Orthopaedic Surgery - Osteoporosis

Basics

Osteoporosis is a systemic skeletal disorder characterized by reduced bone mass and deterioration of bone microarchitecture, resulting in decreased bone strength and an increased risk of fragility fracture.

The disease affects both:

Cortical bone

and

Trabecular bone.

Clinically important fractures most commonly involve the:

Vertebrae

Hip

Distal radius

Proximal humerus

Bone Mineral Density Definition

Bone mineral density is commonly measured using dual-energy X-ray absorptiometry (DEXA or DXA).

The T-score compares the patient’s bone mineral density with that of a healthy young adult reference population.

In postmenopausal women and men aged 50 years or older:

Normal bone density: T-score ≥ –1.0

Low bone mass or osteopenia: T-score between –1.0 and –2.5

Osteoporosis: T-score ≤ –2.5

A fragility fracture may establish clinically important osteoporosis even when the T-score is higher than –2.5.

Z-Score

The Z-score compares the patient’s bone mineral density with that expected for:

People of the same age and sex.

It is particularly useful in:

Premenopausal women

Men younger than 50 years

Children and adolescents

A markedly low Z-score should prompt investigation for secondary causes of reduced bone density.

Prevention

Prevention focuses on preserving bone mass and reducing fracture risk.

Important measures include:

Adequate calcium and vitamin D intake

Regular weight-bearing exercise

Resistance training

Smoking cessation

Avoidance of excessive alcohol

Fall prevention

Treatment of diseases and medications that accelerate bone loss

Nutrition

Adequate nutrition is particularly important during:

Childhood

Adolescence

Early adulthood

because peak bone mass achieved during these periods influences future osteoporosis risk.

Epidemiology

Osteoporosis is a major cause of fragility fractures worldwide.

Older estimates attributed approximately 1.3 million fractures annually to osteoporosis in the United States, with substantial numbers involving the:

Spine

Hip

and

Wrist.

The actual burden has increased as populations have aged.

Age

Fracture risk rises progressively with age and increases particularly sharply in older adults.

Patients older than approximately:

75 years

have a substantially increased risk of hip and other major osteoporotic fractures.

Sex

After approximately age 50, women have a considerably greater lifetime risk of fragility fracture than men.

This is related partly to:

Lower peak bone mass

Accelerated postmenopausal bone loss

Longer life expectancy

Risk Factors

Important risk factors include:

Increasing age

Female sex

Low body weight

Previous fragility fracture

Family history of osteoporosis or hip fracture

Early menopause

Prolonged amenorrhea

Smoking

Excessive alcohol intake

Physical inactivity

Low calcium or vitamin D intake

Ethnicity

Historically, osteoporosis has been recognized particularly often in:

White populations of Northern European ancestry

and

Asian populations.

However, osteoporosis occurs in all racial and ethnic groups, and fracture risk should be assessed individually.

Reproductive Risk Factors

Factors associated with reduced lifetime estrogen exposure include:

Late menarche

Early menopause

Premature ovarian insufficiency

Prolonged amenorrhea

Historically, nulliparity has also been discussed as a possible risk factor.

Low Body Weight

A small body frame or low body mass is associated with:

Lower bone mass and increased fracture risk.

Older criteria sometimes used a body weight below approximately:

127 lb or 58 kg

as a risk marker.

Female Athlete Triad

In physically active women, prolonged low energy availability may contribute to:

Menstrual dysfunction

Reduced bone mineral density

and

Stress fracture risk.

This was historically termed the Female Athlete Triad and is now understood within the broader concept of relative energy deficiency in sport.

Genetics

Bone density has an important hereditary component.

Multiple genes influence:

Peak bone mass

Bone turnover

Calcium metabolism

Fracture susceptibility

Candidate pathways have included genes involving:

Vitamin D signaling

Type I collagen

Wnt signaling, including LRP5/6

The inheritance pattern is complex and polygenic.

Etiology

Osteoporosis may be:

Primary

or

Secondary.

Primary Osteoporosis

Primary osteoporosis includes:

Postmenopausal osteoporosis

and

Age-related osteoporosis.

In many patients, no single secondary cause is identified.

