Models of acute annulus fibrosus (AF) injury consistently produce a mechanical or biological response similar to that of human disc degeneration1–5. These methods are easily implemented, provide repeatable results and have controlled specificity in comparison to global knockout and spontaneous development models. AF injury studies have been conducted in many species including the sheep, rabbit, and rat1–4. The mouse caudal disc is a proposed model, as it degenerates as a result of needle puncture injury, displaying changes consistent with those in humans5. Limited mechanical data for puncture-initiated degeneration is available, however. The primary function of the disc is mechanical — transferring loads, dissipating energy and facilitating joint mobility. Evaluating disc mechanical properties is therefore important for understanding how functional changes can be targeted by potential therapeutics. The objective of this study was to quantify the acute and long term effects of needle puncture injury on mouse caudal disc mechanical function, disc height and nucleus pulposus (NP) glycosaminoglycan (GAG) content.

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