Heparin interacts with candidalysin and neutralizes its cytotoxicity to oral epithelial cells.

Objectives: Candidalysin is a peptide toxin produced by Candida albicans that causes damage to epithelial cells by destabilizing the plasma membrane. This study aimed to evaluate heparin's ability to neutralize candidalysin and protect epithelial cells from lysis.

Methods: The study was conducted using a human oral epithelial cell line and synthetic candidalysin.

Knockdown of sphingomyelin synthase 2 inhibits osteoclastogenesis by decreasing RANKL expression in mouse primary osteoblasts.

Sphingomyelin is a major lipid of the plasma membrane and is enriched in microdomains of the plasma membrane that are critical for signal transduction. However, the function of sphingomyelin in the cell membrane of osteoblasts has not been clarified. Therefore, we examined how sphingomyelin synthase 2 (SMS2) affects osteoclast differentiation by osteoblasts.

RNA interference-mediated knockdown of Smad1 inhibits receptor activator of nuclear factor κB ligand expression induced by BMP-2 in primary osteoblasts.

Objective: BMP-2 induces osteoblast differentiation and activates osteoclast formation. Here, we investigated the role of Smad1, a molecule that signals downstream of BMP-2, in mediating the effects of BMP-2 on osteoclast differentiation induced by 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in osteoblasts.

Design: The effects of 1,25(OH)2D3 and BMP-2 in osteoclasts were examined using polymerase chain reaction and Western blotting to measure changes in target gene and protein expression.

Assessment of alveolar bone mineral density as a predictor of lumbar fracture probability.

Introduction: Osteoporosis and tooth loss have been linked with advancing age, but no clear relationship between these conditions has been proven. Several studies of bone mineral density measurements of the jaw and spine have shown similarities in their rate of age-related deterioration. Thus, measurements of jawbone density may predict lumbar vertebral bone density.

[Osteoporosis and oral biology].

Estrogen deficiency in post-menopausal osteoporosis not only causes decreased bone mass in mandibular bone, but also affect cartilaginous ossification in mandibular condyle. Although the mechanisms of action are not entirely clear, estrogen is thought to promote the programmed cell death of osteoclasts and hence reduce their period of activity. Treatment with estrogen or some agents prevent bone loss in alveolar bone through blocking production of cytokines in osteoblasts and promoting osteoclast apoptosis.