Effect on Dental Hygiene Students of a Substance Use Simulation Conducted with Nursing Students.

Dental professionals have an opportunity to screen for substance use, provide targeted feedback based on patients' oral health, provide patient education, and refer for further assessment as needed. The aim of this study was to assess the impact on dental hygiene students of an interprofessional Screening, Brief Intervention, and Referral to Treatment (SBIRT) educational intervention with standardized patients as a tool for initiating discussions on alcohol and drug use with patients. Starting in 2015, dental hygiene students in two classes at the University of Pittsburgh participated with nursing students in one and a half hours of didactic instruction followed within a ten-week period by SBIRT simulation scenarios utilizing standardized patients, with subsequent debriefing of students by faculty. Students' attitudes were assessed before and after the didactic session and immediately after the SBIRT simulation, using the Alcohol and Alcohol Problems Perceptions Questionnaire and the Drug and Drug Problems Perceptions Questionnaire. All 67 dental hygiene students in the program at the time participated in the educational intervention and surveys. The results showed significant positive changes in role security, defined as the acceptance of SBIRT delivery as part of their role identity as dental hygienists, following the intervention. This study found that the IPE intervention with dental hygiene and nursing students improved the dental hygiene students' attitudes through using SBIRT.

Prevention strategies for dental caries in the adolescent.

The adolescent period presents a challenge for the dental health care professional--dentally, behaviorally, and developmentally. Changes in the frequency, distribution, and rate of progression for dental caries demand a re-evaluation of the treatment paradigm. The purpose of this article is to suggest dental caries preventive strategies for the adolescent dental patient.

Altered Neutrophil Function in Localized Juvenile Periodontitis: Intrinsic or Induced?

Localized juvenile periodontitis (LJP) is an aggressive periodontal disease of familial nature. Neutrophils from a majority of patients with this disease exhibit decreased Chemotaxis with increased adherence, oxidative burst, and degranulation in response to opsonized bacteria. It is proposed that the biological basis for these altered neutrophil functions in LJP may be due either to intrinsic cell abnormalities or to the effect of factors present in the sera of LJP patients, which can modulate neutrophil functions. LJP neutrophils exhibit a lower number of receptors for chemoattractants and GP-110 molecules which are known to facilitate Chemotaxis. Furthermore, these cells exhibit lower signal transduction in response to a biological stimulus. These observations suggest that intrinsic cellular defects may be responsible for altered neutrophil functions in LJP. However, healthy neutrophils, when treated with very low concentrations of proinflammatory cytokines, also exhibit the characteristics of altered or "defective" LJP neutrophils. Additionally, healthy neutrophils, when treated with LJP serum, also exhibit many of the characteristics associated with LJP neutrophils. Attempts to identify these factors have shown that cytokines like TNF-α and/or IL1 ß in LJP sera may be at least partially responsible for modulating neutrophil functions in LJP. These cytokines are primarily produced by activated macrophages, indicating a role for these cells in the etiology of LJP. The hyper-responsiveness of these cells to an immunologic challenge can result in local increases in cytokines leading to excessive bone loss and tissue damage at the site of infection, while systemic elevations in cytokines would lead to decreased neutrophil Chemotaxis, both of which are observed in LJP. Present evidence indicates that neutrophil functions are indeed altered in the majority of LJP patients. However, the biological basis for the alteration may not be due to the neutrophils themselves but, rather, a consequence of an inherent hyperactive immune response during the host-pathogen interaction. J Periodontol 1996;67:337-344.