The role of positive nerve root sedimentation sign in the treatment of patients undergoing lumbar disc herniation.

BACKGROUND: To investigate the efficacy of percutaneous transforaminal endoscopic discectomy (PTED) in the treatment of patients who were diagnosed with lumbar disc herniation (LDH) with positive nerve root sedimentation sign (NRSS). METHODS: A total of 86 patients who underwent LDH were recruited and divided into NRSS-positive group (n = 49) and NRSS-negative group (n = 37). The visual analog scale (VAS), Japanese Orthopaedic Association (JOA), and Oswestry disability index (ODI) were used to evaluate the low back pain and functional recovery and were compared between the two groups. RESULTS: There were no significant differences in the demographic parameters between the two groups. The average area of the dural sac compression in the NRSS-positive group was significantly higher than that in the NRSS-negative group. Patients with a positive NRSS showed a better low back pain relief than those with a negative NRSS at 1 week and 1 month after surgery. The JOA and ODI in the NRSS-positive group were better than those in the NRSS-negative group at 3 months and 6 months postoperatively. The apparent efficiency of JOA and the excellent and good rate of ODI in the negative group was lower than that in the positive group at 6 months after surgery. CONCLUSIONS: Patients undergoing LDH with a positive NRSS showed better pain relief and functional recovery than those with a negative NRSS. The present study suggested that NRSS might be a valuable sign and associated with better clinical outcomes in patients undergoing LDH with the treatment of PTED.

Daidzin inhibits RANKL-induced osteoclastogenesis in vitro and prevents LPS-induced bone loss in vivo.

Osteoclasts are multinuclear giant cells responsible for bone resorption in bone loss diseases, including rheumatoid arthritis, periodontitis, and the aseptic loosening of orthopedic implants. Because of injurious side effects with currently available drugs, it is necessary to continue research novel bone-protective therapies. Daidzin, a naturally occurring isoflavone found in leguminous plants, has numerous beneficial pharmacologic effects, including anti-cancer, anti-cholesterol, and anti-angiocardiopathy, promoting osteoblasts differentiation, and even anti-osteoporosis. However, the effect of daidzin on the regulation of osteoclast activity has not yet been investigated. In this study, our study showed that daidzin significantly inhibited receptor activator of nuclear factor-kB ligand (RANKL)-induced osteoclast differentiation of bone marrow macrophages and the hydroxyapatite-resorbing activity of mature osteoclasts by inhibiting RANKL-induced NF-kB signaling pathway. In addition, daidzin could inhibit the expression of osteoclast marker genes, including nuclear factor of activated T cells cytoplasmic 1 (NFATc1), cellular oncogene fos (c-Fos), tartrate-resistant acid phosphatase (TRAP), and cathepsin K (CTSK). Consistent with in vitro results, daidzin inhibited lipopolysaccharide-induced bone loss by suppressing the osteoclast differentiation. Together our data demonstrated that daidzin inhibits RANKL-induced osteoclastogenesis through suppressing NF-ĸB signaling pathway and that daidzin is a promising agent in the treatment of osteolytic diseases.

Arctigenin inhibits RANKL-induced osteoclastogenesis and hydroxyapatite resorption in vitro and prevents titanium particle-induced bone loss in vivo.

Wear particle-induced bone resorption leads to prosthesis loosening, which is a major complication associated with total joint arthroplasty. Although the exact mechanism remains unclear, wear particle-induced extensive osteoclastogenesis plays a critical role in this process. Thus, a potential treatment of prosthetic loosening is focused on suppressing extensive osteoclast formation and bone resorption, which prevents wear particle-induced osteolysis. Arctigenin isolated from Arctium lappa has numerous beneficial pharmacologic effects, including anti-inflammatory, antiviral, and anticancer activities. Here, we explored the potential impact of arctigenin on titanium (Ti) particle-induced osteolysis in vivo. Our data showed that arctigenin significantly suppressed Ti particle-induced osteolysis and prevented bone destruction compared with Ti group. In addition, the number of osteoclasts reduced after treatment with arctigenin in vivo, indicating osteoclastogenesis might be inhibited by arctigenin. Next, bone marrow-derived macrophages were used to examine osteoclast differentiation, bone resorption, and activation of osteoclast-related signaling pathways. The results showed that arctigenin inhibited RANKL-induced osteoclastogenesis without any cytotoxicity and suppressed osteoclastic marker genes expression and hydroxyapatite resorption activity in a dose-dependent manner. Additionally, arctigenin suppressed receptor activator of nuclear factor κΒ (NF-κB) ligand-induced NF-κB activation, concomitant with retarded IκBɑ degradation and inhibition of p65 nuclear translocation, leading to impaired osteoclastogenesis. Collectively, our results suggest that arctigenin is a promising candidate for the treatment of osteoclast-related osteolytic diseases caused by excessive osteoclast formation.

Andrographolide Exerts Pro-Osteogenic Effect by Activation of Wnt/ß-Catenin Signaling Pathway in Vitro.

BACKGROUND/AIMS: Osteoporosis is a metabolic bone disorders that tortures about millions of people worldwide. Recent studies showed that Andrographolide (AP) is a promising natural compound for the treatment of osteoclast-related bone diseases. However, its potential in treatment of osteoporosis has not been fully explored. METHODS: In this study, the effect of AP on osteoblasts metabolism was investigated via the detection of cell proliferation, cell viability, ALP activity, the expression of osteogenic specific genes including runt-related transcription factor 2 (RUNX2), bone sialoprotein (BSP), osteocalcin (OCN), Bone morphogenic protein-2 (BMP2) and Alkaline phosphatase(ALP) for 3, 5 and 7 days respectively. Further exploration of the association of AP with WNT/ß-catenin signaling pathway was performed by examination of the expression of WNT related genes and proteins. RESULTS: Results showed that AP of 4.46 and 8.92 µM, especially 8.92 µM was beneficial to osteogenic differentiation by upregulating ALP activity and expression of osteogenic related genes (P<0.05). Pathway analyses identify canonical WNT/ß-catenin pathway as an important mediator in AP-induced osteogenesis. CONCLUSION: This study indicates that AP exerts its pro-osteogenic potential via activation of the WNT/ß-catenin in osteoblasts and thus may represent a candidate of therapeutic agent for osteoporosis.