Corpus
Whole body

Bones

Living, remodelling tissue that is also your calcium bank, your blood cell factory and an endocrine organ.

By The Corpus Atlas Editorial TeamUpdated Last reviewed How we source this

206, down from about 270 at birth

Bones in an adult

10 years

Skeleton replaced roughly every

About 99%

Share of body calcium stored in bone

Around age 25–30

Peak bone mass reached by

Overview

Bone is often imagined as inert scaffolding, which is almost exactly wrong. It is a living composite material — collagen fibres for tensile strength, mineral crystals for compressive strength — that is continuously demolished and rebuilt throughout life. Two cell types run the process: osteoclasts dissolve old bone, and osteoblasts lay down new matrix that then mineralises. A third type, the
osteocyteThe mature embedded bone cell that senses mechanical strain and directs remodelling.
, sits embedded within the mineral and acts as the sensor, detecting mechanical strain and directing where remodelling should happen. This is why bone adapts to load and wastes without it, and why the skeleton of a tennis player differs measurably between their two arms. Bone does three further jobs that have nothing to do with structure. It stores 99% of the body's calcium and releases it on hormonal demand, which is why calcium balance and bone density are inseparable. Its marrow manufactures every blood cell. And it functions as an endocrine organ, secreting hormones including osteocalcin and FGF23 that influence phosphate handling, glucose metabolism and more. Peak bone mass is reached in the twenties and slowly declines thereafter — so much of lifelong bone health is determined by how much was built early.

Interesting facts

  • Weight for weight, bone has a higher tensile strength than steel, while being light enough to carry — a consequence of the collagen-mineral composite structure.
  • Osteocytes make up over 90% of bone cells and act as a connected sensory network, detecting strain and signalling where new bone is needed.
  • The skeleton is completely replaced roughly every decade, so the bone you have now is not the bone you had ten years ago.
  • Babies are born with around 270 bones; many fuse during growth, which is why adults have 206.
  • Bone was recognised as an endocrine organ relatively recently — it secretes hormones affecting phosphate regulation, insulin sensitivity and possibly muscle function.
  • Astronauts lose bone density at roughly 1–1.5% per month in microgravity, the clearest demonstration that mechanical loading is what maintains the skeleton.

Common misconceptions

  • Bones are dead, dry structures.
    Bone is highly vascular living tissue with its own nerve supply, continuously remodelling and metabolically active enough to function as an endocrine organ.
  • Drinking milk is the key to strong bones.
    Calcium matters, but mechanical loading matters more. Populations with low dairy intake do not universally have high fracture rates, and calcium supplementation alone has surprisingly modest effects on fracture risk.
  • Osteoporosis is a women's disease.
    It is more common in women, but roughly one in five men over 50 will suffer an osteoporotic fracture, and men have higher mortality after hip fracture. Men are substantially under-diagnosed and under-treated.
  • Running and impact exercise wear out your bones.
    The opposite. Impact loading is one of the strongest stimuli for bone formation. It is joint cartilage that has a more complex relationship with load — bone thrives on it.
  • Cracking your knuckles causes arthritis.
    Studies have found no association. The sound is gas bubbles collapsing in joint fluid, not bone or cartilage damage.
  • Once you have osteoporosis, nothing can be done.
    Treatment reduces fracture risk substantially — by around 40–70% for vertebral fractures depending on the drug — and remains effective in the very old.

Anatomy & how it works

A composite material organised at several scales, with distinct cell populations maintaining an outer shell and inner lattice.

  • Cortical bone

    The dense outer shell providing most of the skeleton's strength and stiffness; about 80% of bone mass.

  • Trabecular (cancellous) bone

    The internal honeycomb lattice found in vertebrae and the ends of long bones; metabolically far more active and lost first in osteoporosis.

  • Osteoblasts

    Bone-forming cells that lay down collagen matrix which subsequently mineralises.

  • Osteoclasts

    Large multinucleated cells that dissolve bone mineral and matrix — the target of most osteoporosis drugs.

