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Evidence-based physiotherapy and rehabilitation resources
Editorial & review policyHuman Anatomy · General anatomy
Bone is the only tissue in the body that rebuilds itself along the lines of the forces you put through it. That single fact explains fracture healing, osteoporosis, why a cast leaves a limb weak, and a great deal of what you will spend your career doing about it.
The dried skeleton in the anatomy laboratory does bone a disservice. It looks like furniture: dry, inert, finished. Living bone is none of those things. It has a blood supply large enough to bleed seriously when broken, nerves that make a fracture agonising, and a cell population that is dismantling and rebuilding it continuously.
You will replace roughly a tenth of your skeleton this year. The femur you have now is not the femur you had a decade ago, even though it has kept the same shape throughout. That shape is maintained by cells reading the forces passing through the bone and adjusting the structure to match.
Why this chapter matters more to you than to most students
Almost everything a physiotherapist does applies force to the skeleton. If bone responds to load, then loading is a treatment — and unloading is a harm. Understanding the mechanism is what separates prescribing exercise from simply encouraging it.
Figure 1 · What bone is for
Notice that the first three functions are mechanical and the last three are metabolic. It is easy to remember bone as a structural material and forget it is also the body's calcium bank and its blood factory. Those two roles explain a great deal of clinical behaviour.
When blood calcium falls, the body will take calcium out of the skeleton to correct it, because a normal blood calcium keeps you alive today and a strong femur only matters tomorrow. Bone always loses that argument. This is why prolonged calcium or vitamin D deficiency weakens the skeleton, and why hormones that regulate calcium have skeletal side effects.
Bone is a composite material, and its properties come from combining two substances that fail in opposite ways.
| Component | Roughly | What it contributes | What happens if it is lost |
|---|---|---|---|
| Mineral calcium hydroxyapatite |
Two thirds by weight | Hardness and stiffness. Resists compression. | The bone becomes soft and bends under load — the pattern seen in rickets and osteomalacia. |
| Organic matrix mostly type I collagen |
One third by weight | Tensile strength and flexibility. Resists being pulled apart. | The bone becomes brittle and shatters, as in osteogenesis imperfecta. |
| Water and cells | The remainder | Nutrition, sensing and the machinery of remodelling. | Without living cells the bone cannot repair or adapt at all. |
The analogy worth carrying is reinforced concrete. Concrete alone is strong in compression and cracks under tension; steel rods alone bend. Put them together and you have something that resists both. Mineral is the concrete, collagen the steel. Remove either and the bone fails, but it fails in a completely different way — which is why two different diseases produce two different fracture patterns.
Figure 2 · The remodelling cycle and the cells that run it
Four cell types maintain the skeleton, and it is worth being precise about which does what, because the names are similar and examiners exploit that.
The cycle they run is continuous and local. A patch of bone is resorbed by osteoclasts, then rebuilt by osteoblasts, and the whole event takes a few months in one small area. Thousands of these are running across your skeleton at any moment. When formation and resorption stay balanced, bone mass holds steady. When resorption outpaces formation, mass falls — which is what osteoporosis is.
A detail worth holding on to
The osteocyte is the sensor. Sitting trapped in its lacuna, connected to its neighbours by fine processes running through canaliculi, it detects the tiny fluid movements caused when bone is loaded — and signals for more bone where the loading is high. It is the cell that makes bone responsive to what you ask a patient to do.
Figure 3 · Bone answers to the load placed on it
The principle is old and it is not controversial: bone adapts its structure to the loads placed on it. Load a bone habitually and it lays down more material along the lines the force travels. Stop loading it and the material is taken away.
