Osteoporosis Differential Diagnoses

  • Author: Dana Jacobs-Kosmin, MD; Chief Editor: Herbert S Diamond, MD   more...
 
Updated: Apr 19, 2012
 
 

Diagnostic Considerations

The differential diagnosis of osteoporosis is very extensive. When dealing with reduced bone density, always rule out the other possible causes of symptoms before treating the patient for osteoporosis. Many patients have a coexisting cause of bone loss.

The differential diagnosis of an atraumatic compression fracture may include osteomalacia, tumor, osteonecrosis, infection, and other bone-softening metabolic disorders. Metastatic bone disease should always be ruled out when one is treating multiple fractures.

Osteoporosis may be confused with osteomalacia, but in osteoporosis, the bones are porous and brittle, while in osteomalacia the bones are soft. This difference in bone consistency is related to the ratio of mineral to organic material. 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.

Often, the presence of a fracture is not only a marker for decreased bone mass but also potentially a symptom of failing health in general and one or more primary disorders in particular. Failure to diagnose and/or make appropriate referrals may create potential legal issues.

Other conditions to be considered include the following:

  • Leukemia
  • Lymphoma
  • Metastases (bony and other)
  • Pathologic fractures secondary to bone metastases from cancer
  • Pediatric osteogenesis imperfecta
  • Renal osteodystrophy

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
Author

Dana Jacobs-Kosmin, MD  Attending Physician, Department of Medicine, Division of Rheumatology, Albert Einstein Medical Center; Clinical Assistant Professor of Medicine, Jefferson Medical College

Dana Jacobs-Kosmin, MD is a member of the following medical societies: American College of Physicians and American College of Rheumatology

Disclosure: Nothing to disclose.

Coauthor(s)

Sucharitha Shanmugam, MD  Consulting Physician, PMA Medical Specialists, Limerick, PA

Sucharitha Shanmugam, MD is a member of the following medical societies: American College of Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD  Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Michael T Andary, MD, MS Professor, Residency Program Director, 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

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Coburn Hobar, MD Clinician in Rheumatology, Hobar Health and Wellness, and Anti-Aging & Wellness Center of Sarasota

Coburn Hobar, MD is a member of the following medical societies: American Academy of Anti-Aging Medicine and American College of Rheumatology

Disclosure: Nothing to disclose.

Robert J Kaplan, MD James E Van Zandt VA Medical Center, Staff Physician, Department of Rehabilitation Medicine

Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

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: Lilly; Aventis; Novartis; Warner Chilcott; Biomimetics; Zimmer; DFine; Innovative Solutions; Honoraria Speaking and teaching; Graftys; Bone Technologies SA; CollPlant Consulting fee Consulting

David Lenrow, MD Vice Chair of Clinical Services, Medical Director, Erdman Clinic; Associate Professor, Department of Rehabilitation Medicine, University of Pennsylvania at Philadelphia

David Lenrow, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Medical Assocation

Disclosure: Nothing to disclose.

Julie Lin, MD Assistant Professor, Department of Rehabilitation Medicine, Weill Medical College of Cornell University; Assistant Attending Physiatrist, Physiatry Department, Hospital for Special Surgery

Julie Lin, MD 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, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation

Disclosure: Nothing to disclose.

Elizabeth A Moberg-Wolff, MD Associate Professor, Department of Physical Medicine and Rehabilitation, Children's Hospital of Wisconsin, Medical College 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

Srinivas R Nalamachu, MD Clinical Assistant Professor, Department of Internal Medicine, Kansas City University of Medicine and Biosciences; President and Medical Director, Internation Clinical Research Institute, Inc; Medical Director, Pain Management Institute

Srinivas R Nalamachu, MD is a member of the following medical societies: International Association for the Study of Pain

Disclosure: Nothing to disclose.

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Miguel A Schmitz, MD Consulting Surgeon, Department of Orthopedics, Klamath Orthopedic and Sports Medicine Clinic

Miguel A Schmitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, Arthroscopy Association of North America, and North American Spine Society

Disclosure: Nothing to disclose.

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.

Curtis W Slipman, MD Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center

Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Shireesha Vuppalanchi, MD Consulting Staff, Methodist Hospital, Indianapolis; Hospitalist, Respiratory and Critical Care Consultants, PC

Disclosure: Nothing to disclose.

William S Whyte II, MD Director of Interventional Spine and Pain Management, Louisiana Pain Physicians

William S Whyte II, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association, Association of Academic Physiatrists, North American Spine Society, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Southern Medical Association

Disclosure: Nothing to disclose.

Jerome D Wiedel, MD Chair, Professor, Department of Orthopedics, University of Colorado Health Sciences Center

Disclosure: Nothing to disclose.