Secondary Osteoporosis

Secondary osteoporosis results from another disease, nutritional abnormality, medication, or lifestyle factor.

Nutritional Causes

Potential contributors include:

Low calcium intake

Vitamin D deficiency

Malnutrition

Restrictive diets

Malabsorption

Excessive alcohol use

Lifestyle Causes

Important lifestyle factors include:

Smoking

Physical inactivity

Low weight-bearing activity

Excessive alcohol consumption

Medical Causes

Secondary osteoporosis may occur with:

Type 1 diabetes mellitus

Cushing syndrome

Chronic kidney disease

Inflammatory bowel disease

Cystic fibrosis

Primary hyperparathyroidism

Hyperthyroidism

Anorexia nervosa

Celiac disease

Idiopathic hypercalciuria

Premature ovarian insufficiency

Other chronic inflammatory, endocrine, gastrointestinal, and hematologic disorders may also contribute.

Medication-Related Causes

Medications associated with bone loss include:

Chronic glucocorticoids

Certain anticonvulsants

Some chemotherapy agents

Long-term excess thyroid hormone replacement

Prolonged lithium therapy in selected patients

Other drugs may also affect bone metabolism depending on dose and duration.

Diagnosis

Signs and Symptoms

Osteoporosis itself is usually:

Asymptomatic until a fracture occurs.

A fragility fracture should immediately raise suspicion for underlying osteoporosis.

Fragility Fracture

A fragility fracture is one occurring after:

Minimal trauma, such as a fall from standing height or less.

Common sites include:

Vertebra

Hip

Distal radius

Proximal humerus

History

Important historical features include:

Prior low-energy fracture

Loss of height

Back pain

Family history of hip fracture

Early menopause

Smoking

Alcohol intake

Diet

Physical activity

Long-term steroid use

Endocrine or gastrointestinal disease

Physical Examination

Many patients have no specific findings until vertebral fractures develop.

Vertebral Compression Fractures

Multiple vertebral compression fractures may cause:

Progressive loss of height

Thoracic kyphosis

Reduced lumbar lordosis

Chronic back pain

Postural Changes

Severe vertebral osteoporosis may produce:

Forward stooping

Reduced trunk height

Prominent abdomen

Altered sagittal balance

DEXA

DEXA is the standard test for measuring bone mineral density.

Common sites include:

Lumbar spine

Femoral neck

Total hip

In selected circumstances, the:

Distal radius

may also be measured.

T-Score Interpretation

The T-score represents the number of standard deviations the patient’s bone mineral density lies above or below the mean of a healthy young reference population.

A lower T-score indicates:

Lower bone density and generally higher fracture risk.

Fracture Risk Assessment

Bone mineral density should be interpreted together with clinical risk factors.

Tools such as fracture-risk calculators can estimate the probability of:

Hip fracture

and

Major osteoporotic fracture

over a defined period.

Laboratory Evaluation

Laboratory testing is used mainly to identify:

Secondary causes of osteoporosis.

Basic Laboratory Studies

Common initial tests include:

CBC

Comprehensive metabolic panel

Serum calcium

Creatinine

Liver function tests when appropriate

Thyroid-stimulating hormone

Additional Testing

Depending on history and examination, testing may include:

25-hydroxyvitamin D

Parathyroid hormone

Phosphate

Serum protein electrophoresis

Testosterone in men

Celiac screening

24-hour urinary calcium

Vitamin D and Parathyroid Hormone

Measurement of:

25-hydroxyvitamin D

and

PTH

is particularly helpful in patients with:

Older age

Chronic kidney disease

Malabsorption

Liver disease

Anticonvulsant use

or suspected metabolic bone disease.

Multiple Myeloma Screening

When unexplained osteoporosis, anemia, renal dysfunction, hypercalcemia, or bone pain is present, evaluation for:

Multiple myeloma

may be appropriate.

Normal routine laboratory studies reduce suspicion but do not absolutely exclude myeloma.

Imaging

Plain Radiographs

Plain radiographs are insensitive for early osteoporosis.

Bone loss may not become visually apparent until approximately:

30% or more of bone mineral has been lost.