You can see this in the femoral neck, where the trabeculae are not arranged randomly but line up along the paths that compression and tension follow through the joint. It is the same arrangement an engineer would choose, arrived at by cells reading local strain.
| Situation | What happens to bone | What it means for you |
|---|---|---|
| Weight-bearing exercise, especially with impact or resistance | Formation is stimulated where the load is applied | The stimulus is local. Loading the legs does little for the wrist. |
| Prolonged bed rest, immobilisation in a cast, non-weight-bearing after surgery | Resorption dominates and bone mass falls | Losses begin within weeks. This is a reason to load early and safely, not to wait for full healing. |
| Swimming and cycling | Good for the heart and muscles; a weak stimulus to bone | Excellent exercise that should not be relied on to protect the skeleton. |
| Long-term corticosteroid treatment | Formation is suppressed and resorption favoured | Ask about it. It changes how cautious you are with loading and falls risk. |
Figure 4 · Classification of bones by shape
Illustration to be added
Six labelled specimens on one plate: long (humerus), short (a carpal bone), flat (sternum or parietal bone), irregular (a lumbar vertebra), sesamoid (patella shown within the quadriceps tendon), pneumatic (maxilla, sectioned to reveal the air sinus). Each named, with a one-line caption slot beneath. Clean line illustration, navy line work on white, bone in warm ivory.
Bones are grouped by shape, and the shape follows the job.
| Type | Description | Examples | Why that shape |
|---|---|---|---|
| Long | Longer than wide, with a shaft and two ends | Humerus, femur, tibia; also the metacarpals and phalanges, despite their size | Acts as a lever. Length multiplies the movement a muscle produces. |
| Short | Roughly cube-shaped | Carpals, tarsals | Allows many small gliding movements while staying stable under load. |
| Flat | Thin, often curved; two plates of compact bone with spongy bone between | Skull vault, sternum, ribs, scapula | Protects, and gives a broad surface for muscle attachment. |
| Irregular | Complex shapes that fit no other group | Vertebrae, hip bone, bones of the face | Shaped by the many things attaching to and passing through them. |
| Sesamoid | Develops within a tendon | Patella, the largest; also small ones at the thumb and great toe | Holds the tendon away from the joint, increasing its leverage and reducing friction. |
| Pneumatic | Contains air spaces | Maxilla, frontal, ethmoid, sphenoid | Lightens the skull and gives resonance to the voice. |
| Accessory or sutural | Extra, inconstant bones | Wormian bones in skull sutures | Normal variants. Worth knowing so they are not mistaken for fractures on imaging. |
Figure 5 · The structure of a long bone
Take the femur as the model, since every long bone follows the same plan.
| Part | What it is | Clinical note |
|---|---|---|
| Diaphysis | The shaft. A thick tube of compact bone around a hollow medullary cavity. | A tube resists bending far better than a solid rod of the same weight. |
| Epiphysis | The expanded end, mostly spongy bone with a thin compact shell, capped by articular cartilage. | The broad end spreads joint load over a wider area, lowering pressure. |
| Metaphysis | The flared region between shaft and end. | Richly supplied with blood, which is why bone infection in children tends to settle here. |
| Epiphyseal plate | The cartilage growth plate, present until skeletal maturity, after which it leaves a visible line. | Growth happens here. Injury to it in a child can disturb growth, so paediatric fractures near a joint are treated with respect. |
| Periosteum | A tough sheath covering the bone except at joint surfaces. Fibrous outer layer, cellular inner layer. | Richly innervated, so it is the source of fracture pain. Its inner layer supplies the cells that heal the fracture. |
| Endosteum | A thin cellular lining of the medullary cavity and the spaces in spongy bone. | Also a source of bone-forming cells. |
| Medullary cavity | The central space, holding marrow. | Red marrow makes blood cells; yellow marrow is mostly fat. Red converts to yellow with age, and back again if the body needs blood cells urgently. |
Both are made of the same material. They differ only in how it is arranged, and the arrangement follows the load.
Dense, solid to the naked eye, forming the outer shell of every bone and the walls of the shaft. Built from osteons — concentric cylinders of bone around a central canal carrying a vessel and nerve. Strong along the direction the osteons run, which is the direction the load usually comes from.
An open lattice of struts called trabeculae, found at the ends of long bones and inside flat and short bones. Light, and arranged along the lines of stress. The spaces hold marrow. Because it has far more surface area exposed to marrow, it turns over faster — so it is lost first in osteoporosis.
Figure 6 · Microscopic structure of compact bone
That last point deserves emphasis, because it explains a clinical pattern you will meet constantly. Spongy bone remodels faster than compact bone, so when bone is being lost the sites richest in spongy bone give way first. Those sites are the vertebral bodies, the femoral neck and the distal radius — which are exactly the three commonest osteoporotic fracture sites.
