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SummaryBackground: Achillodynia is common and includes Achilles tendinopathy, partial Achilles tears and Achilles tendon ruptures. However, we believe an additional pathology should be considered for Achillodynia differentials -the intratendinous tear (ITT). Methods: Examinations of 740 achillodynic patients in one specialist centre were reviewed. ITTs were defined as a clearly visualised echopoor area situated centrally and extending to, but not through the tendon periphery, with pain on palpation and no clinical findings consistent with Achilles rupture. Descriptive statistics were used to analyse differences between pathological sub-groups, and images described qualitatively. Results: 5% (29 males, 8 females) of 740 patients had an ITT. Patients typically presented with a history of sudden onset localised pain and the ability to train but not reach maximal loading. Average age was 36.3 years (range 20-64), significantly lower than mid-tendon tendinopathy (8.48 years; p<0.01). 92% had concurrent Achilles tendinopathy. Elite sportspeople were more highly represented in the ITT than mid-tendon tendi nopathy groups (86.2% ITT group vs 13.8% mid-tendon AT group; p<0.01). Conclusions: ITTs should be actively searched for in patients with Achilles pathology, especially in elite male athletes with a history of high-impact pain. Prospective research is warranted concerning diagnosis and management. Level of evidence: IV.

Background:The intra-tendinous tear is a new pathology that is defined as a discontinuity of fibres situated entirely within the tendon. Prolotherapy involves injecting an irritant, such as hyperosmolar dextrose, to stimulate a tissue healing response and ultimately reduce pain. Methods: 43 consecutive patients diagnosed with an intra-tendinous tear were included (27 males: 16 females, mean (SD) age 41 (11.3). Patients were injected with 0.4ml-1.5ml (mean 0.8ml) of 50% dextrose and 0.5% marcaine mixed in a 1:1 ratio. A 4-6 week period of walking boot immobilisation was followed by progressive rehabilitation (6-8 weeks). Outcomes were assessed with a VISA-A questionnaire at baseline, 3 months and a mean 12.6 (7.0) months post-treatment. Ultrasound scans were conducted before treatment and 5.2 (2.3) weeks later to assess sonographic changes. Results: 30 patients (70%) responded with VISA-A scores increasing by 31 (30.5) points after 3 months (f=0.62, p<0.05) and by 40 (29.3) points after 12.60 (7.0) months (f=0.87, p<0.05). After 5.2 (2.3) weeks, echogenicity was significantly reduced (p<0.05) and 27% of tears were no longer detectable. No significant differences were observed in remaining tears with respect to tear size, tendon thickness or neovascularisation. Conclusion: Treatment resulted in clinically significant improvements and controlled trials are warranted. Level of evidence: IV.

SummaryBackground: The intra-tendinous tear is a new pathology that is defined as a discontinuity of fibres situated entirely within the tendon. Prolotherapy involves injecting an irritant, such as hyperosmolar dextrose, to stimulate a tissue healing response and ultimately reduce pain. Methods: 43 consecutive patients diagnosed with an intra-tendinous tear were included (27 males: 16 females, mean (SD) age 41 (11.3). Patients were injected with 0.4ml-1.5ml (mean 0.8ml) of 50% dextrose and 0.5% marcaine mixed in a 1:1 ratio. A 4-6 week period of walking boot immobilisation was followed by progressive rehabilitation (6-8 weeks). Outcomes were assessed with a VISA-A questionnaire at baseline, 3 months and a mean 12.6 (7.0) months post-treatment. Ultrasound scans were conducted before treatment and 5.2 (2.3) weeks later to assess sonographic changes.

as critical endogenous tissue danger signals. 3 There remains a significant unmet clinical need in the understanding of tendon disorders, largely owing to a lack of in-depth interrogation of the biological mechanisms underpinning the disease process. Objectives To seek evidence of IL-33 expression in early human tendinopathy and thereafter, to explore mechanisms whereby IL-33 may regulate inflammatory mediators and matrix regulation in human tenocytes and a murine tendon model. Methods Fifteen torn supraspinatus tendon (established pathology) and matched intact subscapularis tendon (representing 'early pathology') biopsies were collected from patients undergoing arthroscopic shoulder surgery. Control samples of subscapularis tendon were collected from 10 patients undergoing arthroscopic stabilisation surgery. Human tendon-derived primary cells were derived from hamstring tendon tissue obtained during hamstring tendon ACL reconstruction. The impact of IL-33 upon tenocyte biology ex vivo was measured using quantitative RT-PCR, collagen I and III ELISAs and luminex cytokine multiplexes. In vivo work composed of experiments utilising a murine patellar tendon injury model in WT and ST2-/-. Results IL-33, soluble and membrane bound ST2 transcripts were significantly upregulated in early tendinopathy compared to control or torn tendon biopsies. IL-33 induced dose and time dependent upregulation of total collagen protein accounted for by increased expression of type I but particularly type III collagen mRNA and protein. Following array analysis and consistent with reported IL-33.IL-33 mRNA was elevated on days 1 and 3 post tendon injury in WT mice. This was significantly reduced in injured ST2-/-mice suggesting autocrine regulation. Analysis of collagen synthesis revealed significantly greater expression of collagen 3 at all time points post injury in WT mice compared to uninjured controls or injured ST2-/-mice Importantly injury of WT mice tendons resulted in a significant decrease in biomechanical strength at Day 1 post injury compared to ST2-/-that recovered by days 7 and 21. These data suggest altered collagen matrix synthesis in ST2-/-mice implicating IL-33/ST2 as an early modulator of collagen changes in tendon injury that has biomechanical significance. Administration of rhIL-33 did not affect Collagen 1 synthesis but did significantly increase Collagen 3 synthesis particularly in injured tendons. Moreover, rhIL33 administration significantly reduced ultimate tendon strength at all time points post injection in WT mice suggesting that such changes were of functional impact.Finally we directly targeted IL-33 in vivo. Neutralising antibodies to IL-33 attenuated the collagen I to III switch at days 1 and 3 post injury in WT injured mice resulting in a significant increase in biomechanical strength at day 1 post injury WT mice tendons. Conclusion We herein provide new evidence for a role of IL-33 in the initial steps that lead to the important clinical entity of tendinopathy. Our data implicate IL-33 as an alarmin in ...