Osteomalacia


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Related to Osteomalacia: Paget's disease

osteomalacia

[¦äs·tē·ō·mə′lā·shə]
(medicine)
Failure of bone to ossify due to a reduced amount of available calcium. Also known as adult rickets.

Osteomalacia

 

a bone disease that is manifested by softening and deformity of bone as a result of disturbances in mineral metabolism; usually, the depletion of calcium salts, phosphoric acid, and vitamin D is the cause. Osteomalacia generally occurs in women, especially during pregnancy, in which case the pelvic bones and adjacent portions of the skeleton are particularly affected. Recovery occurs in the postpartum period. Bones may remain permanently deformed after osteomalacia as a result of calcification.

REFERENCE

“Osteomaliatsiia.” In Bol’shaia meditsinskaia entsiklopediia, 2nd ed., vol. 22, Moscow, 1961.
In animals. Osteomalacia in animals is manifested clinically by a decreased and unusual appetite, during which the animal exhibits pica and eats inedible objects. Other symptoms are emaciation and lowered productivity, lameness, loose teeth, sluggishness, curvature or sagging of the spinal column, and bone fractures. The diagnosis is based on analysis of the mineral and vitamin D content of feed; the calcium, phosphorus, and phosphatase content of blood; and roentgenograms of the tail vertebrae. Osteomalacia in animals is prevented by exercise, by regular checks of the feed and inclusion of optimum quantities of minerals and vitamins, and by ultraviolet irradiation while the animals are in their stalls.

REFERENCE

Vnutrennie nezaraznye bolezni zhivotnykh. Edited by A. M. Kolesov. Leningrad, 1972.
References in periodicals archive ?
However, several novel regulators of phosphate homeostasis have been identified as being associated with hypophosphatemia of various types, such as tumor-induced osteomalacia, several hereditary forms of hypophosphatemic rickets, X-linked hypophosphatemia, and autosomal dominant hypophosphatemia (1, 3).
Osteomalacia due to vitamin D depletion: a neglected consequence of intestinal malabsorption.
Calcification of entheses associated with X-linked hypophosphatemic osteomalacia.
Serum 25(OH) D is our best available laboratory aid for diagnosing frank vitamin D deficiency, which causes rickets in children and osteomalacia in adults.
In the past, vitamin D deficiency was identified by a physical rather than a biochemical manifestation--namely, the presence of bone disease, either rickets or the adult equivalent, osteomalacia.
To put this in context, in the UK a level above 25nmol/l is regarded as adequate and below this 'deficient', at which there is an increased risk of bone disease (Lanham-New et al, 2011), levels below 20nmol/l are associated with rickets and osteomalacia (SACN, 2007).
In vitamin D deficiency, osteomalacia, an increase in bone remodeling, and a decrease in bone mineral density (BMD), particularly in the proximal femur, along with an increased risk of osteoporotic fractures, hypocalcemia, hypophosphatemia, and low excretion of urinary calcium may occur.
Aim: Vitamin D deficiency is one of the most important public health problems as a result of osteomalacia, osteoporosis, muscle pain disease, muscle weakness and increased risk of falls and fracture.
Phosphate results can suggest malnutrition or osteomalacia.
This phosphorus-wasting disturbance affects bone metabolism, causing rickets in paediatric patients and osteomalacia in adults [Rowe, 2000].
The adult form of rickets is known as osteomalacia or soft bones.