  • Osteocytes

    Mature cells embedded within mineral, connected into a network that senses mechanical strain and orchestrates remodelling.

  • Periosteum

    The vascular, richly innervated outer membrane — the reason a bone bruise hurts so much and a source of cells for repair.

  • Bone marrow

    Red marrow producing blood cells, and yellow fatty marrow which increases with age.

  • Growth plate (physis)

    The cartilage zone where lengthening occurs in childhood, fusing at the end of puberty.

Remodelling proceeds in discrete units: osteoclasts excavate a cavity, then osteoblasts refill it. In youth, formation slightly exceeds resorption and bone mass rises; from the late twenties the balance tips the other way. Osteocytes govern the process by sensing strain — where loading is high, they suppress the signals that recruit osteoclasts and encourage formation; where loading is absent, resorption dominates. This explains why bone follows
Wolff's lawThe principle that bone adapts its structure to the mechanical loads placed on it.
, adapting its architecture to the loads it habitually experiences, and why bed rest and spaceflight cause rapid loss. The calcium regulation system runs in parallel and can override structural priorities entirely: if blood calcium falls, parathyroid hormone rises and bone is dissolved to correct it, because a normal blood calcium is more immediately essential to survival than a strong skeleton.

Primary functions

  • Providing structural support and a framework for movement
  • Protecting the brain, spinal cord, heart and lungs
  • Acting as levers for muscle to generate movement

Secondary functions

  • Storing and releasing calcium and phosphate under hormonal control
  • Housing bone marrow for blood cell production
  • Secreting hormones including osteocalcin and FGF23
  • Buffering blood pH by releasing alkaline mineral salts
  • Storing certain heavy metals, removing them from circulation

Across a lifetime

Development
Most bone forms by replacing a cartilage template, a process called endochondral ossification. Vitamin D deficiency during growth prevents proper mineralisation, causing rickets.
Childhood
Bone accrues rapidly, with roughly a quarter of adult bone mass laid down during the two years around peak growth in puberty. Childhood and adolescent physical activity is one of the strongest determinants of lifelong bone strength.
Adulthood
Peak bone mass is reached in the mid-to-late twenties, after which a slow decline begins. Relative energy deficiency in sport and eating disorders can cause substantial early bone loss.
Later life
Loss accelerates sharply in women in the years around menopause as oestrogen falls, then continues more slowly. Fracture risk rises steeply, and hip fracture in particular carries high mortality and loss of independence.
Sex differences
Women reach a lower peak bone mass and then lose bone rapidly at menopause, making osteoporosis about four times more common. Men reach a higher peak and decline more gradually, but have higher mortality after hip fracture and are far less likely to be assessed or treated.

Body connections

Bone matters most through fracture, and fracture is not a minor event in later life. Hip fracture carries a mortality of roughly 20–30% within a year and permanently reduces independence for many survivors. Vertebral fractures, often silent, cause height loss, chronic pain and reduced lung capacity. Because bone is also the marrow's home and the body's calcium reservoir, skeletal disease connects outward to haematology, kidney disease and endocrine function — and because bone responds so directly to loading, it is one of the clearest examples of a tissue whose health is determined by how the body is used.

Body connections

How this links to the rest of you

Joints

Bone ends form the joint surfaces, and changes in the underlying bone are central to how osteoarthritis develops.

Spine

Vertebrae are largely trabecular bone, making them the commonest site of osteoporotic fracture — often silent, presenting as height loss and curvature.

Hips & pelvis

Hip fracture is the most consequential osteoporotic fracture, with high mortality and permanent loss of independence in many cases.

Blood

Bone marrow produces every blood cell, so marrow disease and blood disease are the same problem viewed from different angles.

Kidneys

The kidneys activate vitamin D and regulate phosphate; chronic kidney disease reliably disturbs bone metabolism.

Thyroid

Excess thyroid hormone accelerates bone turnover and reduces density, an important risk in over-replacement.

