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A huge percentage of underprivileged kids in Los Angeles County have infectious dental disease that’s gone unchecked, according to a study led by the Herman Ostrow School of Dentistry of the University of Southern California.
In the report, “The Children’s Dental Health Project of Los Angeles County,” researchers Roseann Mulligan and Hazem Seirawan reveal that a staggering 73 percent of disadvantaged kids have untreated caries, the bacterial disease responsible for tooth decay. Dentists screened more than 2,300 children at 59 Head Start centers, Women, Infants and Children (WIC) centers, and elementary and high schools throughout the county.
This groundbreaking study is the most comprehensive study on oral health in underprivileged children ever conducted in Los Angeles County, surveying children of a wide range of ages, races and degrees of caries infection.
A “silent epidemic” with five times the prevalence of asthma, caries is the most common chronic disease in children and can result in serious pain and illnesses affecting parts of the body beyond the mouth, says Mulligan, Chair of the Division of Dental Public Health and Pediatric Dentistry at the Ostrow School of Dentistry. The disease is an infectious process, with bacteria passed between individuals via shared eating utensils, kissing and other forms of contact. The pain caused by the disease is a huge contributor to school absences throughout the county.
The study also explains many of the complex social, logistical and economic factors that make disadvantaged kids more likely to suffer from untreated dental caries. One significant barrier is dental insurance; many kids aren’t covered by Denti-Cal, California’s public dental insurance program, and the parents of those kids that are covered may still have trouble regularly seeing a dentist since only about half of the dentists in Los Angeles County accept Denti-Cal, says Seirawan, research assistant professor at the Ostrow School of Dentistry. Other factors include poor oral hygiene habits, inadequate nutrition, the consumption of bottled versus fluoridated tap water, and more.
The study proposes several suggestions for lessening the impact of dental disease among the county’s underprivileged children. From encouraging better oral health education at the school and community level and supporting the organizations providing care to disadvantaged kids, to helping more dentists serve lower-income communities after they graduate and campaigning for policy changes within local and state government, there’s plenty that members of the community can do to help Los Angeles kids fight dental caries, Mulligan says.
The project was conducted with the help of faculty from the University of California, Los Angeles School of Dentistry and was supported by First 5 LA, the Annenberg Foundation, the California Endowment and the California Wellness Foundation.
Learn more about the study.
See the full report.
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Saturday, March 6, 2010
Friday, March 5, 2010
Periodontal pathogens enhance HIV-1 promoter activation in T cells
Although oral co-infections (e.g. periodontal disease) are highly prevalent in HIV-1 patients and appear to positively correlate with viral load levels, the potential for oral bacteria to induce HIV-1 reactivation in latently infected cells has received little attention. The researchers involved in this study have proved that periodontal pathogens enhanced HIV-1 promoter activation in T-cells, monocytes/macrophages and dendritic cells; however the mechanisms involved in this response remain undetermined.
The objective of this study was to determine the role of Toll-like receptors (TLR) in HIV-1 reactivation induced by periodontal pathogens. The oral Gram-negative but not Gram-positive bacteria enhanced HIV-1LTR activation in BF24 cells. TLR9 activation by F. nucleatum and TLR2 by both Gram-negative bacteria were involved in this response, however TLR4 activation had no effect. Use of NFkB or Sp1 specific chemical inhibitors suggested that these transcription factors are positive and negative regulators of bacterially-induced HIV-1LTR activation, respectively. HIV-1LTR activation and viral replication were similarly induced in THP89GFP cells.
Finally, production of TNFa was enhanced by Gram-negative bacteria and its neutralization reduced HIV-1 reactivation. These results suggest that TLR2 and TLR9 activation by P. gingivalis and F. nucleatum, as well as TNFa produced in response to challenge enhance HIV-1 reactivation in monocytes/macrophages. Increased bacterial growth and emergence of periodontopathogens or their products accompanying chronic oral inflammatory diseases could be risk modifiers for viral replication and transmission, systemic immune activation and AIDS progression in HIV-1 patients.
