Osteoporosis is a skeletal disorder characterized by compromised bone strength resulting in a predisposition to fracture. Osteoporosis-related fractures can lead to pain, disability, and increased healthcare costs. We aimed to explore the guidelines and criteria for selecting medications for osteoporosis.Current Concepts: Osteoporosis medications can be classified mainly as antiresorptive drugs and osteogenesis promoters. The former includes selective estrogen receptor modulators, bisphosphonates, and receptor activators of nuclear factor kappa-B ligand inhibitors, e.g., denosumab. The latter includes human parathyroid hormone, e.g., teriparatide, and the dual-action agent, romosozumab. Selective estrogen receptor modulators (raloxifene or bazedoxifene) can be considered suitable for younger postmenopausal women with low spine bone mineral density. It also can be used for patients with low glomerular filtration rates due to low excretion in urine and patients who need dental care. Bisphosphonate has a residual effect on bone; therefore, osteonecrosis of the jaw and atypical fractures should be considered as side effects for its long-term use. Presently, denosumab is the most potent antiresorptive agent, but its favorable skeletal effects can be reversed quickly after its cessation. Therefore, subsequent antiresorptive treatment is mandatory. Romosozumab is a dual-action agent that simultaneously stimulates bone formation and inhibits bone resorption. It also needs a subsequent antiresorptive treatment.Discussion and Conclusion: Tailored treatment is needed in a patient with osteoporosis. Even in the case of the same bone density, the risk of fracture and the fracture sites differ depending on age. After setting an achievable goal of bone density within a suitable period, the appropriate medication should be selected.

A ~20 kDa heat-labile toxin (BFT) produced by enterotoxigenic B. fragilis induces chemokine responses that are associated with mucosal inflammation. In the present study, we assessed whether the activation of mitogen-activated protein kinase (MAPK) affects the levels of IL-8 and MCP-1 produced by BFT stimulation in human epithelial HT-29 cells. Human intestinal epithelial HT-29 cell lines were incubated with purified BFT. MAPK and AP-1 in HT-29 cells were measured by Western blot and luciferase assay, respectively. The expression of chemokines such as IL-8 and MCP-1 were determined by quantitative RT-PCR, ELISA, and luciferase assay. BFT stimulation activated MAPK such as ERK1/2 and p38 in HT-29 cells. Treatment with MAPK inhibitors attenuated BFT-induced expression of IL-8 and MCP-1. Transfection with mutant genes for Ras or c-Jun did not only suppressed AP-1 reporter genes, but also inhibited BFT-induced expression of IL-8 and MCP-1 reporter genes. These results suggest that Ras and MAPK cascade may act as the upstream signaling for the activation of AP-1, which induce chemokine expression in BFT-stimulated intestinal epithelial cells.
Bacteroides fragilis* ; Bacteroides* ; Blotting, Western ; Chemokines ; Enterotoxins* ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells* ; Genes, Reporter ; HT29 Cells ; Humans* ; Inflammation ; Interleukin-8 ; Luciferases ; Phosphotransferases* ; Protein Kinases ; Transcription Factor AP-1 ; Transfection