A nine-year clinical case study of a resin-bonded fixed partial denture seated on the maxillary anterior teeth.

PATIENT: This report describes the longevity of a resin-bonded fixed partial denture (RBFPD). This denture was seated on the maxillary anterior teeth with minimal tooth preparation. The RBFPD was cast from a silver-palladium alloy (Castwell M.C. 12), and the pontic was veneered with an indirect composite material (Estenia). The retainers were primed with a metal conditioner (V-Primer) and seated with a tri-n-butylborane initiated adhesive resin (Super-Bond C&B). After an observation period of eight years, a fracture occurred in the incisal edge of the central incisor abutment. The fractured area was restored with light-polymerizing composite resin and the anterior guidance was re-adjusted. DISCUSSION: RBFPD abutment teeth with deep vertical overlap should be carefully prepared to avoid abutment tooth fracture. CONCLUSION: The clinical performance of the RBFPD made from a silver-palladium-copper-gold alloy was sufficient when seated with tri-n-butylborane initiated adhesive resin after surface modification using vinyl-thiol primer. CLINICAL SIGNIFICANCE: The use of vinyl-thiol primer and tri-n-butylborane initiated adhesive resin is a clinically reliable bonding system for seating resin-bonded fixed partial denture (RBFPD) made from a silver-palladium-copper-gold alloy. The RBFPD, based on a reliable bonding system, can clinically function for a long time, even if the vertical overlap of the abutment teeth is excessive

Longitudinal MRI follow-up of rheumatoid arthritis in the temporomandibular joint: importance of synovial proliferation as an early-stage sign

This article describes longitudinal magnetic resonance imaging (MRI) observations in a patient with rheumatoid arthritis of the temporomandibular joint. The characteristic findings included marked synovial proliferation, which was observed before the onset of severe bone destruction. MRI is considered to provide valuable information for the early detection of rheumatoid arthritis of the temporomandibular joint

Modeling Low Muscle Mass Screening in Hemodialysis Patients

Introduction: Computed tomography (CT) can accurately measure muscle mass, which is necessary for diagnosing sarcopenia, even in dialysis patients. However, CT-based screening for such patients is challenging, especially considering the availability of equipment within dialysis facilities. We therefore aimed to develop a bedside prediction model for low muscle mass, defined by the psoas muscle mass index (PMI) from CT measurement. Methods: Hemodialysis patients (n = 619) who had undergone abdominal CT screening were divided into the development (n = 441) and validation (n = 178) groups. PMI was manually measured using abdominal CT images to diagnose low muscle mass by two independent investigators. The development group’s data were used to create a logistic regression model using 42 items extracted from clinical information as predictive variables; variables were selected using the stepwise method. External validity was examined using the validation group’s data, and the area under the curve (AUC), sensitivity, and specificity were calculated. Results: Of all subjects, 226 (37%) were diagnosed with low muscle mass using PMI. A predictive model for low muscle mass was calculated using ten variables: each grip strength, sex, height, dry weight, primary cause of end-stage renal disease, diastolic blood pressure at start of session, pre-dialysis potassium and albumin level, and dialysis water removal in a session. The development group’s adjusted AUC, sensitivity, and specificity were 0.81, 60%, and 87%, respectively. The validation group’s adjusted AUC, sensitivity, and specificity were 0.73, 64%, and 82%, respectively. Discussion/Conclusion: Our results facilitate skeletal muscle screening in hemodialysis patients, assisting in sarcopenia prophylaxis and intervention decisions

Cellular and Molecular Bases of the Initiation of Fever

All phases of lipopolysaccharide (LPS)-induced fever are mediated by prostaglandin (PG) E(2). It is known that the second febrile phase (which starts at ~1.5 h post-LPS) and subsequent phases are mediated by PGE(2) that originated in endotheliocytes and perivascular cells of the brain. However, the location and phenotypes of the cells that produce PGE(2) triggering the first febrile phase (which starts at ~0.5 h) remain unknown. By studying PGE(2) synthesis at the enzymatic level, we found that it was activated in the lung and liver, but not in the brain, at the onset of the first phase of LPS fever in rats. This activation involved phosphorylation of cytosolic phospholipase A(2) (cPLA(2)) and transcriptional up-regulation of cyclooxygenase (COX)-2. The number of cells displaying COX-2 immunoreactivity surged in the lung and liver (but not in the brain) at the onset of fever, and the majority of these cells were identified as macrophages. When PGE(2) synthesis in the periphery was activated, the concentration of PGE(2) increased both in the venous blood (which collects PGE(2) from tissues) and arterial blood (which delivers PGE(2) to the brain). Most importantly, neutralization of circulating PGE(2) with an anti-PGE(2) antibody both delayed and attenuated LPS fever. It is concluded that fever is initiated by circulating PGE(2) synthesized by macrophages of the LPS-processing organs (lung and liver) via phosphorylation of cPLA(2) and transcriptional up-regulation of COX-2. Whether PGE(2) produced at the level of the blood–brain barrier also contributes to the development of the first phase remains to be clarified