Chronic tendinopathies represent a major problem in the clinical practice of sports orthopaedic surgeons, sports doctors and other health professionals involved in the treatment of athletes and patients that perform repetitive actions. The lack of consensus relative to the diagnostic tools and treatment modalities represents a management dilemma for these professionals. With this review, the purpose of the ESSKA Basic Science Committee is to establish guidelines for understanding, diagnosing and treating this complex pathology.

The purpose of this investigation was to evaluate if clinical assessment, Ultrasound + Colour Doppler (US + CD) and Ultrasound Tissue Characterisation (UTC) can be useful in detecting plantaris tendon involvement in patients with midportion Achilles tendinopathy. Twenty-three tendons in 18 patients (14 men, mean age: 37 years and 4 women: 44 years) (5 patients with bilateral tendons) with midportion Achilles tendinopathy were surgically treated with a scraping procedure and plantaris tendon removal. For all tendons, clinical assessment, Ultrasound + Colour Doppler (US + CD) examination and Ultrasound Tissue Characterisation (UTC) were performed. At surgery, all 23 cases had a plantaris tendon located close to the medial side of the Achilles tendon. There was vascularised fat tissue in the interface between the Achilles and plantaris tendons. Clinical assessment revealed localised medial activity-related pain in 20/23 tendons and focal medial tendon tenderness in 20/23 tendons. For US + CD, 20/23 tendons had a tendon-like structure interpreted to be the plantaris tendon and localised high blood flow in close relation to the medial side of the Achilles. For UTC, 19/23 tendons had disorganised (type 3 and 4) echopixels located only in the medial part of the Achilles tendon indicating possible plantaris tendon involvement. US + CD directly, and clinical assessment indirectly, can detect a close by located plantaris tendon in a high proportion of patients with midportion Achilles tendinopathy. UTC could complement US + CD and clinical assessment by demonstrating disorganised focal medial Achilles tendon structure indicative of possible plantaris involvement.

The treatment of painful chronic tendinopathy is challenging. Multiple non‐invasive and tendon‐invasive methods are used. When traditional non‐invasive treatments fail, the injections of platelet‐rich plasma autologous blood or cortisone have become increasingly favored. However, there is little scientific evidence from human studies supporting injection treatment. As the last resort, intra‐ or peritendinous open or endoscopic surgery are employed even though these also show varying results. This ESSKA basic science committee current concepts review follows the first part on the biology, biomechanics and anatomy of tendinopathies, to provide a comprehensive overview of the latest treatment options for tendinopathy as reported in the literature.

Partial ruptures in the Achilles tendon are rather uncommon and are often misinterpreted as aggravated Achilles tendinopathy, and not always considered as a differential diagnosis. The aim of this literature review was to characterize typical symptoms, to provide an overview of available diagnosis and treatment options, and to give reference points for future research. There were few studies and sparse knowledge of scientific value, making it difficult to give evidence-based recommendations. Based on the few studies and the authors’ clinical experience, a diagnosis should be based on a patient’s history with a typical sharp onset of pain and inability to fully load the tendon. Previous intratendinous cortisone injections might be present. Clinical findings are a localized tender region in the tendon and often weakness during heel raises. Ultrasound and Doppler examinations show a region with an irregular and bulging superficial tendon line, often together with localized high blood flow. Magnetic resonance Imaging (MRI) shows a hyperintense signal in the tendon on T1 and T2-weighted sequences. First-line therapy should be a conservative approach using a 2 cm heel lift for the first 6 weeks and avoiding tendon stretching (for 12 weeks). This is followed by a reduced heel lift of 1 cm and progressive tendon loading at weeks 7–12. After 12 weeks, the heel lift can be removed if pain-free, and the patient can gradually start eccentric exercises lowering the heel below floor level and gradually returning to previous sport level. If conservative management has a poor effect, surgical exploration and the excision of the partial rupture and suturing is required. Augmentation procedures or anchor applications might be useful for partial ruptures in the Achilles insertion, but this depends on the size and exact location. After surgery, the 12 to 14-week rehabilitation program used in conservative management can be recommended before the patient’s return to full tendon loading activities.

The use of corticosteroids (e.g., dexamethasone) as treatment for tendinopathy has recently been questioned as higher risks for ruptures have been observed clinically. In vitro studies have reported that dexamethasone exposed tendon cells, tenocytes, show reduced cell viability and collagen production. Little is known about the effect of dexamethasone on the characteristics of tenocytes. Furthermore, there are uncertainties about the existence of apoptosis and if the reduction of collagen affects all collagen subtypes. We evaluated these aspects by exposing primary tendon cells to dexamethasone (Dex) in concentrations ranging from 1 to 1000 nM. Gene expression of the specific tenocyte markers scleraxis (Scx) and tenomodulin (Tnmd) and markers for other mesenchymal lineages, such as bone (Alpl, Ocn), cartilage (Acan, Sox9) and fat (Cebpα, Pparg) was measured via qPCR. Cell viability and proliferation was calculated using a MTS Assay. Cell death was measured by LDH assay and cleaved caspase-3 using Western Blot. Gene expression of collagen subtypes Col1, Col3 and Col14 was analyzed using qPCR. Stimulation with Dex decreased cell viability and LDH levels. Dex also induced a significant reduction of Scx gene expression and a marked loss of fibroblast like cell shape. The mRNA for all examined collagen subtypes was found to be down-regulated. Among non-tendinous genes only Pparg was significantly increased, whereas Acan, Alpl and Sox9 were reduced. These results indicate a Dex induced phenotype drift of the tenocytes by reducing scleraxis expression. Reduction of several collagen subtypes, but not cell death, seems to be a feature of Dex induced tissue degeneration.