eMedicine Specialties > Physical Medicine and Rehabilitation > Medical Diseases

Osteoporosis (Secondary): Differential Diagnoses & Workup

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

Differential Diagnoses

Other Problems to Be Considered

The differential diagnosis of osteoporosis is very extensive and includes all the secondary causes (see the information bullet on secondary osteoporosis, under Causes). The differential diagnosis of an atraumatic compression fracture may include osteomalacia, tumor, osteonecrosis, infection, and other bone-softening metabolic disorders.

Workup

Laboratory Studies

  • Biochemical markers of bone turnover reflect bone formation or bone resorption. The following is a list of those currently available:
  • Formation (osteoblast products)
    • Serum
      • Bone specific alkaline phosphatase (BSAP)
      • Osteocalcin (OC)
      • Carboxyterminal propeptide of type I collagen (PICP)
      • Aminoterminal propeptide of type I collagen (PINP)
  • Resorption (osteoclast products)
    • Urine
      • Hydroxyproline
      • Free and total pyridinolines (Pyd)
      • Free and total deoxypyridinolines (Dpd)
      • N -telopeptide of collagen cross-links (NTx)
      • C -telopeptide of collagen cross-links (CTx)
    • Serum
      • Cross-linked C -telopeptide of type I collagen (ICTP)
      • Tartrate-resistant acid phosphatase
      • N -telopeptide of collagen cross-links
      • C -telopeptide of collagen cross-links
  • Of the aforementioned tests, the ones most commonly used in clinical practice are BSAP, OC, urine NTx, and serum CTx. Significant controversy exists regarding their use and concern about intra-assay and interassay variability. At the primary author's institution, a urine NTx value normalized to creatinine excretion from the second urination of the day is used primarily to identify osteopenic patients in a high-turnover state who would benefit from therapy and to monitor the response to therapy in all patients.
  • An important study by Tannenbaum10 evaluated 173 healthy women (ages 46-87 y) for secondary causes of osteoporosis. Fifty-five (32%) were found to have a previously undiagnosed disorder of bone or mineral metabolism. Given that occult disorders are so common among patients with osteoporosis, minimal laboratory screening is indicated in all patients who present with decreased bone mass.
  • In addition to a thorough history and physical examination, the following should be performed:
    • CBC count
    • Chemistry panel: This includes calcium, phosphorus, albumin, and liver enzyme levels.
    • Bone-specific alkaline phosphatase, 25-hydroxyvitamin D, intact parathyroid hormone (PTH), and thyrotropin (if on thyroid replacement) levels: Experts are divided on whether to include thyrotropin testing, regardless of a history of thyroid disease or replacement; however, a recently published study showed reduced femoral neck BMD in women with subclinical hypothyroidism and hyperthyroidism.
    • Twenty-four–hour urinary calcium and creatinine values
    • Erythrocyte sedimentation rate and C-reactive protein value: Some practitioners include these tests, although the utility has not been proven in an evidence-based manner.
    • Testosterone and gonadotropin levels: In younger men with low bone densities, a testosterone profile and gonadotropin value should be obtained.
  • Specialized laboratory testing is guided by clinical suspicion or initial screening test results. A history of milk intolerance or anemia should alert the physician to the possibility of celiac sprue. Patients with anemia, particularly those older than 60 years, should also be evaluated for multiple myeloma with a serum and urine protein electrophoresis. Cushing syndrome is not common but, when present, leads to rapidly progressive osteoporosis; a urine free cortisol value or overnight dexamethasone suppression testing should be ordered if Cushing syndrome is suspected. Serum iron and ferritin values are helpful if malabsorption or hemochromatosis is suspected.

Imaging Studies

  • Several large prospective studies have shown that BMD measurements of the distal and proximal femur and the vertebral bodies can predict the development of the major types of osteoporotic fractures. However, the sensitivity, examination time, cost, and radiation exposure of the different imaging techniques differ greatly. Imaging options include densitometry, quantitative computed tomography (QCT) scanning, single-photon absorptiometry (SPA), dual-photon absorptiometry (DPA), dual energy radiographic absorptiometry (DRA), magnetic resonance imaging (MRI), single-photon emission CT (SPECT) scanning, and bone scanning. Comparison of Densitometry

