Paperis.

© 2026 네오쿤스. All rights reserved.

공지사항이용약관개인정보처리방침환불 정책콘텐츠·제거 요청

상호: 네오쿤스 · 대표자: 김근태 · 사업자등록번호: 751-04-03501 [사업자정보 확인] · 통신판매업 신고: 제 2026-서울서초-3586호 (서초구청)

주소: 서울특별시 서초구 서초대로 266, B103-S36호(서초동) · Tel: 010-7254-2475 · 이메일: support@paperis.app · 고객센터 운영 시간: 평일 10:00–16:00 (한국 시간, 주말·공휴일 제외) · 호스팅 서비스 제공자: Vercel Inc.

Paperis.

Paperis Articles

How Is Bone Alive? — A Site That Builds as It Tears Down, a Warehouse the Body Draws On

Bone is living tissue that tears down old bone and fills the gap with new bone throughout life. The cells that remove, build and sense, the forces and hormones that direct the work, bone's role as the body's calcium store, how bone mass builds in youth and declines with age, and how a broken bone knits

🌱Primer✦AI-generatedMedicine · Nov 3, 2026

Your field's papers, as audio

Pick your fields and journals — Paperis summarizes the key papers and turns them into audio. Listen on your commute.

Start Paperis free →

How Is Bone Alive? — A Site That Builds as It Tears Down, a Warehouse the Body Draws On

A Broken Arm Heals Again

People who fell and broke an arm when they were young remember the day the cast came off. The broken spot has fused back together, and they throw a ball with that arm again. A broken stone does not stick back together on its own. Looking at white bones placed in a museum makes bones look like stone, too, but bones inside the body are living tissue that constantly changes (PMID 3325555).

Bones change even when they are not broken. Throughout life, old bone is slowly torn down a bit at a time and that spot is filled with new bone (PMID 17308163). Lying down for a long time or staying in space for a long period shrinks bones (PMID 33738515). The amount of bone built up during growth is a major factor that determines how easily bones break as people age (PMID 35125324).

This article looks in turn at what bones are made of, who tears them down and who builds them, what commands that work, how bones act as the body's calcium warehouse, how bone mass rises and falls with age, and how a broken bone heals.

Minerals Packed into a Tough Framework

99% of the calcium in the body is found in the bones (PMID 39257024). Inside the bones, calcium forms hard mineral crystals together with phosphorus (PMID 29610149). Those crystals are deposited between protein fibers (PMID 32522695).

Collagen is a tough fibrous protein that holds together tissues throughout the body, and in bones, it serves as the framework where minerals settle. The protein side of bone is mainly collagen and resists pulling forces, while the mineral side provides the hardness that resists pressing forces (PMID 3325555). Bone blends these two materials to withstand both pulling and pressing forces together. Thanks to this, bones support the body to move and surround vital organs (PMID 29865872).

If you cut a bone open, two types of structure are visible. Compact bone is the hard, dense layer that surrounds the exterior of the bone. Cancellous bone is the mesh-like bone filling the interior, where thin bone pillars are intertwined with many gaps. Compact bone is stiffer and reacts slowly even when the applied force changes. Cancellous bone has a much wider surface area for the same volume and is more metabolically active (PMID 3325555). The cancellous bone is also the part that diminishes more when not used for a long time or with aging (PMID 35773785).

The upper end of a thigh bone cut open lengthwise. A thick, solid layer of compact bone forms the outer wall, and the inside of the bone end is filled with spongy bone, a net of fine bony struts.

Bone is a material made by filling a tough protein framework with calcium minerals, and almost all of the body's calcium is contained within those minerals.

Cells That Tear Down, Cells That Build, Cells That Feel

On the bone surface, two cells work in pairs. Osteoclasts are cells that attach to the bone surface, dissolving old bone to tear it down. Osteoblasts are cells that lay down the framework of new bone and fill it with minerals to make bone. These two cells send signals back and forth; when the tearing-down side finishes its work, the building-side takes over that spot (PMID 18406338).

