A review of the risks and relationships between oral health and chronic diseases.

Advances in medical science and in preventive dentistry have changed the context of oral health. The American population is living longer with numerous complex chronic diseases. This paper is to raise awareness about the impact of multiple chronic diseases and their associations with oral diseases. Comorbidities can worsen the course of dental treatment. Inflammation has been the connecting factor in the bidirectional pattern of oral and systemic diseases. High occurrences of chronic diseases generally occur in aging as well as disadvantaged populations. Serious infections, slow healing, prolonged bleeding, and hospitalizations can escalate in patients with uncontrolled chronic diseases. A multidisciplinary team-based approach to patient management can minimize complications and unexpected challenges.

Sickle cell disease: Contributing factors and radiological assessments.

Sickle Cell Disease (SCD) is genetically described as an autosomal blood disorder resulting from the presence of a mutated form of hemoglobin. Morbidity, frequency of crisis, degree of anemia, and organ systems involved vary considerably per patient. Dental health professionals and other specialists commonly request comprehensive medical consultations prior to performing complex periodontal, endodontic, and surgical procedures. In order to have successful dental outcomes and minimize posttreatment dental complications, relevant disease indicators are noted. This review is to raise awareness of the impact of oral diseases in patients with sickle cell disease and to emphasize the importance of full medical disclosure, radiographic interpretation, and a well-documented medical history, and a well-written consultation which can guide treatment planning and greatly improve the course of dental treatment.

Clonotype-specific avidity influences the dynamics and hierarchy of virus-specific regulatory and effector CD4(+) T-cell responses.

A key component of immunity against viruses, CD4(+) T cells expand and differentiate into functional subsets upon primary infection, where effector (Teff) cells facilitate infection control and regulatory (Treg) cells mitigate immunopathology. After secondary infection, Teff cells mount a robust response from the memory pool. Here, we show that Treg-cell responses are diminished upon secondary infection, and Treg-cell response dynamics are associated more with T-cell receptors (TCRs) repertoire and avidity than with epitope specificity. In the murine model, the IA(b) M209 epitope of respiratory syncytial virus is recognized by both CD4(+) Treg and Teff cells, while the IA(b) M226 epitope is recognized almost exclusively by CD4(+) Teff cells expressing high avidity TCR Vß8.1/8.2 and dominating the CD4(+) T-cell response during primary and secondary infections. IA(b) M209 -Teff cells express relatively low avidity TCRs during early primary infection, but high avidity TCR Vß7-expressing IA(b) M209 -Teff cells emerge during the late phase, and become dominant after secondary infection. The emerging high avidity IA(b) M209 -Teff cells outcompete IA(b) M209 -Treg cells that share the same epitope, but have low avidity and are restricted to TCR Vß2 and Vß6 subpopulations. These data indicate that MHC-peptide-TCR interactions can produce different kinetic and functional profiles in CD4(+) T-cell populations even when responding to the same epitope.