Introduction: Pharmacological options to address the imbalance between bone resorption and accrual in osteoporosis include anti-resorptive and osteoanabolic agents. Unique biologic pathways such as the Wnt/β-catenin pathway have been targeted in the quest for new emerging therapeutic strategies.
Areas covered: This review provides an overview of existing pharmacotherapy for osteoporosis in women and explore state-of–the-art and emerging therapies to prevent bone loss, with an emphasis on the mechanism of action, indications and side effects.
Expert opinion: Bisphosphonates appear to be a reliable and cost-effective option, whereas denosumab has introduced a simpler dosing regimen and may achieve a linear increase in bone mineral density (BMD) with no plateau being observed, along with continuous anti-fracture efficacy. Abaloparatide, a parathyroid-hormone-related peptide (PTHrP)-analogue, approved by the FDA in April 2017, constitutes the first new anabolic osteoporosis drug in the US for nearly 15 years and has also proven its anti-fracture efficacy. Romosozumab, a sclerostin inhibitor, which induces bone formation and suppresses bone resorption, has also been developed and shown a significant reduction in fracture incidence; however, concerns have arisen with regard to increased cardiovascular risk. 相似文献
Background: Osteocytic sclerostin inhibits bone formation, and its expression is stimulated by tumor necrosis factor (TNF)‐α. This study investigates sclerostin and TNF‐α expression in rats with diabetes mellitus (DM) and periodontitis. Methods: Rats were divided into control (C), periodontitis (P), and DM + periodontitis (DP) groups. After induction of DM by streptozotocin, periodontitis was induced by ligature. At day 0 (control) and at days 3 and 20 after induction of periodontitis, alveolar bone, osteoclasts, osteoid area, and TNF‐α and sclerostin expression were evaluated. Results: The distance between the cemento‐enamel junction and the alveolar bone crest of the DP group was longer than that of the P group at day 20 after induction of periodontitis, but the number of osteoclasts was not different. Osteoid area decreased in both the P and DP groups by day 3, but whereas sustained osteoid suppression was observed in the DP group at day 20, osteoid formation was increased in the P group. The number of sclerostin‐positive osteocytes increased in both groups at day 3, but the increased number of sclerostin‐positive osteocytes was maintained only in the DP group through day 20. The number of TNF‐α–positive cells increased more in the DP group than in the P group. Conclusions: Enhanced alveolar bone loss, suppressed bone formation, and prevalent TNF‐α expression were characteristic of the DP group compared with the P group. Suppressed bone formation in the DP group was observed simultaneously with increased sclerostin and TNF‐α expression. These results suggest that upregulated osteocytic sclerostin expression in periodontitis accompanied by DM may play a role in suppressed bone formation. 相似文献
In cross-sectional studies, vitamin D deficiency is frequent in spondyloarthritic patients and associated with increased spondyloarthritis (SpA) activity and structural damage. Experimental studies also show that vitamin D interferes with molecular pathways critically involved in SpA, especially regarding entheseal inflammation and ossification (involving cytokines such as IL-23 and sclerostin). Vitamin D deficiency might also affect the course of the disease through periodontal and gut inflammation, leading to increased functional impairment. Therefore, Vitamin D receptor selective agonists could represent a promising therapeutic pathway in this pathology. Randomised-controlled intervention studies are required in order to further elucidate complex relationships between vitamin D deficiency and SpA. 相似文献