Among the cells inside an adult bone, 90 to 95% are a third type of cell, distinct from these two (PMID 21254230). Some of the osteoblasts end up buried right inside the bone they built (PMID 3325555). Osteocytes are cells that formed when osteoblasts became trapped and settled inside the bone they built, connected to each other by thin projections to feel the forces acting on the bone. In adult bone, osteocytes are roughly ten times more numerous than osteoblasts, and osteoclasts are merely a fraction of the osteoblasts (PMID 16036059). Osteocytes live the longest among bone cells, spending decades inside the hard bone (PMID 21254230).

For a long time, osteocytes were considered mere bystanders stuck inside the bone, just holding their ground. As research poured in during the 2000s, it was revealed that osteocytes coordinate the work of both osteoclasts and osteoblasts (PMID 21254230). Osteocytes act as sensors that feel the forces bone receives, while releasing signaling molecules to increase or decrease the work of the tearing-down side and the building-side (PMID 26247020). The ability of osteocytes to directly repair the surrounding bone framework has not yet been fully uncovered (PMID 33537002).

In bone, cells that tear down, cells that build, and cells buried inside the bone that feel forces and coordinate the two live together.

The Never-Ending Construction Site

What happens at a single spot on the bone's surface always follows the same sequence. Bone remodeling is the process of gradually tearing down old bone and filling that spot with new bone, continuing throughout the body's bones for a lifetime. First, osteoclasts melt away the old bone. In the transition phase that follows, other cells appear on the surface. Then osteoblasts lay down new bone, building until they fill the demolished spot entirely (PMID 17308163). The two are tightly coupled so that every wave of demolition is followed by a wave of building (PMID 17308163).

A four-panel picture of remodeling at one spot on a bone surface. Osteoclasts dissolve old bone and leave a pit; in the transition phase other cells appear on the surface; osteoblasts lay down new bone and fill the pit; some end up buried in the bone as osteocytes.

There are three reasons for this construction work. It adjusts the structure to match the forces the bone receives, repairs tiny everyday damages so old bone does not accumulate, and plays a part in keeping calcium in the blood steady (PMID 17308163, PMID 31889637).

Comparing bone to a single building, this building is a construction site where work never ends even after it is built. When the demolition crew, osteoclasts, tears down an old wall a little, the construction crew, osteoblasts, fills that spot with a new wall. Osteocytes living inside the wall feel the weight the building receives and signal where and how much to fix. Routine replacement construction tears down and rebuilds the same spot to keep the building's shape as it is, but when the forces it receives change, the construction changes even the bone's strength and shape (PMID 3325555).

The analogy holds true only up to the sequence of tearing down and building. Real bone has no blueprint, and the amount of construction is decided together by signals traveling within the bone and signals coming from the whole body through the blood (PMID 17308163).

While growing, construction that changes the size and shape of bones happens mostly, and when you become an adult, construction that replaces old bone with new bone is the main work (PMID 28786518). Construction that changes shape drops significantly once the bones are fully grown (PMID 3325555). If the amount torn down and the amount built misalign, bones can become diseased (PMID 26247020).

Bones spend a lifetime tearing down old bone and filling that spot with new bone, and the amount and strength of bone are maintained when the amount torn down and the amount built match (PMID 40847810).

The Building Is Its Own Materials Warehouse

Calcium in the blood is kept within a very narrow range (PMID 40847810). Calcium is the material that makes up bones, and it is also used when cells grow and divide, when blood clots, and when muscles contract (PMID 39257024). The body leaves the job of maintaining this level to hormones.

Hormones are substances made in one part of the body that travel through the blood to a distant place and change what the cells there do. The way hormones travel back and forth like letters is followed from the beginning in "How Hormones Work — Letters Only the Addressee Reads, Replies That Say Stop".

