Whether physical trauma can precipitate tumorigenesis has been debated for more than a century. Orthopaedic literature contains numerous case reports and small series describing musculoskeletal (MSK) tumors at sites of prior injury, including osteosarcoma at old fractures or around fixation, fibrosarcoma/malignant fibrous histiocytoma (MFH/UPS) in chronic traumatic scars, synovial sarcoma after joint/extremity trauma, malignant peripheral nerve sheath tumor (MPNST) in traumatic neuromas, angiosarcoma in chronic osteomyelitis/foreign-body environments, giant cell tumor after bone injury, and desmoid tumor after vertebral fracture. Parallel evidence documents burn-scar malignancies (Marjolin’s ulcers) and other scar-related epithelial cancers. Biologic plausibility rests on sustained inflammation, oxidative DNA damage, pro-angiogenic signaling, extracellular matrix (ECM) remodeling, and foreign body/chronic infection milieus that collectively create a pro-neoplastic niche.206–214,20,79,215 However, causality remains challenging to prove: evidence is dominated by case reports subject to publication and recall bias, with heterogeneous latency definitions and potential reverse causation (occult tumors presenting after minor trauma). Contemporary methodological reviews generally do not support a universal population-level causal link, while acknowledging plausible site-specific risks in chronic injury contexts.50,218 This narrative review synthesizes pathophysiological mechanisms and the reported human evidence, prioritizing musculoskeletal tumors yet summarizing other trauma-associated entities. We conclude that trauma may act as a rare co-factor in tumorigenesis at specific MSK sites, whereas absolute risk after ordinary injury is likely very low; better registry-linked designs are required to quantify risk and define which lesions merit targeted surveillance.
Prof. Thamer Hamdan Mustafa Habeeb Alshawi* (Sun,) studied this question.