{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T23:07:07Z","timestamp":1788995227613,"version":"build-2803163510"},"reference-count":81,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T00:00:00Z","timestamp":1783036800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Insertional Achilles tendinopathy (IAT) accounts for ~20%\u201325% 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-\u03baB)-mediated inflammation, and aberrant tenocyte differentiation drives entheseal degeneration, and, in calcific insertional Achilles tendinopathy (CIAT), dystrophic calcification. Genetic susceptibility modulates individual risk.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Sources of Data<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Areas of Agreement<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Areas of Controversy<\/jats:title>\n                    <jats:p>Management of IAT and CIAT requires a structured, staged approach. There is a lack of high-level evidence base for operative management.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Growing Points<\/jats:title>\n                    <jats:p>mTOR pathway activation drives chondral metaplasia and dystrophic calcification in CIAT; oxidative stress Nicotinamide adenine dinucleotide phosphateoxidase\/mitochondrial reactive oxygen species (ROS) and NF-\u03baB 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Areas Timely for Developing Research<\/jats:title>\n                    <jats:p>High-quality comparative trials across all treatment domains are a priority. Tissue engineering strategies for enthesis regeneration represent a promising direction for the future.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/bmb\/ldag031","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T11:51:50Z","timestamp":1787140310000},"source":"Crossref","is-referenced-by-count":0,"title":["Current concepts and management of insertional Achilles tendinopathy and calcific insertional Achilles tendinopathy"],"prefix":"10.1093","volume":"159","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5327-3702","authenticated-orcid":false,"given":"Nicola","family":"Maffulli","sequence":"first","affiliation":[{"name":"Department of Trauma and Orthopaedic Surgery, Sapienza University of Rome , Piazzale Aldo Moro 5, 00185, Rome ,","place":["Italy"]},{"name":"Centre for Sports and Exercise Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London , Mile End Hospital, 275 Bancroft Road, London, E1 4DG,","place":["United Kingdom"]},{"name":"School of Pharmacy and Bioengineering, Keele University School of Medicine , Stoke-on-Trent , Staffordshire, ST5 5BG,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-2025-993X","authenticated-orcid":false,"given":"Ciaran","family":"Padhiar","sequence":"additional","affiliation":[{"name":"Centre for Sports and Exercise Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London , Mile End Hospital, 275 Bancroft Road, London, E1 4DG,","place":["United Kingdom"]},{"name":"London Independent Hospital , Stepney Green, 1 Beaumont Square, Stepney Green, London, E1 4NL, London ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0352-4534","authenticated-orcid":false,"given":"Nat","family":"Padhiar","sequence":"additional","affiliation":[{"name":"Centre for Sports and 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