Parathyroid hormone comes from the parathyroid glands in the neck and raises the amount of calcium in the blood when it is lacking. When calcium in the blood drops, the parathyroid glands notice this and send out more of this hormone. This hormone first makes the kidneys hold onto more calcium that would otherwise leave in urine. Over the course of hours to days, it increases the work of osteoclasts tearing down bone, taking the calcium and phosphorus inside bones out into the blood. It also makes the kidneys turn vitamin D into its working form so the gut absorbs more calcium. When calcium returns to its normal place, this hormone decreases again (PMID 29597231).

Vitamin D is a substance made in skin that has received sunlight or entered through food, and it helps the gut absorb calcium. Vitamin D gathers more calcium in the gut, reduces the calcium lost in urine, and can also take out calcium stored in bones (PMID 35575431). The amount made in the skin can be greatly reduced by clothing, sunscreen, habits of avoiding sunlight, and living at high latitudes (PMID 35575431). If vitamin D is lacking for a long time, minerals cannot be properly filled into new bone frameworks (PMID 29435763). Conversely, if too much enters, toxicity can occur, so one review notes that vitamin D supplementation can be helpful, but intake should be under medical supervision (PMID 35575431).

Returning to the construction site picture, in this building, the bricks are the warehouse's materials themselves. If calcium in the blood is lacking, the body first adjusts the calcium in the blood even by tearing down bones (PMID 29597231). A single calcium number from a blood test cannot tell us the calcium balance of the bones. Excessively high or low calcium in the blood is a sign that calcium regulation is greatly disturbed, but that alone does not reveal how much calcium is piled up in the bones (PMID 20089499). The calcium balance of bones increases while growing, and can decrease as we age (PMID 20089499).

The same hormone leaves different results in bones depending on the way it is released. If parathyroid hormone is given in short, interrupted bursts—like once a day—building tends to come first, and if it stays high in the blood all the time, tearing down tends to come first (PMID 40847810). In a disease where the parathyroid glands release too much of this hormone, bone turnover speeds up and tilts toward tearing down, the arrangement of the bone worsens, and it can even lead to breaking from a small impact (PMID 40177730). The property of giving it in short bursts is used in drugs that help build bone (PMID 40847810).

Among the hormones directing construction are also sex hormones. Estrogen is a representative female hormone, and it is also made in the male body by converting a portion of male hormones. Estrogen is the main hormone governing bone metabolism in both women and men. When estrogen is lacking, above all, tearing down increases, and building cannot keep up as much, widening the gap between them (PMID 22595550). In men, the male hormone testosterone grows compact bone and makes bones thicker during puberty, and estrogen is essential for making spongy bone and suppressing tearing down (PMID 40120082).

Bone is the body's calcium warehouse, and when calcium in the blood is lacking, hormones open that warehouse.

Use It and It Grows Strong, Don't Use It and It Shrinks

People who have been bedridden for a long time, people with spinal cord injuries who can no longer move their legs, and astronauts who stay in space for a long time all share one thing in common. Their bones shrink (PMID 33738515). Limbs tied up in a cast after a fracture are no different (PMID 33738515).

When movement becomes impossible, bone begins to shrink immediately in both trabecular and cortical bone. The side tearing down relatively increases while the side building decreases (PMID 33738515). Whether the cause was paralysis, space flight, or bed rest, the longer the period of disuse, the more the bone shrank. The patterns of cortical bone thinning and trabecular bone disappearing were also similar (PMID 20637174). However, the degree of shrinkage varied greatly from person to person, and that difference appears to be explained by how much the force acting on the bone decreased compared to before they became immobile (PMID 20637174).

There is also the opposite direction. When the force acting on bone increases, the building work increases, and when the force decreases, bone shrinks and weakens (PMID 28612339). Speaking in terms of a construction site picture, the weight the building receives changes the amount of construction.