Adrenal glands

Cortisol excess — from disease or steroid treatment — is a leading cause of secondary osteoporosis.

Reproductive system

Oestrogen and testosterone both restrain bone resorption, so their loss at menopause or through hypogonadism drives bone loss directly.

Small intestine

Calcium and vitamin D absorption occurs here, so coeliac disease and bowel resection are recognised causes of low bone density.

How lifestyle changes it

Exercise

The most important modifiable factor. Impact and resistance loading stimulate bone formation, while inactivity causes loss — an effect visible within weeks of bed rest. Swimming and cycling, being non-weight-bearing, do relatively little for bone.

Nutrition

Calcium provides the raw material, vitamin D enables its absorption, and protein supplies the collagen matrix. Adequate energy intake is also required; under-fuelling suppresses the hormones that maintain bone.

Hydration

No direct effect on bone density, though it matters for kidney stone risk in people on calcium supplements.

Sleep

Emerging evidence links short sleep and shift work with lower bone density, plausibly through effects on remodelling rhythms and hormones.

Stress

Chronic cortisol elevation suppresses bone formation; this is the mechanism behind steroid-induced osteoporosis and is likely relevant to prolonged psychological stress.

Ageing

Bone mass declines from the late twenties, sharply so after menopause. Falls risk also rises, and it is the combination of weaker bone and more falls that drives fracture rates.

Environment

Smoking accelerates bone loss and impairs fracture healing. Sunlight exposure determines vitamin D status for most people. Microgravity and prolonged immobility cause dramatic loss.

Genetics

Heritability of bone density is high, around 60–80%. A parental hip fracture roughly doubles risk independent of measured density, which is why it appears in fracture risk calculators.

Symptoms & conditions

Rare conditions

  • Paget's disease of bone
  • Osteogenesis imperfecta
  • Osteomalacia and rickets
  • Primary hyperparathyroidism with bone disease
  • Osteonecrosis
  • Fibrous dysplasia
  • Bone sarcoma
  • Renal osteodystrophy

Acute & chronic problems

  • Fragility fracture of hip, wrist or vertebra
  • Stress fracture from repetitive loading
  • Traumatic fracture
  • Bone contusion
  • Growth plate injury in children
  • Osteoporosis and osteopenia
  • Steroid-induced bone loss
  • Non-union or delayed union after fracture
  • Chronic bone pain from Paget's disease or metastases

Early warning signs

  • Losing height, or clothes fitting differently through the torso
  • A fracture from a fall from standing height or less
  • Increasing stoop or upper back curvature
  • New localised bone pain that is worse at night
  • Repeated stress fractures in an athlete
  • Loss of periods in a female athlete, which signals bone-relevant energy deficiency

Risk factors

  • Female sex and early menopause
  • Long-term glucocorticoid use
  • Smoking and heavy alcohol intake
  • Low body weight and eating disorders
  • Parental history of hip fracture
  • Inactivity or prolonged immobility
  • Coeliac disease and inflammatory bowel disease
  • Overactive thyroid or over-replacement
  • Certain drugs including aromatase inhibitors and some antiepileptics

Protective factors

  • Weight-bearing and resistance exercise throughout life
  • Adequate calcium, vitamin D and protein
  • Not smoking and moderating alcohol
  • Building peak bone mass in adolescence
  • Falls prevention including balance training in older adults
  • Treating osteoporosis when diagnosed rather than monitoring indefinitely

Optimise & recover

Prevention

  • Do weight-bearing impact exercise and progressive resistance training — this is the single most effective thing you can do for bone
  • Get enough calcium from food where possible, around 700–1000 mg daily depending on age and local guidance
  • Maintain vitamin D, with supplementation through winter at northern latitudes
  • Eat enough total energy and protein; under-fuelling suppresses bone formation regardless of calcium intake
  • Stop smoking and keep alcohol moderate
  • Ask about a bone density scan if you fracture from a minor fall, take long-term steroids, or have an early menopause
  • Train balance in later life — most fragility fractures require a fall to happen

