Clinical practice guidelines for oral management of Sjögren disease: Dental caries prevention.

Background: Salivary dysfunction in Sjögren disease can lead to serious and costly oral health complications. Clinical practice guidelines for caries prevention in Sjögren disease were developed to improve quality and consistency of care.

Methods: A national panel of experts devised clinical questions in a Population, Intervention, Comparison, Outcomes format and included use of fluoride, salivary stimulants, antimicrobial agents, and nonfluoride remineralizing agents.

Optimizing dry mouth treatment for individuals with Sjögren's syndrome.

A hallmark of the oral component of Sjögren's syndrome (SS) is the complaint of dry mouth thought to be secondary to dysfunction of the salivary glands. This article describes how treatment may be optimized for individuals who have dry mouth.

Small proline-rich protein 1B (SPRR1B) is a biomarker for squamous metaplasia in dry eye disease.

Purpose: Squamous metaplasia occurs in ocular surface diseases like Sjögren's syndrome (SS). It is a phenotypic change whereby epithelial cells initiate synthesis of squamous cell-specific proteins such as small proline-rich protein 1B (SPRR1B) that result in pathologic keratin formation on the ocular surface. The authors hypothesized that inflammation is a key inducer of pathologic keratinization and that SPRR1B represents an analytical biomarker for the study of the molecular mechanisms.

The oral component of Sjögren's syndrome: pass the scalpel and check the water.

The labial salivary gland biopsy is a diagnostic test for the oral component of Sjögren's syndrome (SS) that has been the subject of controversy and re-examination for many years. Despite multiple recent challenges to the significance of this test, when correctly done, it remains one of the most informative, specific, and technically simple tests available for the oral component of SS. Because of compromised salivary gland function, patients with SS are at risk for dental caries.

Tumor necrosis factor-alpha regulation of CD4+CD25+ T cell levels in NOD mice.

The mechanism by which tumor necrosis factor-alpha (TNF) differentially modulates type I diabetes mellitus in the nonobese diabetic (NOD) mouse is not well understood. CD4+CD25+ T cells have been implicated as mediators of self-tolerance. We show (i) NOD mice have a relative deficiency of CD4+CD25+ T cells in thymus and spleen; (ii) administration of TNF or anti-TNF to NOD mice can modulate levels of this population consistent with their observed differential age-dependent effects on diabetes in the NOD mouse; (iii) CD4+CD25+ T cells from NOD mice treated neonatally with TNF show compromised effector function in a transfer system, whereas those treated neonatally with anti-TNF show no alteration in ability to prevent diabetes; and (iv) repeated injection of CD4+CD25+ T cells into neonatal NOD mice delays diabetes onset for as long as supplementation occurred.