What senses this weight is the osteocyte. When the bone bends just a tiny bit from force, fluid flows through the narrow channels around the osteocyte, and that flow appears to wake the osteocyte up (PMID 16036059). Basic research revealing how osteocytes sense force was mainly experiments on rodents like mice (PMID 33738515). That human bone shrinks when not used is a fact observed in humans, and the fine details of cell signals within it are a picture mostly obtained from animals.

Bones that have shrunk from prolonged disuse and bones that have shrunk with age look a lot alike. Both see trabecular bone shrink more, cortical bone thin out, and tearing down increase while building decreases (PMID 35773785). The two differ in which locations' bone shrinks and the speed at which bone is replaced (PMID 35773785).

Bone changes its construction volume to match the force it receives, and when the force is cut off, tearing down outpaces building, causing it to shrink immediately.

Built While Growing, Diminishing As We Age

During puberty, the speed at which minerals build up in the lumbar spine and hip bones becomes four to six times faster than before (PMID 8081064). Peak bone mass is the amount of bone attained when growth is complete, which is the largest amount of bone a person has in their lifetime. Peak bone mass is an important factor that separates the risk of bones becoming weak and breaking as we age (PMID 8081064, PMID 35125324). Osteoporosis is a state where the amount of bone decreases and the inner meshwork becomes sparse, making bones easy to break even from minor impacts. This disease is followed by "Osteoporosis and Fractures — A Thinned Pillar and the Moment of a Fall", and here we look at how the underlying amount of bone rises and falls throughout life.

The main factors determining peak bone mass are race, sex, and genetics. Environmental factors during growth, such as physical activity, calcium and protein intake, body weight, and age at menarche, also play an important role (PMID 35125324). In a position statement by the National Osteoporosis Foundation (NOF), the lifestyle factor evaluated as having the strongest evidence is calcium intake and physical activity during growth periods, including around puberty (PMID 26856587). The American Academy of Pediatrics (AAP) does not recommend routine daily calcium supplements for healthy children and adolescents, and recommends meeting required amounts through food (PMID 25266429).

Bone mineral density is a value measured by shining X-rays on bone to see how many minerals are contained within that area, serving as a representative number to gauge bone amount. The increase in bone amount during growth is mainly due to bones growing larger, while the portion becoming denser is small (PMID 35125324). In long-term controlled studies that increased school physical education time, children who had daily physical education from before puberty until the end of puberty had higher bone mineral and bone density and larger bones than children who had it one to two times a week (PMID 32249382). The review concluded that daily physical education is linked to bone gains and a gradually lower fracture risk (PMID 32249382).

After passing the peak, bones decrease little by little. The age at which the peak is reached differs by bone site and also between men and women (PMID 31576547). In women, bones decrease rapidly around menopause, and in men, they decrease more slowly and steadily (PMID 31576547). Around menopause, estrogen decreases. When estrogen is lacking, breakdown increases above all else (PMID 22595550).

<!-- FIG: Lifetime bone amount — A curve with age on the horizontal axis, rising steeply during puberty, reaching a peak, then descending slowly, with women showing a larger slope around menopause. Shape only, without numerical tick marks -->

As we age, the coordination between the breakdown process and the building process becomes loose. Parathyroid hormone increases, vitamin D in working forms is less produced, and moving the body less also affects bones (PMID 1915689). How much these changes have been confirmed in humans varies by item (PMID 1915689). Along with the amount of bone, the structural meshwork and material properties also change (PMID 31576547).

The amount of bone remaining as we age is determined jointly by two things: the amount built when young and the amount lost afterward (PMID 16568580). As bone amount decreases and quality changes with age, it can lead to the risk of osteoporosis and fractures (PMID 31576547). Age is an actual risk factor, but genetics and lifestyle roles also factor in (PMID 31576547, PMID 35125324). What bone density tests measure, the risks of falls and fractures, and treatments belong to the article covering osteoporosis.

