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Is Chronic Tendon Pain Caused by Neuropathy? Exciting Breakthroughs may Direct Potential Treatment
Tendinopathy significantly impacts the quality of life and imposes a high economic burden, accounting for a large proportion of sports and musculoskeletal injuries. Traditionally considered a collagen-related inflammatory disorder, emerging evidence suggests a critical role of neuropathic processes...
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Published in: | Current pain and headache reports 2024-07 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Tendinopathy significantly impacts the quality of life and imposes a high economic burden, accounting for a large proportion of sports and musculoskeletal injuries. Traditionally considered a collagen-related inflammatory disorder, emerging evidence suggests a critical role of neuropathic processes in chronic tendon pain.
This review aims to evaluate the neuropathic mechanisms in tendinopathy and discuss innovative treatments targeting these pathways.
We analyze recent studies highlighting the tendon innervation, pathological nerve sprouting neuronal ingrowth in tendinopathy, and the associated increase in pain and neuronal mediators.
Chronic tendinopathy exhibits nociceptive sprouting from paratenon into the fibrous tendon proper. Innovative treatments such as Percutaneous Ultrasound-Guided Tenotomy (PUT) or high-frequency ultrasound interventions show promise in targeting these neuropathic components by paratenon separation. These approaches focus on disrupting the pathological innervation cycle.
Chronic tendon pain may be predominantly neuropathic, driven by pathologic neuronal ingrowth from paratenon into the tendon proper. Interventions that accurately target and disrupt these nerve pathways could revolutionize the treatment of tendinopathy. Further research is required to validate these findings and refine treatment modalities to ensure safety and efficacy. |
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ISSN: | 1531-3433 1534-3081 1534-3081 |
DOI: | 10.1007/s11916-024-01299-3 |