The operative management of tendons combined with the application of autologous PRGF may present new possibilities for enhanced healing and functional recovery. This needs to be evaluated in a randomized clinical trial.
Blood platelets become activated and aggregate at the site of vessel injury. Upon activation by thrombin, platelets release storage pools of proteins and growth factors (GFs), including those involved in tissue repair. Our goal was to evaluate the potential beneficial effect of proteins released from platelet-rich clots on tendon healing. PDGF, TGF-P-I, IGF-I, HGF, VEGF and EGF were measured in human platelet-poor plasma (PPP) and in the releasates collected from either platelet-poor or platelet-rich clots prepared in vitro. We then studied the effects of the releasates on human tendon cells in culture. Releasates from both platelet-rich and platelet-poor clots stimulated tendon cell proliferation, in contrast to un-clotted PPP. The mitogenic activity of the supernatants was not decreased by the thrombin inhibitor, hirudin. Cultured tendon cells synthesise VEGF and HGF in the presence of PPP-clots and PRP-clot releasates, thus the synthesised amount was significantly higher with supernatants from platelet-rich clots than supernatants from a platelet-poor clot @ < 0.05). These results suggest that administering autologous platelet-rich clots may be beneficial to the treatment of tendon injuries by inducing cell proliferation and promoting the synthesis of angiogenic factors during the healing process.
Intra-articular administration of PRGF might be beneficial in restoring HA concentration and switching angiogenesis to a more balanced status but does not halt the effects of IL-1beta on synovial cells.
The use of autologous fibrin matrices has been proposed as a therapeutic strategy for the local and physiological delivery of growth factors in the treatment of several clinical conditions requiring tendon healing or tendon graft remodelling. In the present work, we investigated the proliferation, synthesis of type-I collagen and angiogenic factors by tendon cells seeded on platelet-rich (PR) and platelet-poor (PP) matrices. Furthermore, in vivo cellular and vascular effects of each treatment were examined after infiltration in Achilles tendon in sheep. Results showed that the presence of platelets within the fibrin matrices increased significantly the proliferation of tendon cells. Additionally, cultured tendon cells synthesised type I collagen and angiogenic factors such as VEGF and HGF. The synthesis of VEGF, but not of HGF, was significantly higher when platelets were present within the matrix. In the sheep model, the injection of pre-clotted plasma within tendons increased cellular density and promoted neovascularization. These results indicate that administration of fibrin matrices is a safe and easy strategy that may open new avenues for enhancing tissue healing and remodelling and influences the process of regeneration in clinical situations characterised by a poor healing outcome.
Despite the extremely poor prognosis of the case, complete articular cartilage healing was considerably accelerated, and the functional outcome was excellent, allowing a rapid resumption of symptom-free athletic activity. This technique opens new perspectives for human tissue regeneration.
The balance between TGF-beta1 and the pools of platelet-secreted molecules may have important therapeutic implications in the control of angiogenesis and fibrosis.
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