eMedicine Specialties > Physical Medicine and Rehabilitation > Medical Diseases

Osteoporosis (Secondary)

Author: Alana C Serota, MD, Fellow in Metabolic Bone Disease and Osteoporosis, Department of Orthopedics, Hospital for Special Surgery
Coauthor(s): Joseph M Lane, MD, Professor of Orthopedic Surgery, Weill Medical College of Cornell University; Chief, Metabolic Bone Disease Service, Hospital for Special Surgery
Contributor Information and Disclosures

Updated: Jun 25, 2009

Introduction

Background

Osteoporosis, a chronic progressive disease, is the most common metabolic bone disease in the United States. Osteoporosis can affect almost the entire skeleton. Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility.1 The disease often does not become clinically apparent until a fracture occurs. Consequently, many individuals, male and female, experience pain, disability, and diminished quality of life as a result of having osteoporosis. The economic burden of the disease in the United States is considerable and will grow as the population ages.2 Prevention and recognition of the secondary causes of osteoporosis are first-line measures to lessen the impact of osteoporosis. (See images below and Images 1-2.)

Osteoporosis of the spine. Observe the considerab...

Osteoporosis of the spine. Observe the considerable reduction in overall vertebral bone density and note the lateral wedge fracture of L2.

[ CLOSE WINDOW ]
Osteoporosis of the spine. Observe the considerab...

Osteoporosis of the spine. Observe the considerable reduction in overall vertebral bone density and note the lateral wedge fracture of L2.



Osteoporosis of the spine. Note the lateral wedge...

Osteoporosis of the spine. Note the lateral wedge fracture in L3 and the central burst fracture in L5. The patient had suffered a recent fall.

[ CLOSE WINDOW ]
Osteoporosis of the spine. Note the lateral wedge...

Osteoporosis of the spine. Note the lateral wedge fracture in L3 and the central burst fracture in L5. The patient had suffered a recent fall.


A Gallup survey performed by the National Osteoporosis Foundation revealed that 75% of all women aged 45-75 years have never discussed osteoporosis with their physicians; however, treatment to prevent future fractures is available.

Bone mineral density (BMD) in a patient is related to peak bone mass and, subsequently, bone loss. The World Health Organization has established the following definitions of osteoporosis based on bone mass density measurements in white women:

  • Normal - Bone density no lower than 1 standard deviation (SD) below the mean for young adult women (T-score above -1)
  • Low bone mass (osteopenia) - Bone density 1-2.5 SD below the mean for young adult women (T-score between -1 and -2.5)
  • Osteoporosis - Bone density 2.5 SD or more below the normal mean for young adult females (T-score at or below -2.5)

Patients within this group who have already experienced 1 or more fractures are deemed to have severe or established osteoporosis. Although these definitions are necessary to establish the prevalence of osteoporosis, they should not be used as the sole determinant of treatment decisions.

Pathophysiology

Understanding the pathogenesis of osteoporosis starts with knowing how bone formation and remodeling occur. Osteoblasts are osteoid formers, and osteoclasts are bone resorbers. Osteoblasts and osteoclasts are formed in the bone marrow. Bone formation is not static; it is a system that is remodeled constantly. In adults, approximately 25% of trabecular bone is resorbed and replaced every year, compared with only 3% of cortical bone.

Bone is continually remodeled throughout life because bones sustain recurring microtrauma. Bone remodeling occurs at discrete sites within the skeleton and proceeds in an orderly fashion. Bone resorption is always followed by bone formation, a phenomenon referred to as coupling. In osteoporosis, this coupling mechanism is thought to be unable to keep up with the constant microtrauma to trabecular bone.

The hallmark of osteoporosis is a reduction in skeletal mass caused by an imbalance between bone resorption and bone formation. Loss of gonadal function and aging are the 2 most important factors contributing to the development of this condition. Studies have shown that bone loss in women accelerates rapidly in the first years after menopause. The lack of gonadal hormones is thought to up-regulate osteoclast progenitor cells.

In contrast to postmenopausal bone loss, which is associated with excessive osteoclast activity, the bone loss that accompanies aging is associated with a progressive decline in the supply of osteoblasts in proportion to the demand. This demand is ultimately determined by the frequency with which new multicellular units are created and new cycles of remodeling are initiated.

Osteoporosis may be confused with osteomalacia. The normal human skeleton is composed of a mineral component, calcium hydroxyapatite (60%), and organic material, mainly collagen (40%). In osteoporosis, the bones are porous and brittle, while in osteomalacia the bones are soft. This difference in bone consistency is related to the proportion of mineral to organic material content. In osteoporosis, the mineral-to-collagen ratio is within the reference range, whereas in osteomalacia, the proportion of mineral composition is reduced relative to organic mineral content.

