Tendon is a bradytrophic and hypovascular tissue, hence, healing remains a major challenge. The molecular key events involved in successful repair have to be unravelled to develop novel strategies that reduce the risk of unfavourable outcomes such as non-healing, adhesion formation, and scarring. This review will consider the diverse pathophysiological features of tendon-derived cells that lead to failed healing, including misrouted differentiation (e.g. de- or transdifferentiation) and premature cell senescence, as well as the loss of functional progenitors. Many of these features can be attributed to disturbed cell-extracellular matrix (ECM) or unbalanced soluble mediators involving not only resident tendon cells, but also the cross-talk with immigrating immune cell populations. Unrestrained post-traumatic inflammation could hinder successful healing. Pro-angiogenic mediators trigger hypervascularization and lead to persistence of an immature repair tissue, which does not provide sufficient mechano-competence. Tendon repair tissue needs to achieve an ECM composition, structure, strength, and stiffness that resembles the undamaged highly hierarchically ordered tendon ECM. Adequate mechano-sensation and -transduction by tendon cells orchestrate ECM synthesis, stabilization by cross-linking, and remodelling as a prerequisite for the adaptation to the increased mechanical challenges during healing. Lastly, this review will discuss, from the cell biological point of view, possible optimization strategies for augmenting Achilles tendon (AT) healing outcomes, including adapted mechanostimulation and novel approaches by restraining neoangiogenesis, modifying stem cell niche parameters, tissue engineering, the modulation of the inflammatory cells, and the application of stimulatory factors. Cite this article:
The aim of the current study was to assess whether calcaneal broadband ultrasound attenuation (BUA) can predict whole body and regional dual-energy x-ray absorptiometry (DXA)-derived bone mass in healthy, Australian children and adolescents at different stages of maturity. A total of 389 boys and girls across a wide age range (four to 18 years) volunteered to participate. The estimated age of peak height velocity (APHV) was used to classify children into pre-, peri-, and post-APHV groups. BUA was measured at the non-dominant heel with quantitative ultrasonometry (QUS) (Lunar Achilles Insight, GE), while bone mineral density (BMD) and bone mineral content (BMC) were examined at the femoral neck, lumbar spine and whole body (DXA, XR-800, Norland). Associations between BUA and DXA-derived measures were examined with Pearson correlations and linear regression. Participants were additionally ranked in quartiles for QUS and DXA measures in order to determine agreement in rankings.Objectives
Methods
Femoroacetabular impingement (FAI) causes pain
and chondrolabral damage via mechanical overload during movement
of the hip. It is caused by many different types of pathoanatomy,
including the cam ‘bump’, decreased head–neck offset, acetabular
retroversion, global acetabular overcoverage, prominent anterior–inferior
iliac spine, slipped capital femoral epiphysis, and the sequelae
of childhood Perthes’ disease. Both evolutionary and developmental factors may cause FAI. Prevalence
studies show that anatomic variations that cause FAI are common
in the asymptomatic population. Young athletes may be predisposed
to FAI because of the stress on the physis during development. Other
factors, including the soft tissues, may also influence symptoms and
chondrolabral damage. FAI and the resultant chondrolabral pathology are often treated
arthroscopically. Although the results are favourable, morphologies
can be complex, patient expectations are high and the surgery is
challenging. The long-term outcomes of hip arthroscopy are still
forthcoming and it is unknown if treatment of FAI will prevent arthrosis.
Cadaveric models of the shoulder evaluate discrete motion segments
using the glenohumeral joint in isolation over a defined trajectory.
The aim of this study was to design, manufacture and validate a
robotic system to accurately create three-dimensional movement of
the upper body and capture it using high-speed motion cameras. In particular, we intended to use the robotic system to simulate
the normal throwing motion in an intact cadaver. The robotic system
consists of a lower frame (to move the torso) and an upper frame
(to move an arm) using seven actuators. The actuators accurately
reproduced planned trajectories. The marker setup used for motion
capture was able to determine the six degrees of freedom of all
involved joints during the planned motion of the end effector.Objectives
Methods