The Path Broken Bones Take to Mend

When a bone breaks, a vastly greater amount of new bone than usual is built right at that spot (PMID 28786518). The mending process is divided into four overlapping stages. First blood clots and forms a mass, then a cartilaginous callus forms, followed by a bony callus, and finally that callus is remodeled (PMID 38616228).

Inflammation is a response where the body rallies immune cells, causes the area to swell, and reacts against stimuli such as tissue damage, infection, or substances that have entered from outside the body. The moment a bone breaks, blood vessels and the bone framework are severed, triggering inflammation. The gathered inflammatory cells release signaling molecules to call other cells, and this inflammation plays an essential role in ensuring the bone mends properly (PMID 38616228). That process varies depending on age and sex (PMID 38616228).

A callus is a temporary tissue that first fills the gap between broken bone ends; the middle is filled with cartilage and then gradually turns into bone. Near the broken ends, bone is built directly, while in the middle gap, cartilage fills in first and then turns into bone (PMID 35182420). In the final stage, the callus is trimmed through prolonged remodeling to finish the construction (PMID 35182420).

The periosteum is a thin membrane wrapping the outer surface of a bone. The periosteum consists of two layers, and the inner layer among them can make new bone (PMID 3325555). It was only recently confirmed that the cells reconnecting broken bones come mainly from the periosteum and the inner surface inside the bone, and this picture came from studies on genetically modified mice (PMID 30370699).

In the construction site analogy, the callus is a temporary structure hastily put up before rebuilding the main building. It connects things with the temporary structure first, and then tears down and rebuilds according to the usual construction method to return to the original bone. Aging bone also loses the power to carry out this construction. Age-related cellular changes reduce the mending strength, and as inflammation lingers, the final trimming stage grows longer (PMID 35182420). Inflammation is strictly necessary for mending, but prolonged inflammation sides with slowing down healing.

In a single cast-immobilized arm, two construction projects take place at the same time. At the broken site, building increases significantly so the bone is reconnected (PMID 28786518). In the surrounding bone that is bound by the cast and unused, tearing down takes the lead, causing the bone to shrink (PMID 33738515). Even within the same bone, the direction of construction follows the circumstances facing that spot.

A broken bone is first connected using a temporary callus, after which that callus is trimmed according to the usual construction method to return to bone.

Where to Look Further

The ability of osteocytes to directly remodel the bone matrix around them is not yet fully understood (PMID 33537002). Most details of how osteocytes sense mechanical force and send signals also come from animals (PMID 33738515).

The principle that hormones travel like letters and, when results accumulate, replies are sent telling them to stop comes from How Hormones Work — Letters Only the Addressee Reads, Replies That Say Stop. The disease in which bone mass decreases making bones break easily, how to read bone density results, falls and fractures, and classes of treatment are continued in Osteoporosis and Fractures — Porous Pillars and the Moment of Falling. Stories of the places where bones meet, like the knees and lower back, are followed by What Is Knee Osteoarthritis — A Doorframe That Changes With Its Hinge and What Is Lower Back Pain — Wrinkles in the Spine, Unnamed Pain. Muscles aging alongside bones are topics this series will cover in the future.

