Osteoporosis

Also known as: Porous bone disease, Brittle bone disease, Bone thinning, Low bone density, Decreased bone mineral density (low BMD), Systemic skeletal osteoporosis, Primary osteoporosis

Last updated: December 18, 2024

Osteoporosis is a systemic skeletal disease where bone mass is reduced and bone microarchitecture may deteriorate, making bones more fragile. It reflects an imbalance in bone resorption and formation that can lead to net bone loss. Early disease often has few symptoms and may be found on screening or imaging, but fragility fractures of the hip, spine, or wrist can occur, sometimes with back pain or height loss.

Key Facts

•Osteoporosis be described as a systemic skeletal disease in which bone mass is reduced and bone microarchitecture become deteriorated, leading to increased bone fragility
•No symptoms in early disease, with osteoporosis identified after screening or incidental imaging findings
•Diagnosed through history, physical exam, and imaging
•First-line treatment includes exercise, weight management, and activity modification

What It Is

Osteoporosis may be described as a systemic skeletal disease in which bone mass is reduced and bone microarchitecture can become deteriorated, leading to increased bone fragility. The condition typically reflects an imbalance between bone resorption and bone formation, so bone remodeling can favor net loss over time. Bone strength generally depends on both bone mineral density and bone quality, so fracture risk may increase even when symptoms are minimal. Osteoporosis often remains clinically silent until a low-trauma (fragility) fracture occurs, commonly involving the hip, vertebrae, or wrist.

Affected Anatomy

This condition affects several structures in and around the joint:

•Trabecular (cancellous) bone microarchitecture of vertebral bodies (thoracic and lumbar spine)
•Cortical bone of the femoral neck and intertrochanteric region of the proximal femur
•Distal radius metaphysis and cortical shell at the wrist
•Lumbar vertebral endplates and vertebral body anterior column (sites of compression deformity)
•Osteoclasts and osteoblasts within basic multicellular units of bone remodeling surfaces
•Bone marrow cavity and trabecular network of the iliac crest (common reference site for bone turnover research)
•Periosteal and endosteal surfaces of long bones where cortical thinning can occur
•Paraspinal musculature and spinal ligaments that can be secondarily affected by vertebral compression fractures and kyphosis

Common Symptoms

Symptoms can vary in intensity and may change over time. Common experiences include:

•No symptoms in early disease, with osteoporosis often identified after screening or incidental imaging findings
•Back pain that may be acute after a vertebral compression fracture and can become chronic with multiple fractures
•Loss of height over time that may reflect progressive vertebral compression deformities
•Kyphosis (stooped posture) that can occur with multiple thoracic vertebral fractures and may affect balance
•Fragility fractures that can occur after low-energy trauma (such as a fall from standing height), commonly at the hip, wrist, or spine
•Reduced mobility and functional limitation that may follow hip or vertebral fractures and can contribute to deconditioning
•Pain with movement or weight-bearing after a fracture, which may limit gait and daily activities
•Breathing discomfort or reduced pulmonary mechanics that can occur in severe kyphosis due to vertebral fractures

Causes and Risk Factors

Multiple factors can contribute to the development of this condition:

Causes

•Age-related bone loss in which bone resorption may exceed bone formation, often accelerating after midlife
•Postmenopausal estrogen deficiency, which can increase osteoclast activity and typically contributes to rapid early bone loss
•Secondary osteoporosis due to endocrine or metabolic conditions (such as hyperthyroidism, hyperparathyroidism, or malabsorption), which can alter calcium balance and bone remodeling
•Medication-associated bone loss, commonly linked with long-term systemic glucocorticoid exposure that can reduce bone formation and increases resorption
•Nutritional insufficiency or low calcium and vitamin D status, which can impair mineralization and may increase fall and fracture risk through muscle weakness
•Reduced mechanical loading from immobility or low physical activity, which can decrease osteoblastic stimulation and contribute to bone loss

Risk Factors

•Older age, as bone density typically declines with aging and fracture risk generally increases
•Female sex and postmenopausal status, which can be associated with lower peak bone mass and estrogen-related bone loss
•Prior fragility fracture, which may indicate underlying skeletal fragility and can predict future fracture risk
•Family history of osteoporosis or hip fracture, which can reflect genetic influences on peak bone mass and bone quality
•Low body weight or low body mass index, which can be associated with lower bone mass and less protective soft tissue during falls
•Tobacco use, which can adversely affect bone remodeling and is often associated with lower bone density
•Higher alcohol intake, which can impair bone formation and may increase fall risk
•Long-term use of certain medications (such as systemic glucocorticoids, some antiseizure medicines, or aromatase inhibitors), which can contribute to secondary osteoporosis

How It's Diagnosed

Diagnosis typically involves a combination of clinical assessment and imaging studies:

•Clinical history and risk assessment that can include prior fractures, fall history, medication exposures, and family history to estimate fracture probability
•Physical examination that may include height measurement over time, posture assessment for kyphosis, gait and balance evaluation, and focused spine and hip examination for fracture-related pain
•Dual-energy X-ray absorptiometry (DXA) scanning of the hip and lumbar spine, which typically provides bone mineral density values and T-scores used to classify osteoporosis
•Fracture risk estimation tools (such as FRAX) that can integrate clinical risk factors with or without femoral neck BMD to estimate 10-year fracture probability
•Spine imaging (plain radiography) that can identify vertebral compression fractures, height loss patterns, and deformities that may be clinically silent
•Vertebral fracture assessment (VFA) performed with DXA in selected settings, which can detect vertebral fractures with relatively low radiation exposure
•Laboratory evaluation for secondary causes that may include calcium, vitamin D, thyroid function, parathyroid hormone, renal function, and other tests based on clinical context

Treatment Options

Treatment approaches range from conservative measures to surgical interventions, often starting with the least invasive options:

Self-Care and Activity Modification

•Fall risk reduction strategies that can include home safety modifications and balance-focused interventions, which may reduce fracture risk by decreasing falls
•Nutrition optimization that can include adequate calcium and vitamin D consumption from diet and/or supplementation when indicated, which may support bone health and muscle function
•Pharmacologic antiresorptive therapy (such as bisphosphonates), which can reduce bone resorption and may lower vertebral and nonvertebral fracture risk in appropriate patients
•RANKL inhibition (denosumab), which can reduce osteoclast-mediated bone resorption and may be used in selected individuals based on risk profile
•Anabolic or bone-forming therapies (such as teriparatide, abaloparatide, or romosozumab), which can increase bone formation and may be considered for very high fracture risk or multiple fractures
•Vertebral augmentation procedures (vertebroplasty or kyphoplasty) in selected cases of painful vertebral compression fractures, where benefits and risks can vary by patient and timing

Physical Therapy and Exercise

•Weight-bearing and resistance exercise programs that can improve strength and balance and may help maintain bone density, with intensity generally individualized
•Pain management and rehabilitation after fractures, which can include physical therapy, mobility aids, and structured recovery plans to improve function

Medications

•Management of secondary causes and medication review, which can include addressing endocrine disorders or minimizing bone-harming exposures when feasible

Surgery

•Surgical fracture management (such as hip fracture fixation or arthroplasty), which may be required after major fragility fractures to restore mobility and reduce complications

Prognosis and Recovery

The course of this condition varies between individuals:

•Fracture risk may increase over time without risk-factor modification or effective therapy, particularly after an initial fragility fracture.
•Many individuals can have stable disease with appropriate monitoring and risk reduction, although bone density changes may be gradual and variable.
•Hip and vertebral fractures can be associated with substantial morbidity, including reduced mobility and independence, and outcomes often depend on baseline health and rehabilitation access.
•Vertebral compression fractures may lead to chronic pain and progressive kyphosis in some individuals, which can affect balance and quality of life.
•Treatment response can vary, and fracture risk reduction may occur even when bone density gains are modest, reflecting changes in bone remodeling and quality.

Vertebral Compression Fracture(Condition)
Hip Fracture (Proximal Femur Fracture)(Condition)

Frequently Asked Questions

Common symptoms include: No symptoms in early disease, with osteoporosis often identified after screening or incidental imaging findings; Back pain that may be acute after a vertebral compression fracture and can become chronic with multiple fractures; Loss of height over time that may reflect progressive vertebral compression deformities; Kyphosis (stooped posture) that can occur with multiple thoracic vertebral fractures and may affect balance; Fragility fractures that can occur after low-energy trauma (such as a fall from standing height), commonly at the hip, wrist, or spine.

Diagnosis typically involves: Clinical history and risk assessment that can include prior fractures, fall history, medication exposures, and family history to estimate fracture probability; Physical examination that may include height measurement over time, posture assessment for kyphosis, gait and balance evaluation, and focused spine and hip examination for fracture-related pain; Dual-energy X-ray absorptiometry (DXA) scanning of the hip and lumbar spine, which typically provides bone mineral density values and T-scores used to classify osteoporosis; Fracture risk estimation tools (such as FRAX) that can integrate clinical risk factors with or without femoral neck BMD to estimate 10-year fracture probability.

Treatment options range from conservative measures to surgical interventions, including: Fall risk reduction strategies that can include home safety modifications and balance-focused interventions, which may reduce fracture risk by decreasing falls; Weight-bearing and resistance exercise programs that can improve strength and balance and may help maintain bone density, with intensity generally individualized; Nutrition optimization that can include adequate calcium and vitamin D consumption from diet and/or supplementation when indicated, which may support bone health and muscle function; Pharmacologic antiresorptive therapy (such as bisphosphonates), which can reduce bone resorption and may lower vertebral and nonvertebral fracture risk in appropriate patients; RANKL inhibition (denosumab), which can reduce osteoclast-mediated bone resorption and may be used in selected individuals based on risk profile.