Tartrate-resistant acid phosphatase

About: Tartrate-resistant acid phosphatase is a research topic. Over the lifetime, 1115 publications have been published within this topic receiving 45937 citations. The topic is also known as: HPAP & SPENCDI.

Suppressive Effects of the Leaf of Terminalia catappa L. on Osteoclast Differentiation In Vitro and Bone Weight Loss In Vivo

Abstract: Oral administration of Terminalia catappa extract (TCE; 1,000 mg/kg) for 5 wk suppressed bone weight loss and trabecular bone loss in ovariectomized mice. An in vitro experiment showed that TCE (1.3-20 µg/mL) did not increase alkaline phosphatase activity, which would indicate osteoclast formation, in osteoblast-like 3T3-L1 cells. On the other hand, TCE (12.5 µg/mL) markedly decreased the number of tartrate resistant acid phosphatase (TRAP)-positive multinucleated cells, which would indicate osteoclast formation, in a co-culture system (bone marrow cells/osteoblastic UAMS-32 cells). A detailed analysis of the stages of osteoclast differentiation revealed that TCE mainly suppressed the differentiation of bone marrow mononuclear cells into osteoclast progenitor cells in the presence of M-CSF and TGF-β. An additional experiment using fractionated TCE revealed that the water-soluble fraction suppressed the bone weight loss in OVX-mice and osteoclast differentiation in vitro. Therefore, the suppressive effects of TCE on bone weight loss in mice might be due to the suppressive effects of highly polar components on the early stage of osteoclast differentiation.

Isorhamnetin 3-O-neohesperidoside promotes the resorption of crown-covered bone during tooth eruption by osteoclastogenesis.

Abstract: Delayed resorption of crown-covered bone is a critical cause of delayed tooth eruption. Traditional herbal medicines may be good auxiliary treatments to promote the resorption of crown-covered bone. This study was carried out to analyse the effect of isorhamnetin 3-O-neohesperidoside on receptor activator of nuclear factor-kB ligand (RANKL)-induced osteoclastogenesis in vitro and resorption of the crown-covered bone of the lower first molars in mice in vivo. Isorhamnetin 3-O-neohesperidoside promoted osteoclastogenesis and the bone resorption of mouse bone marrow macrophages (BMMs) and upregulated mRNA expression of the osteoclast-specific genes cathepsin K (CTSK), vacuolar-type H + -ATPase d2(V-ATPase d2), tartrate resistant acid phosphatase (TRAP) and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1). NFATc1, p38 and AKT signalling was obviously activated by isorhamnetin 3-O-neohesperidoside in osteoclastogenesis. Isorhamnetin 3-O-neohesperidoside aggravated resorption of crown-covered bone in vivo. In brief, isorhamnetin 3-O-neohesperidoside might be a candidate adjuvant therapy for delayed intraosseous eruption.

Cobalt and Chromium Ions Affect Human Osteoclast and Human Osteoblast Physiology In vitro

Abstract: Introduction: Cobalt-Chromium (Co-Cr) alloys are widely used in biomedicine owing to their resistance to corrosion, mechanical properties, and biocompatibility. Despite the increase in its use in orthopaedic surgery, a number of unique complications (elevated serum levels of Co and Cr ions, development of pseudotumour, neck narrowing, osteolysis and fracture) have been recently reported with Metal-on-Metal (MoM) bearings. The goal of the present study was to assess the effects of Co and Cr ions on human osteoblasts and human osteoclast biology. ` Materials and methods: Peripheral blood mononuclear cells (PBMCs) have been used as a source of osteoclast precursors whilst SaOS-2 cells have been used as osteoblasts. Both cell types have been cultured in the presence of Co2+ or Cr3+ ions. Results: We have found that 100 μM Co2++ induced a significant increase in the number and the size of multinucleated tartrate resistant acid phosphatase positive osteoclasts as well as the number of nuclei per osteoclast. In contrast, 100 μM Cr3+ significantly decreased the number of newly-formed osteoclast but had no effect on the size or the number of nuclei per osteoclast. Interestingly, 100 μM of Co2+ was capable of strongly inhibiting bone resorption whereas 100 μM of Cr3+ had no significant effects on this parameter. The alkaline phosphatase activity was significantly increased by low concentrations of Co2+ and decreased by high concentrations of Cr3+ after 24 h and 48 h. Moreover, the degree of mineralization of a new bone matrix in vitro was significantly reduced when the SaOS-2 cells were exposed to high concentrations of Cr3+, but significantly increased when they were exposed to Co2+. Discussion: These results suggest that long-term exposure to “chronic” levels of metal ions damages the functional behaviour of bone cells and subsequently may affect bone quality.

Bone Degeneration, Inflammation and Secondary Complications of Arthritis: Potential Targets and their Natural Inhibitors.

Abstract: Arthritis is marked by joint deterioration that affects articular cartilage and subchondral bone. Though cartilage degradation does the major damage during arthritis, subsequent bone degeneration cannot be neglected. Recent progress in arthritis research has identified the clinical importance of bone erosion in destructive arthritis. Studies have showed the key role played by osteoclasts and receptor activator of nuclear factor kappaB ligand (RANKL) signaling in bone erosion. Cathepsins and tartrate resistant acid phosphatase (TRAP) are considered key enzymatic factors contributing to bone erosion. Further, reactive oxygen species (ROS) formed at the ruffled border of osteoclasts also causes bone resorption and matrix degradation. Besides, severe inflammation during arthritis induces bone erosion by aiding in Ca2+ removal and activating osteoclastogenesis. The inflammatory cytokines and ROS influence osteoclast differentiation by regulating osteoclast-lineage cells or by acting on other cells to regulate the expression of RANKL and osteoprotegerin (OPG). The enhanced production of pro-inflammatory cytokines and ROS in arthritis stimulates tissue injury by means of oxidative damage leading to vital organ damage and synovial and circulatory cell apoptosis. Thus, blocking enzymatic and non-enzymatic factors responsible for bone erosion and inflammation is considered a prime strategy in the management of arthritis. In this review we provide an overview of the mechanisms of bone erosion, inflammation and associated oxidative stress/damage during arthritis perpetuation along with shedding light on potential targets. The article also describes the possible natural therapeutic agents that could prevent bone loss and inflammation, and related secondary complications of arthritis.