Osteoid Osteoma MCQ — NEET PG Practice Question | NEETPGAI
Osteoid Osteoma
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bone Orthopedics
A 16-year-old male athlete presents with 5 months of progressive deep aching pain in the left proximal tibia, worse at night and sometimes waking him from sleep. The pain is dramatically relieved within 20–30 minutes of taking ibuprofen. Examination reveals point tenderness over the proximal tibial diaphysis. Radiograph and CT imaging show the lesion marked **A** in the diagram: a small (8 mm) round cortical radiolucent nidus with a central focus of mineralization and surrounding dense reactive cortical thickening. Which of the following best explains the dramatic pain relief with NSAIDs in this patient?
A. The reactive sclerosis surrounding the nidus compresses adjacent nerves; NSAIDs reduce inflammatory edema around the lesion
B. The lesion erodes the cortex, causing periosteal irritation; NSAIDs inhibit osteoclast activity and stabilize the cortex
C. The nidus secretes prostaglandins E2 and I2, which mediate bone pain; NSAIDs inhibit COX enzymes and reduce prostaglandin production
D. The central mineralization focus undergoes micronecrosis; NSAIDs promote revascularization of the nidus
Explanation
Why option 1 is correct
The structure marked A — the osteoid osteoma nidus — is a highly vascular lesion that secretes prostaglandins E2 and I2 at elevated concentrations. These prostaglandins are the primary mediators of the characteristic bone pain in osteoid osteoma. NSAIDs (such as ibuprofen) inhibit COX enzymes, thereby suppressing prostaglandin synthesis within the nidus. This mechanism explains the pathognomonic rapid (20–30 minute) and dramatic pain relief that occurs with NSAID use — a hallmark clinical feature of osteoid osteoma. This prostaglandin-mediated pain mechanism is the fundamental reason NSAIDs are so effective in this condition (WHO Bone Tumors 2020).
Why each distractor is wrong
Option 2: While reactive sclerosis does surround the nidus, nerve compression is not the primary pain mechanism in osteoid osteoma. The sclerosis is a response to the lesion, not the source of pain. NSAIDs do not primarily work by reducing edema around the sclerosis.
Option 3: Central mineralization does not undergo micronecrosis as a primary pathology in osteoid osteoma. The nidus is well-vascularized, not ischemic. NSAIDs do not promote revascularization — they reduce prostaglandin-mediated inflammation.
Option 4: Osteoclast inhibition is not the mechanism of NSAID action in osteoid osteoma pain relief. The rapid pain relief (within 20–30 minutes) is far too fast to be explained by changes in osteoclast activity or cortical stabilization.
High-YieldNEET PG
Osteoid osteoma pain is prostaglandin-mediated → NSAIDs work via COX inhibition, not by mechanical or structural changes.
WHO Bone Tumors 2020
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