Osteomalacia Osteomalacia is a metabolic bone disease characterized by inadequate mineralization of

bone.

As a result, the skeleton softens and weakens, causing pain, tenderness to touch, bowing of the bones,
and pathologic fractures.

On physical examination, skeletal deformities (spinal kyphosis and bowed legs) give patients an unusual
appearance and a waddling gait. These patients may be uncomfortable with their appearance and are at
risk 3124 for falls and pathologic fractures, particularly of the distal radius and the proximal femur
(Grossman & Porth, 2014).

Pathophysiology The major defect in osteomalacia is a deficiency of activated vitamin D, which promotes
calcium absorption from the gastrointestinal tract and facilitates mineralization of bone. The supply of
calcium and phosphate in the extracellular fluid is low and does not move to calcification sites in bones.
Osteomalacia may result from failed calcium absorption or from excessive loss of calcium from the body
(e.g., kidney failure). Gastrointestinal disorders (e.g., celiac disease, chronic biliary tract obstruction,
chronic pancreatitis, small bowel resection) in which fats are inadequately absorbed are likely to produce
osteomalacia through loss of vitamin D (along with other fat-soluble vitamins) and calcium, the latter
being excreted in the feces with fatty acids. In addition, liver and kidney diseases can produce a lack of
vitamin D because these are the organs that convert vitamin D to its active form. Severe renal
insufficiency results in acidosis. The body uses available calcium to combat the acidosis, and PTH
stimulates the release of skeletal calcium in an attempt to reestablish a physiologic pH. During this
continual drain of skeletal calcium, bony fibrosis occurs, and bony cysts form. Chronic
glomerulonephritis, obstructive uropathies, and heavy metal poisoning result in a reduced serum
phosphate level and demineralization of bone. Hyperparathyroidism leads to skeletal decalcification and
thus to osteomalacia by increasing phosphate excretion in the urine. Prolonged use of anticonvulsant
medication (e.g., phenytoin [Dilantin], phenobarbital) poses a risk of osteomalacia, as does insufficient
vitamin D (dietary, sunlight). Osteomalacia that results from malnutrition (deficiency in vitamin D often
associated with poor intake of calcium) is a result of poverty, poor dietary habits, and lack of knowledge
about nutrition. It occurs most frequently in parts of the world where vitamin D is not added to food,
where dietary deficiencies exist, and where sunlight is rare (Grossman & Porth, 2014).

Assessment and Diagnostic Findings On x-ray studies, generalized demineralization of bone is evident.
Studies of the vertebrae may show a compression fracture with indistinct vertebral end plates.
Laboratory studies show low serum calcium and phosphorus levels and a moderately elevated ALP. Urine
excretion of calcium and creatinine is low. Bone biopsy demonstrates an increased amount of osteoid, a
demineralized, cartilaginous bone matrix that is sometimes referred to as prebone. Medical
Management Physical, psychological, and pharmaceutical measures are used to reduce the patient’s
discomfort and pain. If the underlying cause of osteomalacia is corrected, the disorder may resolve. If
kidney disease prevents activation of absorbed vitamin D, then supplementation requires the activated
form (calcitriol). If osteomalacia is caused by malabsorption, increased doses of vitamin D, along with
supplemental calcium, are usually prescribed. Exposure to sunlight may be recommended; ultraviolet
radiation transforms a cholesterol substance (7-dehydrocholesterol) present in the skin into vitamin D
(Singer, Bone, Hosking, et al., 2014). If osteomalacia is dietary in origin, the interventions are akin to
those discussed previously in the discussion on osteoporosis. Long-term monitoring of the patient is
appropriate to ensure stabilization or reversal of osteomalacia. Some persistent orthopedic deformities
may need to be treated with braces or surgery (e.g., osteotomy may be performed to correct long bone
deformity).

TOPHI • A nodular deposit of sodium acid urate crystals associated forming in body

Tophi (plural of tophus, Latin for “stone”) are stone-like deposits of

monosodium urate in the soft tissues, synovial tissues, or in bones
near the joints.