Osteocytes, embedded within the mineralized bone matrix, are increasingly recognized as key regulators of bone remodeling in response to mechanical loading. Unlike osteoblasts, which form bone matrix, osteocytes detect mechanical strain and transmit biochemical signals that influence bone formation and resorption. They are highly interconnected and have dendritic processes that extend into canaliculi, allowing them to communicate with other bone cells and the bone surface. Osteocytes are thought to be the primary cells responsible for sensing mechanical strain and orchestrating bone remodeling. Recent studies show that osteocytes are essential for maintaining bone mass under normal loading conditions but may trigger resorption in the absence of load. The Wnt/β-catenin signaling pathway plays a critical role in osteocyte and osteoblast function. This pathway is involved in bone formation, differentiation, and the regulation of bone mass. Osteocytes use this pathway to transmit mechanical signals to the bone surface, while osteoblasts rely on it for differentiation and matrix synthesis. Emerging evidence suggests that the Wnt/β-catenin pathway in osteocytes may be activated by crosstalk with the prostaglandin pathway in response to mechanical loading, leading to reduced expression of negative regulators like Sost and Dkk1. Osteocytes are not merely inactive cells but are highly dynamic, capable of extending and retracting dendritic processes and undergoing deformation in response to mechanical strain. They are also involved in mechanotransduction, with evidence suggesting that cilia may play a role in bone cell mechanosensation. However, the exact mechanisms by which osteocytes sense and transmit mechanical signals remain under investigation. The Wnt/β-catenin pathway is also involved in regulating osteocyte apoptosis. Increased activity of this pathway is associated with reduced apoptosis, and studies have shown that mechanical loading can protect osteocytes from dexamethasone-induced apoptosis. This protective effect is partially mediated through interactions with prostaglandin E2 (PGE2) and the β-catenin signaling pathway. The Wnt/β-catenin pathway also interacts with other signaling pathways, such as the prostaglandin pathway, in response to mechanical loading. These interactions are crucial for the proper regulation of bone remodeling and the maintenance of bone mass. The role of the Wnt/β-catenin pathway in osteocyte biology is increasingly recognized, and further research is needed to fully understand the complex mechanisms by which osteocytes respond to mechanical loading and translate these signals into biochemical responses that regulate bone formation and resorption.Osteocytes, embedded within the mineralized bone matrix, are increasingly recognized as key regulators of bone remodeling in response to mechanical loading. Unlike osteoblasts, which form bone matrix, osteocytes detect mechanical strain and transmit biochemical signals that influence bone formation and resorption. They are highly interconnected and have dendritic processes that extend into canaliculi, allowing them to communicate with other bone cells and the bone surface. Osteocytes are thought to be the primary cells responsible for sensing mechanical strain and orchestrating bone remodeling. Recent studies show that osteocytes are essential for maintaining bone mass under normal loading conditions but may trigger resorption in the absence of load. The Wnt/β-catenin signaling pathway plays a critical role in osteocyte and osteoblast function. This pathway is involved in bone formation, differentiation, and the regulation of bone mass. Osteocytes use this pathway to transmit mechanical signals to the bone surface, while osteoblasts rely on it for differentiation and matrix synthesis. Emerging evidence suggests that the Wnt/β-catenin pathway in osteocytes may be activated by crosstalk with the prostaglandin pathway in response to mechanical loading, leading to reduced expression of negative regulators like Sost and Dkk1. Osteocytes are not merely inactive cells but are highly dynamic, capable of extending and retracting dendritic processes and undergoing deformation in response to mechanical strain. They are also involved in mechanotransduction, with evidence suggesting that cilia may play a role in bone cell mechanosensation. However, the exact mechanisms by which osteocytes sense and transmit mechanical signals remain under investigation. The Wnt/β-catenin pathway is also involved in regulating osteocyte apoptosis. Increased activity of this pathway is associated with reduced apoptosis, and studies have shown that mechanical loading can protect osteocytes from dexamethasone-induced apoptosis. This protective effect is partially mediated through interactions with prostaglandin E2 (PGE2) and the β-catenin signaling pathway. The Wnt/β-catenin pathway also interacts with other signaling pathways, such as the prostaglandin pathway, in response to mechanical loading. These interactions are crucial for the proper regulation of bone remodeling and the maintenance of bone mass. The role of the Wnt/β-catenin pathway in osteocyte biology is increasingly recognized, and further research is needed to fully understand the complex mechanisms by which osteocytes respond to mechanical loading and translate these signals into biochemical responses that regulate bone formation and resorption.