Osteoporosis

Osteoporosis is a condition in which bone strength is reduced, increasing the likelihood of a fragility fracture. It is usually silent until a bone breaks. Assessment therefore focuses on future fracture risk, previous fractures, bone mineral density, falls and treatable causes rather than waiting for pain to appear.

What osteoporosis is Osteoporosis is a systemic skeletal disease in which bone strength is reduced. The bones become more likely to fracture under forces that would not usually break healthy bone. Bone strength depends on both bone mineral density and bone quality. Bone quality includes microscopic structure, turnover, accumulated damage and the properties of the bone material. Osteoporosis is often called a silent disease because it usually causes no symptoms before a fracture. A person cannot reliably feel their bone density falling. The clinical importance of osteoporosis lies in the fractures it makes more likely. Preventing a first fracture and preventing further fractures are therefore the main treatment goals. Bone is living tissue Bone is not a solid, inactive frame. It is living tissue that continually responds to hormones, nutrition, movement, injury and mechanical loading. Specialised cells called osteoclasts remove small areas of old or damaged bone. Osteoblasts then form new bone. This coordinated cycle is called bone remodelling. It repairs microscopic damage and helps bones adapt to changing demands. During childhood and early adulthood, bone formation usually exceeds removal. Peak bone mass is generally reached in early adult life. Later, bone removal can exceed formation. The imbalance becomes more marked after menopause and with some illnesses or medicines. Bone density and bone quality Bone mineral density describes the amount of mineral measured within a defined area of bone. It is an important predictor of fracture risk. Density is not the whole story. Two people with the same DXA result can have different fracture risks because age, falls, previous fractures and bone quality also matter. Microscopic architecture affects how bone distributes force. Thinning and loss of internal struts can weaken bone even when an image still looks reasonably solid. Long term corticosteroid use can increase fracture risk partly through effects that are not fully captured by bone density. This is why modern assessment combines clinical risk factors with bone mineral density rather than treating one scan number as the complete diagnosis. Osteoporosis and fragility fracture are different concepts Osteoporosis describes reduced bone strength or, operationally in many adults, a sufficiently low bone mineral density. A fragility fracture is the clinical event in which a bone breaks after low trauma. A typical example is a fracture after a fall from standing height or less. The two terms are related but are not interchangeable. A person can meet bone density criteria for osteoporosis without having fractured. A person can also sustain a fragility fracture when their T score is above the osteoporosis threshold. Most fractures arise from a combination of bone strength, age, falls and other risks. A fragility fracture should therefore trigger fracture risk assessment even when osteoporosis has not previously been diagnosed. Common fragility fractures Typical sites include the hip, vertebrae, wrist, upper arm and pelvis. Ribs and other bones can also fracture with low trauma. A wrist fracture may be the first visible sign of reduced bone strength. It can occur when someone puts out a hand during a fall. Hip fractures usually follow a fall and can cause major loss of mobility and independence. They require urgent hospital treatment. Vertebral fractures occur when a spinal bone compresses or changes shape. Some cause sudden pain, while others are discovered only after height loss or imaging. One fragility fracture increases the likelihood of another, particularly during the first years after the initial event. Vertebral fractures may be missed Many osteoporotic vertebral fractures do not receive immediate medical attention. They may not cause dramatic pain. Possible clues include new back pain, loss of height, increasing thoracic curvature or difficulty reaching and bending. Several vertebral fractures can shorten the trunk. This can affect balance, breathing, appetite and the space between the ribs and pelvis. Height loss can also result from posture or disc changes, so it does not prove a fracture. When risk factors are present, new back pain, marked height loss or kyphosis may justify vertebral fracture assessment or spinal imaging. Osteoporosis itself usually does not cause general pain Low bone density alone is not usually painful. Pain commonly arises when a fracture occurs or from another musculoskeletal condition. Persistent widespread aching should not automatically be labelled osteoporosis. Osteoarthritis, muscle problems, vitamin D deficiency and other conditions may need consideration. Unexplained focal bone pain can indicate fracture, malignancy, infection or another metabolic bone disorder. This distinction prevents osteoporosis from becoming a catch all explanation for every pain in an older adult. Treatment for osteoporosis aims to reduce future fracture risk. It may not relieve pain caused by osteoarthritis or an old injury. Primary and secondary osteoporosis Primary osteoporosis is associated mainly with ageing and loss of sex hormones, without one separate disease fully explaining the bone loss. Postmenopausal osteoporosis develops partly because reduced oestrogen accelerates