The abnormal bone turnover disrupts normal bone architecture and causes bone pain, bone deformity, deafness, osteoarthritis, and pathological fractures [ 2].
The emergence of bone metastases disrupts normal bone homeostasis by perturbing interactions between bone-forming osteoblasts and bone-resorbing osteoclasts [ 2].
The increase in number and/or activity of bone-resorbing osteoclasts could contribute to excessive bone resorption, disrupts the balance between bone resorption and bone formation, and results in the loss of bone.
Paget's disease of bone (PDB) disrupts normal bone architecture and causes pain, deformity, deafness, osteoarthritis, and fractures.
However, some pertinent questions remain: do these two variants increase wnt ligand binding with the Frizzled protein to activate Wnt-β-catenin signaling; and does mis-function of Frzb in chondrocytes directly lead to OA or Frzb modulation of bone shape, disrupting mechanical loading on cartilage and consequently leading to OA?
Instead, they alter the functions of bone-resorbing (osteoclasts) and bone-forming cells (osteoblasts) and hijack signals coming from the bone matrix, thereby disrupting physiological bone remodeling [ 2, 3].
Metastatic bone disease disrupts the normal homeostasis of bone, a dynamic process that involves the coupled and balanced osteoclast-mediated osteolysis and osteogenesis by osteoblasts (Coleman, 2006).
Breast cancers frequently metastasize to bone, where they disrupt normal bone remodeling to cause bone destruction, pain, pathologic fracture, hypercalcemia, and nerve compression [1].
It is often occurs when the blood supply to bone is disrupted.
