NU 245 · NursingSection 2.5 · Musculoskeletal and skin disorders

Section 7 of 18

Osteoporosis, rickets and osteomalacia

Explain how bone is normally broken down and rebuilt, describe how that balance fails in osteoporosis, and distinguish osteoporosis from the failure of hardening that causes rickets in children and osteomalacia in adults, naming the causes, signs, investigations and nursing priorities of each.

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Why this matters

Osteoporosis gives no early warning: its first sign is often a hip that breaks on the way to the bathroom, or a vertebra that collapses while the patient bends to pick up a bag. Rickets and osteomalacia are equally quiet and are still seen in children who lack sunlight and in adults who cannot absorb vitamin D. These three conditions are not curiosities of the textbook — they decide whether an older adult walks again after a fall, and whether a child’s legs grow straight. Understanding the mechanism lets you recognise the risk on admission, prevent the fall before it happens, and explain to the patient why a daily tablet, a walk in the daylight and a safer bathroom matter more than any single test result.

What you need to know first

You need only the idea from the previous section that bone is living tissue rebuilt throughout life, plus the everyday knowledge that calcium and vitamin D come from food and sunlight. Remodelling, osteoid, the growth plate and the way vitamin D is activated are all defined where they first appear, so no previous physiology course is assumed.

Words to know (5)

Bone remodelling: The lifelong cycle in which osteoclasts remove small patches of old bone and osteoblasts replace them with new bone. When removal works faster than replacement, bone becomes porous and weak, which is what happens in osteoporosis.
Osteoporosis: A disease in which bone strength is reduced, so the bone becomes brittle and breaks under a stress that healthy bone would tolerate. A fall from standing height, a bend or even a cough can break the hip, wrist or spine of a person with advanced osteoporosis.
Fragility fracture: A break caused by a fall from standing height or less, or by a force that would not break a healthy bone. A hip fractured in the bathroom is the classic fragility fracture, and it is often the first sign that osteoporosis was present.
Osteomalacia: Softening of adult bone because the protein framework is laid down normally but is not hardened by calcium and phosphate. An adult with osteomalacia complains of aching bones, muscle weakness and difficulty climbing stairs rather than of deformed legs.
Rickets: The same failure of hardening in a growing child, where it also disturbs the growth plates and produces skeletal deformities. A child with rickets may have bow legs, thickened wrists and ankles, and a walk that looks like a waddle.

One idea at a timeIdea 1 / 5

In one sentence Old bone is removed and new bone is laid down every day, so bone strength depends on which of the two is winning.

Bone is broken down and rebuilt all your life, and peak strength is set around age 30

Bone is living tissue, not a fixed scaffold. Throughout life, small patches of old bone are eaten away by cells called osteoclasts and replaced by new bone made by osteoblasts; this constant renewal is called remodelling. In childhood and adolescence the building side works faster, so bone mass grows and the skeleton becomes denser and stronger. Most people reach their peak bone mass during the third decade of life, at around 30 years. After that the two sides slowly change places: in many people, removal begins to outpace rebuilding, and bone mass falls gradually. Osteoporosis is what happens when that gap has become large. It is a disease in which bone strength is reduced, so the bone becomes weak and brittle and breaks under a stress that healthy bone would tolerate — a fall, a bend, or even a cough. The breaks happen most often in the hip, the wrist and the spine. Because the loss is slow and painless, the disease is invisible until the first fracture, which is why a broken wrist in an older person is treated as a warning about the whole skeleton and not merely as an accident.

For example

Two women fall in the same way at home. The one of 30 bruises her hip; the one of 75 fractures it, because her skeleton has already lost much of the strength it once had.

Pause and check yourself

During which period of life does bone mass increase, and which side of the balance wins afterwards in most older adults?

Show the answer

Bone mass increases during childhood and adolescence until peak mass is reached around age 30; afterwards removal by osteoclasts slowly outpaces rebuilding by osteoblasts, so bone mass falls.