bone resorption. Age related changes affect women and men. Secondary osteoporosis results from another condition, medicine or treatment that weakens bone. Examples include long term systemic corticosteroids, untreated hypogonadism, malabsorption, endocrine disease and some cancer treatments. Many people have more than one contributor. Identifying secondary causes can change both treatment and monitoring. Age Fracture risk rises with age even at the same bone mineral density. Falls become more common, and bone quality and protective responses can change. Older age also increases the consequences of fracture. Recovery may be limited by frailty, muscle weakness or other illnesses. Age does not mean that fracture is inevitable. Exercise, falls prevention and effective osteoporosis treatment can still provide meaningful benefit. Younger adults can develop osteoporosis through major risk factors, but routine population assessment is not usually appropriate. Age should be integrated with the complete risk pattern rather than used as a diagnosis by itself. Sex and menopause Women experience osteoporosis more often than men, partly because their average bones are smaller and menopause accelerates bone loss. Oestrogen helps restrain bone resorption. When oestrogen falls after menopause, remodelling can become unbalanced. Early menopause increases the number of years spent with lower oestrogen exposure. Untreated premature ovarian insufficiency is an important risk factor. Men also develop osteoporosis and sustain substantial numbers of fragility fractures. Their risk is often under recognised. Low testosterone, androgen deprivation therapy and other causes of hypogonadism can contribute to osteoporosis in men. Low body weight and nutrition Low body mass index is associated with increased hip fracture risk. Lower body weight may reflect reduced bone mass, muscle mass or nutritional reserve. Unintentional weight loss can indicate malnutrition, malabsorption, cancer or another illness that needs investigation. Very restrictive diets can reduce calcium, protein and energy intake. These nutrients support bone and muscle health. Higher body weight does not eliminate fracture risk. Diabetes, falls and poor bone quality may still increase risk. Assessment should focus on nutrition and health rather than assuming that one body size is protective or blameworthy. Smoking and alcohol Smoking is associated with lower bone density and increased fracture risk. It can also impair healing after fracture or surgery. Stopping smoking benefits bone, cardiovascular and respiratory health. Support and medication can improve the chance of quitting. Alcohol has a dose related relationship with fracture risk. Higher intake can weaken bone, worsen nutrition and increase falls. Alcohol intake above 14 units each week is a NICE fracture risk factor. NOGG advises limiting intake to no more than two units daily. Reducing alcohol should be discussed realistically, particularly when dependence or withdrawal risk may be present. Family and personal fracture history A parental history of hip fracture increases fracture risk independently of bone density. Genetic factors influence peak bone mass, bone shape, remodelling and other biological features. A previous fragility fracture is one of the strongest predictors of another fracture. Vertebral and hip fractures are particularly important. Multiple previous fractures increase risk beyond that of one fracture. Recent fractures can indicate a period of imminent risk. A health problems in the family or previous fracture should therefore influence assessment even when a DXA result is not severely reduced. Long term corticosteroid treatment Systemic glucocorticoids such as prednisolone can reduce bone formation, increase resorption and weaken muscles. Fracture risk can rise quickly after treatment begins and is not fully explained by measured bone density. Risk depends on dose, duration, underlying disease and other factors. Intermittent repeated courses can also matter. People expected to need prolonged systemic corticosteroids may require early fracture risk assessment and preventive treatment. Inhaled, topical and injected corticosteroids usually have lower systemic exposure, but high cumulative doses and individual circumstances still deserve review. Corticosteroids should not be stopped suddenly when adrenal suppression is possible. Bone protection is planned alongside the treatment that remains medically necessary. Conditions causing secondary osteoporosis Endocrine causes include hyperthyroidism, hyperparathyroidism, Cushing's syndrome, diabetes and untreated hypogonadism. Gastrointestinal causes include coeliac disease, inflammatory bowel disease, chronic liver disease and other forms of malabsorption. Rheumatoid arthritis and other inflammatory conditions increase fracture risk through inflammation, inactivity and sometimes corticosteroid exposure. Chronic kidney disease can alter mineral and bone metabolism. Its management may require specialist interpretation rather than routine osteoporosis treatment alone. Haematological disease, including multiple myeloma, can cause bone loss, pain and fractures through different mechanisms. Neurological disease and immobility can weaken bone and increase falls. Parkinson's disease is one important example. Medicines and treatments affecting bone Aromatase inhibitors used in breast cancer and androgen deprivation therapy used in prostate cancer can accelerate bone loss. Some anticonvulsants, thiazolidinediones and excess thyroid hormone can increase fracture