Tendinopathy affects millions of people in athletic and occupational settings and is a nemesis for patients and physicians. Mechanical loading is a major causative factor for tendinopathy; however, the exact mechanical loading conditions (magnitude, frequency, duration, loading history, or some combinations) that cause tendinopathy are poorly defined. Exercise animal model studies indicate that repetitive mechanical loading induces inflammatory and degenerative changes in tendons, but the cellular and molecular mechanisms responsible for such changes are not known. Injection animal model studies show that collagenase and inflammatory agents (inflammatory cytokines and prostaglandin E1 and E2) may be involved in tendon inflammation and degeneration; however, whether these molecules are involved in the development of tendinopathy because of mechanical loading remains to be verified. Finally, despite improved treatment modalities, the clinical outcome of treatment of tendinopathy is unpredictable, as it is not clear whether a specific modality treats the symptoms or the causes. Research is required to better understand the mechanisms of tendinopathy at the tissue, cellular, and molecular levels and to develop new scientifically based modalities to treat tendinopathy more effectively.

In the absence of major bone and soft tissue lower limb trauma during their athletic career, former elite athletes may not be at increased risk of developing clinical OA. Radiographic signs of OA present at a significantly higher incidence and possibly precede the clinical onset of OA. Age, BMI and occupation are identified as strong predictors of the development of OA in former elite athletes.

Level III, retrospective comparative study.

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Purpose The purpose of the present study was to investigate the mid‐term outcomes of a single‐stage cell‐based procedure in patients with knee focal symptomatic cartilage defects using matrix‐induced culture‐expanded autologous AD‐MSCs. It was hypothesised that the increased number of autologous AD‐MSCs after culture expansion is a safe and efficient cartilage repair procedure, which improves overtime chondrogenesis in cartilage lesions Methods Twenty‐five consecutive patients treated for a symptomatic cartilage defect were prospectively followed for 3 years. The median age of patients was 30.5 (range 16–43) with a median BMI of 23.6 kg/m2 (range 19–29) and an average size of the lesion of 3.5 cm2 (range 2–6). All patients underwent a single‐stage procedure consisting in filling each defect with autologous culture‐expanded mesenchymal stem cells embedded in a trimmed‐to‐fit commercially available biodegradable matrix. Pre‐operative and post‐operative evaluation included knee‐related clinical and functional evaluation based on objective and subjective scores at 6, 12, 24 and 36 months and MRI evaluation of the repair tissue using the MOCART score at 12 and 24 months. Results Clinical outcomes recorded significant improvements (p < 0.05) at the final follow‐up compared with baseline as following: all subcategories of KOOS Score, the IKDC subjective from 40.9 (range 20.7–65.6) to 76.9 (range 42–90.3), Tegner Activity Score from 3 (range 2–4) to 4 (range 3–4), VAS for pain from 6 (range 4–8) to 1 (range 0–3). All patients improve significantly their IKDC objective scores. The MRI findings showed complete filling of the defect and integration to the border zone for 65% of the patients. Two patients underwent post‐operative biopsies and the histological analysis demonstrated the presence of hyaline‐like tissue. Conclusions Adipose‐derived culture‐expanded mesenchymal stem cells were shown to be an efficient and safe single‐stage cell‐based procedure for symptomatic, full‐thickness knee chondral lesions. The findings of the present study demonstrate that all patients presented significant mid‐term clinical, functional and radiological improvement. Level of evidence IV.

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IV.