Read detailed explanations

The cellular tug-of-war: RANKL, oestrogen withdrawal and why the T-score matters

Under the microscope, every remodelling cycle is a short conversation between three cell types. Osteocytes buried in the matrix sense microdamage and signal for repair. Osteoblasts then release two opposing molecules: RANKL, which binds a receptor on osteoclast precursors and drives osteoclastogenesis, and osteoprotegerin, a decoy receptor that mops up RANKL and restrains resorption. The balance between those two signals, more than the number of cells present, decides how much bone is removed. Several hormones move that balance. Oestrogen restrains osteoclast formation, so the fall in oestrogen after the menopause removes a brake and accelerates loss for five to ten years.

Parathyroid hormone, secreted whenever ionised calcium falls, stimulates resorption in order to defend the serum calcium, while calcitriol, the activated form of vitamin D, increases intestinal absorption of calcium and phosphate. In chronic vitamin D deficiency, a low calcium therefore drives a secondary hyperparathyroidism that strips mineral from the skeleton to keep the blood level normal, so density falls while the serum calcium can still look acceptable. Bone is not lost evenly. Trabecular bone, the spongy interior that fills vertebrae, the wrist and the femoral neck, has a large surface area and is lost first; cortical bone, the dense shell of long bones, thins later but contributes to hip fractures. That is why vertebral collapse and wrist fracture tend to appear earlier than mid-shaft fractures. Measurement follows the anatomy.

Dual-energy X-ray absorptiometry compares the patient’s bone mineral density with the mean of a young healthy adult and expresses the difference as a T-score, the number of standard deviations above or below that mean. A score between −1 and −2.5 defines osteopenia; −2.5 or lower defines osteoporosis; and a fragility fracture in the presence of such a score defines severe disease. Because density alone does not capture every risk, tools such as FRAX combine the T-score with age, sex, previous fracture, smoking and corticosteroid use to estimate the ten-year probability of a major fracture.

Osteoid, the growth plate and why one deficiency bends a child and softens an adult

Bone matrix is a protein scaffold, mostly type I collagen, that must be hardened before it can carry load. Hardening happens when crystals of calcium and phosphate, in the form of hydroxyapatite, are deposited along the collagen fibres; the process is called mineralisation. Vitamin D is the gatekeeper. Cholecalciferol made in the skin or taken in food is converted by the liver to 25-hydroxyvitamin D, the form measured in blood, and then by the kidney to calcitriol, the active hormone that makes the gut absorb calcium and phosphate. When any link in that chain fails, the scaffold is laid down normally but never hardens, so osteoid, the unmineralised matrix, accumulates.

Two laboratory clues follow: serum alkaline phosphatase, an enzyme produced by the overactive osteoblasts, rises, and serum phosphate falls because the rising parathyroid hormone drives phosphate out through the kidneys, a phosphaturia. The clinical result depends on age, because a growing child still has epiphyseal growth plates. In rickets, mineralisation fails at the growth plate as well as in the matrix: the cartilage plate widens and becomes irregular, the metaphyses enlarge into the beaded appearance called the rachitic rosary when it affects the rib ends, the wrists and ankles thicken, the skull softens, a finding named craniotabes, and the soft shafts bend under the child’s weight into genu varum, the bow legs.

In an adult the growth plates have closed, so the same deficiency produces osteomalacia instead: generalised bone pain and tenderness, proximal muscle weakness that makes rising from a chair or climbing stairs difficult, a waddling gait, and pseudofractures — thin radiolucent lines called Looser’s zones, where unmineralised bone has cracked under normal load. This is the single most useful distinction to carry to the bedside: rickets is a disease of the growth plate and shows deformities, whereas osteomalacia is a disease of the matrix and shows pain, weakness and pseudofractures.