Biomechanics

An understanding of the biomechanics of bone provides greater appreciation as to why bone may be susceptible to an increased risk of fracture. When vertical loads are placed on bone, such as tibial and femoral metaphyses and vertebral bodies, a substantial amount of bony strength is derived from the horizontal trabecular cross-bracing system. This system of horizontal cross-bracing trabeculae assists in supporting the vertical elements, thus limiting lateral bowing and fractures that may occur with vertical loading. Disruption of such trabecular connections is known to occur preferentially in patients with osteoporosis, particularly in postmenopausal women, making females more at risk than males for vertebral compression fractures.

In 1998, Rosen and Tenenhouse studied the unsupported trabeculae and their susceptibility to fracture within each vertebral body.3 They found an extraordinarily high prevalence of trabecular fracture callus sites within vertebral bodies examined at autopsy, typically 200-450 healing or healed fractures per vertebral body. These horizontal trabecular fractures are asymptomatic, and their accumulation reflects the impact of lost trabecular bone and greatly weakens the cancellous structure of the vertebral body. The reason for preferential osteoclastic severance of horizontal trabeculae is unknown. Some authors have attributed this phenomenon to overaggressive osteoclastic resorption.

Frequency

United States

Most studies assessing the prevalence and incidence of osteoporosis use the rate of fracture as a marker for the presence of this disorder, although BMD also relates to risk of disease and fracture. The risk of new vertebral fractures increases by a factor of 2-2.4 for each SD decrease of bone density measurement. In 1998, statistics from the National Osteoporosis Foundation estimated that more than 10 million men and women in the United States have osteoporosis and nearly 19 million more have low bone mass, placing them at increased risk for osteoporosis and fractures. Women and men with metabolic disorders associated with secondary osteoporosis have a 2- to 3-fold higher risk of hip and vertebral fractures. (See images below and Images 3-4.)

Normal femoral anatomy.

Normal femoral anatomy.

[ CLOSE WINDOW ]
Normal femoral anatomy.

Normal femoral anatomy.



Stable intertrochanteric fracture of the femur.

Stable intertrochanteric fracture of the femur.

[ CLOSE WINDOW ]
Stable intertrochanteric fracture of the femur.

Stable intertrochanteric fracture of the femur.

International

Osteoporosis is a very common metabolic bone disease worldwide, with similar incidence as noted in the United States.

Mortality/Morbidity

Many individuals experience morbidity associated with the pain, disability, and diminished quality of life caused by osteoporosis-related fractures. Hip fractures are known to increase mortality rates in men and women. Secondary complications of hip fractures include nosocomial infections and pulmonary thromboembolism. While the overall prevalence of hip fracture is greater in women than in men, a similar number of men and women die as a consequence of hip fractures because men with hip fractures have a higher mortality rate. The impact of vertebral fractures increases and they increase in number. As posture worsens and kyphosis progresses, patients experience difficulty with balance, back pain, respiratory compromise, and an increased risk of pneumonia. Overall function declines, and patients may lose their ability to live independently.

Race

In 1981, Melton et al reported that the prevalence of hip fractures is higher in white populations, regardless of geographic location.4 Another study indicated that the incidence of hip fractures was lower among African Americans in the United States and South Africa compared to age-matched white populations within the same continent. A study of Japanese American women in Hawaii found a 5% incidence of vertebral fractures each year among individuals aged 80 years.

Sex

Women have a 2-fold increase in the number of fractures resulting from nontraumatic causes, compared with men of the same age. Men have a higher prevalence of secondary osteoporosis, with an estimated 45-60% being a consequence of hypogonadism, alcoholism, or glucocorticoid excess.5 Only 35-40% of osteoporosis diagnosed in men is considered primary in nature.

Age

In 1982, Jensen et al studied Danish women aged 70 years and found a 21% prevalence of vertebral fractures.6 In 1989, Melton et al reported that 27% of women in their study had evidence of vertebral fractures by age 65 years.7 The number of osteoporotic fractures increases with age. Wrist fractures typically occur first, when individuals are aged approximately 50-59 years. Vertebral fractures occur more often in the seventh decade of life, and hip fractures occur more often in the eighth decade of life (see the information bullet on secondary osteoporosis, under Causes.).

