PRP for Carpal Tunnel: Could It Help Relieve Symptoms?
Explore how PRP therapy may support tissue healing and symptom relief in carpal tunnel syndrome by leveraging the growth factors in platelets.
Explore how PRP therapy may support tissue healing and symptom relief in carpal tunnel syndrome by leveraging the growth factors in platelets.
Carpal tunnel syndrome (CTS) causes pain, numbness, and weakness in the hand due to pressure on the median nerve. Traditional treatments range from wrist splints to surgery, but some patients seek alternatives like platelet-rich plasma (PRP) injections, which use components of their own blood to promote healing.
Researchers are exploring whether PRP could reduce inflammation and aid tissue repair in CTS. Understanding how PRP interacts with wrist structures and the biological factors contributing to its effects can help evaluate its potential as a treatment option.
The wrist is a complex region where multiple structures interact to facilitate movement while maintaining stability. In CTS, the primary concern is the median nerve, which runs through the carpal tunnel—a narrow passageway formed by the carpal bones and the transverse carpal ligament. This nerve provides sensation to the thumb, index, middle, and part of the ring finger while also controlling motor function in several hand muscles. When the tunnel becomes constricted due to inflammation or tissue changes, nerve signaling is disrupted, leading to pain, tingling, and weakness.
Surrounding the median nerve are nine flexor tendons, which allow finger movement and pass through the same confined space. These tendons are encased in synovial sheaths that facilitate smooth gliding. In CTS, thickening of these sheaths or increased synovial fluid can further reduce space, worsening nerve compression. Studies using ultrasonography and MRI have shown that individuals with CTS often exhibit an increased cross-sectional area of the median nerve and altered tendon dynamics, reinforcing the role of structural changes in symptom development (Klauser et al., 2009, Radiology).
The transverse carpal ligament, a dense fibrous band spanning the top of the carpal tunnel, plays a key role in wrist stability. While its rigidity provides biomechanical support, excessive pressure within the tunnel can contribute to nerve entrapment. Surgical release aims to modify this structure to relieve pressure, and emerging research suggests that biological interventions like PRP may influence its extracellular matrix composition, potentially altering mechanical properties (Bodor & Flossman, 2020, Muscle & Nerve).
PRP’s therapeutic potential comes from the bioactive molecules within platelets, which aid tissue repair and regeneration. These anucleate cell fragments store growth factors, cytokines, and adhesive proteins in their alpha granules. When activated, platelets release these factors, triggering cellular responses that influence inflammation, angiogenesis, and extracellular matrix remodeling.
Key components of PRP include platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-β), and vascular endothelial growth factor (VEGF). PDGF recruits fibroblasts and mesenchymal cells while stimulating their proliferation. TGF-β regulates collagen deposition, potentially modifying the biomechanical properties of the transverse carpal ligament. VEGF promotes angiogenesis, which may enhance blood supply in ischemic or fibrotic tissues surrounding the median nerve.
PRP also contains adhesive glycoproteins such as fibrin, fibronectin, and vitronectin, which support cell-matrix interactions and provide structural support for regenerating tissues. These proteins help anchor cells at the repair site, creating a scaffold that enhances adhesion and migration. Their presence may be particularly relevant in CTS, where degenerative changes in tendon sheaths and synovial membranes contribute to chronic inflammation and reduced space within the carpal tunnel.
Generating PRP involves controlled steps to isolate and concentrate platelets while preserving their biological activity. The process begins with venous blood collection, typically 15 to 60 milliliters, depending on the intended use. Anticoagulants such as citrate dextrose solution (ACD-A) are added immediately to prevent clotting and keep platelets in a quiescent state until activation at the treatment site. The choice of anticoagulant influences platelet morphology and growth factor release kinetics.
Centrifugation separates blood components based on density. A common two-spin protocol involves an initial low-speed centrifugation (1,500 rpm for 10 minutes) to separate red blood cells from plasma. The plasma layer, still containing platelets and white blood cells, then undergoes a higher-speed centrifugation (3,000 rpm for 10 minutes) to concentrate the platelets while removing platelet-poor plasma. The final product varies in platelet density, typically reaching three to five times baseline levels, depending on centrifugation parameters and the PRP system used.
Another variable in PRP preparation is whether leukocytes are retained or removed. Leukocyte-rich PRP contains white blood cells, which influence inflammation and tissue remodeling, while leukocyte-poor PRP minimizes inflammatory responses. The choice depends on the target tissue and pathology. Some studies suggest leukocyte-rich PRP enhances antimicrobial properties and immune signaling, while others indicate leukocyte-poor PRP may better reduce pro-inflammatory cytokine activity. Standardizing formulations remains a challenge, as different commercial systems yield varying platelet compositions and bioactive profiles.
When PRP is injected into the wrist, its effects depend on how bioactive components interact with local tissues. Upon injection, platelets degranulate, releasing growth factors that diffuse into the extracellular matrix. This process activates fibroblasts, endothelial cells, and tenocytes, modulating collagen synthesis, vascularization, and structural remodeling. In CTS, where fibrosis and altered tendon dynamics contribute to nerve compression, these molecular signals may help restore tissue balance.
The transverse carpal ligament and surrounding tendon sheaths influence the confined space of the carpal tunnel. PRP’s effect on extracellular matrix turnover could impact collagen fiber density and organization, potentially reducing ligament stiffness. Studies suggest PRP promotes a shift toward type III collagen production—associated with early tissue remodeling—which may increase elasticity in previously fibrotic structures. This could reduce compressive forces on the median nerve, improving nerve conduction and alleviating symptoms.