Treatment is two jobs at once: stop the loss and rebuild the bone

Treatment of osteoporosis runs in two directions: slow the removal of bone, or stimulate the building of new bone. The antiresorptive drugs are the first line. Bisphosphonates — alendronate, risedronate, ibandronate and zoledronic acid — bind to bone mineral and cause osteoclasts to stop working and die. Their oral forms are poorly absorbed and can injure the oesophagus, so the nurse teaches the patient to take the tablet on an empty stomach with a full glass of plain water and to stay upright, sitting or standing, for at least thirty minutes before any food or other medicine. Denosumab is a monoclonal antibody that blocks RANKL and is given subcutaneously; because it suppresses resorption strongly, calcium must be adequate before every dose.

The anabolic drugs are reserved for severe disease: teriparatide and abaloparatide are parathyroid hormone fragments given by daily injection, and romosozumab blocks sclerostin in order to increase bone formation. All of them need calcium and vitamin D to be sufficient, otherwise they cannot work. Long-term suppression carries rare but serious risks — osteonecrosis of the jaw and atypical femoral fractures — so any new jaw pain or thigh pain is reported rather than tolerated, and the need for treatment is reviewed periodically. In rickets and osteomalacia the logic is replacement rather than suppression: oral vitamin D for months, with calcium and phosphate added according to the blood results, and treatment of the underlying cause, whether that is coeliac disease, kidney or liver disease, or an antiseizure medicine.

Because correcting the deficiency mobilises calcium, monitoring is needed for hypercalciuria and nephrolithiasis. Nursing care is largely about safety and is similar in both conditions: remove the fall hazards in the room, check vision and footwear, review sedative medicines, encourage daily weight-bearing activity and safe sunlight exposure, relieve pain, and anticipate constipation from immobility, reduced activity and calcium supplements by giving fluids, fibre and prescribed stool softeners.

Explore the diagram

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Three weak bones, two mechanisms

Compare the same bone in three states. In healthy bone, osteoclasts remove old bone and osteoblasts rebuild it at matching rates, so the trabeculae stay thick. In osteoporosis the removal outpaces the rebuilding: the trabeculae thin and the cortex narrows, leaving normally hardened but brittle bone that snaps. In rickets and osteomalacia the framework is built but never hardened, so the bone stays soft and bends. Reading the three panels together separates a loss of bone quantity from a loss of bone quality.

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01 / 4Balanced remodelling

If the drawing is wider than this panel, scroll it sideways. Labels stay readable; the numbered explanations below show the same ideas.

Balanced remodelling

Bone is continuously resorbed by osteoclasts and rebuilt by osteoblasts. In a healthy adult the two rates are matched, so the amount of bone stays stable, and osteocytes direct the repair to the sites of microdamage. Peak bone mass is reached at around 30 years, and everything that happens afterwards is a slow change in this balance rather than a single event.

Schematic, not anatomical: the same block of bone is drawn three times at one size, and the trabeculae are shown as straight lines to make thinning and the fracture visible. The bowing in panel 3 is exaggerated so the effect of a soft framework is obvious; a real long bone bends more gradually.

Key points to remember

Bone is removed and rebuilt throughout life; mass rises to a peak around age 30, then loss slowly outpaces rebuilding in many people.
Osteoporosis is reduced bone strength with normal hardening of what remains; it causes fragility fractures of the hip, wrist and spine and has many risk factors, not one cause.
Osteoporosis is silent until it breaks a bone: look for a collapsed vertebra, height loss and a stooped posture, confirm with bone density, and prevent the next fracture with calcium, vitamin D, weight-bearing exercise and fewer falls.
Rickets and osteomalacia are the same failure of hardening, in a child with active growth plates and in an adult whose plates have closed; the usual cause is vitamin D deficiency, poor absorption or failure of activation.
Rickets gives pain, a waddling walk, thickened wrists and ankles, bow legs and dental problems; osteomalacia gives bone pain, muscle weakness and fractures. Treatment is vitamin D for months, plus calcium or phosphate, plus treating the cause.