Clinical

History

  • Patients who have not sustained a fracture often do not report symptoms that would alert the clinician to suspect a diagnosis of osteoporosis. This disease is a "silent thief" that generally does not become clinically apparent until a fracture occurs. Screening at-risk populations is, therefore, essential.
  • Patients who have sustained a vertebral compression fracture may present with an episode of acute back pain. It should be noted, however, that two thirds of vertebral fractures are asymptomatic. With respect to those that are painful, typical subjective information may include the following:
    • Pain is localized to a specific, identifiable, vertebral level in the midthoracic or lumbar spine.
    • The episode of acute pain may follow a fall or minor trauma.
    • Pain is often accompanied by paravertebral muscle spasms exacerbated by activity and decreased by lying supine.
    • Patients often remain motionless in bed because of fear of causing an exacerbation of pain.
  • Patients who have sustained a hip fracture may experience the following:
    • Patients may have pain in the groin, posterior buttock, anterior thigh, medial thigh, and/or medial knee during weightbearing or attempted weightbearing of the involved extremity.
    • Diminished hip range of motion (ROM) is reported, particularly internal rotation and flexion.
    • Patients may have external rotation of the involved hip while in the resting position.
  • Obtain a thorough history to help determine if the patient has any of the risk factors associated with osteoporosis. Importantly, however, realize that the clinical history may not be completely revealing because the patient may have secondary osteoporosis.
    • Risk factors for osteoporosis, such as advanced age and reduced bone density, have been established by virtue of their direct and strong relationship to the incidence of fractures; however, many other factors have been considered risk factors based on their relationship to bone density value as a surrogate indicator of osteoporosis. Risk factors include the following:
      • Advanced age
      • Female sex
      • White or Asian ethnicity
      • Family history of osteoporosis
      • Body weight less than 127 pounds
      • Amenorrhea
      • Late menarche
      • Early menopause
      • Physical inactivity
      • Alcohol and tobacco use
      • Androgen or estrogen deficiency
      • Calcium deficiency
  • A study by Cummings et al in 1995 evaluated 9516 white women aged 65 years.8 In this study, the subjects were evaluated for an average of 4.1 years and an indirect relationship was observed between the number of risk factors and bone density values. Cummings et al also identified factors that did not increase the risk of fracture, including hair color, number of children breastfed, prior smoking history, or use of short-acting benzodiazepines. One very interesting finding of this study was that dietary intake of calcium was not correlated to the risk of hip fracture; however, the authors of the study did agree with other experts that dietary calcium would only help if the patient was calcium deficient.

Physical

The physical examination should begin with an inspection of the patient. Height measurement with a stadiometer at each visit is useful.

  • Patients with vertebral compression fractures may demonstrate a thoracic kyphosis with an exaggerated cervical lordosis (dowager's hump). This is followed by a loss of lumbar lordosis. After each episode of vertebral compression fracture and progressive kyphosis, the patient's height may decrease by 2-3 cm.
  • Palpation of the spinous processes often does not aid the examiner in localizing point tenderness, but percussion may be helpful in acute or subacute vertebral compression fractures.
  • Patients with hip fractures may show decreased weightbearing on the fractured side or an antalgic gait pattern.
  • Examination of active and passive ROM assists in determining whether spine, hip, wrist, or other osseous pathology may be present.
  • A thorough neurologic examination is essential to rule out spinal cord and/or peripheral nerve compromise.

Causes

Osteoporosis has been divided into several classifications according to etiology and localization in the skeleton. Osteoporosis is initially divided into localized and generalized categories. These 2 main categories are classified further into primary and secondary osteoporosis.

  • Primary osteoporosis occurs in patients in whom a secondary cause of osteoporosis cannot be identified, including juvenile and idiopathic (type I and type II) osteoporosis.
    • Juvenile osteoporosis
      • This condition usually occurs in children or young adults of both sexes.
      • These patients have normal gonadal function. The age of onset usually is 8-14 years.
      • The hallmark characteristic of juvenile osteoporosis is abrupt bone pain and/or a fracture following trauma.
    • Type I osteoporosis (postmenopausal osteoporosis)
      • This condition occurs in women aged 50-65 years.
      • This type of osteoporosis is characterized by a phase of accelerated bone loss.
      • This bone loss occurs primarily from trabecular bone. In this phase, fractures of the distal forearm and vertebral bodies are common.
    • Type II osteoporosis (age-associated or senile)
      • This condition occurs in women and men older than 70 years.
      • This form of osteoporosis represents bone loss associated with aging. Fractures occur in cortical and trabecular bone.
      • In addition to wrist and vertebral fractures, hip fractures are often seen in patients with type II osteoporosis.
  • Secondary osteoporosis occurs when an underlying disease, deficiency, or drug causes osteoporosis, which are as follows:
    • Genetic (congenital)
      • Cystic fibrosis
      • Ehlers-Danlos syndrome
      • Glycogen storage disease
      • Gaucher disease
      • Hemochromatosis
      • Homocystinuria
      • Hypophosphatasia
      • Idiopathic hypercalciuria
      • Marfan syndrome
      • Menkes steely hair syndrome
      • Osteogenesis imperfecta
      • Porphyria
      • Riley-Day syndrome
      • Hypogonadal states (see below)
    • Hypogonadal states
      • Androgen insensitivity
      • Anorexia nervosa/bulimia nervosa
      • Female athlete triad
      • Hyperprolactinemia
      • Panhypopituitarism
      • Premature menopause
      • Turner syndrome
      • Klinefelter syndrome
    • Endocrine9
      • Acromegaly
      • Adrenal insufficiency
      • Cushing syndrome
      • Estrogen deficiency
      • Diabetes mellitus
      • Hyperparathyroidism
      • Hyperthyroidism
      • Pregnancy
    • Deficiency states
      • Calcium deficiency
      • Magnesium deficiency
      • Protein deficiency
      • Vitamin D deficiency9
      • Bariatric surgery
      • Celiac disease
      • Gastrectomy
      • Malabsorption
      • Malnutrition
      • Parenteral nutrition
      • Primary biliary cirrhosis
    • Inflammatory diseases
      • Inflammatory bowel disease
      • Ankylosing spondylitis
      • Rheumatoid arthritis
    • Hematologic and neoplastic
      • Hemochromatosis
      • Hemophilia
      • Leukemia
      • Lymphoma
      • Multiple myeloma
      • Sickle cell anemia
      • Systemic mastocytosis
      • Thalassemia
      • Metastatic disease
    • Drug-induced
      • Anticonvulsants (ie, phenytoin, phenobarbital)
      • Antipsychotic drugs
      • Antiretroviral drugs
      • Cyclosporines and tacrolimus
      • Cytotoxic drugs
      • Furosemide
      • Glucocorticoids and corticotropin5
      • Gonadotropin-releasing hormone analogs
      • Heparin
      • Lithium
      • Methotrexate
      • Selective serotonin reuptake inhibitors
      • Thyroxine (excessive)
    • Miscellaneous
      • Alcoholism
      • Amyloidosis
      • Chronic metabolic acidosis
      • Congestive heart failure
      • Depression
      • Emphysema
      • End-stage renal disease
      • HIV disease/AIDS
      • Idiopathic scoliosis
      • Immobility
      • Multiple sclerosis
      • Ochronosis
      • Organ transplantation
      • Sarcoidosis
      • Weightlessness

