Rheumatic diseases can cause multi-system and multi-organ functional damage, and in recent years, the prognosis of patients has been significantly improved with the improvement of the diagnosis and treatment of the primary disease. However, secondary osteoporosis, especially glucocorticoid-induced osteoporosis (GIOP), has become an increasingly important issue affecting the quality of life of patients. How to correctly recognize GIOP and how to make early diagnosis and standardized treatment have not yet attracted sufficient attention in clinical practice. The purpose of this article is to raise awareness of GIOP, to carry out early and effective prevention and treatment, and to avoid as much as possible the emergence of GIOP and serious consequences such as fractures. 1. Great importance should be attached to the problem of GIOP in patients with rheumatic diseases. Over the years, people have gained a great understanding of the etiology, pathogenesis and treatment of common rheumatic diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and dry syndrome (SS), but the high prevalence of osteoporosis in these patients has not attracted clinical attention. Glucocorticoids are widely used in the treatment of many rheumatic diseases, and osteoporosis is one of their most serious side effects. giOP is the most common of the drug-induced osteoporosis. a placebo-controlled study conducted by Mckenzie et al. in 2000 demonstrated that the application of small doses of glucocorticoids (equivalent to 7.5 mg/d of prednisone) can lead to a decrease in bone mineral density (BMD). Most scholars now believe that even physiological doses of glucocorticoids can cause bone loss and that there is no such thing as a safe dose of glucocorticoids; the higher the dose, the more bone loss. It is important to note that the effect of glucocorticoids on BMD is dose- and time-dependent, with bone loss being most pronounced in the first year of treatment (12%-20%) and approximately 3% per year thereafter, with trabecular bone being more significantly affected than cortical bone. A study by Angeli A et al. showed that 37% of postmenopausal women treated with glucocorticoids had asymptomatic vertebral fractures [3]. Therefore, the presence or absence of complaints such as pain should not be the only focus in this group of patients, but changes in BMD should be closely followed. the study by Kaji H et al. is of more interest to us, namely, the higher risk of fracture in GIOP compared to postmenopausal patients with primary osteoporosis at the same BMD [4]. Another issue that deserves to be explored is that some patients with rheumatic diseases develop reduced BMD or osteoporosis at the beginning of the disease or before the use of glucocorticoids due to abnormal autoimmune function and the production of multiple inflammatory factors in the organism [5, 6]. Therefore, osteoporosis should be prevented and treated at the beginning of the disease. For patients who already have osteoporosis, it is more important to strengthen prevention and control measures when applying glucocorticoids and to closely monitor the changes in bone mass of patients. 2. Timely evaluation of the risk of osteoporosis occurrence is a prerequisite for proper prevention and treatment of GIOP. 2.1 Pay attention to the high-risk group of osteoporosis: Rheumatology has made many breakthroughs in recent years in pathogenesis, early diagnosis and standardized treatment, which have led to significant improvement in the prognosis of the disease. However, over the years, people have always focused mainly on the diagnosis and treatment of the disease itself, while not enough attention has been paid to the study of GIOP and other related complications, which has considerably affected the quality of life of patients. The development of rheumatology today has required rheumatologists to pay sufficient attention to the diagnosis and treatment of complications such as GIOP, to promptly select sensitive methods to test people at high risk of developing GIOP, and to give targeted treatment according to the results to maximize the prevention of osteoporosis and possible fractures and improve the quality of life of patients. In patients with rheumatic diseases, in addition to the drug factor of receiving glucocorticoid therapy, other factors that predispose to osteoporosis include gender, age, previous history of fracture and trauma, etc. Therefore, in addition to the dose and duration of glucocorticosteroid application, other risk factors for osteoporosis should be evaluated in clinical practice. 2.2 Timing of BMD testing: At present, people do not pay enough attention to the importance of BMD testing, and there is no uniform understanding of the timing of BMD testing and the instruments to be used for testing. Some domestic and international expert consensus suggests that in order to identify patients with osteoporosis, a variety of bone metabolism indicators such as serum alkaline phosphatase, osteocalcin and plasma antitartaric acid phosphatase can be tested in the clinical setting. However, the universal indicators for diagnosing osteoporosis remain the occurrence of fragility fractures and/or reduced BMD (although BMD reflects only 70% of bone strength, there is a lack of means to directly measure bone strength). Methods for detecting BMD include dual-energy x-ray absorptiometry, ultrasonography, or quantitative computed tomography, with dual-energy x-ray absorptiometry being the currently internationally accepted method for detecting BMD. Regarding the timing of BMD testing, we should refer to the American College of Rheumatology (ACR) guidelines for osteoporosis, which state that BMD testing is required when patients are to be treated with glucocorticoids (equivalent to prednisone ≥ 5 mg/day) for more than 3 months or when they are to be treated with long-term glucocorticoids, and should be reviewed every 6-12 months for the purpose of determining the presence or absence of osteoporosis and providing a baseline value for monitoring BMD after glucocorticoid use. The purpose is to determine the presence of osteoporosis and to provide a baseline value for monitoring changes in BMD after glucocorticoid use. 3. The treatment of GIOP is not yet standardized. The treatment of GIOP is an important topic that rheumatologists often face, and there are still some misconceptions in this regard in the past. 3.1 Insufficient understanding of the timing of the treatment of GIOP: The ACR recommendations on the prevention and treatment of GIOP suggest that even the application of small doses of glucocorticoids can lead to bone loss or osteoporosis [7]. 