Go deeper

Worked example

A 78-year-old woman with sudden back pain after bending. A woman of 78 feels a sharp pain in the middle of her back while bending to pick up a shopping bag. She has no history of a fall and no injury. She is 4 cm shorter than she was five years ago, has a small frame, went through the menopause at 50, and eats very little dairy. Her X-ray shows a wedge-shaped collapse of a thoracic vertebra.

Explain how a bag can break a bone. The force needed to lift a bag is trivial for healthy bone; a vertebral collapse at that moment tells you the bone had already lost much of its strength. The mechanism is the imbalance you studied: after the peak around age 30, removal of old bone slowly outpaces the building of new bone, and the gap widens after the menopause.
Read her risk profile. Female sex, age 78, a small body frame, menopause at 50, a diet very low in calcium and no reported weight-bearing activity are several risks acting together. This is not one cause but a cumulative profile, and it is exactly why risk is assessed from the history rather than from a single test.
Why the spine rather than the leg. The vertebrae are rich in the spongy interior bone that has the largest surface for removal, so it is lost early. That is why a vertebra can collapse under ordinary load and why the patient loses height and becomes stooped, often before any hip fracture occurs.
Ask what else could soften the bone. Sudden bone pain in an older adult is not always osteoporosis. Vitamin D deficiency, coeliac disease, kidney or liver disease and antiseizure medicines can produce osteomalacia, which also causes bone pain and fractures. Her vitamin D, calcium, phosphate, alkaline phosphatase and renal function are therefore checked before the diagnosis is closed.
Set the nursing priorities. Relieve the acute pain and assess its characteristics after analgesia, because the pain of a collapsed vertebra is severe. Prevent constipation, which follows immobility and calcium supplements. Prevent the next fracture by reviewing the home for fall hazards, checking vision and footwear, encouraging safe daily weight-bearing activity and sunlight, and teaching the prescribed medicines that slow bone removal and the calcium and vitamin D that must accompany them.

The collapsed vertebra is the disease announcing itself. The important clinical move is not to treat the X-ray but to treat the whole skeleton: confirm the diagnosis, exclude a hardening problem such as osteomalacia, supply calcium and vitamin D, start the prescribed medicine that slows bone removal, and build a fall-prevention plan with the patient. That is what turns one fracture into a prevented second fracture.

Common misconception

Many beginners collapse osteoporosis, rickets and osteomalacia into one idea: “weak bones caused by too little calcium, so calcium tablets will fix it.” That model hides three different mechanisms. In osteoporosis the amount and architecture of bone are lost because removal outpaces rebuilding, and the bone that remains is normally hardened; in rickets and osteomalacia the amount of framework may be normal but it is not hardened, so the bone is soft. This is why osteoporosis is usually painless until it breaks, while osteomalacia causes aching bones and muscle weakness. It is also why calcium alone does not treat either condition: bone cannot be rebuilt without vitamin D and without treating the cause, and soft bone cannot harden without vitamin D to absorb the minerals at all.

Check your reasoning

A man of 70 has taken prednisone for three years for a lung condition. He now has a wrist fracture after a minor fall, and he tells you he has stopped dairy products and never goes outside. Using this section, explain his likely diagnosis, what else must be excluded, and the three things you would teach him before discharge.

Reveal an answer

The likely diagnosis is osteoporosis. Long-term corticosteroid treatment interferes with bone rebuilding, his age and sex add risk, avoiding dairy removes the calcium supply, and staying indoors removes both weight-bearing activity and the sunlight the skin needs to make vitamin D — several causes acting on the same balance. A fracture from a minor fall at his age is by definition a fragility fracture. Before concluding, you must exclude a failure of hardening: his vitamin D, calcium, phosphate and alkaline phosphatase are checked, because osteomalacia also causes bone pain and fractures and is treated differently. The three teaching points are: take the calcium and vitamin D prescribed, and explain that vitamin D is what allows calcium to be absorbed; restart safe weight-bearing activity and regular daylight exposure rather than complete rest; and take the prescribed medicine for bone exactly as directed while reducing fall risks at home. He also needs to know that his prednisone dose can only be changed by the prescriber, never stopped suddenly.