More on Osteoporosis (Secondary)

Overview: Osteoporosis (Secondary)
Differential Diagnoses & Workup: Osteoporosis (Secondary)
Treatment & Medication: Osteoporosis (Secondary)
Follow-up: Osteoporosis (Secondary)
Multimedia: Osteoporosis (Secondary)
References
Further Reading
[ CLOSE WINDOW ]

References

  1. Ahmed SF, Elmantaser M. Secondary osteoporosis. Endocr Dev. 2009;16:170-190. [Medline].

  2. [Best Evidence] Majumdar SR, Lier DA, Beaupre LA, et al. Osteoporosis case manager for patients with hip fractures: results of a cost-effectiveness analysis conducted alongside a randomized trial. Arch Intern Med. Jan 12 2009;169(1):25-31. [Medline].

  3. Rosen CJ, Tenenhouse A. Biochemical markers of bone turnover. A look at laboratory tests that reflect bone status. Postgrad Med. Oct 1998;104(4):101-2, 107-10, 113-4.

  4. Melton LJ 3rd, Sampson JM, Morrey BF, Ilstrup DM. Epidemiologic features of pelvic fractures. Clin Orthop Relat Res. Mar-Apr 1981;43-7. [Medline].

  5. Migliaccio S, Brama M, Malavolta N. Management of glucocorticoids-induced osteoporosis: role of teriparatide. Ther Clin Risk Manag. Apr 2009;5(2):305-10. [Medline]. [Full Text].

  6. Jensen GF, Christiansen C, Boesen J, et al. Epidemiology of postmenopausal spinal and long bone fractures. A unifying approach to postmenopausal osteoporosis. Clin Orthop. Jun 1982;(166):75-81. [Medline].

  7. Melton LJ 3d, Kan SH, Frye MA, et al. Epidemiology of vertebral fractures in women. Am J Epidemiol. May 1989;129(5):1000-11. [Medline].

  8. Cummings SR, Nevitt MC, Browner WS, et al. Risk factors for hip fracture in white women. Study of Osteoporotic Fractures Research Group. N Engl J Med. Mar 23 1995;332(12):767-73. [Medline]. [Full Text].

  9. Mann GB, Kang YC, Brand C, et al. Secondary causes of low bone mass in patients with breast cancer: a need for greater vigilance. J Clin Oncol. Jun 22 2009;[Medline].

  10. Tannenbaum C, Clark J, Schwartzman K, et al. Yield of laboratory testing to identify secondary contributors to osteoporosis in otherwise healthy women. J Clin Endocrinol Metab. Oct 2002;87(10):4431-7.

  11. Jilka RL, Hangoc G, Girasole G, et al. Increased osteoclast development after estrogen loss: mediation by interleukin-6. Science. Jul 3 1992;257(5066):88-91. [Medline].

  12. [Best Evidence] Kastner M, Straus SE. Clinical decision support tools for osteoporosis disease management: a systematic review of randomized controlled trials. J Gen Intern Med. Dec 2008;23(12):2095-105. [Medline].

