skip to main content

OPG Function — MFDS Part 1 MCQ

Instant feedback + full explanation. One question, done properly.

HardPhysiologyOPG FunctionMFDS Part 1

During alveolar bone remodelling, osteoblast-lineage cells increase their secretion of osteoprotegerin (OPG). RANKL and macrophage colony-stimulating factor expression remain unchanged, but NFATc1 induction and multinucleated osteoclast formation decrease. Which molecular action of OPG most directly accounts for these findings?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: D — Sequestration of RANKL, preventing its ligation of RANK on osteoclast precursors

OPG is a soluble decoy receptor produced by osteoblast-lineage cells. It binds RANKL and prevents RANKL from ligating RANK on monocyte-lineage osteoclast precursors. This reduces downstream signalling, including NFATc1 induction, and therefore inhibits osteoclast differentiation, activation and bone resorption. OPG does not act as a RANK agonist, so B is incorrect. It does not stimulate RANKL production or potentiate macrophage colony-stimulating factor signalling; those effects would favour osteoclastogenesis, making C and D incorrect. OPG also has no direct matrix-degrading action: mineralised bone is resorbed by mature osteoclasts through acidification and proteolytic enzymes, so E is incorrect.

Reference: Takahashi N, Maeda K, Ishihara A, Uehara S, Kobayashi Y. Regulatory mechanism of osteoclastogenesis by RANKL and Wnt signals. Front Biosci (Landmark Ed). 2011;16:21–30. https://pubmed.ncbi.nlm.nih.gov/21196156/