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Osteoporosis. Lateral radiograph demonstrates multiple osteoporotic vertebral compression fractures. Kyphoplasty has been performed at one level.
Osteoporosis. Lateral radiograph of the patient seen in the previous image following kyphoplasty performed at 3 additional levels.
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 fracture in L3 and the central burst fracture in L5. The patient had suffered a recent fall.
Normal femoral anatomy.
Stable intertrochanteric fracture of the femur.
Percutaneous vertebroplasty, transpedicular approach.
Asymmetric loss in vertebral body height, without evidence of an acute fracture, can develop in patients with osteoporosis. These patients become progressively kyphotic (as shown) over time, and the characteristic hunched-over posture of severe osteoporosis develops eventually.
In kyphoplasty, a KyphX inflatable bone tamp is percutaneously advanced into the collapsed vertebral body (A). It is then inflated, (B) elevating the depressed endplate, creating a central cavity, and compacting the remaining trabeculae to the periphery. Once the balloon tamp is deflated and withdrawn, the cavity (C) is filled under low pressure with a viscous preparation of methylmethacrylate (D).
Reduction in kyphotic angulation after kyphoplasty.
Osteoporosis is defined as a loss of bone mass below the threshold of fracture. This slide (methylmethacrylate embedded and stained with Masson's trichrome) demonstrates the loss of connected trabecular bone.
The bone loss of osteoporosis can be severe enough to create separate bone "buttons" with no connection to the surrounding bone. This easily leads to insufficiency fractures.
Inactive osteoporosis is the most common form and manifests itself without active osteoid formation.
Osteoporosis that is active contains osteoid seams (red here in the Masson's trichrome).
Woven bone arising directly from surrounding mesenchymal tissue.
This image depicts bone remodeling with osteoclasts resorbing one side of a bony trabecula and osteoblasts depositing new bone on the other side.
Osteoclast, with bone below it. This image shows typical distinguishing characteristics of an osteoclast: a large cell with multiple nuclei and a "foamy" cytosol.
In this image, several osteoblasts display a prominent Golgi apparatus and are actively synthesizing osteoid. Two osteocytes can also be seen.
Severe osteoporosis. This radiograph shows multiple vertebral crush fractures. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.
This radiograph of the spine shows a lateral wedge fracture of L3 (yellow asterisk) and compression fracture of L5 (red asterisk) in an osteoporotic patient who suffered a recent fall. More detailed imaging, usually with computed tomography (CT) scanning, is often needed to better evaluate compression fractures and to determine the urgency of surgical interventions.
Lateral spine radiograph depicting osteoporotic wedge fractures of L1-L2. Source: Wikimedia Commons.
Dual-energy computed tomography (CT) scan in a patient with involutional osteoporosis. Insufficiency fractures of the sacrum and the pubic rami are seen on an isotopic bone scan as a characteristic H, or Honda, sign (arrows), which appears as intense radiopharmaceutical uptake at the fracture sites.
Schematic example of an early bone densitometer: the QDR-1000 System (spine scan). (From: Third National Health and Nutrition Examination Survey Bone Densitometry Manual. Rockville, Md: Westat, Inc; 1989 [revised].)
Bone density scanner. This machine measures bone density to check for osteoporosis in the elderly and other vulnerable subjects. Source: Wikimedia Commons.
Example of a dual energy x-ray absorption (DXA) scan. This image is of the left hip bone. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.
Example of a dual energy x-ray absorption (DXA) scan. This image is of the lumbar spine. Source: Government of Western Australia Department of Health. http://www.imagingpathways.health.wa.gov.au/includes/dipmenu/osteo/image.html.
Table 1. WHO Definition of Osteoporosis Based on BMD Measurements by DXA
Definition Bone Mass Density Measurement T-Score
NormalBMD within 1 SD of the mean bone density for young adult womenT-score ≥ –1
Low bone mass (osteopenia)BMD 1–2.5 SD below the mean for young-adult womenT-score between –1 and –2.5
OsteoporosisBMD ≥2.5 SD below the normal mean for young-adult womenT-score ≤ –2.5
Severe or “established” osteoporosisBMD ≥2.5 SD below the normal mean for young-adult women in a patient who has already experienced ≥1 fracturesT-score ≤ –2.5 (with fragility fracture[s])
Sources:



(1) World Health Organization (WHO). WHO scientific group on the assessment of osteoporosis at primary health care level: summary meeting report. Available at: http://www.who.int/chp/topics/Osteoporosis.pdf. Accessed February 6, 2012.[8]



(2) Kanis JA. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: synopsis of a WHO report. WHO Study Group. Osteoporos Int. Nov 1994;4(6):368-81.[7]



(3) Czerwinski E, Badurski JE, Marcinowska-Suchowierska E, Osieleniec J. Current understanding of osteoporosis according to the position of the World Health Organization (WHO) and International Osteoporosis Foundation. Ortop Traumatol Rehabil. Jul-Aug 2007;9(4):337-56.[6]



BMD = bone mass density; DXA = dual x-ray absorptiometry; SD = standard deviation; T-score = a measurement expressed in SD units from a given mean that is equal to a patient's BMD measured by DXA minus the value in a young healthy person, divided by the SD measurement in the population.[9] .