  13. Sinaki M, Mikkelsen BA. Postmenopausal spinal osteoporosis: flexion versus extension exercises. Arch Phys Med Rehabil. Oct 1984;65(10):593-6. [Medline].

  14. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. AJNR Am J Neuroradiol. Nov-Dec 1997;18(10):1897-904. [Medline]. [Full Text].

  15. National Osteoporosis Foundation. Executive Summary of Osteoporosis. Washington, DC: Osteoporosis International;1998.

  16. National Osteoporosis Foundation. Physician's guide to prevention and treatment of osteoporosis. Washington, DC;1998.

  17. Hosking D, Chilvers CE, Christiansen C, et al. Prevention of bone loss with alendronate in postmenopausal women under 60 years of age. Early Postmenopausal Intervention Cohort Study Group. N Engl J Med. Feb 19 1998;338(8):485-92. [Medline]. [Full Text].

  18. Odvina CV, Zerwekh JE, Rao DS, et al. Severely suppressed bone turnover: a potential complication of alendronate therapy. J Clin Endocrinol Metab. Mar 2005;90(3):1294-301.

  19. Body JJ, Gaich GA, Scheele WH, et al. A randomized double-blind trial to compare the efficacy of teriparatide [recombinant human parathyroid hormone (1-34)] with alendronate in postmenopausal women with osteoporosis. J Clin Endocrinol Metab. Oct 2002;87(10):4528-35.

  20. Dempster DW, Cosman F, Kurland ES, et al. Effects of daily treatment with parathyroid hormone on bone microarchitecture and turnover in patients with osteoporosis: a paired biopsy study. J Bone Miner Res. Oct 2001;16(10):1846-53.

  21. Neer RM, Arnaud CD, Zanchetta JR, et al. Effect of parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med. May 10 2001;344(19):1434-41. [Medline]. [Full Text].

  22. Kurland ES, Heller SL, Diamond B, et al. The importance of bisphosphonate therapy in maintaining bone mass in men after therapy with teriparatide [human parathyroid hormone(1-34)]. Osteoporos Int. Dec 2004;15(12):992-7.

  23. Finkelstein JS, Hayes A, Hunzelman JL, et al. The effects of parathyroid hormone, alendronate, or both in men with osteoporosis. N Engl J Med. Sep 25 2003;349(13):1216-26. [Medline]. [Full Text].

  24. Cosman F, Nieves J, Zion M, et al. Daily and cyclic parathyroid hormone in women receiving alendronate. N Engl J Med. Aug 11 2005;353(6):566-75. [Medline]. [Full Text].

  25. Deal C, Omizo M, Schwartz EN, et al. Combination teriparatide and raloxifene therapy for postmenopausal osteoporosis: results from a 6-month double-blind placebo-controlled trial. J Bone Miner Res. Nov 2005;20(11):1905-11. [Medline].

  26. Ste-Marie LG, Schwartz SL, Hossain A, et al. Effect of teriparatide [rhPTH(1-34)] on BMD when given to postmenopausal women receiving hormone replacement therapy. J Bone Miner Res. Feb 2006;21(2):283-91. [Medline].

  27. American Journal of Medicine. Consensus Development Conference on Osteoporosis. Hong Kong, April 1-2, 1993. Am J Med. Nov 30 1993;95(5A):1S-78S. [Medline].

  28. American Journal of Medicine. Consensus development conference: diagnosis, prophylaxis, and treatment of osteoporosis. Am J Med. Jun 1993;94(6):646-50. [Medline].

  29. Baillie SP, Davison CE, Johnson FJ, Francis RM. Pathogenesis of vertebral crush fractures in men. Age Ageing. Mar 1992;21(2):139-41.

  30. Blake GM, Fogelman I. Long-term effect of strontium ranelate treatment on BMD. J Bone Miner Res. Nov 2005;20(11):1901-4. [Medline].

  31. Blake JM, Collins JA, Reid RL, et al. The SOGC statement on the WHI report on estrogen and progestin use in postmenopausal women. J Obstet Gynaecol Can. Oct 2002;24(10):783-90, 793-802.

  32. Boden SD. Diagnostic imaging of the spine. In: Weinstein JN, Rydevik BL, Sonntag VKH, eds. Essentials of the Spine. New York: Raven Press;1995: 97-110.

  33. Body JJ, Facon T, Coleman RE, et al. A study of the biological receptor activator of nuclear factor-kappaB ligand inhibitor, denosumab, in patients with multiple myeloma or bone metastases from breast cancer. Clin Cancer Res. Feb 15 2006;12(4):1221-8. [Medline].

  34. Bostrom MP, Lane JM. Future directions. Augmentation of osteoporotic vertebral bodies [published erratum appears in Spine 1998 Sep 1;23(17):1922]. Spine. Dec 15 1997;22(24 Suppl):38S-42S. [Medline].