Bone develops in two ways. Both end with the same tissue; they differ in what was there before.
Figure 7 · Intramembranous and endochondral ossification
Illustration to be added
Two rows. Top row, intramembranous, four stages: mesenchymal condensation, ossification centre with osteoblasts, woven bone spicules, mature compact plates of a flat skull bone. Bottom row, endochondral, five stages: hyaline cartilage model, periosteal bony collar, primary ossification centre in the diaphysis with vascular invasion, secondary centres appearing in both epiphyses, and the mature bone with growth plates remaining. Cartilage pale blue, bone warm ivory, vessels red.
| Intramembranous ossification | Endochondral ossification | |
|---|---|---|
| Forms in | Fibrous membrane directly | A cartilage model, which is replaced |
| Which bones | Flat bones of the skull vault, most of the face, the clavicle | Nearly all the rest: long bones, vertebrae, pelvis, base of the skull |
| Sequence | Mesenchymal cells cluster and become osteoblasts, which lay down matrix directly. Woven bone forms, then is remodelled into compact plates. | A cartilage model forms, a bony collar appears around the shaft, the primary centre appears in the middle, then secondary centres appear in each end. |
| Growth afterwards | By adding bone at the edges and surfaces | In length at the growth plate, in width by adding at the surface |
| Why it matters | Skull bones are separated at birth by fontanelles, allowing the head to mould during delivery and the brain to grow. | Growth plates are cartilage and therefore weaker than the bone around them. In a child they fail before the ligaments do. |
The consequence you must not forget
In an adult, a violent twist at the ankle tears a ligament. In a child, the ligament is stronger than the growth plate, so the plate gives way instead. A child with a painful ankle after an injury and tenderness over the bone end should be assumed to have a growth plate injury until imaging says otherwise — not treated as a sprain.
A long bone must get longer and thicker at the same time, and it does the two by different mechanisms.
Length comes from the epiphyseal plate. On the epiphyseal side, cartilage cells divide and enlarge, pushing the end away from the shaft. On the diaphyseal side, that cartilage is calcified and replaced by bone. The plate itself stays roughly the same thickness while the bone lengthens beneath it. When growth finishes the plate is fully ossified and fuses, leaving the epiphyseal line.
Width comes from the periosteum, which adds bone to the outer surface, while the endosteum removes it from inside. The shaft therefore grows wider without becoming impossibly heavy, and the medullary cavity enlarges to match.
Why bones stop growing when they do
Growth hormone and thyroid hormone drive growth at the plate through childhood. The sex hormones at puberty cause a growth spurt and then close the plates. Because oestrogen closes plates more strongly, girls generally finish growing earlier than boys. Once the plate has fused, no amount of anything will make a bone longer.
Figure 8 · Blood supply of a long bone
Illustration to be added
A long bone with the nutrient artery entering the shaft obliquely through its foramen, dividing into ascending and descending branches; metaphyseal and epiphyseal vessels entering near each end; periosteal vessels supplying the outer shaft; and the anastomoses between them. A second smaller panel showing the femoral neck, with the retinacular vessels running up the neck to the head and a fracture line drawn across them to explain avascular necrosis. Arteries in red on navy line work.
A long bone receives blood from four sources: a nutrient artery entering the shaft obliquely, metaphyseal and epiphyseal vessels entering near the ends, and periosteal vessels supplying the outer layers of the shaft. In a healthy bone these anastomose, so damage to one is survivable.
The trouble comes where they do not. At a few sites the supply runs in one direction only, and a fracture across that point cuts off everything beyond it. The bone downstream dies — avascular necrosis.
| Site | What goes wrong | Consequence |
|---|---|---|
| Femoral head | Most of its supply runs up the femoral neck. A displaced neck fracture divides those vessels. | The head may die and collapse. It is a large part of why displaced neck fractures in older adults are often replaced rather than fixed. |
| Scaphoid | Blood enters from the distal end and runs backwards through the bone. | A fracture across the waist strands the proximal fragment. Scaphoid fractures are slow to unite and are treated cautiously. |
| Talus | Largely covered in articular cartilage, leaving little surface for vessels to enter. | Neck fractures risk necrosis of the body of the talus. |
These three come up in every examination, and they are worth learning as a principle rather than a list: where blood enters a bone from one direction only, a fracture across that path is dangerous.