Table 2. Types of Primary Osteoporosis
Type of Primary OsteoporosisCharacteristics
Juvenile osteoporosis
  • Usually occurs in children or young adults of both sexes
  • Normal gonadal function
  • Age of onset: usually 8-14 years
  • Hallmark characteristic: abrupt bone pain and/or a fracture following trauma
Idiopathic osteoporosis
  • Postmenopausal osteoporosis (type I osteoporosis)
  • Occurs in women aged 50-65 years
  • Characterized by a phase of accelerated bone loss, primarily from trabecular bone
  • Fractures of the distal forearm and vertebral bodies common
  • Age-associated or senile osteoporosis (type II osteoporosis)
  • Occurs in women and men older than 70 years
  • Represents bone loss associated with aging
  • Fractures occur in cortical and trabecular bone
  • Wrist, vertebral, and hip fractures often seen in patients with type II osteoporosis
Table 3. Causes of Secondary Osteoporosis in Adults
Cause Examples
Genetic/congenital
  • Renal hypercalciuria – one of the most important secondary causes of osteoporosis; can be treated with thiazide diuretics
  • Cystic fibrosis
  • Ehlers-Danlos syndrome
  • Glycogen storage disease
  • Gaucher disease
  • Marfan syndrome
  • Menkes steely hair syndrome
  • Riley-Day syndrome
  • Osteogenesis imperfecta
  • Hemochromatosis
  • Homocystinuria
  • Hypophosphatasia
  • Idiopathic hypercalciuria
  • Porphyria
  • Hypogonadal states
Hypogonadal states
  • Androgen insensitivity
  • Anorexia nervosa/bulimia nervosa
  • Female athlete triad
  • Hyperprolactinemia
  • Panhypopituitarism
  • Premature menopause
  • Turner syndrome
  • Klinefelter syndrome
Endocrine disorders[24]
  • Cushing syndrome
  • Diabetes mellitus
  • Acromegaly
  • Adrenal insufficiency
  • Estrogen deficiency
  • Hyperparathyroidism
  • Hyperthyroidism
  • Hypogonadism
  • Pregnancy
  • Prolactinoma
Deficiency states
  • Calcium deficiency
  • Magnesium deficiency
  • Protein deficiency
  • Vitamin D deficiency[24, 25]
  • Bariatric surgery
  • Celiac disease
  • Gastrectomy
  • Malabsorption
  • Malnutrition
  • Parenteral nutrition
  • Primary biliary cirrhosis
Inflammatory diseases
  • Inflammatory bowel disease
  • Ankylosing spondylitis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
Hematologic and neoplastic disorders
  • Hemochromatosis
  • Hemophilia
  • Leukemia
  • Lymphoma
  • Multiple myeloma
  • Sickle cell anemia
  • Systemic mastocytosis
  • Thalassemia
  • Metastatic disease
Medications
  • Anticonvulsants: phenytoin, barbiturates, carbamazepine (these agents are associated with treatment-induced vitamin D deficiency)
  • Antipsychotic drugs
  • Antiretroviral drugs
  • Aromatase inhibitors: exemestane, anastrozole
  • Chemotherapeutic/transplant drugs: cyclosporine, tacrolimus, platinum compounds, cyclophosphamide, ifosfamide, high-dose methotrexate[26]
  • Furosemide
  • Glucocorticoids and corticotropin[27] : prednisone (≥5 mg/day for ≥3 mo)[28]
  • Heparin (long term)
  • Hormonal/endocrine therapies: gonadotropin-releasing hormone (GnRH) agonists, luteinizing hormone-releasing hormone (LHRH) analogues, depomedroxyprogesterone, excessive thyroxine
  • Lithium
  • Selective serotonin reuptake inhibitors (SSRIs)
Miscellaneous
  • Alcoholism
  • Amyloidosis
  • Chronic metabolic acidosis
  • Congestive heart failure
  • Depression
  • Emphysema
  • Chronic or end-stage renal disease
  • Chronic liver disease
  • HIV/AIDS
  • Idiopathic scoliosis
  • Immobility
  • Multiple sclerosis
  • Ochronosis
  • Organ transplantation
  • Pregnancy/lactation
  • Sarcoidosis
  • Weightlessness
Sources:



(1) American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocr Pract. Nov-Dec 2003;9(6):544-64.[21]



(2) Kelman A, Lane NE. The management of secondary osteoporosis. Best Pract Res Clin Rheumatol. Dec 2005;19(6):1021-37.[22]



Table 4. Prevalence of Osteoporosis Among Racial and Ethnic Groups
Race/Ethnicity Sex (age ≥50 y) % Estimated to have osteoporosis % Estimated to have low bone mass
Non-Hispanic white; AsianWomen2052
Men735
Non-Hispanic blackWomen5*
Men419
HispanicWomen1049
Men323
Source:  National Osteoporosis Foundation. Fast facts. Available at: http://www.nof.org/node/40. Accessed: February 16, 2012.[42]



* Low bone density is present in an additional 35% of black women, increasing their risk of developing osteoporosis.



Table 5. Comparison of Densitometry Techniques and Cost-Effectiveness
Single-photon absorptiometry Dual-photon absorptiometry Dual-energy x-ray absorptiometry Quantitative computed tomography
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



Source:  Nayak S, Roberts MS, Greenspan SL. Cost-effectiveness of different screening strategies for osteoporosis in postmenopausal women. Ann Intern Med. Dec 6 2011;155(11):751-61.[68]
Table 6. Baseline Studies for Baseline Conditions in Osteoporosis
Baseline test Disorder
Complete blood count (CBC)CBC results may reveal anemia, as in sickle cell disease (patients with anemia, particularly those older than 60 years, should also be evaluated for multiple myeloma), and may raise the suspicion for alcohol abuse (in conjunction with results from serum chemistry tests and liver function tests)
Serum chemistry levelsCalcium levels can reflect underlying disease states (eg, severe hypercalcemia may reflect underlying malignancy or hyperparathyroidism; hypocalcemia can contribute to osteoporosis)



levels of serum calcium, phosphate, and alkaline phosphatase are usually normal in persons with primary osteoporosis, although alkaline phosphatase levels may be elevated for several months after a fracture



levels of serum calcium, phosphate, alkaline phosphatase, and 25(OH) vitamin D may be obtained to assess osteomalacia



Creatinine levels may decrease with increasing parathyroid hormone (PTH) levels or may be elevated in patients with multiple myeloma



Creatinine levels are also used to estimate creatinine clearance, which may indicate reduced renal function in elderly patients



Magnesium is very important in calcium homeostasis[71] ; decreased levels of magnesium may affect calcium absorption and metabolism



Serum iron and ferritin levelsThese tests are helpful when malabsorption or hemochromatosis are suspected
Liver function testsIncreased levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), bilirubin, and alkaline phosphatase may indicate alcohol abuse
Thyroid-stimulating hormone (TSH) levelThyroid dysfunction has been associated with osteoporosis and should therefore be ruled out[72]
25-Hydroxyvitamin D levelThis test assesses for vitamin D insufficiency; inadequate vitamin D levels can predispose persons to osteoporosis
Table 7. Tests for Secondary Causes of Osteoporosis
Tests for Secondary Causes of Osteoporosis Disorder
24-Hour urine calcium levelThis study assesses for hypercalciuria to help rule out benign familial hypocalciuric hypercalcemia (FHH), in which urinary calcium levels are low
Parathyroid hormone (PTH) levelAn intact PTH result is essential in ruling out hyperparathyroidism; an elevated PTH level may be present in benign FHH
Thyrotropin level (if on thyroid replacement)Experts are divided on whether to include thyrotropin testing, regardless of a history of thyroid disease or replacement; however, one study showed reduced femoral neck bone mineral density (BMD) in women with subclinical hypothyroidism and hyperthyroidism[72]
Testosterone and gonadotropin levels in younger men with low bone densitiesThese tests may help evaluate a sex hormone deficiency as a secondary cause of osteoporosis
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levelsSome practitioners include ESR and CRP values in the workup, although their utility in this setting has not been proven in an evidence-based manner
Urinary free cortisol level and tests for adrenal hypersecretionThese tests are used to exclude Cushing syndrome, which, although uncommon, can lead to rapidly progressive osteoporosis when the condition is present; a urine free cortisol value or overnight dexamethasone suppression test should be ordered in suspected cases
Serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP)These are used to identify multiple myeloma
Antigliadin and antiendomysial antibodiesThese tests can help identify celiac disease
Serum tryptase and urine N-methylhistamineThese tests help identify mastocytosis and are used to exclude the presence of multiple myeloma; serum tryptase may be performed to rule out plasma cell dyscrasias
Bone marrow biopsyThis study is obtained when a hematologic disorder is suspected
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