Developing entrustable professional activities for general dentistry at the University of North Carolina.

INTRODUCTION: As part of curriculum innovation, the University of North Carolina (UNC) Adams School of Dentistry identified core entrustable professional activities (EPAs) that graduates must demonstrate for practice readiness. This paper describes the development of the UNC EPAs and the perceptions of the general dentistry faculty. METHODS: Upon establishing a blueprint of knowledge, skills, and attitudes of UNC graduates, using a distributed leadership approach, faculty teams developed EPAs focused on the patient care process. The American Dental Education Association Compendium of Clinical Competency Assessments and Commission on Dental Accreditation Standards informed the team's work. Perceptions of the assessment framework were examined using a questionnaire completed by 13 general dentistry faculty considering the importance, accuracy, and agreement of each EPA, associated domains of competence, and encounter management on a 6-point rating scale. RESULTS: Distributed leadership was a useful strategy in EPA development to disperse decision-making and build ownership. Through multiple iterations, four EPAs (assessment, plan of care, collaborative care, and provision of care) with associated sub-EPAs emerged. EPAs included a description, required knowledge and skills, and rubrics for assessment. The general dentistry faculty reported a high level of importance, accuracy, and agreement with EPAs, domains of competence, and encounter management. DISCUSSION: EPAs provide a standardized manner to describe the comprehensive work dentists perform, shifting away from individual competencies. The UNC EPAs provide the foundation for longitudinal measures of competence preparing graduates for independent practice. With limited EPAs frameworks available in dentistry, we aim to inform the development and implementation of EPAs across dental education.

Interferon activated gene 204 protects against bone loss in experimental periodontitis.

BACKGROUND: Periodontal destruction can be the result of different known and yet-to-be-discovered biological pathways. Recent human genetic association studies have implicated interferon-gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)-1ß levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis. METHODS: Periodontitis was induced in Ifi204-/- (IFI16 murine homolog) and Aim2-/- mice using the ligature model. Chimeric mice were created to identify the main source cells of Ifi204 in the periodontium. IFI16-silenced human endothelial cells were treated with periodontal pathogens in vitro. Periodontal tissues from Ifi204-/- mice were evaluated for alveolar bone (micro-CT), cell inflammatory infiltration (MPO+ staining), Il1b (qRT-PCR), and osteoclast numbers (cathepsin K+ staining). RESULTS: Ifi204-deficient mice> exhibited >20% higher alveolar bone loss than wild-type (WT) (P < 0.05), while no significant difference was found in Aim2-/- mice. Ifi204's effect on bone loss was primarily mediated by a nonbone marrow source and was independent of Aim2. Ifi204-deficient mice had greater neutrophil/macrophage trafficking into gingival tissues regardless of periodontitis development compared to WT. In human endothelial cells, IFI16 decreased the chemokine response to periodontal pathogens. In murine periodontitis, Ifi204 depletion elevated gingival Il1b and increased osteoclast numbers at diseased sites (P < 0.05). CONCLUSIONS: These findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.