Brucellosis is a common zoonosis, and osteoarthritis is the most common chronic complication of brucellosis. Development of brucellosis osteoarthritis involves multiple organs, tissues, and cells. grows and multiplies in intrinsic cells of the skeleton, including osteoblasts, osteocyte and osteoclasts, which results in sustained release of bacteria that leads to exacerbation of the immune response. Concurrently, activation of the immune system caused by invasion with may affect the dynamic balance of the skeleton. A variety of and models have been employed to study osteoarthritis, such as using bone marrow-derived macrophages to establish cell models and mice to develop animal models of osteoarthritis. However, limited studies on the molecular pathological mechanisms of osteoarthritis have been performed and inadequate animal models have been developed due to the challenging parameters of research. This paper reviews recent advances in the clinical features, molecular pathological mechanisms, and animal models of osteoarticular infections. This review underscores the complexity of the pathogenesis of osteoarticular infections and highlights inflammation as a contributing factor to bone loss caused by . Additionally, the significant proliferation of in skeletal resident cells also is an important factor leading to bone loss. A deeper understanding of the molecular pathological mechanism of osteoarthrosis and their animal models could provide robust support for the prevention and treatment of osteoarticular disease.