2007 European League Against Rheumatism EULAR Expert Recommendations for Glucocorticoid Therapy in Rheumatic Diseases states that those with prednisone doses ≥7.5 mg/day for more than 3 months should be supplemented with Calcium and vitamin D, and measures including improvement of lifestyle habits, appropriate weight-bearing physical activity, smoking cessation and avoidance of alcohol abuse should be given. The decision to add bisphosphonates should be based on the presence of risk factors for GIOP, including reduced bone mineral density, female age, advanced age, postmenopause, and low body mass index, with patients on higher glucocorticoid doses and with reduced bone mineral density being more likely to develop fractures. 3.2 Overemphasis on the importance of calcium supplementation at the expense of active vitamin D3: As early as 1996, Buckley et al. demonstrated that the combination of calcium and vitamin D prevented bone loss in RA patients treated with low-dose glucocorticoids, but that calcium alone did not prevent bone loss in patients with GIOP. A recent meta-analysis further showed that active vitamin D3 may prevent bone loss and reduce the incidence of vertebral fractures [but blood and urine calcium levels need to be monitored during treatment and the dose adjusted at any time. These findings suggest that calcium combined with active vitamin D3 therapy is effective in preventing and treating GIOP caused by low-dose glucocorticoids. However, there are some misconceptions about the relationship between calcium supplementation and GIOP, one of which is that GIOP is equivalent to calcium deficiency and that glucocorticoids only cause osteoporosis through calcium loss and that adequate calcium supplementation can prevent osteoporosis; another is that blood calcium is used to determine whether a patient has osteoporosis. It should be noted that normal blood calcium is not the same as normal calcium in the bones, and some patients with GIOP may still have normal blood calcium levels even if they have a severe fracture. Therefore, GIOP should not be judged based on blood calcium levels, and BMD testing should be emphasized. In addition, GIOP is also affected by age, low body weight, low sex hormones, smoking and excessive alcohol consumption, excessive coffee and carbonated beverages, lack of physical activity, lack of vitamin D in the diet (low light exposure or low intake), combined diseases affecting bone metabolism (such as diabetes, thyroid and parathyroid diseases, etc.) and the application of other drugs affecting bone metabolism (such as immunosuppressive drugs, etc.). GIOP should be treated in a comprehensive manner, and the rational application of active vitamin D3 and bisphosphonates should be emphasized, with the aim of increasing bone mass, enhancing bone strength and preventing fractures. 3.3 The need for treatment such as anti-bone resorption drugs should be fully recognized. A large number of studies have shown that bisphosphonates can effectively prevent and treat GIOP and reduce the risk of fracture. For example, alendronate, pamidronate and risedronate can increase the BMD of proximal femur and spine, and alendronate and risedronate can reduce the risk of vertebral fracture, so the above drugs can be used as the first-line drugs for the prevention and treatment of GIOP, and should be used according to the guidelines for patients who need long-term application of glucocorticoids and reduced BMD. The role of calcitonin in the treatment of GIOP is controversial, and it has been suggested that calcitonin increases spinal BMD in patients on long-term glucocorticoids, but does not increase hip bone mass or reduce the risk of vertebral fractures diagnosed by imaging. The results showed a 1.75% increase in lumbar BMD but a 3.76% decrease in femoral neck BMD in the calcitonin group; however, the bisphosphonate group showed a 4.34% and 2.52% increase in lumbar and femoral neck BMD, respectively. Most expert consensus currently includes calcitriol as a second-line agent for patients who are contraindicated to bisphosphonates or who present with significant bone pain. Other current treatments for GIOP include sex hormone replacement therapy (HRT) and parathyroid hormone (PTH1-34), but large prospective controlled studies are lacking to confirm their positive effects on increasing BMD and reducing fracture risk. Recently, in order to reduce the gastrointestinal adverse effects of bisphosphonates and to reduce the number of doses, several new drugs for the treatment of primary osteoporosis have been used abroad or have entered clinical trials, including intravenous ibandronate (a nitrogenous bisphosphonate that inhibits osteoclast-mediated bone resorption), Zoledronic acid (a third-generation bisphosphonate that inhibits pyrophosphate synthetase activity) and Denosumab (an anti-human IgG2 monoclonal antibody that inhibits osteoclast differentiation with high affinity for RANKL), which will also provide additional approaches for the treatment of GIOP. In conclusion, GIOP has become a topic of great concern in the field of rheumatology, and the importance of the diagnosis and treatment of GIOP will benefit many rheumatology patients, and the correct understanding of the characteristics of GIOP and mastering the principles of standardized treatment is the key.