Knogleresorption

Knogleresorption, or bone resorption, is the biological process by which mineralized bone tissue is dissolved and minerals are released into the bloodstream. It is a key component of bone remodeling, a lifelong balance between resorption and formation that maintains skeletal strength and mineral homeostasis. Osteoclasts, specialized multinucleated cells, mediate resorption. They attach to the bone surface, secrete hydrogen ions to acidify the resorption lacuna, and release proteolytic enzymes that break down the organic matrix, enabling mineral dissolution. Osteoblasts later refill resorption pits with new bone matrix, completing a remodeling cycle.

Regulation occurs through the RANK/RANKL/osteoprotegerin system, M-CSF, and hormonal signals. Parathyroid hormone and vitamin D stimulate resorption, while estrogen and calcitonin tend to inhibit it. The balance between resorption and formation can be disrupted by aging, endocrine disorders, inflammation, nutrition, and medications.

Clinical relevance: excessive resorption relative to formation leads to reduced bone mass and increased fracture risk, as seen in osteoporosis. Localized resorption occurs in osteolytic metastases or hyperparathyroidism. Conditions such as Paget disease involve dysregulated remodeling with phases of resorption and formation.

Assessment may use bone turnover markers such as CTX and P1NP, alongside imaging like DXA to measure bone density and detect structural changes. Management depends on underlying causes and may include antiresorptive therapies such as bisphosphonates or denosumab, along with lifestyle measures. Potential adverse effects of antiresorptives include hypocalcemia, osteonecrosis of the jaw, and atypical femoral fractures.