Osteoporosis Disease

BASICS

DESCRIPTION
A multifactorial skeletal disease characterized by severe bone loss, disruption of skeletal micro-architecture, and disturbed bone quality sufficient to predispose to atraumatic fractures of the vertebral column, upper femur, distal radius, proximal humerus, pubic rami and ribs. Five types recognized:
  • Postmenopausal (Type I): The most common form in Caucasian and Asian women. Due to excessive and prolonged acceleration of bone resorption following menopausal loss of estrogen secretion.
  • Involutional (Type II): Occurs in both sexes above age 75. Due to a subtle, prolonged imbalance between rates of bone resorption and formation. A mixture of Types I and II is common.
  • Idiopathic: A rare form of primary osteoporosis occurring in premenopausal women and in men below age 75. Not related to secondary causes or risk factors predisposing to bone loss.
  • Juvenile: A rare form of variable severity in prepubertal children. Self-limited with cessation of fractures at puberty.
  • Secondary: Due to extrinsic factors
  • System(s) affected: Musculoskeletal, Endocrine/Metabolic
  • Genetics: Familial predisposition. More common in Caucasians and Orientals than in Black and Latino ethnic groups.
  • Incidence/Prevalence in USA:
    • 30–40% cumulatively in women, 5–15% in men
    • Prevalence of idiopathic and juvenile types unknown
    • Secondary osteoporosis cumulatively 5–10%, both sexes
  • Predominant age: Elderly
  • Predominant sex: Female > Male
SIGNS AND SYMPTOMS
  • Back ache/pain; acute/chronic
  • Loss of height
  • Kyphosis/scoliosis
  • Atraumatic fractures
  • No peripheral bone deformities
  • Sclerae not blue/green/grey
  • Restrictive lung disease
  • Gastrointestinal symptoms
  • Depression, loss of self esteem
  • Excess mortality, 5–20% during 1–5 years post acute fracture
CAUSES
  • Postmenopausal (Type I): Hypoestrogenemia
  • Involutional (Type II): Unknown
  • Idiopathic: Unknown
  • Juvenile: Unknown
  • Secondary: Eating disorders, corticosteroid excess, rheumatoid arthritis, chronic liver/kidney disease, malabsorption syndromes, systemic mastocytosis, hyperparathyroidism, hyperthyroidism, elite athletes/ballet dancers with hypoestrogenism, a variety of hypogonadal states, idiopathic hypercalciuria, chronic anticoagulant use, chronic antiseizure medication and others
  • Aging: Bone loss is a consequence of aging; osteoporosis occurs in individuals who fail to achieve optimal skeletal mass at maturity or lose bone rapidly thereafter (e.g., excessive postmenopausal and/or involutional bone loss, or conditions/risk factors that increase bone loss)
RISK FACTORS
  • Dietary - inadequate calcium or vitamin D; excessive phosphate/protein
  • Physical - immobilization, sedentary lifestyle
  • Social - alcohol, cigarettes, caffeine
  • Medical - chronic diseases, malabsorption, endocrinopathies (see also secondary osteoporosis in Description)
  • Iatrogenic - corticosteroids, excess thyroid hormone replacement, chronic anticoagulant or antiseizure medication use, chemotherapy, loop diuretics, radiation therapy
  • Genetic/familial - suboptimal bone mass at maturity, "familial fast bone losers"