Fracture healing is the same remodelling machinery running at speed. It happens in overlapping stages rather than tidy steps.
| Stage | Roughly | What happens | What it means clinically |
|---|---|---|---|
| Haematoma | Hours to days | Bleeding from bone and periosteum forms a clot; inflammatory cells arrive. | The pain and swelling of the first days. The clot is the scaffold, not waste. |
| Soft callus | Days to about 3 weeks | Fibrous tissue and cartilage bridge the gap. | The fracture is uniting but cannot bear load. Protection matters most here. |
| Hard callus | About 3 to 12 weeks | The soft callus is replaced by woven bone through endochondral ossification. | Clinical union. Loading can usually begin and is a stimulus, not a threat. |
| Remodelling | Months to years | Woven bone is replaced by organised lamellar bone; the excess callus is trimmed along the lines of load. | Strength keeps improving long after discharge, and it improves faster in a limb that is used. |
Three things reliably slow this down, and all three are worth asking about: a poor blood supply at the site, movement between the fragments, and infection. Smoking, poor nutrition, diabetes and some medicines slow it further.
It is one of the most metabolically active tissues you have. Every clinical property that matters — healing, adaptation, loss with disuse — follows from it being alive.
Spongy bone is not inferior compact bone. It is a lattice arranged along the lines of stress, giving strength for very little weight. It is lost first in osteoporosis because it turns over faster, not because it was ever poorly built.
The anchor is simple: intramembranous forms in a membrane, and is mostly skull. Endochondral forms in cartilage — chondral is the clue — and is nearly everything else.
Until the plates fuse, the growth plate is the weak link, not the ligament. The same force produces a sprain in an adult and a plate injury in a child.
The stimulus is mechanical load, and it is local. Swimming and cycling are excellent for many things and weak stimuli to the skeleton. If bone is the target, the load has to reach the bone you are targeting.
Clinical union is not full strength. Remodelling continues for months, and it continues faster in a limb that is being used than in one being protected.
Ten questions on this chapter. Tap one to see the answer and the reasoning.
Answer: (B) Collagen provides tensile strength and flexibility; mineral provides hardness and resists compression. Lose the collagen and bone becomes brittle, as in osteogenesis imperfecta.
Answer: (C) The osteocyte. Trapped in its lacuna and linked to neighbours through canaliculi, it detects the fluid movement produced when bone is loaded.
Answer: (C) Bone responds to local load. Removing load from that limb tips the cycle towards resorption in that limb, while the rest of the skeleton continues as normal.
Answer: (B) The patella, and it is the largest sesamoid in the body. It develops within the quadriceps tendon and improves the leverage of that tendon at the knee.
Answer: (B) The metaphysis is richly vascular, and the arrangement of its vessels slows flow, which favours organisms settling there.
Answer: (B) Intramembranous ossification, directly within a fibrous membrane. This is why the newborn skull has fontanelles between bones that have not yet met.
Answer: (B) Appositional growth. The periosteum adds bone to the outside while the endosteum resorbs it from the inside, so the shaft widens and the marrow cavity enlarges with it.
Answer: (B) The retinacular vessels run along the neck to reach the head. A displaced fracture divides them, and the head can die and collapse.
Answer: (C) Hard callus, when woven bone has replaced the soft callus. Load then becomes a stimulus to remodelling rather than a threat to the repair.
Answer: (B) Spongy bone has far more surface exposed to marrow, so it remodels faster and is lost first when resorption outpaces formation.
Everything on this page, in one screen
| Book | What it adds here |
|---|---|
| B D Chaurasia's Handbook of General Anatomy Chaurasia and Garg |
The chapter on the skeleton covers this material in the order used above, and is closely matched to Indian examinations. |
| Anatomy and Human Movement: Structure and Function Palastanga, Field and Soames |
Best for the mechanical side: why trabeculae line up as they do and what that means for loading. |
| BRS Cell Biology and Histology Gartner |
For the microscopic detail of the osteon and the four cell types, if you want more than this chapter gives. |
| Principles of Bone Biology | A reference work, not a textbook. Worth knowing it exists if you go on to research bone. |
Reviewed by the Physiotherapist India Team. · Human Anatomy contents