Recovery

  • Fracture healing takes six to twelve weeks for initial union and up to a year for full remodelling; protected loading accelerates it, complete immobility slows it
  • Weight-bearing as permitted is part of the treatment, not a risk — bone needs load to heal well
  • After a fragility fracture, ensure osteoporosis is actually assessed and treated; the majority of patients are still discharged without it
  • Stress fractures need relative rest plus correction of the cause — usually training load, sometimes energy availability or bone density

Bone rehabilitation has two distinct aims: restoring loading capacity after injury, and reducing fracture risk by improving both bone strength and the likelihood of falling. Progressive resistance and impact training builds density in the specific bones loaded, so programmes must target the sites at risk — the hip and spine in particular. The LIFTMOR trial demonstrated that supervised high-intensity resistance and impact training is safe and effective even in postmenopausal women with low bone mass, overturning the long-held assumption that they must avoid heavy loading. Balance and gait training reduces falls, which addresses the other half of the fracture equation.

Movement library

  • Thoracic extension work

    Counters the stooped posture that follows vertebral fractures and reduces further forward-flexion loading on the spine.

    Beginner
  • Balance and gait training

    Directly reduces fall frequency, which is what converts low bone density into an actual fracture.

    Beginner
  • Tai chi

    Reasonable trial evidence for reducing falls in older adults, with good adherence and low injury risk.

    Beginner
  • Progressive heavy resistance training

    Squats, deadlifts and presses at meaningful loads build hip and spine density; shown safe in postmenopausal women with low bone mass under supervision.

    Intermediate
  • Impact loading — hopping and jumping

    Brief, high-magnitude, varied-direction impacts are potent bone stimuli; a few dozen hops daily produce measurable hip effects.

    Intermediate
  • Weighted stair climbing and walking

    Accessible weight-bearing loading for those not ready for heavy lifting.

    Beginner
  • Hip abductor strengthening

    Supports hip stability and reduces fall risk, targeting the site of the most consequential fractures.

    Beginner
  • Hip flexor and pectoral stretching

    Addresses the postural tightness that accompanies a stooped thoracic spine after vertebral fracture.

    Beginner
  • Avoid loaded spinal flexion

    Deep loaded forward bending and twisting are best avoided with known vertebral fragility, as they increase compression fracture risk.

    Beginner

Massage does not affect bone density. It has a supportive role for the muscular pain that accompanies vertebral fracture and postural change, but firm pressure directly over an area of known fragility or recent fracture should be avoided.

Habits worth building

  • Add short bursts of impact into daily life — stair climbing, a few hops while the kettle boils
  • Get outside for sunlight in summer months and supplement vitamin D in winter
  • Review your home for trip hazards and lighting if you are over 65 — falls prevention is bone protection

Nutrition, devices & products

Calcium and vitamin D are necessary but not sufficient — supplementation alone has a surprisingly modest effect on fracture risk, and the evidence is strongest in people who are deficient or institutionalised. Protein deserves more attention than it usually gets: bone is roughly half collagen by volume, and higher protein intake is associated with better bone density, contradicting the older concern that protein leaches calcium. Adequate total energy is essential; relative energy deficiency suppresses the hormonal environment bone needs, which is why low bone density is common in endurance athletes and people with eating disorders despite high activity levels.

Foods to prioritise

  • Calcium from dairy, fortified plant milks, tinned fish with bones, tofu and leafy greens
  • Vitamin D from sunlight in summer and supplementation in winter
  • Protein at around 1.0–1.2 g per kg body weight, higher in older adults
  • Vitamin K from green leafy vegetables, involved in bone matrix protein function
  • Magnesium and potassium from fruit, vegetables and nuts
  • Adequate overall energy intake, particularly in athletes