DIAGNOSIS

LABORATORY
  • CBC, multi-panel tests usually normal
  • Alkaline phosphatase (bone specific and total) may be transiently increased following fractures
  • Serum and/or urine protein electrophoresis normal
  • Thyroid function tests and urinary free cortisol normal in primary types
  • Serum osteocalcin, if high, indicates high turnover type
  • Urine calcium normal (except if idiopathic hypercalciuria)
  • Serum and urinary pyridinoline and N- and C-telopeptide collagen crosslinks, if high, indicate high turnover type
Drugs that may alter lab results:
  • Hepatotoxins: changes in total alkaline phosphatase
  • Estrogens: changes in thyroid function tests
Disorders that may alter lab results:
  • Multiple myeloma or other neoplasia
  • Osteomalacia
  • Hyperparathyroidism
  • Hyperthyroidism
PATHOLOGICAL FINDINGS
  • Reduced skeletal mass, trabecular bone more so than cortical bone. Thinned/loss of trabecular connections.
  • Osteoclast and osteoblast number variable
  • No evidence of other metabolic bone diseases and no increase in unmineralized osteoid
  • Marrow normal or atrophic
SPECIAL TESTS
N/A
IMAGING
  • Plain film "early" changes: increased width of intervertebral spaces, relative accentuation of cortical plates, vertical striations of vertebral bodies
  • Plain film "late" changes: cortical plate fractures, vertebral compression, wedge and crush fractures, peripheral fractures at ends of long bones, rib fractures
  • Bone scan: increased uptake at previous fracture sites
  • Bone mineral density (BMD). Data Analysis: Normative data for DXA, QUS, and QCT are incorporated into each instrument, allowing calculation of T and Z scores. T scores represent the number of standard deviations (SD) a measurement deviates from the mean for young normal (age 25-40) controls of same sex and in some cases, ethnic group. T scores indicate severity of bone loss as follows: T scores of ±1 SD are normal; a T score between -1 and -2 indicates an osteopenic state; T scores below -2 indicate established osteoporosis with high risk of fracture. Z scores indicate number of standard deviations compared to age matched controls and are not generally used to determine severity or need for treatment.
  • Whole body DXA: BMD of whole body, lumbar spine, forearm, and upper femur
  • Peripheral (p) DXA: BMD of the calcaneus, distal tibia, and distal radius. Partial correlation with whole body DXA but does not accurately quantitate changes from baseline during treatment
  • Quantitative CT (QCT): Quantitates either trabecular or cortical bone mass (or both) of lumbar spine
  • Quantitative ultrasound (QUS): Uses US attenuation at calcaneus. Correlates partially with whole body and peripheral DXA, but does not reflect changes during treatment. May be influenced by microarchitecture as well as BMD
DIAGNOSTIC PROCEDURES
Bone biopsy needed rarely, to rule out other metabolic bone diseases. Sometimes used to quantitate bone loss, utilizing quantitative histomorphometric technique.

TREATMENT

APPROPRIATE HEALTH CARE
  • Usually outpatient
  • Inpatient care for acute back pain, especially for new vertebral fractures and for acute treatment of upper femoral and pelvic fractures
  • Nursing home or home care may be needed following peripheral fractures
GENERAL MEASURES

As required by pain and disability, e.g., heat, analgesics, physical therapy. Decrease falls. Avoid excessive psychotropic effects of drugs.

SURGICAL MEASURES

N/A

ACTIVITY
  • Maintain ambulation, walking 1 mile twice a day, if possible, swimming, tricycling
  • Avoid exercises and maneuvers that increase compressive forces and mechanical stress on spine and peripheral bone sites
  • Rehabilitation procedures for back muscle spasm, to increase agility (e.g., decrease falls), and encourage ambulation
DIET
  • Reducing diet if overweight
  • Calcium intake 1500 mg/day from all sources, if not hypercalciuric or with past medical history of calcium stones
  • Avoid excess phosphate or protein intake, i.e., avoid phosphoric-acid-containing beverages and excess meat intake
  • 600–1000 IU vitamin D daily from all sources
PATIENT EDUCATION

Teaching resources and patient literature available from National Osteoporosis Foundation, 2100 M St., Suite 602, Washington, DC 20037

FOLLOW UP

PREVENTION/AVOIDANCE
  • General guidelines: Diet, exercise, calcium, vitamin D
  • Prevention during the osteopenic phase (prolonged, usually asymptomatic phase prior to fracturing)
    • Identification of osteopenia
    • Correction of treatable medical conditions and other risk factors; will also help achieve optimal skeletal mass during development
    • HRT if postmenopausal and no absolute contraindications
    • Low dose alendronate (Fosamax) 5 mg qd, if no contraindications
    • Raloxifene (Evista) 60 mg qd
POSSIBLE COMPLICATIONS
  • Severe disabling pain
  • Dorsal/lumbar neurologic deficits secondary to vertebral fracture (rare)
  • Respiratory and GI symptoms
  • Invalidism/death secondary to complications
EXPECTED COURSE AND PROGNOSIS
  • With treatment, 80% of patients stabilize skeletal manifestations; increase bone mass, increase mobility, and have reduced pain
  • 20% of vertebral and upper femoral fractures may lead to chronic care and/or premature death

MISCELLANEOUS

ASSOCIATED CONDITIONS
  • Corticosteroid excess
  • Rheumatoid arthritis
  • Chronic liver/kidney disease
  • Malabsorption syndromes
  • Systemic mastocytosis
  • Hyperparathyroidism; Hyperthyroidism including iatrogenic
  • Various hypogonadal states
  • Seizure disorder under treatment
  • Eating disorders
AGE-RELATED FACTORS

Pediatric: Juvenile osteoporosis not discussed herein
Geriatric: Postmenopausal/involutional/mixed types
Others: Primary types uncommon in African Americans. Patients with British, North European, Scandinavian, and Asian ancestry most susceptible.

PREGNANCY

Rare acute osteoporosis of pregnancy, not discussed here

OTHER NOTES

N/A

ABBREVIATIONS

BMD = bone mineral density
HRT = hormone replacement therapy

Clinical Investigations

ROLE OF HOMOEOPATHY

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