Question:

The primary metabolic bone disorder in scurvy is:

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Vitamin C builds collagen, so scurvy fails to form osteoid matrix; rickets instead fails to mineralize.
Updated On: Jun 24, 2026
  • Decreased mineralization
  • Decreased osteoid matrix formation
  • Increased bone resorption
  • Decreased bone mass with normal mineralization and osteoid formation
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The Correct Option is B

Solution and Explanation

Step 1: Recall the biochemistry of scurvy. Scurvy is vitamin C (ascorbic acid) deficiency. Vitamin C is an essential cofactor for prolyl and lysyl hydroxylase, the enzymes that hydroxylate proline and lysine during collagen synthesis. Without it, collagen cannot be properly cross linked and stabilised.

Step 2: Apply this to bone. Bone osteoid (the organic matrix laid down by osteoblasts) is mostly type I collagen. In scurvy, defective collagen synthesis means the osteoblasts cannot form normal osteoid matrix. So the primary defect is impaired osteoid (collagen) matrix formation, not a mineral problem.

Step 3: Contrast with rickets and osteomalacia. There the matrix (osteoid) is laid down normally but fails to mineralize because of vitamin D or phosphate problems, giving decreased mineralization (option A). That is the opposite of scurvy, where the matrix itself is deficient.

Step 4: Address the remaining distractors.
Increased bone resorption is the dominant feature of hyperparathyroidism, not the primary defect of scurvy.
Decreased bone mass with normal mineralization and osteoid (option D) describes osteoporosis, where both matrix and mineral are normal in quality but reduced in quantity; scurvy specifically impairs matrix quality.

Step 5: The core lesion of scurvy is failure of osteoid (collagen) matrix formation.

The correct answer is option B, Decreased osteoid matrix formation.
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