Arch Orthop Trauma Surg. 2026 Feb 2;146(1):34. doi: 10.1007/s00402-025-06140-z.
ABSTRACT
INTRODUCTION: Symptomatic neuromas result from disorganized nerve growth at the site of amputation, causing pain that affects recovery and quality of life. In patients with diabetes mellitus (DM), nerve regeneration is impaired, compounded by comorbidities such as obesity, hypertension, and hyperlipidemia. Surgical approaches including targeted muscle reinnervation (TMR) and regenerative peripheral nerve interface (RPNI) have shown promise for managing symptomatic neuroma, but their effectiveness in diabetic patients is uncertain due to unique challenges in nerve regeneration. This narrative review explores the protective effects of DM on symptomatic neuroma formation and to evaluate the implications for surgical intervention.
MATERIALS AND METHODS: A systematic search of PubMed was conducted, and relevant studies discussing symptomatic neuroma formation in amputees were included.
RESULTS: Symptomatic neuromas were reported in 9.5-50% of amputees involving 9.5% of upper extremity, and 3.8% of lower extremity amputees. Younger age and proximal amputations were identified as significant risk factors. While it is suggested that Interleukin (IL)-10 and brain-derived neurotropic factor (BDNF) levels are involved in protecting against symptomatic neuroma formation, IL-1β and IL-6 promote neuroma formation. Although evidence is mixed, some evidence suggests that DM and diabetic peripheral neuropathy decrease symptomatic neuroma formation by impairing axonal regeneration, altering the extracellular matrix and modulating inflammatory responses.
CONCLUSIONS: Although surgical approaches such as TMR and RPNI have shown potential in reducing neuroma-related pain, further studies are needed to ensure that this benefit extends to diabetic patients whose disease puts them at increased risk of postoperative complications. Additional studies are required to confirm these findings and optimize surgical strategies for high-risk patient populations.
PMID:41627521 | DOI:10.1007/s00402-025-06140-z