Platelet-rich plasma (PRP) has been utilized in surgery for 2 decades; there has been a recent interest in the use of PRP for the treatment of sports-related injuries. PRP contains growth factors and bioactive proteins that influence the healing of tendon, ligament, muscle, and bone. This article examines the basic science of PRP, and it describes the current clinical applications in sports medicine. This study reviews and evaluates the human studies that have been published in the orthopaedic surgery and sports medicine literature. The use of PRP in amateur and professional sports is reviewed, and the regulation of PRP by antidoping agencies is discussed.

Platelet-Rich Plasma From Basic Science to Clinical Applications

Muscle injuries are one of the most common traumas occurring in sports. Despite their clinical importance, few clinical studies exist on the treatment of these traumas. Thus, the current treatment principles of muscle injuries have either been derived from experimental studies or been tested only empirically. Although nonoperative treatment results in good functional outcomes in the majority of athletes with muscle injuries, the consequences of failed treatment can be very dramatic, possibly postponing an athlete's return to sports for weeks or even months. Moreover, the recognition of some basic principles of skeletal muscle regeneration and healing processes can considerably help in both avoiding the imminent dangers and accelerating the return to competition. Accordingly, in this review, the authors have summarized the prevailing understanding on the biology of muscle regeneration. Furthermore, they have reviewed the existing data on the different treatment modalities (such as medication, therapeutic ultrasound, physical therapy) thought to influence the healing of injured skeletal muscle. In the end, they extend these findings to clinical practice in an attempt to propose an evidence-based approach for the diagnosis and optimal treatment of skeletal muscle injuries.

Muscle Injuries: Biology and Treatment

/pdf/from-basic-science-to-clinical-applications-3358bp6t1n.pdf

From Basic Science to Clinical Applications

After injury, muscle healing occurs through different phases, including (1) degeneration and inflammation, (2) muscle regeneration, and (3) development of fibrosis.

The severity and type of muscle injury influence the healing process.

Enhancement of muscle regeneration and prevention of muscle fibrosis can improve muscle healing.

Growth factors, including basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), and nerve growth factor (NGF), can improve muscle regeneration, but the post-injury healing process remains incomplete.

The use of anti-fibrosis agents that antagonize the effect of transforming growth factor-β1 (TGF-β1) can prevent fibrosis and improve muscle healing, resulting in nearly complete recovery.

Optimal muscle recovery may require the use of novel technologies, such as gene therapy and tissue engineering, to achieve both high levels and long-term persistence of these growth factors and cytokines within the injured muscle.

Muscle injury presents a challenging problem in traumatology, as injured muscles heal very slowly and often with incomplete functional recovery. It has been observed that injured muscles can initiate regeneration promptly, but the healing process is often inefficient and hindered by the formation of scar tissue, which may contribute to the tendency for muscle injury to recur. The enhancement of muscle regeneration and the prevention of muscle fibrosis through the use of biological approaches are being investigated in an effort to improve muscle healing after injury. In this Current Concepts Review, we will outline the structure and histological organization of skeletal muscle and describe the basic physiology of skeletal muscle contraction. We will subsequently summarize the biological and pathological processes that occur in skeletal muscle after injury (i.e., degeneration, inflammation, regeneration, and fibrosis) and present the clinical treatments currently available for injured skeletal muscle. Finally, we will discuss current trends in research, which include the improvement of regeneration and the inhibition of fibrosis in injured skeletal …

Muscle injuries and repair: current trends in research.

Transforming growth factor-β1 (TGF-β1) is thought to play a crucial role in fibrotic diseases. This study demonstrates for the first time that TGF-β1 stimulation can induce myoblasts (C2C12 cells) to express TGF-β1 in an autocrine manner, down-regulate the expression of myogenic proteins, and initiate the production of fibrosis-related proteins in vitro. Direct injection of human recombinant TGF-β1 into skeletal muscle in vivo stimulated myogenic cells, including myofibers, to express TGF-β1 and induced scar tissue formation within the injected area. We also observed the local expression of this growth factor by myogenic cells, including regenerating myofibers, in injured skeletal muscle. Finally, we demonstrated that TGF-β1 gene-transfected myoblasts (CT cells) can differentiate into myofibroblastic cells after intramuscular transplantation, but that decorin, an anti-fibrosis agent, prevents this differentiation process by blocking TGF-β1. In summary, these findings indicate that TGF-β1 is a major stimulator that plays a significant role in both the initiation of fibrotic cascades in skeletal muscle and the induction of myogenic cells to differentiate into myofibroblastic cells in injured muscle.