  35. Bronk J, Urabe K, Liang T, et al. The effects of age on fracture repair in a rat femur model. Trans Orthop Res Soc. 1996;42:200.

  36. Brown JP, Josse RG. 2002 clinical practice guidelines for the diagnosis and management of osteoporosis in Canada. CMAJ. Nov 12 2002;167(10 Suppl):S1-34.

  37. Bruni V, Dei M, Filicetti MF, et al. Predictors of bone loss in young women with restrictive eating disorders. Pediatr Endocrinol Rev. Jan 2006;3 Suppl 1:219-21.

  38. Burlet N, Reginster JY. Strontium ranelate: the first dual acting treatment for postmenopausal osteoporosis. Clin Orthop Relat Res. Feb 2006;443:55-60.

  39. Campistol JM, Holt DW, Epstein S, et al. Bone metabolism in renal transplant patients treated with cyclosporine or sirolimus. Transpl Int. Sep 2005;18(9):1028-35.

  40. Caplan GA, Scane AC, Francis RM. Pathogenesis of vertebral crush fractures in women. J R Soc Med. Apr 1994;87(4):200-2.

  41. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D3 and calcium to prevent hip fractures in the elderly women. N Engl J Med. Dec 3 1992;327(23):1637-42. [Medline].

  42. Cole A, Herzog R. The lumbar spine: Imaging options. In: Cole A, Herring S, eds. The Low Back Pain Handbook. Philadelphia, PA: Hanley and Belfus, Inc;1997; 179-81.

  43. Cybulski GR. Methods of surgical stabilization for metastatic disease of the spine. Neurosurgery. Aug 1989;25(2):240-52. [Medline].

  44. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med. Sep 4 1997;337(10):670-6. [Medline].

  45. Delmas PD. Biochemical markers of bone turnover. J Bone Miner Res. Dec 1993;8 Suppl 2:S549-55. [Medline].

  46. Delmas PD. Hormone replacement therapy in the prevention and treatment of osteoporosis. Osteoporos Int. 1997;7 Suppl 1:S3-7. [Medline].

  47. Delmas PD, Bjarnason NH, Mitlak BH, et al. Effects of raloxifene on bone mineral density, serum cholesterol concentrations, and uterine endometrium in postmenopausal women. N Engl J Med. Dec 4 1997;337(23):1641-7. [Medline].

  48. Deramond H, Depriester C, Galibert P, Le Gars D. Percutaneous vertebroplasty with polymethylmethacrylate. Technique, indications, and results. Radiol Clin North Am. May 1998;36(3):533-46. [Medline].

  49. Eastell R. Assessment of bone density and bone loss. Osteoporosis Int. 1996;6 Suppl 2:S3-5.

  50. Favur MJ. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. 3rd ed. Philadelphia, Pa: Lippincott-Raven;116, 249.

  51. Francis RM, Peacock M, Marshall DH, et al. Spinal osteoporosis in men. Bone Miner. Mar 1989;5(3):347-57.

  52. Frye MA, Melton LJ 3d, Bryant SC, et al. Osteoporosis and calcification of the aorta. Bone Miner. Nov 1992;19(2):185-94. [Medline].

  53. Gangi A, Kastler BA, Dietemann JL. Percutaneous vertebroplasty guided by a combination of CT and fluoroscopy. AJNR Am J Neuroradiol. Jan 1994;15(1):83-6. [Medline].

  54. Haden ST, Fuleihan GE, Angell JE, et al. Calcidiol and PTH levels in women attending an osteoporosis program. Calcif Tissue Int. Apr 1999;64(4):275-9. [Medline].

  55. Hassager C, Fabbri-Mabelli G, Christiansen C. The effect of the menopause and hormone replacement therapy on serum carboxyterminal propeptide of type I collagen. Osteoporos Int. Jan 1993;3(1):50-2. [Medline].

  56. Heaney RP, Avioli LV, Chestnut C, et al. Is bone the cause of osteoporotic fracture or its consequence?. J Bone Miner Res. 1988;3:79S.

  57. Jackson JA, Kleerekoper M. Osteoporosis in men: diagnosis, pathophysiology, and prevention. Medicine (Baltimore). May 1990;69(3):137-52. [Medline].

  58. Johnson BE, Lucasey B, Robinson RG, Lukert BP. Contributing diagnoses in osteoporosis. The value of a complete medical evaluation. Arch Intern Med. May 1989;149(5):1069-72.

  59. Kanis J, Johnell O, Gullberg B, et al. Risk factors for hip fracture in men from southern Europe: the MEDOS study. Mediterranean Osteoporosis Study. Osteoporos Int. 1999;9(1):45-54.

  60. Kanis JA, Melton LJ 3rd, Christiansen C. The diagnosis of osteoporosis. J Bone Miner Res. Aug 1994;9(8):1137-41. [Medline].

