In many inflammatory conditions, such as rheumatoid arthritis (RA), psoriatic arthritis, and periodontitis, bone degradation is a substantial contributor to morbidity and disability. [1][2][3] Patients with RA have a considerably worse quality of life and an increased risk of passing away.Bone tissues are constantly renewing, and this provides a mechanism for adjusting the skeleton to changing biomechanical stresses and repairing bone damage. Bone remodeling is dependent on maintaining a delicate equilibrium between the activities of 2 primary cell types: osteoclasts, which are responsible for bone resorption, and osteoblasts/osteocytes, which are responsible for bone formation. There is communication between these cells, which allows them to coordinately pair their activities and guarantee that osteoclast-generated resorption lacunae are filled with new bone formed by osteoblasts. This is necessary in order to keep bone homeostasis during the process of bone remodeling. [4][5][6] Numerous pharmacological and targeted treatments have been researched in patients with RA, and a growing number of them have been given the go-ahead for use in clinical settings. Recent research has looked at their impacts on bone mineral density (BMD) and bone metabolism, both of which may have an influence on clinical symptoms and the overall quality of life of RA patients.Because structural damages play a vital role in diagnostic processes, the diagnosis of bone erosions in RA is important. Furthermore, because bone erosions are symptomatic of a bad result, they impact the treatment decision. 7 This review presents an overview of the effects of disease-modifying antirheumatic drugs (DMARDs) on bone homeostasis in patients with RA.