Osteomalacia

• Caused in adults but a deficiency in Vitamin D which causes;
• Decreased calcium and phosphate absorption from the gut
• Mobilisation of calcium and phosphate from the bone
• PTH causes excretion of phosphate in the urine therefore calcium levels will be close to normal and phosphate levels will be decreased

 

Predisposing conditions for Ricket’s or osteomalacia

 

• Inadequate synthesis or dietary deficiency of Vitamin D
  • Inadequate exposure to sunlight
  • Limted dietary intake of fortified foods
  • Poor maternal nutrition
  • Dark skin pigmentation
• Decreased absorption of fat-soluable Vitamin D
  • Cholestatic liver disease
  • Pancreatic insufficiency
  • Biliary tree obstruction
  • Extensive small bowel disease
• Derangements in Vitamin D metabolism
  • Increased degradation of vitamin D and 25(OH)D seen with drugs which induce cytochrome P450 enzymes
  • Impaired synthesis of 25(OH)D in diffuse liver disease
  • Decreased synthesis of 1,25(OH)₂D
    • Advanced renal disease
    • Inherited deficiency in renal-a1-hydroxylase (Vitamin D-dependant rickets type I)
• End organ resistance to 1,25(OH)₂D
  • Inherited absence or defective receptors for acute metabolite of Vit D (Vitamin D-dependant rickets type II)
• Phosphate depletion
  • Poor absorption of phosphate due to chronic use of antacids – binding by aluminium hydroxide
  • Excess renal excretion of phosphate (X-linked hypophosphatemic rickets)

 

Morphology

 

• The basic derangement in both rickets and osteomalacia is an excess of unmineralised matrix
• Rickets in children is made more complicated by inadequate provisional calcification of epiphyseal cartilage deranging endochondrial bone growth
• The following sequence occurs in Rickets;
• Overgrowth of epiphyseal cartilage due to inadequate provisional calcification and failure of the cartilage to mature and disintegrate
• Persistence of distorted irregular masses of cartilage, many of which may project into the bone cavity
• Disruption of orderly replacement of cartilage by osteoid matrix with enlargement of he osteochondral junction
• Abnormal growth of capillaries and fibroblasts in the disorganised zone due to microfractures and stresses
• Deformation of the skeleton due to loss of structural rigidity

 

• During nonambulatory stage of infancy, the head and chest sustain the greatest stresses
• The softened occipital bones can become flattened and the parietal bones can become pushed forward with pressure
• An excess of osteoid produces frontal bossing of the head
• Pigeon breast deformity of the chest
• In the ambulatory child, deformities arise in the spine, pelvis and long bones causing lumbar lordosis and bowing of the legs

 

• In adults the lack of vitamin D deranges normal bone modelling
• The newly formed osteoid matrix laid down by osteoblasts is inadequately mineralised thus producing the persistant osteoid characteristics of osteomalacia
• The contours of the bone isn’t affected but the bone is weak and vulnerable to fractures
• Most affected areas are vertebrae and femoral necks

 

• Persistent mineralisation eventually leads to a loss of skeletal mass referred to as osteopenia. It can be difficult to differentiate osteomalacia from other osteopenias including osteoporosis