  61. Kelepouris N, Harper KD, Gannon F, et al. Severe osteoporosis in men. Ann Intern Med. Sep 15 1995;123(6):452-60.

  62. Kelman A, Lane NE. The management of secondary osteoporosis. Best Pract Res Clin Rheumatol. Dec 2005;19(6):1021-37. [Medline].

  63. Kimble RB, Vannice JL, Bloedow DC, et al. Interleukin-1 receptor antagonist decreases bone loss and bone resorption in ovariectomized rats. J Clin Invest. May 1994;93(5):1959-67. [Medline].

  64. LaCroix AZ. Estrogen with and without progestin: benefits and risks of short-term use. Am J Med. Dec 19 2005;118(12 Suppl 2):79-87.

  65. Lee N, Radford-Smith G, Taaffe DR. Bone loss in Crohn's disease: exercise as a potential countermeasure. Inflamm Bowel Dis. Dec 2005;11(12):1108-18. [Medline].

  66. Lee WY, Oh KW, Rhee EJ, et al. Relationship between subclinical thyroid dysfunction and femoral neck bone mineral density in women. Arch Med Res. May 2006;37(4):511-6. [Medline].

  67. Lieberman IH, Dudeney S, Reinhardt MK, Bell G. Initial outcome and efficacy of "kyphoplasty" in the treatment of painful osteoporotic vertebral compression fractures. Spine. Jul 15 2001;26(14):1631-8.

  68. Lindsay R. Osteoporosis: Review of the evidence for prevention, diagnosis and treatment and cost-effectiveness analysis. Osteoporosis Int. 1998;8 Suppl 4:S1-S88.

  69. Majumbar S. QMR in assessment of trabecular bone mineral density and structure. Presented at: 4th International Symposium on Osteoporosis;March 1993.

  70. Manolagas SC, Jilka RL. Bone marrow, cytokines, and bone remodeling. Emerging insights into the pathophysiology of osteoporosis. N Engl J Med. Feb 2 1995;332(5):305-11. [Medline].

  71. Marie PJ. Strontium as therapy for osteoporosis. Curr Opin Pharmacol. Dec 2005;5(6):633-6.

  72. McClung MR, Lewiecki EM, Cohen SB, et al. Denosumab in postmenopausal women with low bone mineral density. N Engl J Med. Feb 23 2006;354(8):821-31.

  73. Melton LJ, Crowson CS, Khosla S, O''Fallon WM. Fracture risk after surgery for peptic ulcer disease: a population-based cohort study. Bone. Jul 1999;25(1):61-7.

  74. Melton LJ, Riggs BL. The Osteoporotic Syndrome: Detection, Prevention, and Treatment. New York: Grune and Stratton;1983: 45-72.

  75. Minkin C. Bone acid phosphatase: tartrate-resistant acid phosphatase as a marker of osteoclast function. Calcif Tissue Int. May 1982;34(3):285-90. [Medline].

  76. Naessen T, Persson I, Adami HO, et al. Hormone replacement therapy and the risk for first hip fracture. A prospective, population-based cohort study. Ann Intern Med. Jul 15 1990;113(2):95-103. [Medline].

  77. National Osteoporosis Foundation. Understanding Osteoporosis: A Survey of American Women. Gallup Survey. Washington, DC;1991.

  78. Neer RM. Osteoporosis. In: DeGroot LJ, ed. Endocrinology. Philadelphia, Pa: WB Saunders; 1994:. 1228-58.

  79. Nicola N, Lins E. Vertebral hemangioma: retrograde embolization-stabilization with methyl methacrylate. Surg Neurol. May 1987;27(5):481-6. [Medline].

  80. Okinaga H, Matsuno A, Okazaki R. High risk of osteopenia and bone derangement in postsurgical patients with craniopharyngiomas, pituitary adenomas and other parasellar lesions. Endocr J. Dec 2005;52(6):751-6.

  81. Panigrahi K, Delmas PD, Singer F, et al. Characteristics of a two-site immunoradiometric assay for human skeletal alkaline phosphatase in serum. Clin Chem. May 1994;40(5):822-8. [Medline].

  82. Parfitt AM. Morphologic basis of bone mineral measurements: transient and steady state effects of treatment in osteoporosis. Miner Electrolyte Metab. 1980;4:273-87.

  83. Parfitt AM. Trabecular bone architecture in the pathogenesis and prevention of fracture. Am J Med. Jan 26 1987;82(1B):68-72. [Medline].

  84. Parfitt AM, Mundy GR, Roodman GD, et al. A new model for the regulation of bone resorption, with particular reference to the effects of bisphosphonates. J Bone Miner Res. Feb 1996;11(2):150-9. [Medline].

  85. Peris P, Guañabens N, Monegal A, et al. Aetiology and presenting symptoms in male osteoporosis. Br J Rheumatol. Oct 1995;34(10):936-41.