Foods to limit

  • Heavy alcohol intake, which impairs bone formation and increases falls
  • Very high sodium intake, which increases urinary calcium loss
  • Excessive caffeine in the context of low calcium intake
  • Prolonged very low energy dieting, which suppresses bone formation
SupplementEvidenceNote
Vitamin DStrongClearly required to prevent osteomalacia and correct deficiency; fracture prevention evidence is strongest when combined with calcium in deficient or older institutionalised populations.
CalciumModerateNecessary for bone mineralisation, but supplementation in already-replete people has modest effects on fracture risk and may raise kidney stone risk. Food sources are preferable.
ProteinModerateHigher intakes are associated with better bone density and reduced hip fracture risk; the old concern that protein harms bone is not supported.
Vitamin K2EmergingBiologically plausible role in matrix proteins with some Japanese trial data; Western trials have been less convincing.
Collagen peptidesEmergingSmall trials suggest modest bone density effects; the evidence base is early and mostly industry-funded.
Strontium supplementsLimitedOver-the-counter strontium is not the prescription form studied, inflates density readings artefactually, and carries cardiovascular concerns.

Devices & wearables

  • DXA scanners for bone density measurement
  • Vibration platforms, with mixed and generally weak evidence for density gains
  • Hip protectors, which reduce hip fracture risk in high-risk care home residents
  • Walking aids and home adaptations for falls prevention
  • Fall detection devices, useful for reducing the consequences of falls rather than preventing them
  • Activity trackers, relevant because step count and impact loading both matter for bone

Professional treatments

  • DXA bone density scanning and FRAX fracture risk assessment
  • Vertebral fracture assessment imaging
  • Blood tests for secondary causes including calcium, vitamin D, thyroid and coeliac screening
  • Fracture liaison services to ensure treatment after a fragility fracture
  • Surgical fracture fixation and joint replacement
  • Vertebroplasty or kyphoplasty in selected vertebral fractures

Educational mention only, not a recommendation: Bisphosphonates such as alendronate and zoledronic acid as first-line treatment, Denosumab, a twice-yearly injection — must not be stopped abruptly due to rebound bone loss, Teriparatide and abaloparatide, which build bone rather than just slowing loss, Romosozumab, which both builds bone and reduces resorption, Hormone replacement therapy, which preserves bone at menopause, Vitamin D and calcium as adjuncts rather than treatments.

When to seek medical care

Any fracture from a fall from standing height or less in an adult over 50 should trigger a bone density assessment — this is a fragility fracture, it predicts further fractures, and it is still frequently missed. Losing height, developing a stoop, or sudden severe back pain after minimal trauma all suggest possible vertebral fracture. If you take long-term steroids, have had an early menopause, or have coeliac disease or an overactive thyroid, ask about assessment rather than waiting for a fracture. New bone pain that is worse at night, particularly with weight loss, needs prompt investigation.

Seek care promptly if you notice

  • Inability to bear weight after a fall, particularly in an older adult
  • Sudden severe back pain after minimal or no trauma
  • Bone pain that is worse at night or unrelated to activity
  • Bone pain with unexplained weight loss, night sweats or a history of cancer
  • Fever with localised bone pain, swelling and redness
  • Back pain with new leg weakness, numbness or bladder or bowel changes
  • Progressive height loss or increasing spinal curvature

Research & frequently asked questions

Current research

  • The LIFTMOR trial and subsequent work have overturned the long-standing advice that postmenopausal women with low bone mass should avoid heavy loading — supervised high-intensity resistance and impact training improved bone density and function without excess injury.
    1

    Journal of Bone and Mineral Research · 2018

    High-Intensity Resistance and Impact Training Improves Bone Mineral Density and Physical Function in Postmenopausal Women With Osteopenia and Osteoporosis

    The LIFTMOR randomised trial demonstrating improvements in lumbar spine and femoral neck bone density and functional performance with supervised heavy loading, with a very low adverse event rate.

  • Sequential and combination drug strategies are an active area, with evidence that starting with a bone-building agent before an antiresorptive produces better density gains than the reverse order.
    2

    The Lancet · 2019

    Osteoporosis

    Review quantifying fracture risk reduction with available therapies and documenting the large treatment gap, with most patients receiving no bone-directed therapy after a fragility fracture.