Source Papers

  • "Bone structure and function." (1987) — PMID 3325555 — Bones are living, constantly changing tissues; collagen provides tensile strength while minerals provide compressive strength; compact bone is slow while spongy bone has a high surface area and metabolic activity; bone cells originate from osteoblasts, and shape-shaping construction stops at maturity (though 1915689 and 35773785 document shape changes on the periosteal side of adults → phrased as "greatly reduced"), while routine remodeling occurs in the same spot for a lifetime and adaptive remodeling alters strength, density, and shape, with the inner layer of the periosteum creating new bone.
  • "Bone remodeling." (2006) — PMID 17308163 — Lifelong remodeling occurs in three stages: resorption, reversal, and formation, which adjusts architecture to mechanical forces, repairs microdamage, and maintains calcium, regulated systemically and locally, with formation tightly coupled to follow every resorption.
  • "Disuse Osteoporosis: Clinical and Mechanistic Insights." (2022) — PMID 33738515 — Bone loss occurs from spinal cord injury, post-fracture immobilization, bed rest, and spaceflight; both spongy and compact bone decrease immediately after immobilization (with relative increases in resorption and decreases in formation); basic research mainly uses rodent models, and osteocytes sense mechanical force.
  • "Acquisition of peak bone mass." (2022) — PMID 35125324 — Gains in bone mass during growth are primarily driven by increases in bone size, and peak bone mass is a core determinant of subsequent bone mass and fragility fractures, driven mainly by race, sex, and genetics, with physical activity, calcium, protein, body weight, and age at menarche also playing important roles.
  • "Biology of calcium homeostasis regulation in intestine and kidney." (2025) — PMID 39257024 — 99% of the body's calcium resides in bone, and calcium is used for bone, cell division, blood clotting, and muscle contraction.
  • "Mechanism of Bone Mineralization." (2018) — PMID 29610149 — Bone mineralization requires calcium ions and inorganic phosphate, and bone serves as a reservoir for essential minerals.
  • "Alkaline phosphatase: Structure, expression and its function in bone mineralization." (2020) — PMID 32522695 — Mineral crystals are deposited between collagen fibers.
  • "Bone Mechanical Properties in Healthy and Diseased States." (2018) — PMID 29865872 — The mechanical properties of bone support movement and protect internal organs.
  • "Similarities Between Disuse and Age-Induced Bone Loss." (2022) — PMID 35773785 — Both disuse and aging lead to preferential loss of spongy bone, thinning of compact bone, increased resorption, and decreased formation, with differences in site specificity and turnover rates.
  • "The amazing osteocyte." (2011) — PMID 21254230 — Osteocytes account for 90–95% of bone cells in adults and are the longest-lived bone cells (living for decades), functioning as coordinators of remodeling rather than "passive sitters," with a surge of data over the past decade.
  • "Osteoclast-osteoblast communication." (2008) — PMID 18406338 — The two cells exchange signals, and factors from osteoclasts drive the transition from resorption to formation.
  • "Osteocyte and bone structure." (2003) — PMID 16036059 — Osteocytes outnumber osteoblasts by roughly 10-fold, osteoclasts are a subset of osteoblasts, and fluid flow generated by deformation appears to mechanically activate osteocytes.
  • "Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells." (2015) — PMID 26247020 — Osteocytes act as force sensors and coordinators of remodeling, and imbalances between resorption and formation lead to bone diseases such as osteoporosis.
  • "Control of Bone Matrix Properties by Osteocytes." (2020) — PMID 33537002 — The ability of osteocytes to alter the bone scaffold is still incompletely understood.
  • "Post-natal bone physiology." (2020) — PMID 31889637 — Remodeling aids in calcium regulation, the repair of routine microdamage, and shaping during growth.
  • "The biology of normal bone remodelling." (2017) — PMID 28786518 — Childhood is dominated by shaping, whereas adulthood is dominated by remodeling, and bone formation increases significantly following a fracture.
