Knogleturnover

Knogleturnover, or bone turnover, is the ongoing process in which old bone is resorbed by osteoclasts and new bone is formed by osteoblasts. This remodeling keeps skeletal strength, helps regulate mineral balance (calcium and phosphate), and repairs microdamage from daily loading. Remodeling occurs in localized units where a site of old bone is removed and replaced with new tissue, a cycle that maintains bone mass over time.

Key cellular players are osteoclasts, osteoblasts, and osteocytes. Osteoclasts create resorption pits; osteoblasts fill these pits with osteoid that later mineralizes. Osteocytes, embedded in bone, regulate turnover in response to mechanical strain and hormonal signals. The process is tightly coupled by signaling pathways, notably RANKL-RANK interactions that promote osteoclast formation, with osteoprotegerin (OPG) acting as a decoy receptor. Wnt/β-catenin signaling promotes osteoblast activity, and its inhibitor sclerostin modulates formation in response to load.

Turnover is regulated by hormones and nutrients. Parathyroid hormone increases remodeling in response to low calcium, while estrogen deficiency accelerates turnover, particularly in postmenopausal women. Vitamin D supports mineralization and calcium balance; calcitonin can suppress resorption in some contexts.

Turnover markers in blood or urine, such as the resorption marker CTX (C-terminal telopeptide) and the formation marker P1NP (procollagen type I N-terminal propeptide), reflect dynamic remodeling and are used to monitor therapy. Imaging with DXA measures bone density, not turnover itself, but turnover contributes to observed changes over time.

Clinical relevance: altered knogleturnover is central to osteoporosis, osteomalacia, Paget’s disease, and metastatic lesions. Treatments aim to rebalance remodeling: antiresorptives (bisphosphonates, denosumab) reduce resorption, while anabolic agents (teriparatide, romosozumab) stimulate formation.