    Open table in new window

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    Table
    SPADPADRAQCT Scanning
    Time5-15 min20-30 min5-10 min10-30 min
    Cost$50-150$150-300$100-200$150-300
    Sites ScannedRadius, forearm,
    calcaneus    		Spine, hip (anteroposterior)Spine (lateral), hip,
    radius    		Spine (lateral), hip,
    radius
    SPADPADRAQCT Scanning
    Time5-15 min20-30 min5-10 min10-30 min
    Cost$50-150$150-300$100-200$150-300
    Sites ScannedRadius, forearm,
    calcaneus    		Spine, hip (anteroposterior)Spine (lateral), hip,
    radius    		Spine (lateral), hip,
    radius
  • QCT scanning of the spine is the most sensitive method for diagnosing osteoporosis because it measures trabecular bone within the vertebral body. Because the expense and radiation dose associated with QCT scanning are high and its reproducibility is relatively poor, it is not an ideal technique when repeated measurements are needed to detect small changes in bone density. Additionally, a method is currently available to translate QCT results into fracture risk, making it less clinically useful overall.
  • SPA of the proximal forearm provides precision and offers low radiation exposure, but this test is relatively insensitive for detecting the early stages of osteoporosis because it measures cortical bone, not trabecular bone.
  • DPA is a means of measuring BMD in the spine and proximal femur. Use of DPA is very limited because of poor reproducibility, prolonged scanning times, and artifacts caused by vascular calcifications.
  • DRA is the method of choice to assess bone density of the lumbar spine and proximal femur. Although DRA is not as sensitive as QCT scanning for detecting early trabecular bone loss, it does provide rapid scanning times, lower costs, and greater precision. First-generation DRA scanners measured spinal bone density in just the anteroposterior view. This resulted in measurements of not just the trabecular-rich vertebral bodies, but also of the cortical-rich spinal elements. New-generation DRA scanners are capable of measuring spinal bone density in the lateral view, thus eliminating measurement of the cortical-rich structures. This improvement results in more accurate measurements of trabecular bone density and greater sensitivity for detecting osteoporosis.
  • MRI can be useful in the assessment of metabolic bone disease. MRI can be used to discriminate between acute and chronic fractures of the vertebrae and occult stress fractures of the proximal femur. These osteoporotic fractures demonstrate characteristic changes in the bone marrow that distinguish them from other uninvolved parts of the skeleton and the adjacent vertebrae.
  • Bone scanning assesses the function and tissue metabolism of organs by using a radionuclide (technetium Tc 99m) that emits radiation in proportion to its attachment to a target structure.
    • Bone scanning is a nonspecific modality, but it is very sensitive for detecting bony abnormalities because an increase in osteoblastic activity (as seen in compression fractures) results in an increase of the radionuclide tracer concentration.
    • Images may be obtained in 3 phases of the bone scanning process. These phases are the immediate-flow study, the immediate static blood pool study, and the delayed static study.
    • Acute fractures are visible in all phases of bone scanning and may remain beyond the reference range for up to 2 years.
  • SPECT scanning represents a tomographic (CT-like) bone imaging technique that offers improved image contrast and more accurate lesion localization than planar bone scanning.
    • SPECT scanning is helpful when accurate localization of skeletal lesions within large and/or anatomically complex bony structures is required. This localization is possible because SPECT can visualize bony structures that would overlap on planar images (eg, separating vertebral body, facet and pars interarticularis lesions).
    • SPECT imaging increases the sensitivity and specificity of bone scanning for detection of lumbar spine lesions by 20-50% over planar techniques.
  • When evaluating patients for osteoporosis, plain radiography may be indicated if a fracture is already suspected or if patients have lost more than 1.5 inches of height. A scoliosis series is useful for detecting occult vertebral fractures. Radiography is better for evaluating cortical bone than trabecular bone. Because osteoporosis predominantly affects trabecular bone, radiography does not reveal osteoporotic changes until they affect the cortical bone. Cortical bone is not affected by osteoporosis until more than 30% of bone loss has occurred, so radiography is an insensitive tool to diagnose osteoporosis.

Other Tests

  • If vertebroplasty or kyphoplasty is performed for fixation of a vertebral compression fracture, a common practice at the primary author's institution is to perform a bone biopsy.

Histologic Findings

Osteoblasts are derived from mesenchymal stem cells, whereas osteoclasts are derived from hematopoietic precursors. The 2 types of cells are dependent on each other for production. In fact, the development of osteoclasts from hematopoietic precursors cannot be accomplished unless mesenchymal cells are present. Mesenchymal cells with the potential to become osteoblasts also have the potential to become fibroblasts, chondrocytes, adipocytes, or muscle cells. This potential for differentiation allows the osteoblast to secrete the same cytokines and colony-stimulating factors produced by fibroblasts.

Hematopoietic granulocyte-macrophage colony-forming units (CFUs) produce osteoclasts and give rise to monocytes and macrophages. As such, the osteoclasts produce the same cytokines that monocytes produce. Interleukin (IL)–6 is produced, in part, by osteoblasts that stimulate osteoclastic activity. This phenomenon is one proposed mechanism for certain diseases that exhibit increased bone resorption. Two examples of diseases that result in osteoporosis by this mechanism are multiple myeloma and rheumatoid arthritis.

Jilka et al have demonstrated that IL-6 regulates osteoclasts, and the scientific community gained insight into the role played by cytokines in the development of osteoporosis.11  The investigators studied mice, either removing the mice's ovaries or performing sham operations. IL-6 levels and the number of granulocyte-macrophage CFUs were measured. IL-6 and granulocyte-macrophage CFU levels were much higher in the ovariectomized mice. This finding provided evidence that estrogen inhibits the secretion of IL-6, and IL-6 contributes to the recruitment of osteoclasts from the monocyte cell line, thus contributing to osteoporosis. IL-1 has also been shown to be involved in the production of osteoclasts.

The production of IL-1 is increased in bone marrow mononuclear cells from ovariectomized rats. Administering IL-1 receptor antagonist to these animals prevents the late stages of bone loss induced by the loss of ovarian function, but it does not prevent the early stages of bone loss. The increase in the IL-1 in the bone marrow does not appear to be a triggered event, but is a result of removal of the inhibitory effect of sex steroids on IL-6 and other genes directly regulated by sex steroids.

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
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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

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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

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