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Diagnostic Imaging · Musculoskeletal System

Bone remodeling

Bone turnover

Bone remodeling is a continuous physiological process of skeletal renewal in which old bone is resorbed and replaced by new bone. In a healthy organism, this cycle takes 3–4 months and is in strict balance, ensuring the mechanical strength of bones throughout life.

Cycle durationNormally, complete renewal of a small area of bone takes 3 to 4 months.
Skeletal massCortical bone accounts for 80% of skeletal mass, while spongy (trabecular) bone accounts for 20%.
Risk of imbalanceExcessive resorption or incomplete filling of lacunae with new tissue leads to osteoporosis.
Basis of mineralizationVitamin D, calcium, phosphorus, and normal pH are critical for bone hardening.
4 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Cellular participants: builders and destroyers

Bone tissue balance is maintained by the coordinated work of two main cell types. The process is ongoing, forming the so-called basic multicellular unit.

  • Osteoclasts (osteoclasts) are responsible for the resorption (destruction) of old bone. They form lacunae in the tissue. This process is single-stage: osteoclasts remove the mineral component and collagen simultaneously.
  • Osteoblasts (osteoblasts) take over from osteoclasts to fill the resulting voids. Their work takes place in two stages. First, they secrete osteoid (osteoid), an unmineralized matrix. Then, mineralization of this matrix occurs.

During the formation of new bone, some osteoblasts become trapped within their own matrix. These cells transform into osteocytes (osteocytes).

Conditions for proper mineralization

For soft osteoid to turn into strong bone tissue, strict biochemical conditions must be met in the body. Key factors for normal mineralization include:

  1. Presence of the active form of vitamin D ($1,25(OH)_2D_3$).
  2. Adequate intake of calcium (Ca).
  3. Normal levels of phosphorus (P) and the enzyme alkaline phosphatase (alkaline phosphatase).
  4. Normal acidity level (pH).

If these conditions are violated, serious mineralization defects develop. In childhood, a lack of building blocks leads to rickets (rickets), while in adults a similar defect causes osteomalacia (osteomalacia).

Test your knowledge on the topicTasks from the "Diagnostic Radiology" course bank — instant answers and explanations.

Remodeling pathologies

Any disruption in the balance between bone destruction and formation leads to diseases:

  • Osteoporosis (osteoporosis): occurs when resorption is too active or osteoblasts cannot cope with completely filling the lacunae. The result is a catastrophic loss of bone mass.
  • Paget's disease (Paget's disease): a state of abnormally high bone turnover (high turnover state) in which bone renews too quickly and chaotically.
  • Osteopetrosis (osteopetrosis): a genetic defect in which osteoclast function is impaired. Normal resorption ceases, leading to abnormal modeling and pronounced tissue sclerosis. Paradoxically, such dense-looking bones become extremely fragile and prone to frequent fractures.

Mechanism of bone growth and development

During embryonic development, the skeleton is laid down as a cartilaginous framework. Further maturation proceeds via two pathways: endochondral (endochondral) and desmal/intramembranous (desmal) ossification.

Growth of long tubular bones is ensured by primary (in the center) and secondary (in the epiphyses) ossification centers. The mechanism of endochondral ossification:

  1. Cartilage cells hypertrophy and accumulate glycogen.
  2. Cells degenerate, and a provisional zone of calcification (provisional zone of calcification) is formed.
  3. Deep layers of perichondral cells turn into osteoblasts, creating primary spongiosa (primary spongiosa).
  4. Vessels and new osteoblasts penetrate the matrix, secrete osteoid, and mineralize it.

Bone lengthening occurs in the metaphyses (metaphyses), directly adjacent to the physis (physis)—the cartilaginous growth plate. This zone remains active until skeletal maturity is reached. If the process is temporarily stopped due to severe illness or starvation, the zone of provisional calcification remains as a scar. On an X-ray, this looks like thin white lines—Harris growth arrest lines (Harris growth arrest line).

Macrostructure and types of bone tissue

An anatomically long tubular bone is divided into three parts: epiphysis (epiphysis), the articular end; metaphysis (metaphysis), the transition zone; and diaphysis (diaphysis), the central shaft. Inside the bone lies the marrow space (marrow space) containing hematopoietic bone marrow. It is lined on the inside by the endosteum (endosteum), and on the outside the bone is protected by the periosteum (periosteum). Articular surfaces are covered by highly organized articular cartilage, which appears on MRI as a bright hyperintense rim.

All bone tissue is divided into two types:

  • Cortical (compact) bone (cortical bone): forms the outer framework and accounts for 80% of skeletal mass.
  • Trabecular (spongy) bone (trabecular bone): a lacy structure at the ends of long bones and in the axial skeleton. It accounts for only 20% of the mass, but provides a colossal surface area for cellular activity. Its trabeculae are located strictly along the load vectors to protect the skeleton from tension by muscle pull and body weight.

Briefly: answers to topical questions

What hormones regulate the balance between bone resorption by osteoclasts and its formation by osteoblasts?

The balance between bone resorption and formation is regulated by a complex of hormones affecting cellular activity.

  • Sex hormones (including estrogens)—regulate the OPG/RANK/RANKL triad; their deficiency increases resorption.
  • Parathyroid hormone (PTH)—stimulates osteoclasts, causing bone matrix resorption and the release of calcium into the blood.
  • Calcitonin—an antagonist of parathyroid hormone; stimulates osteoblast activity and decreases osteoclast activity.
  • Vitamin D ($1,25(OH)_2D_3$)—essential for normal mineralization.

Growth hormone, thyroid hormones, and glucocorticoids are also involved in regulating remodeling.

How to memorize

OsteoCLASTS — Crash (destroy old tissue). OsteoBLASTS — Build (build new bone).

Class and exam questions

What is osteoid?

This is an organic unmineralized matrix secreted by osteoblasts during the first stage of new bone formation. Subsequently, it becomes saturated with calcium and phosphorus, turning into hard bone.

Why do bones break in osteopetrosis even though they are sclerotic?

In this pathology, osteoclasts do not work, due to which old bone is not resorbed. Abnormal compaction (sclerosis) occurs, the internal microarchitecture of the tissue is disrupted, causing the bone to lose its elasticity and become mechanically fragile.

Where does longitudinal growth of a long bone take place?

Longitudinal growth occurs in the metaphysis, in the zone adjacent to the cartilaginous growth plate (physis). This process continues until growth stops and the plates close (skeletal maturity).

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What else to study on this topic

  • Biochemical mechanisms of single-stage resorption by osteoclasts
  • Histological structure of the epiphyseal growth plate (physis)
  • Differences between endochondral and desmal ossification pathways
  • Hormonal regulation of calcium, phosphorus, and vitamin D levels
  • Mechanism of formation of Harris growth arrest lines at the cellular level

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