Where this comes from

MUSKULOSKELETAL SYSTEM PATHOLOGIES lecture notes (supplied), Level 200 nursing · Lines 426–472: osteoporosis definition and causes (remodelling by osteoclasts and osteoblasts, oversupply of osteoclasts or undersupply of osteoblasts, peak bone mass in the third decade and loss afterwards), risk factors (sex, age, ancestry, family history, body frame; sex hormones, thyroid, parathyroid and adrenal glands; low calcium intake and eating disorders; gastrointestinal surgery; corticosteroids; coeliac disease, inflammatory bowel disease, kidney or liver disease, cancer, multiple myeloma, rheumatoid arthritis; sedentary lifestyle, alcohol and tobacco), complications (hip, wrist and spine fractures, vertebral collapse, back pain, height loss and stooped posture), symptoms, diagnosis, prevention (calcium 1,000 mg rising to 1,200 mg; vitamin D 600 IU rising to 800 IU after 70; exercise) and treatment, nursing diagnosis and interventions.
MUSKULOSKELETAL SYSTEM PATHOLOGIES lecture notes (supplied) — rickets and osteomalacia · Lines 473–518: definition of rickets and osteomalacia, the roles of calcium, phosphorus and vitamin D, causes (low vitamin D, poor diet and inadequate sun exposure, surgery removing stomach or intestine, coeliac disease and destruction of the villi, liver or kidney disease preventing vitamin D activation, antiseizure drugs), signs and symptoms (pain, waddling walk, thickened ankles, wrists and knees, bow legs, soft skull, dental problems, poor growth, fragile bones), diagnosis, management and treatment (vitamin D for months, calcium and phosphate supplements, treating the cause, painkillers, braces, surgery), complications and nursing diagnosis and interventions.
Beyond the supplied notes: correction of two source values, and the mechanism they describe · the notes give “20 to 50 ng/mL or 400 IU” as one recommendation, but 20–50 ng/mL is a target serum 25-hydroxyvitamin D concentration (about 50–125 nmol/L) while 400 IU is a dose, not a concentration; the notes’ own prevention text gives 600 IU a day rising to 800 IU after 70, which is the conventional adult intake, and this section uses that figure. The notes also present a complication of osteomalacia as “kidney failure” caused by calcium clumping in the bloodstream; in vitamin D deficiency the serum calcium is low, not high, and the renal risk is hypercalciuria and kidney stones, chiefly during or after treatment, not kidney failure from a high blood calcium. Both corrections are labelled here rather than echoed in the lesson.
Beyond the supplied notes: standard physiology and pharmacology of bone turnover and vitamin D · RANKL and osteoprotegerin signalling with osteoclastogenesis, oestrogen withdrawal and secondary hyperparathyroidism, trabecular versus cortical bone, and dual-energy X-ray absorptiometry with the T-score thresholds for osteopenia (−1 to −2.5) and osteoporosis (at or below −2.5); osteoid and mineralisation, hepatic 25-hydroxylation and renal calcitriol, alkaline phosphatase and phosphaturia, rickets at the epiphyseal growth plate with the rachitic rosary, craniotabes and genu varum, and Looser’s zones in osteomalacia; and the bisphosphonate, denosumab, teriparatide, abaloparatide and romosozumab classes with their administration precautions. The supplied notes list these conditions and their management but do not explain the cellular mechanisms, which are uncontroversial standard teaching.

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About this course and its sources

The musculoskeletal and neurological lessons build on the supplied Level 200 nursing notes. Reproductive, respiratory, skin and nursing-response lessons use cited external references. Diagrams are original educational schematics. Sections that go beyond the supplied notes say so in their sources. Specialist clinical and French-language editorial review remain pending.