Osteoblasts synthesize and secrete the bone matrix, which later mineralizes to form new bone tissue. Their primary function is essential for bone growth and repair.

Osteocytes are mature bone cells that reside in lacunae and help maintain the bone matrix. They also communicate via canaliculi to coordinate bone remodeling.

Osteoclasts break down bone tissue through the process of bone resorption. This function is vital for the continuous remodeling and repair of bone.

Osteoblasts are responsible for creating new bone by secreting the bone matrix and initiating its mineralization. Their activity is essential for growth, repair, and overall maintenance of the skeletal system.

Bone remodeling is the continuous process where old bone is resorbed and new bone is formed. This process is critical for repairing micro-damages and maintaining the strength and integrity of bones.

Osteocytes use their extensive network of canaliculi to sense mechanical stress within the bone. This mechanosensory function helps regulate bone remodeling in response to changes in mechanical load.

Canaliculi are tiny channels that connect the lacunae where osteocytes reside. They allow for the exchange of nutrients and signaling molecules between cells, essential for coordinated bone maintenance.

Osteoclasts originate from hematopoietic stem cells, setting them apart from osteoblasts that come from mesenchymal stem cells. This difference in origin is key to their function in bone resorption.

Osteoclasts are specialized in breaking down bone tissue, a process known as bone resorption. This activity is fundamental to bone remodeling and maintaining calcium balance in the body.

Osteoblasts synthesize new bone matrix and are the key players in forming new bone tissue during remodeling. Their activity follows osteoclast-mediated resorption to ensure balanced bone renewal.

Collagen type I is the primary protein component of the bone matrix produced by osteoblasts. It provides the structural framework necessary for mineral deposition and overall bone strength.

Osteocytes are central to the regulation of bone remodeling by sensing mechanical changes and communicating with both osteoblasts and osteoclasts. Their signaling ensures that bone formation and resorption are well balanced.

Canaliculi are tiny channels that connect osteocyte lacunae, allowing for the transfer of nutrients and signaling molecules. This network is crucial for maintaining bone health and proper remodeling.

RUNX2 is a key transcription factor that drives the differentiation of mesenchymal stem cells into osteoblasts. Its expression is essential for proper bone formation and skeletal development.

Parathyroid hormone (PTH) helps regulate blood calcium levels by indirectly stimulating osteoclast activity through osteoblast signaling. This results in increased bone resorption, which releases calcium into the bloodstream.

The RANK/RANKL/OPG system is pivotal in regulating bone resorption. RANKL promotes osteoclast differentiation by binding to RANK, while OPG, acting as a decoy, prevents this interaction and thus regulates osteoclast activity.

Osteocytes communicate through canaliculi to sense mechanical stress and coordinate remodeling. Impaired communication disrupts this feedback loop, reducing the bone's ability to adapt to stress and potentially leading to weakened bone structure.

Osteoporosis occurs when bone resorption outpaces bone formation, leading to reduced bone mass. An imbalance that favors osteoclast activity results in excessive bone loss and increased susceptibility to fractures.

The Wnt/β-catenin signaling pathway is fundamental to osteoblast differentiation and bone formation. Many bone anabolic therapies aim to modulate this pathway to enhance bone mass and strength.

Mechanical forces are primarily detected by osteocytes, which use their network to sense strain and stress. This information is then relayed to osteoblasts and osteoclasts to adjust bone formation and resorption accordingly.