risk. Sedatives, antipsychotics, some antidepressants and blood pressure medicines may increase falls, even when their direct effect on bone is uncertain. Proton pump inhibitors have been associated with fracture risk in some studies, but they should not be stopped without reviewing why they are needed. A medication review considers both bone metabolism and falls risk. Necessary treatment should not be removed simply because an association exists. Who should have fracture risk assessment UK guidance uses targeted case finding rather than relying only on symptoms. NICE advises considering fracture risk assessment in all women aged 65 or over and all men aged 75 or over. Younger women and men should be assessed when risk factors are present. Examples include previous fragility fracture, systemic glucocorticoid use, falls, low BMI, smoking and parental hip fracture. NOGG recommends FRAX assessment in postmenopausal women and men aged 50 or over who have a clinical risk factor. People under 50 are not assessed routinely unless major risk factors exist, such as premature menopause, high dose glucocorticoids or previous major fragility fracture. Every fragility fracture is a prevention opportunity Anyone with a suspected fragility fracture should have their future fracture risk considered. The fracture should be treated, but care should not stop when the cast is removed or the operation is complete. A fracture liaison service can identify people after fractures, arrange assessment and ensure treatment and falls interventions are not missed. This secondary prevention approach matters because the risk of another fracture is highest soon after the first. Treatment may sometimes begin without waiting for DXA when the fracture history and clinical risk make the need sufficiently clear. FRAX FRAX is a calculator that estimates the ten year probability of hip fracture and major osteoporotic fracture. Major osteoporotic fracture in FRAX refers to clinical vertebral, hip, forearm or proximal humerus fracture. The calculation includes age, sex, body mass index and selected risk factors. Femoral neck bone mineral density can be added when available. FRAX can be used without a DXA result as an initial step. The result can help decide whether bone density measurement or treatment is appropriate. It is a risk estimation tool, not a diagnostic test. A percentage does not state what will definitely happen to an individual. QFracture QFracture is another validated tool developed using UK primary care data. It estimates cumulative risk of hip fracture and major osteoporotic fracture using a wider set of coded clinical variables. Bone mineral density cannot be entered into QFracture. Its output is not directly interchangeable with FRAX. NICE permits either tool within its validated age range. Local pathways and national treatment thresholds determine how the result is used. A calculator cannot replace clinical judgement when risk factors are severe, recent or incompletely represented. Limitations of risk calculators FRAX does not fully account for fracture number, recency, falls frequency or every effect of high dose corticosteroids. Risk can be underestimated in people with multiple or recent vertebral fractures and some secondary causes. A ten year estimate can also understate immediate risk in a frail older person who has recently fractured. QFracture and FRAX use different methods, so their percentages should not be substituted into each other's treatment thresholds. The most useful explanation combines numbers with context. A clinician may describe how many people out of 100 with a similar profile are expected to fracture. DXA scanning Dual energy X ray absorptiometry, usually shortened to DXA, measures bone mineral density using a low dose of ionising radiation. The hip and lumbar spine are commonly scanned. The forearm may be used when hip or spine measurement is unsuitable. The test is quick and non invasive. The person lies on a table while the scanner passes over the selected areas. DXA measures mineral content projected over an area. It does not directly display microscopic bone quality. Its result is combined with age, fracture history and other clinical risks. Understanding the T score A T score compares the measured bone density with the average peak bone density of a young healthy reference population. A T score of minus 1 means the result is one standard deviation below the young adult reference average. In postmenopausal women and men aged 50 or over, a T score of minus 2.5 or lower at an accepted site supports the densitometric diagnosis of osteoporosis. A T score between minus 1 and above minus 2.5 is commonly called osteopenia or low bone mass. A T score of minus 1 or above is usually described as within the expected normal range for this classification. A T score is not a fracture forecast by itself Lower T scores are associated with higher fracture risk, but no value creates a sharp biological boundary. Someone with a T score of minus 2.4 is not suddenly safe while someone at minus 2.5 is destined to fracture. Many fragility fractures occur in people whose bone density lies in the osteopenic range because that group is large and other risks contribute. Age, previous fracture, falls, corticosteroids and health problems in the family can justify treatment even when the T score is not below minus 2.5. A small numerical change on repeat scanning may reflect measurement variation rather than true biological change. Z scores and younger adults A Z score compares bone density with people of a similar age and sex rather