Abstract
Tendinopathy is the term used to refer to tendon disorders. Spontaneous adult tendon healing results in scar tissue formation and fibrosis with suboptimal biomechanical properties, often resulting in poor and painful mobility. The biomechanical properties of the tissue are negatively affected. Adult tendons have a limited natural healing capacity, and often respond poorly to current treatments that frequently are focused on exercise, drug delivery, and surgical procedures. Therefore, it is of great importance to identify key molecular and cellular processes involved in the progression of tendinopathies to develop effective therapeutic strategies and drive the tissue toward regeneration. To treat tendon diseases and support tendon regeneration, cell-based therapy as well as tissue engineering approaches are considered options, though none can yet be considered conclusive in their reproduction of a safe and successful long-term solution for full microarchitecture and biomechanical tissue recovery. In vitro differentiation techniques are not yet fully validated. This review aims to compare different available tendon in vitro differentiation strategies to clarify the state of art regarding the differentiation process.
Highlights
Tendons connect muscles to bones and allow movements
An interesting study of Mehr et al [160] showed that Tcn mRNA and protein expression was upregulated, in vitro, in the portion of tendon subjected to compression with respect to the portion not directly affected by mechanical stimulation
The results showed that amniotic epithelial stem cells (AECs) tenogenic differentiation accelerated to take half the time compared to poly (lactic-co-glycolic) acids (PLGA) fleeces cultured only with AECs
Summary
Tendons connect muscles to bones and allow movements. Lesions and inflammation can occur in tendons because of mechanical stress, aging, genetic predisposition, or lesions and inflammation [1]. The epitenon is a thin connective tissue sheath that surrounds the entire tendon below the paratenon that contains the vascular, lymphatic, and nervous structures. TSCPs can be sorted on CD44 positivity [26] and express MSC markers Stro 1 and CD146 and tenogenic markers α-smooth muscle actin (α-Sma) and tenomodulin (Tnmd) [21,27,28] The characteristics of this cell population are affected with age; in particular, their number and self-renewal potential decrease with time [26]. This could explain the low ability of adult tendons to spontaneous healing
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