• Clinical science

Osteomalacia and rickets

Abstract

Bone softening caused by impaired mineralization manifests as either osteomalacia or rickets. Osteomalacia affects adults exclusively, as their growth plates have already fused. Rickets affects children, whose growth plates are still open. The most common cause of both osteomalacia and rickets is vitamin D deficiency, resulting from inadequate intake, malabsorption, or lack of exposure to sunlight. Patients with osteomalacia usually present with bone pain and tenderness, while patients with rickets exhibit bone deformities and impaired growth. Over time, both conditions may lead to bending of the long bones or even pathologic fractures. Treatment consists of administering vitamin D and ensuring sufficient calcium intake.

Etiology

Vitamin D‑dependent forms

Vitamin D‑independent forms (rare)

References:[1][2][3][4][5][6]

Pathophysiology

For more information on calcium metabolism, see calcium homeostasis.

References:[2][7]

Clinical features

Osteomalacia

Rickets

References:[8][9]

Diagnostics

Laboratory tests

Calcium
Phosphate
Alkaline Phosphatase
Parathyroid hormone

(See laboratory evaluation of bone disease.)

  • Vitamin D-dependent rickets

X‑ray

Osteomalacia

Rickets

References:[8][9]

Differential diagnoses

Congenital pseudoarthrosis of the tibia

References:[8]

The differential diagnoses listed here are not exhaustive.

Treatment

  • Vitamin D deficiency: administration of Vitamin D
    • Also indicated in infants who are exclusively breastfed
    • The healing of both osteomalacia and rickets requires adequate daily intake of calcium.
  • Defective vitamin D metabolism or vitamin D‑independent forms
    • Treatment of underlying disease

References:[2][8]