Thrombocytopenia alters early but not late repair in a mouse model of Achilles tendon injury.

Abstract

Besides their hemostatic function, platelets can express key factors involved in tissue healing. However, the role of platelets in tendon healing following acute injury is poorly understood. We investigated this role by injecting male C57BL/6 mice with an antiplatelet antibody to induce thrombocytopenia. Placebo animals received serum only. The right Achilles tendon was sectioned and sutured using the 8-strand technique that allows immediate weight bearing. Platelet depletion did not alter the accumulation of neutrophils and macrophages or cell proliferation. A slight increase in vascularization was observed 7 days postinjury in tendons from thrombocytopenic mice relative to placebo animals, but the effect had disappeared by day 14. Furthermore, collagen content had a tendency to decrease in Achilles tendons under thrombocytopenia when compared with placebo treatment at 7 days posttrauma. This was correlated with a decline in maximal stress sustained by tendons at day 14 but not after 28 days. The impact of thrombocytopenia was otherwise negligible, as force relaxation and stiffness were similar in the two groups. Our findings demonstrate that platelets modulate early tendon repair following rupture, although the effect is limited over time. Nevertheless, platelets are not essential for the recruitment of inflammatory cells, proliferation, angiogenesis, and tendon maturation.