There are three types of primary osteoporosis, including idiopathic (adult type), postmenopausal osteoporosis (type I), and senile osteoporosis (type II). The treatment of secondary osteoporosis focuses on the primary cause and is beyond the scope of this article. Once a patient has this disease, he or she will have to take medication and injections for years and years, and will have repeated fractures during treatment. 1. Pathologically speaking, osteoporosis consists of two main aspects, one is the decrease in the number of bone cells, and the other is the decrease in bone matrix (minerals). The best state of treatment for osteoporosis is that the bone cells increase and the bone matrix increases, but after understanding the etiology, this is almost mission impossible. 2. Etiologically, there are two reasons for the decrease in bone cells: the decrease in gonadotropin after aging, the conversion of bone marrow stromal stem cells to adipocytes, and the decrease in differentiation of osteoblast precursor cells; the second is the increase in osteoclast activity, which causes bone cell death. There are also two reasons for the decrease in bone matrix: first, aging and the reduced ability of osteoblasts to secrete bone matrix; second, the enhanced uptake of bone matrix by osteoclasts. To use an analogy, bone cells are like a machine, and osteoporosis is like an aging machine in a factory, which not only has a reduced ability to produce products, but also has an increasing rate of machine obsolescence. To add insult to injury, there is a bad egg called osteoclast that not only destroys the machine but also the product. At this level, the best treatment for osteoporosis is to increase the differentiation of osteoblasts and decrease the activity of osteoclasts, but this is also almost an impossible task after understanding the regulation of osteoblasts. 3. In terms of cellular activity regulation, the regulatory factors of osteoblasts (bone cells) and osteoclasts are mainly various hormones of the body. The main growth-regulating hormones that promote osteoblast differentiation into bone are growth hormones such as glucocorticoids, thymosin, thyroid hormone, insulin, insulin-like growth factor (IGF-1), transforming growth factor-β (TGF-β), etc. Unfortunately, these factors are not available in the body. Unfortunately, the levels of these factors decrease with age and act on various tissue cells throughout the body, making them almost impossible to use clinically. The hormones that inhibit osteoclast activity are mainly sex hormones and calcium-regulating hormones such as estrogen, testosterone, calcitonin, and parathyroid hormone. Unfortunately, these factors also decrease with ageing. Slightly fortunately, these factors can be applied clinically, although with various negative effects. In fact, the current therapeutic strategy is focused on both increasing calcium absorption in the intestine and inhibiting bone resorption by osteoclasts. Without making a difference in osteoblasts, the most critical cell, that is, the machine production capacity is increased, osteoporosis treatment is still an unachievable task. 4. In terms of calcium absorption, many links are needed to truly treat osteoporosis. The calcium content of the current commercially available calcium supplements are basically sufficient, but the necessary active vitamin D3 (1,25-(OH)2 VitaminD3) to complete the intestinal absorption of calcium, otherwise eat more calcium, even the calcium supplements as a meal is also very limited absorption. The 25-position OH of vitamin D3 requires the metabolism of kidney cells in order to be activated, and elderly people have reduced kidney function and limited activation capacity, and limited ability to turn food calcium into blood calcium. Taking a step back, even if blood calcium is sufficient, if bone cells have limited ability to synthesize matrix and cannot turn into bone calcium, it still cannot treat osteoporosis and will only be metabolized. Just like if the production capacity of a machine is limited, even sufficient raw materials are wasted and osteoporosis treatment is still an unachievable task. 5. In terms of inhibiting the activity of osteoclasts, there are two main types of drugs, one is hormonal and the other is diphosphonates. Hormonal drugs include sex hormones and calcium-regulating hormones. Sex hormones (estrogen, testosterone) are the most effective, but unfortunately increase the risk of reproductive cancers and should only be used in special cases. Calcitonin is more effective for pain relief and was widely used in the 1990s and 2000s. The FDA recommends very cautious use for osteoporosis due to the increased risk of cardiovascular disease. Diphosphonates (mainly sodium allantoin phosphate and zolay phosphate) are relatively small molecules with better signaling effects, but require long-term administration. Current studies have found that RANKL signaling plays a key role in osteogenic and osteoblastic activities and can be a therapeutic target. Currently, RANKL modulators are mostly biologics and their efficacy and safety are still under study. It is still unfortunate that even if the osteoclast, the bad guy who destroys the machine and the product, is caught, the capacity will still be low when the aging and scrap rate of the machine is high and osteoporosis treatment becomes an unfinishable task. Therefore, in terms of treatment, it is difficult for the bones that have become osteoporotic to become normal again, and medication only prevents further aggravation of osteoporosis to the maximum extent. 6. Even if osteoporosis treatment is difficult, we can act in two aspects, one is prevention and the other is treatment. In terms of prevention, ① exercise is the best prevention, because exercise will constantly stimulate bone tissue, and bone tissue will not easily lose calcium; ② long-term estrogen replacement therapy will be started within 3 years after menopause, and long-term preventive calcium supplementation will be insisted on to safely and effectively prevent osteoporosis. The aim of treatment is to prevent further aggravation of osteoporosis by ① inhibiting bone resorption (estrogen, sodium allantoin phosphate, etc.); ② increasing calcium absorption (calcium supplements, active VitD, etc.).