Fluoride Fluoride ions are highly electronegative, displacing the hydroxyl groups of apatite, and the fluorapatite formed in bone is not easily dissolved and absorbed, resulting in increased bone density and hardness. Clinically, it has been reported (31) that sodium fluoride significantly reduces the incidence of vertebral fractures (relative risk 0.3), with the common side effect of bone irritation symptoms, and the commonly used dosage forms are sodium fluoride, glutamine monofluorophosphate plus calcium. It has also been reported that fluorine-induced bone formation is non-physiological, with a crystalline composition different from the original bone, irregular arrangement, abnormal proliferation of uncalcified bone-like tissue, low bone strength, and brittle quality, which instead increases extra-vertebral fractures. Raloxifene is an active drug with both estrogen agonism and estrogen antagonism, the so-called selective estrogen receptor modulator. It has estrogenic properties in bone, but antagonist effects in the breast and endometrium. It has been shown (33) that raloxifene reduces bone resorption, increases lumbar spine and greater trochanter bone density by 2.4%, decreases serum LDL cholesterol concentrations, and has no side effect of stimulating endometrial growth. Parathyroid hormone (PTH), plays an important role in maintaining the body’s calcium and phosphorus balance through bone calcium mobilization, intestinal calcium absorption and urinary phosphorus excretion. (1) Promotes increased osteoclast activity, resulting in increased bone resorption and higher blood calcium; (2) Promotes VitD activation, resulting in increased bone 1 ,25-(OH)2D3 production, indirectly promoting intestinal calcium absorption and reducing urinary calcium excretion, with high direct bone formation and bone anabolic effects. pTH is effective in low turnover type II osteoporosis. A 13% increase in lumbar spine BMD and a 3% increase in greater trochanter BMD and a significant decrease in the incidence of vertebral deformities have been reported (34) with PTH for 3 years, but the effect on fracture incidence is unclear. Vitk2 increases the concentration of osteocalcin, a VitK-dependent non-collagenous protein that is an indicator of bone formation, and has the effect of stimulating osteoblasts to promote bone formation. takashi found that Vitk2 caused apoptosis of osteoclasts, which inhibited bone resorption. However, Vitk has factors related to increased blood clotting and should be used with caution in patients with a hypercoagulable state. There are many other drugs for the treatment of osteoporosis, such as calcium-enhancing flavonoids, protein-synthesizing hormones, Eprafon, and sequential treatment regimens (ADRF), but in general, the effects are not very satisfactory, so I will not repeat them here.