  • "Advances in Parathyroid Hormone-based medicines." (2025) — PMID 40847810 — Blood calcium is maintained within a narrow range, balanced remodeling preserves bone density and strength, intermittent administration favors formation, and continuous elevation favors resorption.
  • "Physiology of the Calcium-Parathyroid Hormone-Vitamin D Axis." (2018) — PMID 29597231 — Low calcium leads to increased parathyroid hormone, which prompts renal reabsorption (rapid), osteoclastic resorption to release bone calcium (hours to days), and renal production of active vitamin D to enhance intestinal absorption, which is suppressed once normal levels are restored.
  • "Vitamin D: sources, physiological role, biokinetics, deficiency, therapeutic use, toxicity..." (2022) — PMID 35575431 — Vitamin D increases intestinal absorption, reduces urinary loss, and mobilizes bone calcium, while skin synthesis decreases due to clothing, sunscreen, sun avoidance, and high latitudes, and excessive amounts cause toxicity, requiring expert supervision.
  • "Functions of vitamin D in bone." (2018) — PMID 29435763 — Active vitamin D deficiency or resistance reduces the minerals required for normal bone matrix calcification, leading to conditions like osteomalacia.
  • "Calcium metabolism in health and disease." (2010) — PMID 20089499 — Hypercalcemia and hypocalcemia indicate severe regulatory disturbances but do not alone reflect the calcium balance, which shifts between positive, neutral, and negative states depending on growth and aging.
  • "Bone in Parathyroid Diseases Revisited..." (2025) — PMID 40177730 — Hyperparathyroidism increases bone turnover skewed toward resorption, leading to microarchitectural deterioration, decreased bone density, and fragility fractures.
  • "Estrogen and the skeleton." (2012) — PMID 22595550 — Estrogen is a primary regulator of bone metabolism in both women and men, and its deficiency leads primarily to increased resorption and a gap between resorption and formation.
  • "Testosterone and Male Bone Health: A Puzzle of Interactions." (2025) — PMID 40120082 — Testosterone is essential for compact bone growth in adolescent males, while estradiol is required for spongy bone formation and the suppression of resorption.
  • "Osteocyte Mechanobiology." (2017) — PMID 28612339 — Increased mechanical force boosts bone formation, while reduced loading is consistently linked to bone loss and fragility.
  • "Immobilization and bone structure in humans." (2010) — PMID 20637174 — Paralysis, spaceflight, and bed rest all share duration as a primary determinant, resulting in similar shapes characterized by thinned compact bone and reduced spongy bone, with large individual variations that appear explained by the magnitude of load reduction compared to pre-immobilization levels.
  • "Peak bone mass." (1994) — PMID 8081064 — Peak bone mass is the amount of bone tissue at skeletal maturity and an important determinant of osteoporotic fracture risk, with the rate of areal bone mineral density accumulation peaking at 4 to 6 times baseline during puberty, and DXA measuring areal values.
  • "The National Osteoporosis Foundation's position statement on peak bone mass development and lifestyle factors..." (2016) — PMID 26856587 — Among lifestyle factors, calcium intake and physical activity have a grade A level of evidence (especially in late childhood and around puberty).
  • "Optimizing bone health in children and adolescents." (2014) — PMID 25266429 — Routine calcium supplementation is not recommended for healthy children and adolescents, who are advised to meet their requirements through diet.
  • "Exercise and Peak Bone Mass." (2020) — PMID 32249382 — In long-term controlled intervention studies, children who engaged in daily school physical education throughout puberty showed greater bone mineral density and bone size than those who did so 1 to 2 times a week, and their fracture incidence rate ratio 8 years later was less than half of that predicted by age (benefits appear to "carry over").
  • "The Aging Skeleton." (2019) — PMID 31576547 — Gradual bone loss follows peak bone mass, with peak ages varying by site and sex, accelerating around menopause in women and progressing more gradually in men, altering both quantity and quality through genetic and epigenetic factors and leading to osteoporosis and fracture risks.