than with young adults. It can be more informative in premenopausal women, younger men and children, where a T score diagnosis may be inappropriate. A markedly low Z score can prompt investigation for secondary causes. The interpretation depends on age, clinical context, scan quality and specialist standards. This lesson focuses mainly on the T score because it is commonly used in postmenopausal women and men aged 50 or over. When DXA is used NICE advises using FRAX or QFracture before routine bone density measurement in most adults. DXA is particularly useful when the calculated risk lies near a treatment threshold and the result could change management. It is also used when treatment may rapidly reduce bone density, such as some breast or prostate cancer therapies. Younger adults with major risk factors may need direct DXA assessment. DXA may not be needed before treatment after some fragility fractures when clinical risk is already clearly high. Investigating secondary causes Assessment includes what the person describes, examination and selected laboratory tests. Common tests may include full blood count, kidney and liver function, calcium, phosphate, alkaline phosphatase, thyroid function and vitamin D. Further tests depend on the presentation. Coeliac screening, parathyroid hormone, sex hormones or myeloma investigations may be appropriate. Persistent focal bone pain, anaemia, high calcium, kidney impairment or unexplained weight loss should not be attributed automatically to osteoporosis. A low DXA result can occur in osteomalacia and other disorders, so the cause must be interpreted rather than assumed. Weight bearing exercise Weight bearing activity means supporting body weight through the skeleton. Walking, stair climbing, dancing and suitable impact exercise are examples. Mechanical loading signals bone to maintain strength. It also supports muscle and physical function. The most appropriate level depends on age, fracture history, balance and other health conditions. A person with severe vertebral osteoporosis may need professional guidance before high impact activity or loaded spinal flexion. Exercise should build confidence and capacity rather than create fear of movement. Muscle strengthening and balance Muscle strengthening exercise supports bone and helps generate the forces that stimulate adaptation. Stronger legs and trunk can improve transfers, walking and protective responses during a loss of balance. Balance training can reduce falls risk. Tai chi and structured balance programmes may suit some people. A falls focused programme should be tailored and progressed. General advice to be careful is not an effective intervention. People with recurrent falls may need physiotherapy, medication review, vision assessment and home hazard evaluation. Calcium adequacy Calcium is a major mineral component of bone. Adults in the UK have a reference nutrient intake of about 700 milligrams daily. Dietary sources include dairy products, calcium set tofu, fortified alternatives, some fish and selected green vegetables. The exact calcium content varies, and some people need dietary assessment to determine whether intake is adequate. Supplements are used when diet is insufficient or when a treatment pathway requires them. More is not automatically better. Excess supplementation can cause gastrointestinal effects and may be unsuitable in some kidney or calcium disorders. Vitamin D adequacy Vitamin D supports calcium absorption and bone mineralisation. It also contributes to muscle function. Sunlight exposure and diet provide vitamin D, but UK production from sunlight is limited during autumn and winter. General UK advice commonly includes a daily supplement during autumn and winter. People at higher deficiency risk may need supplementation throughout the year. NOGG advises at least 800 international units daily when vitamin D insufficiency or clear risk factors are present in people at fracture risk. Deficiency should be corrected before intravenous bisphosphonate or denosumab treatment because severe hypocalcaemia can occur. Nutrition beyond calcium Bone health requires adequate energy and protein as well as calcium and vitamin D. Protein supports the muscles that protect the skeleton and assist recovery after fracture. Unintentional weight loss, poor appetite, swallowing difficulty or food insecurity should prompt nutritional assessment. A varied diet with adequate protein, fruit, vegetables and micronutrients is preferable to relying on one supplement. Calcium and vitamin D do not replace effective anti osteoporosis medicine when fracture risk is high. Smoking cessation and alcohol moderation Stopping smoking reduces several health risks and may improve bone and fracture healing. Behavioural support and licensed cessation treatment can improve success. Alcohol intake should remain within low risk guidance, and NOGG advises no more than two units daily for people at osteoporosis risk. Reducing alcohol can also improve balance, sleep, nutrition and medicine safety. People who may be dependent on alcohol need medically supported reduction because abrupt withdrawal can be dangerous. Falls prevention Bone strength is only one side of fracture prevention. Many hip and wrist fractures begin with a fall. A falls assessment explores previous falls, dizziness, vision, feet, footwear, muscle strength, balance and environmental hazards. Medicines that lower blood pressure, sedate or impair coordination may need review. Home changes can include improved lighting, removal of loose obstacles and appropriate rails. Changes