Spinal Findings

Moderate or severe osteoporosis may demonstrate:

Generalized osteopenia

Vertebral compression fractures

Biconcave vertebral bodies

Anterior wedging

Long-Bone Findings

Long bones may demonstrate:

Cortical thinning

Relative widening of the medullary canal

Generalized reduction in bone density

Occult Fractures

Fragility fractures may occasionally be occult on initial radiographs.

Additional imaging may include:

MRI

CT

Bone scintigraphy

or

Repeat radiographs

depending on the suspected site.

MRI is particularly useful for detecting:

Occult hip fracture

Acute vertebral compression fracture

Sacral insufficiency fracture

Pathophysiology

Normal bone undergoes continuous remodeling.

The remodeling cycle includes:

Osteoclastic resorption of old bone

followed by

Recruitment of osteoblasts

Deposition of new osteoid

and

Mineralization.

Remodeling Imbalance

In osteoporosis, bone resorption exceeds bone formation over time.

Each remodeling cycle results in:

A small net loss of bone mass.

Repeated cycles eventually reduce:

Trabecular connectivity

Cortical thickness

Mechanical strength

Postmenopausal Bone Loss

Estrogen deficiency increases:

Osteoclast activity and bone turnover.

This produces accelerated bone loss, particularly in the years following menopause.

Hyperparathyroidism

Excess parathyroid hormone can increase:

Bone-remodeling activation and resorption, contributing to secondary osteoporosis.

Differential Diagnosis

Important differential diagnoses include:

Osteomalacia

Multiple myeloma

Leukemia

Paget disease of bone

Osteogenesis imperfecta

Hyperparathyroid bone disease

Osteomalacia

Osteomalacia represents defective:

Mineralization of osteoid

rather than simply reduced bone quantity.

Vitamin D deficiency is a common cause.

Neoplastic Disease

Myeloma and other malignancies may produce:

Diffuse osteopenia

Pathologic fractures

Bone pain

and should be considered when clinical features are atypical.

Treatment

General Principles

Treatment aims to:

Prevent fractures

Maintain or improve bone density

Reduce fall risk

Correct secondary causes

Preserve mobility and independence

Exercise

Regular exercise is important.

Beneficial programs include:

Weight-bearing exercise

Resistance training

Balance training

These interventions may produce modest improvements in bone mineral density and reduce fall risk.

Fall Prevention

Particularly in older adults, fracture prevention requires attention to:

Vision

Footwear

Home hazards

Balance impairment

Sedating medications

Muscle weakness

Calcium

Adequate calcium intake should be ensured, preferably through diet when possible.

Total daily intake from food and supplements is commonly targeted around:

1,000–1,200 mg per day in many older adults, depending on age and sex.

Excessive supplementation should be avoided.

Vitamin D

Vitamin D should be sufficient to support:

Calcium absorption and bone mineralization.

Supplementation is individualized according to:

Diet

Sun exposure

Serum 25-hydroxyvitamin D

Age

Comorbidities

Older fixed recommendations often used approximately 800 IU daily.

Bisphosphonates

Bisphosphonates are first-line antiresorptive medications for many patients at elevated fracture risk.

They act primarily by:

Reducing osteoclast-mediated bone resorption.

Common Bisphosphonates

Examples include:

Alendronate

Risedronate

Ibandronate

Zoledronic acid

Administration may be:

Weekly

Monthly

or

Intravenous at longer intervals, depending on the drug.

Fracture Reduction

Bisphosphonates reduce the risk of:

Vertebral fracture

and, for several agents,

Hip and other nonvertebral fractures.

The exact degree of risk reduction varies by medication and patient population.

Bisphosphonate Requirements

Patients should have adequate:

Calcium

and

Vitamin D

and clinically important hypocalcemia should be corrected before treatment.

Bisphosphonate Adverse Effects

Potential complications include:

Upper gastrointestinal irritation with oral agents

Acute-phase reaction after intravenous therapy

Hypocalcemia

Rare long-term complications include:

Atypical femoral fracture

and

Medication-related osteonecrosis of the jaw.

Denosumab

Denosumab is a monoclonal antibody against:

RANKL.

It suppresses osteoclast formation and activity.

It is useful in selected patients with:

High fracture risk

or intolerance to other therapies.

