147- What is rickets?
Rickets is a disorder of epiphyseal growth plate characterized by defective
development and impaired mineralization of growth plate as a result of abnor-
mal mineral homeostasis. The defective development of epiphyseal growth
plate is due to lack of apoptosis of hypertrophic chondrocytes, which is essen-
tial for invasion by the bone cells (osteoblasts and osteoclasts) for the new bone
formation. Impaired apoptosis is the result of hypophosphatemia, as optimal
levels of serum phosphate are required for caspase-9-mediated apoptosis of
hypertrophic chondrocytes. Failure of removal of hypertrophic chondrocytes
results in secondary defect in osteoid synthesis and hence impaired mineraliza-
tion. Besides the involvement of epiphyseal growth plate, there is a generalized
defective mineralization (osteomalacia) of bone matrix in rickets.- What is the difference between rickets and osteomalacia?
The difference between rickets and osteomalacia are summarized in the table
given below.Parameters Rickets Osteomalacia
Site of involvement Growth plate and bone matrix Bone matrix
Deformities Common (genu valgum, genu varum) Uncommon (bowing)
Presentation Bone pain, deformities, and poor linear
growthBone pain, fracturesFractures Uncommon Common
Radiology Epiphysis: indistinct and irregular margins Cortical thinning
Physis: widening of growth plate Looser’s zone
Metaphysis: cupping, fraying, and splaying Osteopenia
Diaphysis: cortical thinning, Looser’s zone Triradiate pelvis- How to classify rickets?
Rickets can be classified as vitamin D-deficient, vitamin D-dependent, or vita-
min D-resistant. In addition, rickets can also be classified on the basis of abnor-
malities of mineral homeostasis as calcipenic or phosphopenic rickets. Since
hypophosphatemia is considered as the common denominator for all types of
rickets, a new classification based on the mechanism of hypophosphatemia, i.e.,
PTH-dependent and FGF 23-dependent has been recently proposed.- How does vitamin D deficiency cause rickets?
Although the most common cause of rickets is vitamin D deficiency, neither
vitamin D nor its receptor (VDR) is directly involved in the development of
rickets. This is evidenced in VDR knockout mice where administration of
intravenous calcium and phosphate is associated with healing of rachitic
lesions. Vitamin D deficiency is associated with hypophosphatemia, low
normal calcium, and secondary hyperparathyroidism. Decreased calcium5 Rickets–Osteomalacia