  • "Osteoporosis-an update." (2005) — PMID 16568580 — Osteoporosis depends on two processes: the acquisition of peak bone mass and subsequent bone loss.
  • "Age-related bone changes." (1991) — PMID 1915689 — Aging uncouples resorption and formation, accompanied by increases in parathyroid hormone, decreases in active vitamin D, and reduced activity, though the degree of human confirmation varies by item.
  • "Osteoimmunology of Fracture Healing." (2024) — PMID 38616228 — Healing occurs in four overlapping stages—hematoma, soft callus, hard callus, and callus remodeling—where inflammation is crucial for robust healing, varying by age and sex.
  • "Fracture Healing in the Setting of Endocrine Diseases, Aging, and Cellular Senescence." (2022) — PMID 35182420 — Healing proceeds via cartilage intermediaries in the center, direct bone formation near the fracture ends, and a final chronic remodeling phase, with aging and lingering inflammation (inflammaging) impairing healing and prolonging the remodeling phase.
  • "Cellular biology of fracture healing." (2019) — PMID 30370699 — Studies in genetically modified mice have recently confirmed that the periosteum and endosteum are the primary sources of bone-forming cells.
Sources (36)
  • Bone structure and functionPMID 3325555
  • Bone remodelingPMID 17308163
  • Disuse Osteoporosis: Clinical and Mechanistic InsightsPMID 33738515
  • Acquisition of peak bone massPMID 35125324
  • Biology of calcium homeostasis regulation in intestine and kidneyPMID 39257024
  • Mechanism of Bone MineralizationPMID 29610149
  • Alkaline phosphatase: Structure, expression and its function in bone mineralizationPMID 32522695
  • Bone Mechanical Properties in Healthy and Diseased StatesPMID 29865872
  • Similarities Between Disuse and Age-Induced Bone LossPMID 35773785
  • The amazing osteocytePMID 21254230
  • Osteoclast-osteoblast communicationPMID 18406338
  • Osteocyte and bone structurePMID 16036059
  • Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone CellsPMID 26247020
  • Control of Bone Matrix Properties by OsteocytesPMID 33537002
  • Post-natal bone physiologyPMID 31889637
  • The biology of normal bone remodellingPMID 28786518
  • Advances in Parathyroid Hormone-based medicinesPMID 40847810
  • Physiology of the Calcium-Parathyroid Hormone-Vitamin D AxisPMID 29597231
  • Vitamin D: sources, physiological role, biokinetics, deficiency, therapeutic use, toxicityPMID 35575431
  • Functions of vitamin D in bonePMID 29435763
  • Calcium metabolism in health and diseasePMID 20089499
  • Bone in Parathyroid Diseases RevisitedPMID 40177730
  • Estrogen and the skeletonPMID 22595550
  • Testosterone and Male Bone Health: A Puzzle of InteractionsPMID 40120082
  • Osteocyte MechanobiologyPMID 28612339
  • Immobilization and bone structure in humansPMID 20637174
  • Peak bone massPMID 8081064
  • The National Osteoporosis Foundation's position statement on peak bone mass development and lifestyle factorsPMID 26856587
  • Optimizing bone health in children and adolescentsPMID 25266429
  • Exercise and Peak Bone MassPMID 32249382
  • The Aging SkeletonPMID 31576547
  • Osteoporosis-an updatePMID 16568580
  • Age-related bone changesPMID 1915689
  • Osteoimmunology of Fracture HealingPMID 38616228
  • Fracture Healing in the Setting of Endocrine Diseases, Aging, and Cellular SenescencePMID 35182420
  • Cellular biology of fracture healingPMID 30370699
📚 Bones and Joints — What Holds Us Up and Lets Us Move
1 / 4
  1. 1.How Is Bone Alive? — A Site That Builds as It Tears Down, a Warehouse the Body Draws On
  2. 2.Osteoporosis and Fractures — A Hollowed Pillar and the Moment of the Fall
  3. 3.What Is Knee Osteoarthritis? — The Door Frame That Changes With the Hinge
  4. 4.What Is Low Back Pain? — Wrinkles in the Spine, Pain Without a Name
Next →Osteoporosis and Fractures — A Hollowed Pillar and the Moment of the Fall

This article is AI-generated from research papers for general information and does not replace professional advice. Spotted an error? Let us know

© 2026 Neokuns (Paperis). Sharing links is welcome; republishing the full text requires prior permission.