Transforming Growth Factor-β1 Induces the Differentiation of Myogenic Cells into Fibrotic Cells in Injured Skeletal Muscle: A Key Event in Muscle Fibrogenesis

The detection and transmission of the temporal quality of intracellular and extracellular signals is an essential cellular mechanism. It remains largely unexplored how cells interpret the duration information of a stimulus. In this paper, through an integrated quantitative and computational approach we demonstrate that crosstalk among multiple TGF-β activated pathways forms a relay from SMAD to GLI1 that initializes and maintains SNAILl expression, respectively. This transaction is smoothed and accelerated by another temporal switch from elevated cytosolic GSK3 enzymatic activity to reduced nuclear GSK3 enzymatic activity. The intertwined network places SNAIL1 as a key integrator of information from TGF-β signaling subsequently distributed through upstream divergent pathways; essentially cells generate a transient or sustained expression of SNAIL1 depending on TGF-β duration. Other signaling pathways may use similar network structure to encode duration information.

/pdf/pathway-crosstalk-enables-cells-to-interpret-tgf-b-duration-17vlnmr827.pdf

Pathway crosstalk enables cells to interpret TGF-β duration

The detection and transmission of the strength and temporal quality of intracellular and extracellullar signals is an essential cellular mechanism. While TGF-β signaling is one of the most thoroughly studied signaling pathways, the mechanisms by which cells translate TGF-β signals remain unclear. In this paper, through an integrated quantitative and computational approach we demonstrate that crosstalk among multiple TGF-β activated pathways forms a relay from SMAD to GLI1 that initializes and maintains SNAILl expression, respectively. This transaction is smoothed and accelerated by another temporal switch from elevated cytosolic GSK3 enzymatic activity to reduced nuclear GSK3 enzymatic activity. This nested relay mechanism places SNAIL1 as a key integrator of information from TGF-β signaling subsequently distributed through divergent pathways; essentially cells generate a transient or sustained expression of SNAIL1 depending on TGF-β duration. Our results provide a mechanistic understanding of a long-standing paradox that TGF-β can both suppress and promote cancer development.

/pdf/cells-interpret-temporal-information-from-tgf-b-through-a-2x6d3v4cvu.pdf

Cells Interpret Temporal Information From TGF-β Through A Nested Relay Mechanism

The detection and transmission of the temporal quality of intracellular and extracellular signals is an essential cellular mechanism. It remains largely unexplored how cells interpret the duration information of a stimulus. In this paper, we performed an integrated quantitative and computational analysis on TGF-β induced activation of SNAIL1, a key transcription factor that regulates several subsequent cell fate decisions such as apoptosis and epithelial-to-mesenchymal transition. We demonstrate that crosstalk among multiple TGF-β activated pathways forms a relay from SMAD to GLI1 that initializes and maintains SNAILl expression, respectively. SNAIL1 functions as a key integrator of information from TGF-β signaling distributed through upstream divergent pathways. The intertwined network serves as a temporal checkpoint, so that cells can generate a transient or sustained expression of SNAIL1 depending on TGF-β duration. Furthermore, we observed that TGF-β treatment leads to an unexpected accumulation of GSK3 molecules in an enzymatically active tyrosine phosphorylation form in Golgi apparatus and ER, followed by accumulation of GSK3 molecules in an enzymatically inhibitive serine phosphorylation in the nucleus. Subsequent model analysis and inhibition experiments revealed that the initial localized increase of GSK3 enzymatic activity couples to the positive feedback loop of the substrate Gli1 to form a network motif with multi-objective functions. That is, the motif is robust against stochastic fluctuations, and has a narrow distribution of response time that is insensitive to initial conditions. Specifically for TGF-β signaling, the motif ensures a smooth relay from SMAD to GLI1 on regulating SNAIL1 expression.

/pdf/pathway-crosstalk-enables-cells-to-interpret-tgf-b-duration-f7cpnf6fgj.pdf

Pathway crosstalk enables cells to interpret TGF-β duration.

Muscle injuries represent a large number of professional and recreational sports injuries. Muscle strains habitually occur after an eccentric contraction, which often leads to an injury located in the myotendinous junction. Treatment varies widely, depending on the severity of the trauma, but has remained limited mostly to rest, ice, compression, elevation, antiinflammatory drugs, and mobilization. The authors' research group aims to develop new biologic approaches to improve muscle healing after injuries, including muscle strains. To achieve this goal, the authors investigated several parameters that will lead to the development of new strategies to enhance muscle healing. The authors first evaluated natural muscle healing after strain injuries and showed that muscle regeneration occurs in the early phase of healing but becomes impaired with time by the development of tissue fibrosis. Several growth factors capable of improving muscle regeneration were investigated; basic fibroblast growth factor, insulin-like growth factor, and nerve growth factors were identified as substances capable of enhancing muscle regeneration and improving muscle force in the strained injured muscle. The current study should aid in the development of strategies to promote efficient muscle healing and complete recovery after strain injury.

Use of growth factors to improve muscle healing after strain injury.

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Pathway crosstalk enables cells to interpret TGF-β duration

Cells Interpret Temporal Information From TGF-β Through A Nested Relay Mechanism

Pathway crosstalk enables cells to interpret TGF-β duration.

Use of growth factors to improve muscle healing after strain injury.