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Osteomalacia (rickets)
Classification and external resources
ICD-10 M83
ICD-9 268.2
DiseasesDB 9351
MedlinePlus 000376
eMedicine ped/2014 radio/610
Patient UK Osteomalacia
MeSH D010018

Osteomalacia is the softening of the bones caused by defective bone mineralization secondary to inadequate levels of available phosphate and calcium, or because of overactive resorption of calcium from the bone as a result of hyperparathyroidism (which causes hypercalcemia).[1] Osteomalacia in children is known as rickets, and because of this, use of the term "osteomalacia" is often restricted to the milder, adult form of the disease. Signs and symptoms can include diffuse body pains, muscle weakness, and fragility of the bones.

The most common cause of osteomalacia is a deficiency in vitamin D, which is normally derived from sunlight exposure and, to a lesser extent, from the diet.[2] Nursing home residents (and the elderly in general) are at particular risk for vitamin D deficiency, as both the efficiency of vitamin D synthesis in the skin and the absorption of vitamin D from the intestine decline with age. The most specific screening test for vitamin D deficiency in otherwise healthy individuals is a serum 25(OH)D level.[3]

Measures to prevent and treat osteomalacia revolve around intake of vitamin D and calcium supplements. Vitamin D should always be repleted in conjunction with calcium supplementation since most of the consequences of vitamin D deficiency are a result of impaired mineral ion homeostasis.[4]

General characteristics[edit]

Osteomalacia is a generalized bone condition in which there is inadequate mineralization of the bone. Many of the effects of the disease overlap with the more common osteoporosis, but the two diseases are significantly different. There are two main causes of osteomalacia: (1) insufficient calcium absorption from the intestine because of lack of dietary calcium or a deficiency of, or resistance to, the action of vitamin D; and (2) phosphate deficiency caused by increased renal losses.

Osteomalacia is derived from Greek: osteo- which means "bone", and malacia which means "softness". In the past, the disease was also known as malacosteon and its Latin-derived equivalent, mollities ossium. Osteomalacia is associated with increase in osteoid maturation time.


The causes of adult osteomalacia are varied, but ultimately result in a vitamin D deficiency:

Signs and Symptoms[edit]

  • Weak bones
  • Bone pain
  • Muscle weakness
  • Hypocalcemia
  • Compressed vertebrae
  • Pelvic flattening
  • Easy fracturing
  • Bone softening
  • Bending of bones

Clinical features[edit]

Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs, spreading later to the arms and ribs. The pain is symmetrical, non-radiating and is accompanied by sensitivity in the involved bones. Proximal muscles are weak, and there is difficulty in climbing up stairs and getting up from a squatting position.

Due to demineralization bones become less rigid. Physical signs include deformities like triradiate pelvis[8] and lordosis. The patient has a typical "waddling" gait. However, those physical signs may derive from a previous osteomalacial state, since bones do not regain their original shape after they become deformed.

Pathologic fractures due to weight bearing may develop. Most of the time, the only alleged symptom is chronic fatigue, while bone aches are not spontaneous but only revealed by pressure or shocks.

It differs from renal osteodystrophy, where the latter shows hyperphosphatemia.

Biochemical findings[edit]

Biochemical features are similar to those of rickets. The major factor is an abnormally low vitamin D concentration in blood serum.

Major typical biochemical findings include:[9]

Furthermore, a technetium bone scan will show increased activity (also due to increased osteoblasts).

Comparison of bone pathology
Condition Calcium Phosphate Alkaline phosphatase Parathyroid hormone Comments
Osteoporosis unaffected unaffected normal unaffected decreased bone mass
Osteopetrosis unaffected unaffected elevated unaffected[citation needed] thick dense bones also known as marble bone
Osteomalacia and rickets decreased decreased elevated elevated soft bones
Osteitis fibrosa cystica elevated decreased elevated elevated brown tumors
Paget's disease of bone unaffected unaffected variable (depending on stage of disease) unaffected abnormal bone architecture

Radiographic characteristics[edit]

Radiological appearances include:


Nutritional osteomalacia responds well to administration of 10,000 IU weekly of vitamin D for four to six weeks. Osteomalacia due to malabsorption may require treatment by injection or daily oral dosing[10] of significant amounts of vitamin D.


  1. ^ TheFreeDictionary > osteomalacia Citing: Mosby's Medical Dictionary, 8th edition. Copyright 2009
  2. ^ MedlinePlus Medical Encyclopedia: Osteomalacia
  3. ^ al.], ed. Dan L. Longo ... [et (2012). Harrison's principles of internal medicine. (18th ed. ed.). New York: McGraw-Hill. ISBN 978-0-07174889-6. 
  4. ^ . ISBN 978-0-07174889-6.  Missing or empty |title= (help)
  5. ^ "Autoimmunity research foundation, Science behind Vitamin D". Retrieved 2011-07-19. 
  6. ^ Pack, Alison (2008). "Bone health in people with epilepsy: is it impaired and what are the risk factors". Seizure 17 (2): 181–6. doi:10.1016/j.seizure.2007.11.020. PMID 18187347. 
  7. ^ Albany, Costantine; Servetnyk, Zhanna (2009). "Disabling osteomalacia and myopathy as the only presenting features of celiac disease: a case report". Cases Journal 2 (1): 20. doi:10.1186/1757-1626-2-20. PMC 2626577. PMID 19128487. 
  8. ^ Chakravorty, N. K. (1980). "Triradiate deformity of the pelvis in Paget's disease of bone.". Postgraduate Medical Journal 56 (653): 213–5. doi:10.1136/pgmj.56.653.213. PMC 2425842. PMID 7393817. 
  9. ^ Holick, Michael F. (19 July 2007). "Vitamin D Deficiency". New England Journal of Medicine 357 (3): 266–281. doi:10.1056/NEJMra070553. 
  10. ^ Eisman, John A. (1988). "6 Osteomalacia". Baillière's Clinical Endocrinology and Metabolism 2: 125–55. doi:10.1016/S0950-351X(88)80011-9. 

See also[edit]