should not create new restrictions or hazards. Walking aids require correct sizing and technique. Fear of falling can itself reduce activity and worsen strength. Bisphosphonates as first line treatment Bisphosphonates reduce osteoclast mediated bone resorption. This helps preserve bone density and lowers fracture risk. Oral alendronic acid and risedronate are common first line choices. Intravenous zoledronate is another cost effective option. Choice depends on fracture risk, kidney function, swallowing, gastrointestinal disease, adherence and personal preference. Zoledronate is particularly useful after hip fracture and when oral dosing is unsuitable. Bisphosphonates reduce risk rather than guaranteeing that no fracture will occur. Taking oral bisphosphonates safely Oral bisphosphonates are poorly absorbed and can irritate the oesophagus. They are usually taken after an overnight fast with plain water before food, drinks or other medicines. The person remains sitting or standing upright for the specified period, commonly at least 30 minutes. Exact instructions vary by drug and formulation. The prescription and patient leaflet should be followed. Difficulty swallowing, oesophageal disease or inability to remain upright may make oral treatment unsuitable. Kidney function and calcium Bisphosphonates require kidney assessment because some are unsuitable in severe renal impairment. The threshold differs between medicines, so kidney function is interpreted against the specific product guidance. Low blood calcium must be corrected before treatment. Vitamin D deficiency is a common contributor. Intravenous zoledronate can cause a short lived flu like reaction, particularly after the first infusion. These considerations guide safe choice. They do not mean that everyone with kidney disease is excluded from fracture treatment. Atypical femoral fracture An atypical femoral fracture is a rare stress type fracture in the shaft or upper portion of the thigh bone. It has been associated with prolonged bisphosphonate treatment and, rarely, denosumab. The absolute risk is small compared with the number of common fragility fractures prevented in appropriately selected high risk patients. Some people develop persistent thigh, hip or groin pain for weeks or months before a complete fracture. New unexplained pain in these areas during long term antiresorptive treatment should be reported and assessed, often with imaging of both femurs. Osteonecrosis of the jaw Osteonecrosis of the jaw involves delayed healing and exposed or damaged jawbone. It is a rare complication at osteoporosis doses of bisphosphonates or denosumab. Risk is much higher with the intensive doses used for some cancers. Dental infection, invasive procedures, smoking, corticosteroids and poor oral health can increase risk. Good oral hygiene and routine dental care are encouraged. Planned dental treatment should be discussed with the dentist and prescribing team. Jaw pain, swelling, loose teeth, discharge or a non healing mouth sore should be reported promptly. Balancing rare risks with fracture prevention Rare adverse effects can sound frightening when presented without context. Hip and vertebral fractures are common and can cause pain, disability, loss of independence and death. For a person at high fracture risk, the expected benefit of appropriate antiresorptive treatment usually greatly exceeds the rare risk of atypical femoral fracture or jaw osteonecrosis. The balance changes with treatment duration, new illness and changing fracture risk. This is why planned review matters. People should not stop effective treatment independently after reading about a rare complication. Denosumab Denosumab is a monoclonal antibody that blocks RANK ligand, an important signal for osteoclast formation and activity. It is given by subcutaneous injection every six months. Denosumab reduces vertebral, non vertebral and hip fractures in appropriate patients. It may be used when bisphosphonates are unsuitable or according to an individual treatment pathway. Calcium and vitamin D status, kidney disease and the risk of hypocalcaemia require assessment before dosing. Denosumab must not be stopped or delayed casually The effect of denosumab reverses relatively quickly when doses are missed or treatment ends. Bone turnover can rebound above the previous level, and bone mineral density can fall rapidly. Multiple vertebral fractures have occurred after stopping or substantially delaying ongoing denosumab. A long term plan must therefore exist before the first injection. Six monthly appointments should be treated as time critical. Denosumab should not be stopped without specialist review and planned follow on antiresorptive treatment. Follow on treatment after denosumab When denosumab ends, another medicine is usually required to limit rebound bone loss. NOGG recommends intravenous zoledronate six months after the last denosumab injection, with further management guided by specialist protocols and bone turnover monitoring where available. The precise plan depends on treatment duration, kidney function, previous fractures and access to monitoring. A bisphosphonate treatment holiday cannot simply be applied to denosumab. Anyone who misses a planned injection should contact the prescribing service promptly rather than waiting for the next routine review. Hormone replacement therapy Hormone replacement therapy can prevent bone loss and reduce fractures while it is being taken. NOGG advises considering HRT as a first line option in selected postmenopausal women aged 60 or under who have high