Treatment should not be stopped abruptly without another antiresorptive strategy because rapid rebound bone loss and vertebral fractures may occur.

Selective Estrogen Receptor Modulators

SERMs such as:

Raloxifene

can reduce the risk of:

Vertebral fractures

in selected postmenopausal women.

They have less established benefit for:

Hip fracture prevention.

Estrogen Therapy

Estrogen reduces postmenopausal bone loss and fracture risk.

However, routine use solely for osteoporosis treatment is limited by risks that may include:

Venous thromboembolism

Stroke

Cardiovascular effects

Certain hormone-sensitive cancers

depending on formulation and patient characteristics.

Calcitonin

Calcitonin inhibits osteoclast activity.

Its role in long-term osteoporosis treatment is now limited because:

Fracture-prevention benefit is modest or uncertain compared with newer therapies.

Anabolic Therapy

Bone-forming therapies may be used in patients at very high fracture risk.

Examples include:

Teriparatide

Abaloparatide

and, in selected patients,

Romosozumab.

Teriparatide

Teriparatide is a recombinant parathyroid hormone analog that stimulates:

New bone formation

when administered intermittently.

It is generally reserved for patients with:

Severe osteoporosis

Multiple fragility fractures

Very high fracture risk

or failure of other therapy.

Romosozumab

Romosozumab inhibits:

Sclerostin

and has both:

Anabolic and antiresorptive effects.

It may be considered in selected very-high-risk patients, with attention to cardiovascular risk.

Surgery

Surgical treatment is directed toward:

Completed or impending fragility fractures, rather than the osteoporosis itself.

Hip Fractures

Hip fractures usually require operative management such as:

Internal fixation

or

Arthroplasty

depending on fracture pattern and patient factors.

Vertebral Compression Fractures

Most osteoporotic vertebral fractures are initially treated nonoperatively with:

Analgesia

Activity modification

Gradual mobilization

Osteoporosis treatment

Vertebroplasty and Kyphoplasty

Vertebral cement augmentation may be considered in carefully selected patients with:

Persistent severe pain from an acute or subacute vertebral compression fracture despite appropriate conservative treatment.

Routine prophylactic cement injection into unfractured vertebrae is not recommended.

Follow-Up

Patients require periodic reassessment of:

Fracture risk

Medication adherence

Adverse effects

Falls

Calcium and vitamin D status

Secondary causes

Repeat DEXA

Bone density testing is generally repeated after an interval sufficient to detect clinically meaningful change.

The interval is individualized according to:

Baseline bone density

Treatment

Age

Fracture risk

Referral

Referral to an endocrinologist or metabolic bone specialist should be considered for:

Very low bone density

Recurrent fractures despite therapy

Unusual osteoporosis at a young age

Suspected secondary osteoporosis

Complex endocrine or metabolic disease

A T-score alone should not be the sole determinant for referral.

Prognosis

Earlier recognition and treatment can substantially reduce fracture risk.

The prognosis depends on:

Baseline bone density

Age

Previous fractures

Fall risk

Secondary causes

Response to therapy

Complications

The major complication is:

Fragility fracture.

Vertebral Fractures

Vertebral fractures can lead to:

Chronic pain

Progressive kyphosis

Loss of height

Reduced pulmonary capacity

Impaired mobility

Hip Fractures

Hip fractures are particularly serious and may result in:

Loss of independence

Prolonged rehabilitation

Institutionalization

Increased mortality

Wrist and Upper-Extremity Fractures

Distal radius and proximal humerus fractures may impair:

Self-care

Balance aid use

Upper-extremity function

Patient Monitoring

Patients should be monitored for:

New fragility fractures

Loss of height

Back pain

Falls

Medication adverse effects

Changes in bone mineral density

Evidence of secondary osteoporosis

Key Principle

Osteoporosis is a systemic disorder of reduced bone strength caused by low bone mass and deterioration of bone microarchitecture.

Management focuses on:

Identifying patients at high fracture risk, correcting secondary causes, ensuring adequate calcium and vitamin D, encouraging weight-bearing and resistance exercise, reducing falls, and using antiresorptive or anabolic therapy when indicated.