Bone remodeling

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Simplified illustration of the process of bone tissue remodeling. The multinucleated osteoclasts break down the bone matrix and the osteoblasts rebuild it via the intermediate stage of the osteoid .

The bone remodeling ( English bone (re) modeling , bone tissue (re) modeling ' ) is a continuous process, in the course of which old bone tissue is broken down by osteoclasts and formed anew by osteoblasts at the same (remodeling) or another (modeling) location. About 3% of the cortical bone and 25% of the trabecular bone are remodeled in this way every year; within 7 to 10 years, the equivalent of the total human bone mass is broken down and newly synthesized .


Degradation of bone substance when the foot is immobilized after a fracture of the 5th metatarsal bone : on the left the image immediately after the fracture, on the right approx. 5 weeks later after immobilization.

Bone remodeling serves to maintain a stable and functional skeletal system that would quickly wear out without this repair mechanism. An essential mechanism is to repair structural damage ( micro cracks ) that arise from everyday movements and stress, while at the same time adapting the micro- architecture to the stress. The adaptation of the bone to its load was first demonstrated by Julius Wolff using the example of cancellous bone architecture and is the subject of Wolff's law of 1892.

In the same way, the bone remodeling also takes over the restoration of the fully functional bone at the end of the fracture healing . The callus made of braided bone is gradually replaced by lamellar bones that are adapted to the direction of loading .

Since the bones, in addition to their function in the musculoskeletal system, represent the body's largest reservoir for calcium and phosphate , the demineralization or breakdown of bone tissue is also of great importance for calcium homeostasis : By increasing the osteoclast activity that takes place in the context of bone remodeling in the event of an acute calcium deficiency, calcium can be made available quickly without losing bone substance in the long term.


In the course of remodeling , osteoclasts “dig” themselves into the bone matrix with the help of various lytic enzymes ( Cathepsin K , MMP-3 and 9 , ALP ) and form pits on the surface of the trabeculae ( Howship's lacunae ) or drill channels inside the cortex. Following this resorption, osteoblasts secrete new collagenous skeletal skeleton ( osteoid ) in large fields of at least 50 cells , which gradually calcifies and thus forms new bone matrix. Some of the osteoblasts are enclosed by the mineralizing matrix and later differentiate into osteocytes .


At the center of the regulation of the bone remodeling are the osteocytes , which run through the entire bone tissue with their cell processes in the canaliculi and exchange information with one another via gap junctions : They record the mechanical stresses via shear forces on their cell surface, which arise when extracellular fluid is deformed when the bone is deformed is pressed through the lacuno-canalicular system . The radially stretched fine threads with which the cell membranes are attached to the walls of the canaliculi could also have a mechanosensory function. In addition, osteocytes detect microscopic damage to the bone tissue in their vicinity. They integrate all this information with chemical signals from the local environment and the endocrine system . Osteoblasts sometimes play a synergistic role in regulation. Osteocytes can have an effect on bone formation and breakdown via the following mechanisms:

  • Secretion of sclerostin , which inhibits the proliferation and differentiation of progenitor cells into osteoblasts as well as osteoblast activity (released when there is insufficient mechanical stress; parathyroid hormone inhibits secretion)
  • Secretion of M-CSF , which promotes the proliferation of osteoclast precursor cells
  • Expression of the membrane protein RANKL , whose binding to RANK , a membrane receptor of the osteoclasts, is a prerequisite for their activation (parathyroid hormone promotes expression)
  • Secretion of osteoprotegerin which, as a decoy receptor, occupies the RANKL and makes it ineffective

In addition, the osteocytes can stimulate phosphate excretion in the kidneys via the endocrine secretion of FGF23 . The local osteocytes react to microscopic damage to the bone tissue with apoptosis , while the surrounding osteocytes increasingly express RANKL, so that the damaged area is quickly cleared of osteoclasts. The osteoblasts coordinate their activity with one another via gap junctions. The mechanisms by which osteoclast activity is coupled to osteoblast activity are poorly understood.

Parathyroid hormone is used to provide acute calcium in the context of calcium homeostasis . Chronically increased PTH levels initially cause increased bone turnover and later the loss of bone substance, since the RANKL-mediated osteoclast activation outweighs the increased osteoblast activity resulting from the reduced inhibition by sclerostin. In the case of intermittently elevated hormone levels, such as can be brought about by daily injections, the main effect of PTH, on the other hand, is the inhibition of sclerostin secretion, which can be used therapeutically to gain bone substance.

Calcitriol (activated vitamin D) promotes the differentiation of osteoclasts from precursor cells on the one hand and the activity of the osteoblasts on the other. Overall, it mostly causes the build-up of bone substance, of which the increase in the calcium supply through its effects on the intestines and kidneys has the greater share.

Estrogens and androgens inhibit the apoptosis of osteocytes, they also inhibit the formation and activation and promote the apoptosis of osteoclasts. The protection against bone loss mediated in this way diminishes with menopause , which explains the increased risk of osteoporosis in older women compared to men of the same age.


  • Renate Lüllmann-Rauch: pocket textbook histology . 5th edition. Thieme, Stuttgart 2015, ISBN 978-3-13-129245-2 , Chapter 8.4 Bones .
  • AG Porras, SD Holland, BJ Gertz: Pharmacokinetics of alendronate. In: Clinical Pharmacokinetics Volume 36, Number 5, May 1999, pp. 315-328, ISSN  0312-5963 . PMID 10384857 . (Review).
  • MM Cohen: The new bone biology: pathologic, molecular, and clinical correlates. In: American journal of medical genetics. Part A Volume 140, Number 23, December 2006, pp. 2646-2706, ISSN  1552-4825 . doi: 10.1002 / ajmg.a.31368 . PMID 17103447 . (Review).
  • GA Rodan, TJ Martin: Role of osteoblasts in hormonal control of bone resorption - a hypothesis. In: Calcified tissue international , Volume 33, Number 4, 1981, pp. 349-351, PMID 6271355 , ISSN  0171-967X .

Individual evidence

  1. Bone Health and Osteoporosis. (PDF; 25 MB) US Department of Health and Human Services under the general direction of the Office of the Surgeon General, 2004, p. 22. According to: F. Rauch, FH Glorieux: Osteogenesis imperfecta. In: Lancet Volume 363, Number 9418, April 2004, pp. 1377-1385, ISSN  1474-547X . doi: 10.1016 / S0140-6736 (04) 16051-0 . PMID 15110498 . (Review).
  2. P. Reuter: Der Große Reuter: Springer universal dictionary medicine, pharmacology and dentistry. German-English . Birkhäuser, 2005, ISBN 3-540-25104-9 , p. 742,