Nicola Maffulli, Ciaran Padhiar, Nat Padhiar, Otto Chan, Francesco Oliva, Filippo Spiezia
Journal: British medical bulletin 2026;159(1):
PMID: 42716511
BACKGROUND
Insertional Achilles tendinopathy (IAT) accounts for ~20%-25% of all Achilles tendinopathy presentations. Diagnosis is primarily clinical, supported by weight-bearing radiographs, ultrasound, and magnetic resonance image. At the molecular level, activation of the mammalian target of rapamycin (mTOR) pathway, reactive oxygen species (ROS), nuclear factor kappa B (NF-κB)-mediated inflammation, and aberrant tenocyte differentiation drives entheseal degeneration, and, in calcific insertional Achilles tendinopathy (CIAT), dystrophic calcification. Genetic susceptibility modulates individual risk.
SOURCES OF DATA
A narrative literature review was conducted, searching PubMed, Embase, and the Cochrane Library for studies addressing the epidemiology, clinical presentation, imaging, pathophysiology, genetics, and treatment of IAT and CIAT, prioritizing randomized controlled trials, systematic reviews, and meta-analyses, to March 2026.
AREAS OF AGREEMENT
Insertional and calcific Achilles tendinopathy markedly impair athletic performance and quality of life. Modified eccentric loading and extracorporeal shock wave therapy have better evidence-based outcomes. There is genetic susceptibility.
AREAS OF CONTROVERSY
Management of IAT and CIAT requires a structured, staged approach. There is a lack of high-level evidence base for operative management.
GROWING POINTS
mTOR pathway activation drives chondral metaplasia and dystrophic calcification in CIAT; oxidative stress Nicotinamide adenine dinucleotide phosphateoxidase/mitochondrial reactive oxygen species (ROS) and NF-κB signalling are parallel, interacting mechanisms that are targetable pharmacologically. The modified Zadek calcaneal osteotomy is effective for appropriately selected CIAT patients, even without excision of intratendinous calcific deposits.
AREAS TIMELY FOR DEVELOPING RESEARCH
High-quality comparative trials across all treatment domains are a priority. Tissue engineering strategies for enthesis regeneration represent a promising direction for the future.
© The Author(s) 2026. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact [email protected] for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact [email protected].
Medical:
Miscellaneous:
Full Text Sources:
© Copyright 2026, Nutrition Evidence
We use cookies to improve your experience and analyze site traffic with Google Analytics. By continuing to use our site, you agree to our use of cookies. Learn more.