History and exam
Key diagnostic factors
common
advanced age
The risk of osteoporotic fractures increases significantly with age for both men and women.[8] It is estimated that 50% of white women and 20% of white men aged >50 years will sustain an osteoporotic fracture at some point during their lifetime.[10] In women, the lifetime risk of clinically significant osteoporotic vertebral compression fracture increases sixfold from menopause to age 85 years.[21]
ethnicity
Rates of fracture differ by ethnic/racial population and skeletal site.[11] For fracture at any site in women, after adjusting for BMD, weight, and other co-variates, non-Hispanic white and Hispanic-American women have the highest risk for fracture, followed by Native Americans, African Americans, and Asian Americans. For hip fracture in men, the age-adjusted incidence is highest for non-Hispanic white men, similar among Hispanic-American and black men, and lowest in Asian men.[11][12][13]
previous osteoporotic vertebral compression fracture
Women with a previous history of osteoporotic compression fracture have a fivefold increased risk of developing subsequent compression fractures.[22]
acute back pain
Patients may report sudden dull or sharp back pain from atraumatic activities such as standing from a seated position, bending forwards, or coughing and sneezing. Pain is characteristically exacerbated by movement.
Other diagnostic factors
common
history of long-term corticosteroid use
Prolonged or repeated use of oral or high-dose inhaled glucocorticoids is associated with osteoporosis.[11][31] The mechanisms of corticosteroid-induced osteoporosis are multifactorial and include osteoclast activation, osteoblast inhibition, decreased gastrointestinal and renal calcium absorption, and decreased gonadotrophin secretion.[32]
bone-losing medications
In addition to corticosteroids, several other medications are associated with reduced bone mass: aromatase inhibitors (e.g., letrozole, exemestane, anastrozole); gonadotrophin-releasing hormone agonists (e.g., leuprorelin); immunosuppressants; anticonvulsants (e.g., phenobarbital, phenytoin); cytotoxic drugs; lithium; long-term heparin; depot medroxyprogesterone acetate.
Some drugs increase the risk of fracture including levothyroxine (decreased bone density), loop diuretics (impair calcium absorption in kidney), and proton-pump inhibitors (reduce calcium absorption).[31][39][40] Medications that cause sedation (e.g. antidepressants, opioid analgesics) or postural hypotension (antihypertensives) increase the risk of falls.[40][41]
kyphotic deformity
Patients may have a local kyphosis at the site of the fracture. This may lead to loss of height, the perception that the patient's abdomen is more prominent, and neck pain caused by the need to extend the neck to look forwards. Severe kyphosis may lead to dyspnoea.[11][55]
Sagittal balance is lost when the gravity line passes in front of the hip joint when the pelvis is fully extended. It is compensated for by using walking aids, or by flexion of the hip and knee joints.
loss of lumbar lordosis
Fractures in the lumbar region may result in lessening of the curvature of the lumbar lordosis.
localised tenderness
There may be localised tenderness at the fracture site if the fracture is recent.
loss of standing height
Patients with multiple osteoporotic spinal compression fracture may report a loss of standing height.
loss of sagittal balance
This is consequent on the other diagnostic factors and means that the patient can no longer stand upright with the head balanced over the hips without bending the knees. This is a potent source of back pain.
Loss of sagittal balance causes intolerance of standing still or walking slowly. Sometimes this can be compensated for by walking fast, or by using impromptu walking aids, such as a supermarket trolley or a child's pushchair.
Risk factors
strong
older age
The risk of osteoporotic spinal compression fracture increases significantly with age for both men and women.[8] It is estimated that 50% of white women and 20% of white men aged >50 years will sustain an osteoporotic fracture at some point during their lifetime.[10] In women, the lifetime risk of clinically significant osteoporotic vertebral compression fracture increases sixfold from menopause to age 85 years.[21] Rates of fracture differ by ethnic/racial population and skeletal site.[11] For fracture at any site in women, after adjusting for bone mineral density, weight, and other co-variates, non-Hispanic white and Hispanic-American women have the highest risk for fracture, followed by Native Americans, African Americans, and Asian Americans. For hip fracture in men, the age-adjusted incidence was highest for non-Hispanic white men, similar among Hispanic-American and black men, and lowest in Asian men.[11][12][13]
previous osteoporotic vertebral compression fracture
Women with a previous history of osteoporotic spinal compression fracture have a fivefold increase in risk of developing subsequent compression fractures.[22]
low body weight
A small, thin body frame is associated with an increased risk of vertebral fractures.[23]
recent weight loss
Increases the likelihood of osteoporotic fragility fractures.[1] However, this is also a clinical indicator of possible malignancy and pathological fracture.
