BackgroundArticular cartilage displays a poor repair capacity. The aim of cell-based therapies for cartilage defects is to repair damaged joint surfaces with a functional replacement tissue. Currently, chondrocytes removed from a healthy region of the cartilage are used but they are unable to retain their phenotype in expanded culture. The resulting repair tissue is fibrocartilaginous rather than hyaline, potentially compromising long-term repair. Mesenchymal stem cells, particularly bone marrow stromal cells (BMSC), are of interest for cartilage repair due to their inherent replicative potential. However, chondrocyte differentiated BMSCs display an endochondral phenotype, that is, can terminally differentiate and form a calcified matrix, leading to failure in long-term defect repair. Here, we investigate the isolation and characterisation of a human cartilage progenitor population that is resident within permanent adult articular cartilage.Methods and FindingsHuman articular cartilage samples were digested and clonal populations isolated using a differential adhesion assay to fibronectin. Clonal cell lines were expanded in growth media to high population doublings and karyotype analysis performed. We present data to show that this cell population demonstrates a restricted differential potential during chondrogenic induction in a 3D pellet culture system. Furthermore, evidence of high telomerase activity and maintenance of telomere length, characteristic of a mesenchymal stem cell population, were observed in this clonal cell population. Lastly, as proof of principle, we carried out a pilot repair study in a goat in vivo model demonstrating the ability of goat cartilage progenitors to form a cartilage-like repair tissue in a chondral defect.ConclusionsIn conclusion, we propose that we have identified and characterised a novel cartilage progenitor population resident in human articular cartilage which will greatly benefit future cell-based cartilage repair therapies due to its ability to maintain chondrogenicity upon extensive expansion unlike full-depth chondrocytes that lose this ability at only seven population doublings.

Iliotibial band (ITB) syndrome is a common overuse injury in runners and cyclists. It is regarded as a friction syndrome where the ITB rubs against (and 'rolls over') the lateral femoral epicondyle. Here, we re-evaluate the clinical anatomy of the region to challenge the view that the ITB moves antero-posteriorly over the epicondyle. Gross anatomical and microscopical studies were conducted on the distal portion of the ITB in 15 cadavers. This was complemented by magnetic resonance (MR) imaging of six asymptomatic volunteers and studies of two athletes with acute ITB syndrome. In all cadavers, the ITB was anchored to the distal femur by fibrous strands, associated with a layer of richly innervated and vascularized fat. In no cadaver, volunteer or patient was a bursa seen. The MR scans showed that the ITB was compressed against the epicondyle at 30° of knee flexion as a consequence of tibial internal rotation, but moved laterally in extension. MR signal changes in the patients with ITB syndrome were present in the region occupied by fat, deep to the ITB. The ITB is prevented from rolling over the epicondyle by its femoral anchorage and because it is a part of the fascia lata. We suggest that it creates the illusion of movement, because of changing tension in its anterior and posterior fibres during knee flexion. Thus, on anatomical grounds, ITB overuse injuries may be more likely to be associated with fat compression beneath the tract, rather than with repetitive friction as the knee flexes and extends.

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In recent years it has become increasingly clear that articular cartilage harbours a viable pool of progenitor cells and interest has focussed on their role during development and disease. Analysis of progenitor numbers using fluorescence-activated sorting techniques has resulted in wide-ranging estimates, which may be the result of context-dependent expression of cell surface markers. We have used a colony-forming assay to reliably determine chondroprogenitor numbers in normal and osteoarthritic cartilage where we observed a 2-fold increase in diseased tissue (P  < 0.0001). Intriguingly, cell kinetic analysis of clonal isolates derived from single and multiple donors of osteoarthritic cartilage revealed the presence of a divergent progenitor subpopulation characterised by an early senescent phenotype. Divergent sub-populations displayed increased senescence-associated β–galactosidase activity, lower average telomere lengths but retained the capacity to undergo multi-lineage differentiation. Osteoarthritis is an age-related disease and cellular senescence is predicted to be a significant component of the pathological process. This study shows that although early senescence is an inherent property of a subset of activated progenitors, there is also a pool of progenitors with extended viability and regenerative potential residing within osteoarthritic cartilage.

To define the anatomical relationships of the nerves to the common arthroscopy portals at the elbow an arthroscope was introduced into 20 cadaver elbows and the positions of the nerves were then determined by dissection. In all cases the posterior interosseous nerve lay close to the radiohumeral joint and to the anterolateral portal. Pronation of the forearm displaced the nerve away from the arthroscope. The median nerve passed consistently within 14 mm of the arthroscope when it was introduced through the anteromedial portal. The branches supplying the superficial forearm flexor muscles were at risk.