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The short‐term results after treatment with sclerosing polidocanol injections have been shown to be good in patients with chronic painful mid‐portion Achilles tendinosis. This study aimed to evaluate the longer‐term effects on tendon thickness, structure and vascularity, patient satisfaction with treatment, and pain during tendon loading activity. Ultrasonography (US) + colour Doppler (CD) was used for evaluation of the tendon, and the patients graded the amount of pain during tendon loading activity on a VAS. Forty‐two patient's tendons (23 men and 19 women, mean age 53 years) with a long duration (mean 32 months) of pain symptoms from mid‐portion Achilles tendinosis (US + CD showed a localised thickening, structural changes and neovascularisation), were at three (mean) occasions (6–8 weeks in between) treated with US and CD guided injections of the sclerosing substance polidocanol, targeting the area with neovessels ventral to the tendon. After treatment, 37 patients were satisfied with the results of the treatment and back to previous (before injury) activity level. At the 2‐year follow‐up (mean 23 months), 38 patients were satisfied with the results of the treatment, and there was a significant reduction in VAS (from 75 to 7; P < 0.05). US showed a significant reduction in the mean mid‐portion tendon thickness (from 10 to 8 mm, P < 0.05) and a “more normal” structure. CD showed no, or a few, remaining neovessels in the majority of the successfully treated tendons. In conclusion, treatment with sclerosing polidocanol injections in patients with chronic painful mid‐portion Achilles tendinosis showed remaining good clinical results at a 2‐year follow‐up. Decreased tendon thickness and improved structure after treatment, might indicate a remodelling potential?

Objectives Spondyloarthritides (SpA) are characterised by both peripheral and axial arthritis. The hallmarks of peripheral SpA are the development of enthesitis, most typically of the Achilles tendon and plantar fascia, and new bone formation. This study was undertaken to unravel the mechanisms leading towards enthesitis and new bone formation in preclinical models of SpA. Results First, we demonstrated that TNFΔARE mice show typical inflammatory features highly reminiscent of SpA. The first signs of inflammation were found at the entheses. Importantly, enthesitis occurred equally in the presence or absence of mature T and B cells, underscoring the importance of stromal cells. Hind limb unloading in TNFΔARE mice significantly suppressed inflammation of the Achilles tendon compared with weight bearing controls. Erk1/2 signalling plays a crucial role in mechanotransduction-associated inflammation. Furthermore, new bone formation is strongly promoted at entheseal sites by biomechanical stress and correlates with the degree of inflammation. Conclusions These findings provide a formal proof of the concept that mechanical strain drives both entheseal inflammation and new bone formation in SpA.

Despite the high prevalence of tendon pathology in athletes, the underlying pathogenesis is still poorly understood. Various aetiological theories have been presented and rejected in the past, but the tendon cell response model still holds true. This model describes how the tendon cell is the key regulator of the extracellular matrix and how pathology is induced by a failed adaptation to a disturbance of tissue homeostasis. Such failure has been attributed to various kinds of stressors (eg, mechanical, thermal and ischaemic), but crucial elements seem to be missing to fully understand the pathogenesis. Importantly, a disturbance of tissue pressure homeostasis has not yet been considered a possible factor, despite it being associated with numerous pathologies. Therefore, we conducted an extensive narrative literature review on the possible role of intratendinous pressure in the pathogenesis of tendon pathology. This review explores the current understanding of pressure dynamics and the role of tissue pressure in the pathogenesis of other disorders with structural similarities to tendons. By bridging these insights with known structural changes that occur in tendon pathology, a conceptual model was constituted. This model provides an overview of the possible mechanism of how an increase in intratendinous pressure might be involved in the development and progression of tendon pathology and contribute to tendon pain. In addition, some therapies that could reduce intratendinous pressure and accelerate tendon healing are proposed. Further experimental research is encouraged to investigate our hypotheses and to initiate debate on the relevance of intratendinous pressure in tendon pathology.

Achilles tendinopathy is a painful overuse injury that is extremely common in athletes, especially those who participate in running and jumping sports. In addition to pain, Achilles tendinopathy is accompanied by alterations in the tendon's structure and mechanical properties, altered lower extremity function, and fear of movement. Cumulatively, these impairments limit sport participation and performance. A thorough evaluation and comprehensive treatment plan, centered on progressive tendon loading, is required to ensure full recovery of tendon health and to minimize the risk of reinjury. In this review, we will provide an update on the evidence-based evaluation, outcome assessment, treatment, and return-to-sport planning for Achilles tendinopathy. Furthermore, we will provide the strength of evidence for these recommendations using the Strength of Recommendation Taxonomy system.

Both acute and chronic tendon injuries are disabling sports medicine problems with no effective treatment at present. Sustained oxidative stress has been suggested as the major factor contributing to fibrosis and adhesion after acute tendon injury as well as pathological changes of degenerative tendinopathy. Numerous in vitro and in vivo studies have shown that the inhibition of oxidative stress can promote the tenogenic differentiation of tendon stem/progenitor cells, reduce tissue fibrosis and augment tendon repair. This review aims to systematically review the literature and summarize the clinical and pre-clinical evidence about the potential relationship of oxidative stress and tendon disorders. The literature in PubMed was searched using appropriate keywords. A total of 81 original pre-clinical and clinical articles directly related to the effects of oxidative stress and the activators or inhibitors of oxidative stress on the tendon were reviewed and included in this review article. The potential sources and mechanisms of oxidative stress in these debilitating tendon disorders is summarized. The anti-oxidative therapies that have been examined in the clinical and pre-clinical settings to reduce tendon fibrosis and adhesion or promote healing in tendinopathy are reviewed. The future research direction is also discussed.

