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. 2026 May 30;21:263. doi: 10.1186/s13023-026-04412-4

Table 3.

Therapeutic strategy for ocular complications in PDB based on pathogenic mechanism

Ocular Complication Dominant Mechanism Role of Systemic Therapy
(Bis/Denosumab)
Necessity of Ocular-Specific Therapy Therapeutic Synergy & Timing
Vascular Optic Neuropathy Vascular “Steal” / Hyperemia Direct & Primary: Suppresses pagetic hypermetabolism/hypervascularity to reverse ischemia Adjunct: Corticosteroids may be used acutely to reduce optic nerve edema/inflammation; severe cases may consider vascular embolization Concurrent/Sequential: Start systemic anti-resorptive urgently; consider short-term steroids for acute presentation
Compressive Optic Neuropathy Bony Stenosis / Mechanical Foundational/Preventive: Halts progression of hyperostosis; does not reverse existing compression Necessary & Definitive: Surgical decompression is indicated for progressive or severe compression Sequential: Optimize systemic control preoperatively to reduce bleeding risk; surgery addresses fixed anatomy
Orbital GCT causing Ptosis Mass Effect Variable/Adjuvant: Denosumab may induce tumor regression; bisphosphonates control background PDB activity Necessary & Definitive: Surgical excision is primary treatment for symptomatic mass effect Combined/Neoadjuvant: Consider denosumab to shrink tumor preoperatively; surgery for definitive removal
AS with CNV Local Neovascularization Indirect/Supportive: Manages systemic disease but has no direct effect on CNV Necessary & Primary: Intravitreal anti-VEGF injections are standard care for active CNV Parallel: Treat systemic disease and ocular CNV independently but concurrently
Cataract Age-related / Multifactorial No Role Necessary & Definitive: Cataract surgery when visually significant Independent: Ocular surgery proceeds based on ophthalmic indication, independent of PDB status if bone is inactive

Abbreviations: Paget’s disease of bone (PDB), Bisphosphonates (Bps), Giant Cell Tumor (GGT), Angioid Streaks (AS), Choroidal Neovascularization (CNV), Anti-Vascular Endothelial Growth Factor (anti-VEGF)