Comparison of the acute inflammatory response of two commercial platelet-rich plasma systems in healthy rabbit tendons.

BACKGROUND: Numerous studies have shown platelet-rich plasma (PRP) preparations differ with respect to the inclusion of certain blood components, which may affect the host's cellular response. HYPOTHESIS: This study evaluated the inflammatory effect of Biomet GPS III leukocyte-rich PRP (LR-PRP) versus MTF Cascade leukocyte-poor PRP (LP-PRP) after intratendinous injection in an animal model. The authors anticipated that LR-PRP would incite a greater acute inflammatory response than LP-PRP. STUDY DESIGN: Controlled laboratory study. METHODS: A total of 17 skeletally mature New Zealand White rabbits were tested. In all cases, healthy patellar tendons were treated. In the control animals, one patellar tendon was injected with 2 mL autologous whole blood, and the other was injected with 2 mL sterile saline. Seven total tendons were injected with whole blood, and 7 tendons were injected with saline. In the experimental animals, one patellar tendon was injected with 2 mL LR-PRP, and the other was injected with 2 mL LP-PRP. Ten tendons were injected with LR-PRP, and 10 tendons were injected with LP-PRP. Animals were euthanized at 5 or 14 days after injection. Tendons were harvested and stained using hematoxylin and eosin and scored semi-quantitatively for total white blood cells (WBCs), mononuclear cells (macrophages and lymphocytes), polymorphonuclear cells (PMNs), vascularity, fiber structure, and fibrosis. RESULTS: At 5 days after injection, tendons treated with LR-PRP had significantly greater overall tendon scores (6.3 ± 1.79 vs 1.8 ± 1.64, P = .012), as well as mean scores for fiber structure (1.4 ± 0.22 vs 0.50 ± 0.50, P = .012), denoting disrupted composition, total WBCs (1.1 ± 0.89 vs 0.10 ± 0.22, P = .014), mononuclear cells (macrophages and lymphocytes) (0.80 ± 0.45 vs 0.10 ± 0.22, P = .014), vascularity (1.7 ± 0.27 vs 0.80 ± 0.16, P = .008), and fibrosis (1.0 ± 0.35 vs 0.3 ± 0.45, P = .037) compared with tendons treated with LP-PRP. Otherwise, there were no significant differences in mononuclear cells (P = .590), PMN cells (P = 1.00), total WBCs (P = .811), vascularity (P = .650), or total tendon score (P = .596) in any of the treatment groups at 14 days. CONCLUSION: Compared with leukocyte-poor Cascade PRP, leukocyte-rich GPS III PRP causes a significantly greater acute inflammatory response at 5 days after injection. There is no significant difference in the inflammatory response or cellularity regardless of the injection type at 14 days after intratendinous injection. CLINICAL RELEVANCE: Platelet-rich plasma injections are frequently prepared using commercial systems and are administered for clinical treatment of chronic tendinopathy. It is important to characterize the cellular responses elucidated by different injection preparations to further understand their effect on tissue healing and aid clinical decision making. Future investigations are necessary to apply these findings to the clinical setting.

Incidence and risk factors for injuries to the anterior cruciate ligament in National Collegiate Athletic Association football: data from the 2004-2005 through 2008-2009 National Collegiate Athletic Association Injury Surveillance System.

BACKGROUND: Injuries to the anterior cruciate ligament (ACL) are common in athletic populations, particularly in athletes participating in football, soccer, and skiing. PURPOSE: The purpose of this study was to analyze the National Collegiate Athletic Association (NCAA) Injury Surveillance System (ISS) men's football ACL injury database from the playing seasons of 2004-2005 through 2008-2009 to determine the incidence and epidemiology of complete injury to the ACL in NCAA football athletes. STUDY DESIGN: Descriptive epidemiology study. METHODS: The NCAA ISS men's football database was reviewed from the 2004-2005 through 2008-2009 seasons using the specific injury code, "Anterior cruciate ligament (ACL) complete tear." The injury rate was computed for competition and practice exposures. Ninety-five percent confidence intervals (CIs) for the incident rates were calculated using assumptions of a Poisson distribution. Pairwise, 2-sample tests of equality of proportions with a continuity correction were used to estimate the associations of risk factors such as event type, playing surface, season segment, and football subdivision. Descriptive data were also described. RESULTS: The ACL injury rate during games (8.06 per 10,000 athlete-exposures [AEs] 95% CI, 6.80-9.42) was significantly greater than the rate during practice (0.8 per 10,000 AEs 95% CI, 0.68-0.93). Players were 10.09 (95% CI, 8.08-12.59) times more likely to sustain an ACL injury in competition when compared with practices. When practice exposures were analyzed separately, the injury rate was significantly greater during scrimmages (3.99 per 10,000 AEs 95% CI, 2.29-5.94) compared with regular practices (0.83 per 10,000 AEs 95% CI, 0.69-0.97) and walk-throughs (0 per 10,000 AEs 95% CI, 0-0.14). There was an incidence rate of 1.73 ACL injuries per 10,000 AEs (95% CI, 1.47-2.0) on artificial playing surfaces compared with a rate of 1.24 per 10,000 AEs (95% CI, 1.05-1.45) on natural grass. The rate of ACL injury on artificial surfaces is 1.39 (95% CI, 1.11-1.73) times higher than the injury rate on grass surfaces. CONCLUSION: Between 2004 and 2009, NCAA football players experienced a greater number of ACL injuries in games compared with practices, in scrimmages compared with regular practices, and when playing on artificial turf surfaces. This latter finding will need to be confirmed by additional studies.

Estradiol protects against hippocampal damage and impairments in fear conditioning resulting from transient global ischemia in mice.

Estradiol protects against hippocampal damage and some learning impairments resulting from transient global ischemia in rats. Here, we seek to validate a mouse model of transient global ischemia and evaluate the effects of estradiol on ischemia-induced hippocampal damage and behavioral impairments. Female C57Bl6/J mice were ovariectomized and implanted with estradiol- or oil-secreting capsules. One week later, mice experienced 15-min of 2-vessel occlusion (2-VO) or sham surgical procedures. Five days later, mice were exposed to a fear conditioning protocol in which a specific context and novel tone were paired with mild footshock. Twenty-four hours following conditioning, contextual fear was assessed by measuring freezing behavior in the conditioned context (in the absence of the tone). This was followed by assessment of cue fear by measuring freezing behavior to the conditioned tone presented in a new context. When tested in the conditioned context, oil-treated mice that experienced 2-VO exhibited a significant reduction in freezing behavior whereas estradiol-treated mice that experienced 2-VO showed no disruption in freezing behavior. Freezing behavior when presented with the conditioned tone was unaffected by either surgery or hormone treatment. These findings suggest that global ischemia causes impairments in performance on the hippocampally-dependent contextual fear task but not conditioned cue-based fear. Furthermore, estradiol prevented the ischemia-induced impairment in contextual fear conditioning. Fluoro-Jade (FJ) staining revealed neuronal degeneration throughout the dorsal hippocampus of mice that experienced 2-VO. Estradiol treatment reduced the number of FJ+ cells in CA1 and CA2, but not in CA3 or in the dentate gyrus. Together, these findings suggest that 15 min of global ischemia causes extensive hippocampal neurodegeneration and disrupts contextual fear conditioning processes in mice and that estradiol protects against these adverse effects.