fracture risk and low baseline malignant and thromboembolic risk. The decision also considers menopausal symptoms, womb status, cardiovascular risk and personal preference. HRT is not a universal osteoporosis medicine. Benefits and risks change with age, time since menopause and individual history. When HRT is stopped, fracture risk should be reassessed and another treatment considered when indicated. Selective oestrogen receptor modulators Selective oestrogen receptor modulators, or SERMs, act like oestrogen in some tissues and block it in others. Raloxifene can reduce vertebral fracture risk in postmenopausal women. Evidence for hip fracture prevention is less convincing. It may increase hot flushes and venous thromboembolism risk. A SERM may suit selected women when its benefits and limitations fit their risk profile. It is not used in men and is unsuitable when blood clot risk is high. Bone forming treatments Some medicines primarily stimulate new bone formation. Teriparatide and abaloparatide act through parathyroid hormone pathways. Romosozumab both increases bone formation and reduces resorption. These treatments are generally reserved for people at very high fracture risk, particularly those with vertebral fractures, or when other treatment is unsuitable. They have defined treatment durations and require follow on antiresorptive therapy to preserve gains. Specialist assessment is needed because eligibility, contraindications and sequencing are important. How long bisphosphonates are used Osteoporosis is a long term condition, but bisphosphonate prescriptions should not continue indefinitely without review. NOGG recommends planning oral bisphosphonate treatment for at least five years before reassessing fracture risk. Intravenous zoledronate is generally planned for at least three years before reassessment. Longer treatment is often appropriate for people who remain at high risk, including those with hip or vertebral fractures or ongoing glucocorticoid exposure. A fixed duration cannot be applied safely to every patient. Treatment holidays Bisphosphonates remain in bone after dosing stops, so some lower risk people can have a planned temporary pause after several years. This is commonly called a treatment holiday. It is an active monitoring strategy, not discharge from care. Higher risk people may benefit from continuing treatment rather than taking a pause. Risk is reassessed after a medicine specific interval, sooner if a new fracture occurs or risk factors change. Treatment holidays apply to selected bisphosphonate users. They do not apply to denosumab. Monitoring treatment Review includes adherence, administration technique, adverse effects, new fractures, falls and changes in health. A fracture during treatment does not automatically prove that the medicine failed. No treatment prevents every fracture. Clinicians check whether doses were taken correctly, whether enough time has passed and whether a secondary cause is present. Repeat DXA can help in selected circumstances, but changes must exceed measurement variability to be meaningful. Bone turnover markers are sometimes used by specialists to assess response or guide treatment transitions. New fracture while taking treatment A new fracture deserves prompt reassessment because risk may now be very high. The clinician confirms the fracture mechanism, treatment adherence and whether the medicine was absorbed or administered correctly. Secondary causes, vitamin D deficiency and falls risk are reviewed. Treatment may continue, change to another antiresorptive or escalate to a bone forming medicine. The response should not be an automatic unsupervised doubling or stopping of treatment. Managing vertebral fracture pain An acute vertebral fracture can cause severe localised back pain and muscle spasm. Assessment confirms the diagnosis and excludes neurological compression, cancer, infection and other serious causes. Pain relief, safe movement and early rehabilitation are important. Prolonged bed rest worsens muscle and bone loss. Physiotherapy can support posture, back extensor strength and safe activity after the acute phase. Anti osteoporosis treatment reduces future fracture risk but does not act as immediate analgesia. Fracture prevention is combined care Effective prevention combines bone directed treatment, nutrition, exercise and falls management. A strong bone can still break during major trauma, and a person with moderate bone loss can fracture during a fall. The plan therefore addresses both the chance of falling and the chance that a fall causes a fracture. Vision, medication, muscle strength, home environment and confidence can matter as much as one scan result. The person's priorities and ability to follow treatment determine whether the plan works in practice. The main goal The goal of osteoporosis care is not simply to improve a T score. The aim is to prevent hip, vertebral and other fragility fractures while minimising treatment burden and harm. A good plan identifies treatable causes, explains risk clearly and matches treatment to individual fracture probability. It includes a safe long term strategy for medicines, especially denosumab. It also recognises every fragility fracture as an opportunity to prevent the next one.

Osteoporosis is usually silent until a fragility fracture occurs. Bone mineral density is important, but future fracture risk also depends on age, previous fractures, falls, medicines and secondary causes. Treatment therefore combines risk assessment, bone strengthening medicine when indicated and active falls prevention.