Emerging therapies

  • Sclerostin inhibition with romosozumab, offering dual anabolic and antiresorptive action
  • Cathepsin K and other novel resorption targets
  • Optimised treatment sequencing and drug holiday protocols
  • Investigation of bone as an endocrine organ, including osteocalcin's metabolic roles

Scientific controversies

  • Calcium supplementation has been questioned on cardiovascular safety grounds, with conflicting analyses; the pragmatic conclusion is to prioritise dietary calcium and reserve supplements for those with genuinely low intake.
  • Whether to screen the general population for osteoporosis, and at what age, differs between national guidelines despite broadly similar evidence.
  • Bisphosphonate drug holidays are widely practised without strong trial evidence on optimal duration, and rare atypical femoral fractures have driven considerable — arguably disproportionate — reluctance to treat.

Julius Wolff proposed in 1892 that bone architecture adapts to mechanical load, a principle now understood at the cellular level through osteocyte strain sensing. Rickets was one of the great diseases of industrial cities, and the discovery of vitamin D and food fortification in the 1920s and 1930s nearly eliminated it in developed countries — though it has re-emerged in some populations with limited sun exposure. Bisphosphonates were originally industrial chemicals used to prevent scale in water pipes before their affinity for bone mineral was exploited therapeutically.

Frequently asked questions

What is the best exercise for bones?

Loading that is heavy, impactful and varied in direction. Progressive resistance training and jumping or hopping are the most effective; walking helps but far less. Swimming and cycling do very little for bone because they are not weight-bearing.

Is heavy lifting safe with osteoporosis?

Under supervision, yes — and it is beneficial. The LIFTMOR trial specifically tested high-intensity resistance and impact training in postmenopausal women with low bone mass and found improvements in density and function without excess injury. Loaded spinal flexion is the movement to avoid.

Do I need calcium supplements?

Only if your dietary intake is low. Food sources are preferable, supplementation in already-replete people has modest fracture benefit, and there are questions about kidney stones and cardiovascular safety at high supplemental doses.

How much vitamin D do I need for bones?

Enough to avoid deficiency, which for most people at northern latitudes means a supplement of around 10 µg (400 IU) daily through the winter months. Very high doses do not confer extra bone benefit and intermittent large doses have performed poorly in trials.

Can men get osteoporosis?

Yes, and it is badly under-recognised. Around one in five men over 50 will have an osteoporotic fracture, and men have higher mortality after hip fracture than women. Men are far less likely to be assessed or treated.

Does osteoporosis hurt?

Not usually, which is why it is called a silent disease. It causes no pain until a fracture occurs. Vertebral fractures can also be painless, showing up only as gradual height loss and increasing stoop.

How long does a broken bone take to heal?

Initial union typically takes six to twelve weeks depending on the bone and your age, with remodelling continuing for up to a year. Controlled loading speeds healing; smoking and poor nutrition slow it considerably.

Explore further

Glossary

Osteoblast
The bone-forming cell that lays down collagen matrix for mineralisation.
Osteoclast
The cell that dissolves bone, and the target of most osteoporosis medications.
Osteocyte
The mature embedded bone cell that senses mechanical strain and directs remodelling.
Cortical bone
The dense outer shell providing most of the skeleton's mechanical strength.
Trabecular bone
The inner honeycomb lattice, metabolically active and lost early in osteoporosis.
Osteoporosis
Reduced bone mass and disrupted architecture leading to increased fracture risk.
Fragility fracture
A fracture from a fall from standing height or less — a marker of underlying bone fragility.
DXA
Dual-energy X-ray absorptiometry, the standard scan for measuring bone mineral density.
Wolff's law
The principle that bone adapts its structure to the mechanical loads placed on it.

Trusted organisations & further reading

Medical disclaimer

This page is for general education and does not replace personalised medical advice. If you have concerning symptoms, or before starting a new supplement, medication or exercise programme, speak with a qualified healthcare professional.