Question:hard
The primary metabolic bone disorder in scurvy is:
The primary metabolic bone disorder in scurvy is:
Show Hint
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
Show Solution
The Correct Option is B
Solution and Explanation
Anchor the answer in what vitamin C actually does. Ascorbic acid powers the hydroxylation of proline and lysine residues, a step that lets collagen fibres cross link and gain tensile strength. Strip away vitamin C and collagen production falters everywhere collagen is needed.
Bone is one such place. The osteoid, the unmineralized organic scaffold that osteoblasts secrete before calcium is deposited, is built chiefly from type I collagen. In scurvy that scaffold cannot be assembled properly, so the fundamental bone lesion is failure to form normal osteoid matrix. The mineral handling machinery is not the problem here, the protein framework is.
This is precisely where scurvy parts ways with rickets and osteomalacia. In those vitamin D or phosphate disorders the osteoid is manufactured fine but never gets calcified, so the defect is decreased mineralization, the mirror image of scurvy. Increased resorption is the language of parathyroid excess, not vitamin C lack. And the description of low bone mass with otherwise normal mineral and matrix simply restates osteoporosis, a quantity problem rather than the matrix quality problem of scurvy.
So the defining metabolic bone defect in scurvy is the breakdown of osteoid matrix formation.
\[\boxed{\text{Decreased osteoid matrix formation}}\]
Bone is one such place. The osteoid, the unmineralized organic scaffold that osteoblasts secrete before calcium is deposited, is built chiefly from type I collagen. In scurvy that scaffold cannot be assembled properly, so the fundamental bone lesion is failure to form normal osteoid matrix. The mineral handling machinery is not the problem here, the protein framework is.
This is precisely where scurvy parts ways with rickets and osteomalacia. In those vitamin D or phosphate disorders the osteoid is manufactured fine but never gets calcified, so the defect is decreased mineralization, the mirror image of scurvy. Increased resorption is the language of parathyroid excess, not vitamin C lack. And the description of low bone mass with otherwise normal mineral and matrix simply restates osteoporosis, a quantity problem rather than the matrix quality problem of scurvy.
So the defining metabolic bone defect in scurvy is the breakdown of osteoid matrix formation.
\[\boxed{\text{Decreased osteoid matrix formation}}\]
Was this answer helpful?
0
