Platelet Rich Plasma for Hamstring Tears
Proximal hamstring injuries are common in athletes and frequently result in prolonged rehabilitation, time missed from play, and a significant risk of reinjury.1,2 Reports of acute hamstring strains without avulsion in dancers have suggested recovery times for return-to-play ranging from 30 to 76 weeks.1 The healing process associated with hamstring injuries and with injured skeletal muscle is inefficient as compared to that associated with injuries of other tissue such as bone. This inefficiency is driven by structural adaptations that maximize load-carrying capacity under prolonged ischemic conditions.3 Vascular supply from associated muscle and surrounding tissues typically does not extend beyond the proximal third of the tendon.3,4 Because oxygen consumption is low and energy generation is anaerobic, the resulting metabolic rate is slow and healing capacity is limited.3
Tendons are damaged when subjected to loads that exceed their tensile or physiologic threshold. This can occur in response to massive trauma or to repetitive overload if insufficient time is allowed for tissue recovery. The risk for tendon rupture is highest when tension is applied rapidly and obliquely.3 The highest forces have been recorded during eccentric contraction.3,5 Tendons respond to this nonphysiologic overload with tendon sheath inflammation, intratendinous degeneration, or a combination of both.1,6
Muscle and tendon recover from injury through tissue remodeling that can lead to inefficient regeneration and infiltration by scar tissue.7,8 The first phase involves an increase in vascular permeability, initiation of angiogenesis, chemotactic migration of inflammatory cells (notably neutrophils initially then followed by macrophages) to the region of injury, and induction of local tenocytes to synthesize collagen and extracellular matrix (ECM).7,8 After several days, type III collagen synthesis peaks as tenocyte proliferation continues. At roughly six weeks, the healing tissue begins to remodel. Regional cellularity decreases as up-regulation of synthesis of collagen and other proteins takes place. Tissue gradually transitions from cellular to fibrous in nature as tenocytes align in the direction of stress forces. Production of collagen type I increases as production of type III drops off. At approximately 10 weeks, fibrous tissue begins to remodel and mature. These processes continue through the course of a full year, resulting in tendon tissue with scar-like properties. As tissue matures, tenocyte metabolism decreases—either through intrinsic mechanisms contained within an intact peritenon or through extrinsic mechanisms involving invasion by cells from the surrounding tissue. Extrinsic pathways related to peritenon disruption and more severe injuries lead to greater scarring and adhesion and resultant disruption of the normal gliding of the tendon within the sheath.9,10
Traditional hypotheses have attributed pain in tendinopathy to an inflammatory process. Studies of chronically painful achilles and patellar tendons have shown no evidence of inflammation. Histologically, healing appears to be disordered and haphazard, with an absence of inflammatory cells but presence of hypercellularity, scattered vascular in-growth, and collagen degeneration. The etiology of pain within tendons has not been conclusively elucidated, but evidence suggests that mechanical collagen breakdown, abnormal lactate levels, neurotransmitter imbalance, the presence of pro-inflammatory prostaglandins, and neural centralization may be involved.3
Tendon recovery is frequently incomplete in severe or full-thickness tears, due to the proliferation and up-regulation of fibroblasts, which induce formation of excessive scar tissue that leads to suboptimal tissue integrity and functionality.8 Research suggests that throughout tendon repair, trophic substances, such as growth factors released from damaged tissue, may regulate the healing response. It has been hypothesized that autologous growth factors found in platelets may augment the healing of musculoskeletal soft-tissue abnormalities.8,11-13
An understanding of the role of platelets in tissue healing has led to the use of autologous platelet concentrates for therapeutic purposes. Degranulation and subsequent release of growth factors from platelets can be induced and the isolated growth factors can be delivered directly into injured tissue to stimulate a physiologic response. Platelet-rich plasma (PRP) is easy to produce through centrifugation of peripheral blood and separation of the resulting component. As an autologous substrate, PRP has limited potential to harm.11,14 The therapeutic response of the percutaneous implantation of PRP into tendon, muscle, ligament, cartilage, intervertebral disc, and fascia has generally been positive.15
Numerous growth-factor peptides have been identified in both the dense granules and the alpha granules of platelets, which bind to membrane-bound receptors, thereby activating intracellular second-messenger pathways.11,16,17 Bioactive functions associated with platelet-derived growth factors (PDGFs) include angiogenesis, chemotaxis, cell recruitment, cellular proliferation, cellular differentiation, and ECM synthesis.12 Some researchers have suggested that, due to the complexity of healing pathways and tissue regeneration, the synergistic interaction of multiple growth factors at physiologic concentrations may be superior to the action of a single exogenous growth factor.12,18
A 48-year-old female sustained a severe left proximal hamstring tear while water skiing. Her left leg became hyperextended when she attempted to drop her right ski and the ski caught the water, aggressively forcing her left hip into eccentric hyperflexion. Subsequently, she felt a tearing sensation localized to the left ischial tuberosity region at the origin of the left common hamstring tendon. She immediately experienced pain and transient numbness in the left lower extremity. Initially, she did not seek care, instead relying on rest and oral nonsteroidal anti-inflammatory drugs (NSAIDs) for two and one-half weeks. During this time, although symptom intensity decreased, pain and dysfunction persisted with ambulation, prolonged sitting, and exertional activity. Nocturnal pain interrupted the patient’s sleep patterns. In addition, the patient experienced subjective weakness and instability of the affected leg as well as localized swelling at the site of injury.
Sixteen days after the injury, the patient consulted an orthopaedic surgeon because of the persistence of pain and functional limitation. The consulting physician identified pain on palpation, which was localized to the left buttock and aggravated by resisted knee flexion. Left hamstring strength was rated 4/5 and left lower extremity sensory and vascular exams were normal.