout the study, teeth exhibiting obvious loss of bone were exited from study and treated with conventional mechanical therapy. At the end of the pretreatment period both patient groups had a similar mean rate of alveolar bone loss. In individuals given placebo tablets, the rate of bone loss was significantly (P <.05) less than baseline at 6 and 12 months of treatment, but not thereafter. Individuals given flurbiprofen twice daily had a significant (P <.05) decrease in rate of bone loss compared to baseline at 6, 12 and 18 months of treatment. In addition we found that at 12 and 18 months of flurbiprofen use the rate of bone loss in the flurbiprofen treated individuals was significantly less than in the placebo patients. However at 24 months of the treatment period there was no difference in the rate of bone loss between the placebo and flurbiprofen treated patients. These data suggest that the NSAID flurbiprofen, as an inhibitor of cyclooxygenase, can inhibit human alveolar bone loss as measured radiographically. This finding suggests that pharmacologic agents whose main action is the blocking of host responses involved in the disease process may become adjuncts to anti‐infective therapy in the management of bone resorption diseases such as Periodontitis. (J Periodontol 1989;60:485–490)
Price and Quantity Policies in a Simple Political Economy Framework
Authors: Gulati Sumeet 
Published: October 2010

Abstract
The literature of the second-best demonstrated the difference between exogenous price and quantity distortions. However, it is not always realistic to assume that distortions are beyond the policy makers control. Are price and quantity distortions different even if they are endogenized using a political economy setting? In this paper, I postulate a government that uses trade and pollution policy to maximize a weighted welfare function where domestic producers get a higher weight than consumers. International trade is regulated by either a tariff or a quota, and pollution is regulated using a pollution tax. I find that if the government has full control on both trade and pollution policy, endogenously created quantitative distortions (quantitative restrictions) have the same effect as price distortions (tariffs).