Osteoporosis is a metabolic skeletal disease defined as a reduction of bone mineral density below a defined lower limit of normal.
The World Health Organisation (WHO) defines osteoporosis as a T-score less than -2.5 SD. However, Z-scores are more reliable than T-scores (which are defined against adult white females) as they compare with normal people of same age and gender - see dual-energy x-ray absorptiometry (DEXA) for additional discussion of T and Z scores.
Osteoporosis per se is asymptomatic and is most often diagnosed when individuals are evaluated on the basis of risk factors or following presentation with fragility fracture.
Osteoporosis is essentially decreased bony tissue per unit volume of bone. There is no microstructural and biochemical change as occurs in osteomalacia or rickets. Hence the mineral-to-osteoid ratio is normal (c.f. osteomalacia in which the mineral-to-osteoid ratio is decreased).
Osteoporosis can be localised or diffuse and be divided into:
primary: no cause is identifiable
- postmenopausal (type 1): occurs in 50-65-year-olds females; disproportionate loss of cancellous bone as compared to cortical bone resulting in more involvement of cancellous bone-rich areas, like vertebrae and ends of long bones
- senile (type 2): occurs in the elderly; proportionate loss of cortical and cancellous bones affecting long bones
- idiopathic juvenile osteoporosis
secondary (type 3): occurs due to a range of causes including
- endocrine disease (e.g. Cushing syndrome, hyperthyroidism, hyperparathyroidism, diabetes mellitus) 7
- chronic illness (e.g. COPD, chronic liver disease, multiple sclerosis, coeliac disease) 7
- medications (e.g. steroids, phenytoin)
- thalassaemia major 4
- nutritional disturbances 6 (e.g. malnutrition, anorexia)
There is a different list of secondary causes for juvenile osteoporosis with some overlap with adult causes.
Decreased bone density can be appreciated by decreased cortical thickness and loss of bony trabeculae in the early stages in radiography. Bones like the vertebra, long bones (proximal femur), calcaneum and tubular bones are usually looked at for evidence of osteoporosis.
- not a sensitive modality, as more than 30-50% bone loss is required to appreciate decreased bone density on a radiograph
- vertebral osteoporosis manifests as
- loss of trabeculae in proximal femur area, which is explained by Singh's index (and can also be seen in the calcaneum)
- in tubular bones (especially metacarpals), there will be thinning of the cortex
- cortical thickness <25% of the whole thickness of metacarpal signifies osteoporosis (normally 25-33%)
Bone mineral density measurement
Bone mineral density (BMD) measurement is the method of estimation of calcium hydroxyapatite. Multiple x-ray based, gamma-ray based and ultrasonic methods are available:
- radiographic absorptiometry (RA)
- single photon and x-ray absorptiometry (SPA)
dual energy x-ray absorptiometry (DEXA)
- most commonly-used and most reliable
- quantitative computed tomography can be used
Bone marrow signal takes on a heterogeneous appearance with rounded focal fatty lesions replacing normal marrow with coalescence often occurring 5:
- T1: heterogeneously hyperintense
- T2: variable signal
Treatment and prognosis
As osteoporosis decreases bone strength, patients are at an increased risk of fracture, often with minimal trauma, and commonly at the pelvis, hip and wrist.
Oral bisphosphonates are the most commonly prescribed medications and are effective in reducing the risk of further osteoporotic fracture. There are a range of other medications that can also be used, including intravenous bisphosphonates, selective estrogen receptor modulators (e.g. raloxifene), denosumab, strontium ranelate, calcitonin, and parathyroid hormone-based treatments (e.g. teriparatide) 8.
Bisphosphonates and denosumab have been associated with rare, but serious, side effects including bisphosphonate-related atypical femoral fractures and bisphosphonate-related osteonecrosis of the jaw.
- 1. Sutton D. Textbook of radiology and imaging. Churchill Livingstone. ISBN:0443071098. Read it at Google Books - Find it at Amazon
- 2. Anil G, Guglielmi G, Peh WC. Radiology of osteoporosis. Radiol. Clin. North Am. 2010;48 (3): 497-518. doi:10.1016/j.rcl.2010.02.016 - Pubmed citation
- 3. Hodsman PM. Diagnosis and management of involutional osteoporosis. Can Fam Physician. 2013;25: 467-72. Free text at pubmed - Pubmed citation
- 4. Toumba M, Skordis N. Osteoporosis syndrome in thalassaemia major: an overview. Journal of osteoporosis. 2010: 537673. doi:10.4061/2010/537673 - Pubmed
- 5. Christopher J. Hanrahan, Lubdha M. Shah. MRI of Spinal Bone Marrow: Part 2, T1-Weighted Imaging-Based Differential Diagnosis. (2012) American Journal of Roentgenology. 197 (6): 1309-21. doi:10.2214/AJR.11.7420 - Pubmed
- 6. Wolfgang D. Radiology Review Manual. (2011) ISBN: 9781609139438
- 7. Andreu-Arasa VC, Chapman MN, Kuno H, Fujita A, Sakai O. Craniofacial Manifestations of Systemic Disorders: CT and MR Imaging Findings and Imaging Approach. (2018) Radiographics : a review publication of the Radiological Society of North America, Inc. 38 (3): 890-911. doi:10.1148/rg.2018170145 - Pubmed
- 8.Tu KN, Lie JD, Wan CKV, Cameron M, Austel AG, Nguyen JK, Van K, Hyun D. Osteoporosis: A Review of Treatment Options (2018), P T. 2018 Feb; 43(2): 92–104. Pubmed
Metabolic bone disease
- bone mineralisation
- osteosclerosis (differential diagnosis / mnemonic)
- pituitary gland-related
- thyroid gland-related