  86. Poór G, Atkinson EJ, O''Fallon WM, Melton LJ 3rd. Predictors of hip fractures in elderly men. J Bone Miner Res. Dec 1995;10(12):1900-7.

  87. Prescrire International. Strontium: new drug. Postmenopausal osteoporosis: too many unknowns. Prescrire Int. Dec 2005;14(80):207-11.

  88. Price PA, Parthemore JG, Deftos LJ. New biochemical marker for bone metabolism. Measurement by radioimmunoassay of bone GLA protein in the plasma of normal subjects and patients with bone disease. J Clin Invest. Nov 1980;66(5):878-83. [Medline].

  89. Reginster JY, Seeman E, De Vernejoul MC, et al. Strontium ranelate reduces the risk of nonvertebral fractures in postmenopausal women with osteoporosis: Treatment of Peripheral Osteoporosis (TROPOS) study. J Clin Endocrinol Metab. May 2005;90(5):2816-22.

  90. Rupp RE, Ebraheim NA, Coombs RJ. Magnetic resonance imaging differentiation of compression spine fractures or vertebral lesions caused by osteoporosis or tumor. Spine. Dec 1 1995;20(23):2499-503; discussion 2504. [Medline].

  91. Seeman E, Melton LJ, O''Fallon WM, Riggs BL. Risk factors for spinal osteoporosis in men. Am J Med. Dec 1983;75(6):977-83.

  92. Segrest JP, Cunningham LW. Variations in human urinary O-hydroxylysyl glycoside levels and their relationship to collagen metabolism. J Clin Invest. Aug 1970;49(8):1497-509. [Medline].

  93. Siddall PJ, Cousins MJ. Spinal pain mechanisms. Spine. Jan 1 1997;22(1):98-104.

  94. Solomon L. Osteoporosis and fracture of the femoral neck in the South African Bantu. J Bone Joint Surg [Br]. Feb 1968;50(1):2-13. [Medline].

  95. Stein E, Shane E. Secondary osteoporosis. Endocrinol Metab Clin North Am. Mar 2003;32(1):115-34, vii.

  96. Steinmann J, Tingey CT, Cruz G, Dai Q. Biomechanical comparison of unipedicular versus bipedicular kyphoplasty. Spine. Jan 15 2005;30(2):201-5.

  97. Tilyard MW, Spears GF, Thomson J, Dovey S. Treatment of postmenopausal osteoporosis with calcitriol or calcium. N Engl J Med. Feb 6 1992;326(6):357-62.

  98. Wasnich R. Bone mass measurement: prediction of risk. Am J Med. Nov 30 1993;95(5A):6S-10S.

  99. White AH, Derby R, Wynne G. Epidural injections for the diagnosis and treatment of low-back pain. Spine. Jan-Feb 1980;5(1):78-86. [Medline].

  100. Yasuda Y, Kaleta J, Brömme D. The role of cathepsins in osteoporosis and arthritis: rationale for the design of new therapeutics. Adv Drug Deliv Rev. May 25 2005;57(7):973-93.

  101. Yaturu S, DjeDjos S, Alferos G, Deprisco C. Bone mineral density changes on androgen deprivation therapy for prostate cancer and response to antiresorptive therapy. Prostate Cancer Prostatic Dis. 2006;9(1):35-8.

[ CLOSE WINDOW ]

Keywords

secondary osteoporosis, osteoporosis, bone density, bone loss, bone disease, hip fracture, Forteo, alendronate, bisphosphonate, osteoporosis treatment, osteoporosis exercise, bone mass, bone densitometry, bone mineral density, broken hip, hip fractures, teriparatide, metabolic bone disease, vertebral compression fracture

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Alana C Serota, MD, Fellow in Metabolic Bone Disease and Osteoporosis, Department of Orthopedics, Hospital for Special Surgery
Alana C Serota, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph M Lane, MD, Professor of Orthopedic Surgery, Weill Medical College of Cornell University; Chief, Metabolic Bone Disease Service, Hospital for Special Surgery
Joseph M Lane, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of University Professors, American Federation for Aging Research, American Orthopaedic Association, American Society for Bone and Mineral Research, Association of Bone and Joint Surgeons, Medical Society of the State of New York, Musculoskeletal Tumor Society, National Osteoporosis Foundation, North American Spine Society, and Orthopaedic Research Society
Disclosure: P & G; Roche; Lilly: Aventis: Novartis: Spinewave; biomimetics; Zimmer; DFine; Innovative Solutions; Honoraria Speaking and teaching

Medical Editor

Elizabeth A Moberg-Wolff, MD, Associate Professor and Pediatric PM&R Fellowship Director, Department of Physical Medicine and Rehabilitation, Medical College of Wisconsin; Program Director, Tone Management and Mobility, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin
Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
Disclosure: Medtronic Neurological Grant/research funds Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Michael T Andary, MD, MS, Residency Program Director, Professor, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine
Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists
Disclosure: allergan Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.