Obesity and lipid metabolism play critical roles in the development of osteoporosis. Osteoporosis is a common bone disease that causes significant health and social burdens. It is characterized by reduced bone mass and increased fracture risk. The disease can be primary or secondary, with postmenopausal women, elderly men, and diabetic patients being at high risk. Current treatments focus on promoting osteogenesis and inhibiting osteoclasts, but their effectiveness is limited. The review explores the mechanisms linking lipid metabolism, inflammation, and oxidative stress to osteoporosis. Bone marrow mesenchymal stem cells (BM-MSCs) can differentiate into osteoblasts or adipocytes, with a balance between these processes. Lipids influence this balance through pathways such as PPARγ and Wnt/β-catenin. Excess lipids can impair osteogenesis by increasing inflammation and oxidative stress, which promote osteoclast activity and bone resorption. Obesity reduces antioxidant enzyme activity, leading to oxidative stress and inhibiting osteogenesis. Vitamin D deficiency is also linked to osteoporosis, as it affects lipid metabolism and bone remodeling. Lipid metabolism disorders are common in osteoporosis, particularly in postmenopausal women, diabetic patients, and obese individuals. High triglyceride levels, high cholesterol, and imbalanced lipid profiles negatively affect bone mineral density. Conversely, high-density lipoprotein cholesterol (HDL-C) is beneficial for bone health. Oxidized lipids contribute to inflammation and osteoclast differentiation, while bile acids like ursodeoxycholic acid may help prevent osteoporosis. The review highlights the complex interplay between lipid metabolism, inflammation, and oxidative stress in osteoporosis. Proper lipid regulation, reduced inflammation, and antioxidant support are essential for improving bone mass and treating osteoporosis. The study emphasizes the importance of understanding these mechanisms to develop more effective therapies for osteoporosis.Obesity and lipid metabolism play critical roles in the development of osteoporosis. Osteoporosis is a common bone disease that causes significant health and social burdens. It is characterized by reduced bone mass and increased fracture risk. The disease can be primary or secondary, with postmenopausal women, elderly men, and diabetic patients being at high risk. Current treatments focus on promoting osteogenesis and inhibiting osteoclasts, but their effectiveness is limited. The review explores the mechanisms linking lipid metabolism, inflammation, and oxidative stress to osteoporosis. Bone marrow mesenchymal stem cells (BM-MSCs) can differentiate into osteoblasts or adipocytes, with a balance between these processes. Lipids influence this balance through pathways such as PPARγ and Wnt/β-catenin. Excess lipids can impair osteogenesis by increasing inflammation and oxidative stress, which promote osteoclast activity and bone resorption. Obesity reduces antioxidant enzyme activity, leading to oxidative stress and inhibiting osteogenesis. Vitamin D deficiency is also linked to osteoporosis, as it affects lipid metabolism and bone remodeling. Lipid metabolism disorders are common in osteoporosis, particularly in postmenopausal women, diabetic patients, and obese individuals. High triglyceride levels, high cholesterol, and imbalanced lipid profiles negatively affect bone mineral density. Conversely, high-density lipoprotein cholesterol (HDL-C) is beneficial for bone health. Oxidized lipids contribute to inflammation and osteoclast differentiation, while bile acids like ursodeoxycholic acid may help prevent osteoporosis. The review highlights the complex interplay between lipid metabolism, inflammation, and oxidative stress in osteoporosis. Proper lipid regulation, reduced inflammation, and antioxidant support are essential for improving bone mass and treating osteoporosis. The study emphasizes the importance of understanding these mechanisms to develop more effective therapies for osteoporosis.