The objective of this study was to determine the role of Toll-like receptors (TLR) in HIV-1 reactivation induced by periodontal pathogens. The oral Gram-negative but not Gram-positive bacteria enhanced HIV-1LTR activation in BF24 cells. TLR9 activation by F. nucleatum and TLR2 by both Gram-negative bacteria were involved in this response, however TLR4 activation had no effect. Use of NFkB or Sp1 specific chemical inhibitors suggested that these transcription factors are positive and negative regulators of bacterially-induced HIV-1LTR activation, respectively. HIV-1LTR activation and viral replication were similarly induced in THP89GFP cells.
Finally, production of TNFa was enhanced by Gram-negative bacteria and its neutralization reduced HIV-1 reactivation. These results suggest that TLR2 and TLR9 activation by P. gingivalis and F. nucleatum, as well as TNFa produced in response to challenge enhance HIV-1 reactivation in monocytes/macrophages. Increased bacterial growth and emergence of periodontopathogens or their products accompanying chronic oral inflammatory diseases could be risk modifiers for viral replication and transmission, systemic immune activation and AIDS progression in HIV-1 patients.
Successful treatment of periodontal disease lowered preterm birth incidences
Previous studies have explored the effect of periodontal treatment, irrespective of efficacy of treatment, in reducing infant prematurity. In a study titled "Risk of Preterm Birth Is Reduced with Successful Periodontal Treatment," lead researcher M. Jeffcott, and colleagues S. Parry and M. Sammel (all from the University of Pennsylvania, Philadelphia) and G. Macones (Washington University, St. Louis, Missouri) determined whether a reduction in infant prematurity was associated with successful periodontal treatment.
Pregnant subjects between 6 and 20 weeks gestation (using standard pregnancy dating criteria) were eligible for screening and enrollment. Eight hundred and seventy-two subjects with and without periodontal disease were followed. One hundred and sixty subjects with periodontal disease were treated with scaling and root planing. Subjects received periodontal examinations before and after scaling and root planing. Subjects were classified post-hoc according to the results of periodontal treatment: successful treatment ("non-exposure") or unsuccessful treatment ("exposure").
Groups were compared using standard bivariate statistics, odds ratios, and logistic regression analysis. Dichotomous outcomes were compared with chi-square where appropriate.
The primary study outcome for this clinical trial was the occurrence of spontaneous preterm birth <35 weeks. Subjects without periodontal disease had 7.2 percent rate of prematurity less than 35 weeks gestation; subjects with periodontal disease had 23.4 percent rate of prematurity <35 weeks gestation. Pregnant women who were refractory to scaling and root planing were significantly more likely to have preterm infants. Subjects who were successfully treated for their periodontal disease had a significantly lower incidence of preterm birth less than 35 weeks gestation.
Pregnant subjects between 6 and 20 weeks gestation (using standard pregnancy dating criteria) were eligible for screening and enrollment. Eight hundred and seventy-two subjects with and without periodontal disease were followed. One hundred and sixty subjects with periodontal disease were treated with scaling and root planing. Subjects received periodontal examinations before and after scaling and root planing. Subjects were classified post-hoc according to the results of periodontal treatment: successful treatment ("non-exposure") or unsuccessful treatment ("exposure").
Groups were compared using standard bivariate statistics, odds ratios, and logistic regression analysis. Dichotomous outcomes were compared with chi-square where appropriate.
The primary study outcome for this clinical trial was the occurrence of spontaneous preterm birth <35 weeks. Subjects without periodontal disease had 7.2 percent rate of prematurity less than 35 weeks gestation; subjects with periodontal disease had 23.4 percent rate of prematurity <35 weeks gestation. Pregnant women who were refractory to scaling and root planing were significantly more likely to have preterm infants. Subjects who were successfully treated for their periodontal disease had a significantly lower incidence of preterm birth less than 35 weeks gestation.
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