Tendon pain remains an enigma. Many clinical features are consistent with tissue disruption—the pain is localised, persistent and specifically associated with tendon loading, whereas others are not—investigations do not always match symptoms and painless tendons can be catastrophically degenerated. As such, the question ‘what causes a tendon to be painful?’ remains unanswered. Without a proper understanding of the mechanism behind tendon pain, it is no surprise that treatments are often ineffective. Tendon pain certainly serves to protect the area—this is a defining characteristic of pain—and there is often a plausible nociceptive contributor. However, the problem of tendon pain is that the relation between pain and evidence of tissue disruption is variable. The investigation into mechanisms for tendon pain should extend beyond local tissue changes and include peripheral and central mechanisms of nociception modulation. This review integrates recent discoveries in diverse fields such as histology, physiology and neuroscience with clinical insight to present a current state of the art in tendon pain. New hypotheses for this condition are proposed, which focus on the potential role of tenocytes, mechanosensitive and chemosensitive receptors, the role of ion channels in nociception and pain and central mechanisms associated with load and threat monitoring.

BackgroundRecent investigation of human tissue and cells from positional tendons such as the rotator cuff has clarified the importance of inflammation in the development and progression of tendon disease. These mechanisms remain poorly understood in disease of energy-storing tendons such as the Achilles. Using tissue biopsies from patients, we investigated if inflammation is a feature of Achilles tendinopathy and rupture.MethodsWe studied Achilles tendon biopsies from symptomatic patients with either mid-portion tendinopathy or rupture for evidence of abnormal inflammatory signatures. Tendon-derived stromal cells from healthy hamstring and diseased Achilles were cultured to determine the effects of cytokine treatment on expression of inflammatory markers.ResultsTendinopathic and ruptured Achilles highly expressed CD14+ and CD68+ cells and showed a complex inflammation signature, involving NF-κB, interferon and STAT-6 activation pathways. Interferon markers IRF1 and IRF5 were highly expressed in tendinopathic samples. Achilles ruptures showed increased PTGS2 and interleukin-8 expression. Tendinopathic and ruptured Achilles tissues expressed stromal fibroblast activation markers podoplanin and CD106. Tendon cells isolated from diseased Achilles showed increased expression of pro-inflammatory and stromal fibroblast activation markers after cytokine stimulation compared with healthy hamstring tendon cells.ConclusionsTissue and cells derived from tendinopathic and ruptured Achilles tendons show evidence of chronic (non-resolving) inflammation. The energy-storing Achilles shares common cellular and molecular inflammatory mechanisms with functionally distinct rotator cuff positional tendons. Differences seen in the profile of ruptured Achilles are likely to be attributable to a superimposed phase of acute inflammation and neo-vascularisation. Strategies that target chronic inflammation are of potential therapeutic benefit for patients with Achilles tendon disease.

Overuse tendinopathy is problematic to manage clinically. People of different ages with tendons under diverse loads present with varying degrees of pain, irritability, and capacity to function. Recovery is similarly variable; some tendons recover with simple interventions, some remain resistant to all treatments.The pathology of tendinopathy has been described as degenerative or failed healing. Neither of these descriptions fully explains the heterogeneity of presentation. This review proposes, and provides evidence for, a continuum of pathology. This model of pathology allows rational placement of treatments along the continuum.A new model of tendinopathy and thoughtful treatment implementation may improve outcomes for those with tendinopathy. This model is presented for evaluation by clinicians and researchers.

Correspondence to Professor Tero AH Järvinen, Faculty of Medicine and Health Technologies, Tampere University and Department of Orthopedics & Traumatology, Tampere University Hospital, Tampere, Finland; tero.jarvinen@tuni.fi Tendinopathy is the most common disorder in sports medicine. [...]from a biological perspective, it is somewhat counterintuitive to assume that eradication of neovessels—those originally induced by cells struggling to survive under hypoxic conditions—could offer a viable long-term solution for tendinopathy. Funding This work was funded by the Academy of Finland, Päivikki and Sakari Sohlberg Foundation, and The Competitive State Research Financing of the Expert Responsibility Area of Tampere University Hospital.

Platelet-Rich Plasma (PRP) has been widely used in orthopaedic surgery and sport medicine to treat tendon injuries. However, the efficacy of PRP treatment for tendinopathy is controversial. This paper focuses on reviewing the basic science studies on PRP performed under well-controlled conditions. Both in vitro and in vivo studies describe PRP’s anabolic and anti-inflammatory effects on tendons. While some clinical trials support these findings, others refute them. In this review, we discuss the effectiveness of PRP to treat tendon injuries with evidence presented in basic science studies and the potential reasons for the controversial results in clinical trials. Finally, we comment on the approaches that may be required to improve the efficacy of PRP treatment for tendinopathy.