muramidase and Osteoporosis

The aim of this study was to examine how the composition and properties of saliva change in people with osteoporosis who have received antiresorptive (AR) treatment, compared to patients with osteoporosis who have not yet received this treatment.. The study population consisted of 38 patients with osteoporosis using AR drugs (Group I) and 16 patients with osteoporosis who had never used AR drugs (Group II). The control group consisted of 32 people without osteoporosis. Laboratory tests included determination of pH and concentrations of Ca, PO. There were no statistically significant differences between the saliva of Group I and Group II. No statistically significant correlation was found between the amount of time using AR therapy (Group I) and the tested parameters of the saliva. Significant differences were found between Group I and the control group. The concentrations of PO. The saliva of people with osteoporosis subjected to AR therapy and those not subjected to AR therapy did not show statistically significant differences in terms of the examined parameters of the saliva. However, the saliva of patients with osteoporosis taking and not taking AR drugs was significantly different compared to the saliva of the control group.

Topics: Bone Density Conservation Agents; Humans; Hydrocortisone; Immunoglobulin A, Secretory; Muramidase; Neopterin; Osteoporosis; Saliva

Maintenance of healthy bone requires the balanced activities of osteoclasts (OCs), which resorb bone, and osteoblasts, which build bone. Disproportionate action of OCs is responsible for the bone loss associated with postmenopausal osteoporosis and rheumatoid arthritis. NF-κB inducing kinase (NIK) controls activation of the alternative NF-κB pathway, a critical pathway for OC differentiation. Under basal conditions, TRAF3-mediated NIK degradation prevents downstream signaling, and disruption of the NIK:TRAF3 interaction stabilizes NIK leading to constitutive activation of the alternative NF-κB pathway.. Using transgenic mice with OC-lineage expression of NIK lacking its TRAF3 binding domain (NT3), we now find that alternative NF-κB activation enhances not only OC differentiation but also OC function. Activating NT3 with either lysozyme M Cre or cathepsinK Cre causes high turnover osteoporosis with increased activity of OCs and osteoblasts. In vitro, NT3-expressing precursors form OCs more quickly and at lower doses of RANKL. When cultured on bone, they exhibit larger actin rings and increased resorptive activity. OC-specific NT3 transgenic mice also have an exaggerated osteolytic response to the serum transfer model of arthritis.. Constitutive activation of NIK drives enhanced osteoclastogenesis and bone resorption, both in basal conditions and in response to inflammatory stimuli.

Topics: Animals; Arthritis; Binding Sites; Blotting, Western; Bone Density; Bone Marrow Cells; Cathepsin K; Cells, Cultured; Female; Macrophages; Male; Mice; Mice, Transgenic; Muramidase; NF-kappa B; NF-kappaB-Inducing Kinase; Osteocalcin; Osteoclasts; Osteolysis; Osteoporosis; Protein Binding; Protein Serine-Threonine Kinases; RANK Ligand; Reverse Transcriptase Polymerase Chain Reaction; TNF Receptor-Associated Factor 3