family history of low bone mass/osteoporotic fractures
Heredity affects peak bone mass, and a greater peak bone mass before age-related bone loss can lower the risk of subsequent fracture.[24]
smoking
white or Asian race
Of women aged ≥50 years, 20% of white and Asian women, 10% of Latin women, and 5% of black women are estimated to have osteoporosis. International Osteoporosis Foundation: facts and statistics Opens in new window
postmenopausal status
secondary amenorrhoea
Has been associated with low oestrogen before the menopause and can lead to decreased bone mineral density. Can be a consequence of anorexia nervosa or exercise-induced amenorrhoea.[28]
alcohol (>2 units/day)
corticosteroid use
Prolonged or repeated use of oral or high-dose inhaled glucocorticoids is associated with osteoporosis.[11][31] The mechanisms of corticosteroid-induced osteoporosis are multifactorial and include osteoclast activation, osteoblast inhibition, decreased gastrointestinal and renal calcium absorption, and decreased gonadotrophin secretion.[32]
glucocorticoid excess
Fifty percent of people with Cushing syndrome experience fractures, especially vertebral fractures.[32]
hyperthyroidism
Hyperthyroidism increases osteoclast activity.[33]
Risk of fracture is greater with clinically evident hyperthyroidism than with subclinical hyperthyroidism.
vitamin D deficiency
low calcium intake
In a study of 36,282 women, those assigned to placebo had a greater loss of bone mineral density than those given calcium and vitamin D supplementation.[34]
rheumatoid arthritis and other autoimmune connective tissue diseases
These and other inflammatory conditions can cause generalised osteopenia, periarticular osteopenia, and focal subchondral erosions. The synovial tissue proliferation in rheumatoid arthritis promotes the development of osteoclast-like cells from mononuclear cell precursors. Osteoclast-like cells cause focal osteolysis at the articular surfaces, and thus the inflammatory synovial process can extend to the periarticular bone and marrow, promoting increased osteoclast activity and subsequent osteopenia.
endocrine disorders (e.g., hypogonadism, hyperparathyroidism, hyperprolactinaemia, acromegaly, hypercortisolism, hyperthyroidism)
Endocrine disorders constitute the most frequent cause of secondary osteoporosis in men and women. They are relatively common and should be considered in the differential diagnosis and management of osteopenia. The pathogenesis of hormone-induced bone loss involves several components of the bone remodelling cycle, and in many cases is not fully understood.
gastrointestinal diseases (e.g., inflammatory bowel disease, coeliac disease, malabsorption syndromes, post-bariatric surgery)
People with inflammatory bowel disease are often treated with corticosteroids, which can interfere with the development and maintenance of healthy bones. Bone loss increases with the amount and length of corticosteroid therapy. Furthermore, in people with severe inflammation of the small bowel, or if the small bowel is removed, there may be difficulty absorbing calcium and vitamin D.[35] The underlying inflammatory state is also a risk factor for osteoporosis.[35]
liver diseases (e.g., biliary sclerosis, sclerosing cholangitis, alcoholic cirrhosis, autoimmune hepatitis)
Metabolic bone disease and increased risk of bone fracture commonly complicate chronic liver disease. Osteoporosis is uncommon in patients with early liver disease, but affects up to 50% of patients with cirrhosis.[36] The cause of bone loss in patients with chronic liver disease is generally thought to be multifactorial.
dietary disorders (e.g., anorexia nervosa/bulimia, inadequate diet, total parenteral nutrition)
Patients with dietary disorders can experience nutritional and hormonal problems that negatively impact bone density. Low body weight in women causes the body to stop producing oestrogen, resulting in amenorrhoea. Low oestrogen levels contribute to significant losses in bone density. In addition, individuals with anorexia can produce excessive amounts of cortisol, which is known to trigger bone loss.
neurological disorders (e.g., stroke, multiple sclerosis, Parkinson's disease, spinal cord injury, long-term immobilisation)
In many neurological disorders, bone density will be affected by loss of motor function and subsequent disuse. Stroke is one of the major causes of disuse osteoporosis (bone loss resulting from inadequate stress or pressure on the bones) in the ageing population.[37]
renal disease
Causes complex bone disease with histological features of osteoporosis, osteomalacia, osteosclerosis, and osteitis fibrosa cystica.
type 1 diabetes mellitus
In type 1 diabetes, bone mass and bone strength are reduced, resulting in up to a five-times greater risk of fractures throughout life.[38] Bone fragility in diabetes can result from cellular abnormalities, matrix interactions, immune and vascular changes, and musculoskeletal maladaptation to chronic hyperglycaemia.[38] Insulin-like growth factors and other cytokines may influence diabetic bone metabolism.
organ transplantation
The contributing factors in organ transplant patients include disturbances of bone metabolism in the pre-transplant period and immunosuppressive therapy, including corticosteroids, after the transplantation.
bone-losing medications
In addition to corticosteroids, several other medications are associated with reduced bone mass: aromatase inhibitors (e.g., letrozole, exemestane, anastrozole); gonadotrophin-releasing hormone agonists (e.g., leuprorelin); immunosuppressants; anticonvulsants (e.g., phenobarbital, phenytoin); cytotoxic drugs; lithium; long-term heparin; depot medroxyprogesterone acetate.
Some drugs increase the risk of fracture including levothyroxine (decreased bone density), loop diuretics (impair calcium absorption in kidney), and proton-pump inhibitors (reduce calcium absorption).[31][39][40] Medications that cause sedation (e.g. antidepressants, opioid analgesics) or postural hypotension (antihypertensives) increase the risk of falls.[40][41]
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