Cholesteatoma produces bone erosion through enzymatic and cellular mechanisms. Which combination best describes the primary mediators?
- A Collagenase (MMP-1) and osteoclast activation via RANKL upregulation by cholesteatoma keratinocytes ✓
- B Cathepsin K secreted by cholesteatoma epithelium acting directly on collagen
- C Elastase degrading the elastin framework of the temporal bone
- D Plasminogen activator dissolving the organic matrix of ossicles
Explanation
Cholesteatoma keratinocytes produce matrix metalloproteinases (especially MMP-1/collagenase, MMP-2, and MMP-9) that degrade the collagen matrix of surrounding bone. Simultaneously, these keratinocytes upregulate RANKL (receptor activator of nuclear factor kappa-B ligand) and pro-inflammatory cytokines (IL-1, TNF-α, IL-6) that activate osteoclasts, which directly resorb the calcified bone matrix. This combined enzymatic degradation plus osteoclast-mediated resorption explains the aggressive, progressive bone destruction seen with cholesteatoma — more than with chronic infection alone.
Reference: Dhingra Diseases of Ear, Nose and Throat, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.