Clinically relevant anatomical risk factors for ACL injury have widely been deemed to be nonmodifiable. The lab's current work has challenged this perception by characterizing how knee structure risk factors and the ACL respond to exercise perturbations throughout adolescence and early adulthood. With both resistive and non-resistive voluntary cage wheel running, we have recently shown that the mouse knee joint and ACL can structurally and functionally adapt to moderate to strenuous physical activity throughout adolescence and into adulthood. The majority of these adaptations are positive and if translatable to humans could offer hope to clinicians, athletes, parents, coaches and athletic trainers that knee injuries may be reduced with habitual physical activity early on.
Current dogma is that over abduction of the knee during a pivot-shift or jump-landing results in a single overload failure of the ACL. Presently we are testing whether the majority of these injuries could in fact be more a consequence of accumulated fatigue damage. Characterizing how fatigue-damage accumulates and may result in catastrophic tissue failure in the short-term, may allow researchers to identify clinical intervention windows during growth in the long-term, wherein the tissue may be biologically repaired before exceeding some failure threshold. To accomplish this, the lab has developed a novel in vivo animal model to submaximally fatigue the ACL over time, while hierarchically characterizing the physiologic response of the ACL and its entheses to repetitive loading over time.
In tandem with ‘preventative research arm’, the lab are also characterizing the bony changes that occur in the joint from the time of injury up until the time of primary ACL reconstructive surgery. Bone mineral density (BMD) measures taken after injury and at various time points following ACL reconstructive surgery suggest there is significant bone loss about the knee joint following injury that is never fully recovered post-surgery. However, BMD data is not localized to the bony matrix at the point of ACL insertion (wherein an ACL graft would be placed). Establishing multiscalar osseous changes occurring within the mineralized fibrocartilaginous, cortical and trabecular matrices comprising the ACL femoral and tibial entheses post-injury up until the point of reconstructive surgery, will help identify a clinical window wherein the homeostatic state of bone is suitable for primary graft fixation and effective osseointegration. The lab hopes to inform clinicians of when an auto- or allo-graft is most likely to biologically integrate with a patient’s existing epi/metaphyseal bone tissue to provide a structurally-sound ACL graft, reducing the probability of a primary graft failure and rupture downstream. This information can then be used to improve pre-surgical rehabilitative protocols prior to reconstructive surgery so that patients are in the best position possible to receive a graft when their existing epi/metaphyseal bone is at its most ‘optimal’ post-injury state. Using a novel in vivo ACL rupture animal model, researchers are investigating the physiological response to injury in the interest of improving patient outcomes.
Patton DM, Martin CT, Casden M, Jepsen KJ, Ashton-Miller JA, Wotys EM, Schlecht SH*. State of the mineralized tissue comprising the femoral ACL enthesis in young women with an ACL failure. J Orthop Res; 2021; doi:10.1002/jor.25130.
Chen J, Shao W, Kim J, Schlecht SH, Baek SY, Jones A, Ahn T, Ashton-Miller J, Banaszak Holl M, Wojtys E*. On an ACL failure mechanism. Am J Sports Med; 2019; 47:2067-2076.
Schlecht SH*, Martin CT, Ochocki DN, Wojtys EM, Ashton-Miller JA. Morphology of mouse anterior cruciate ligament-complex changes following exercise during pubertal growth. J Orthop Res; 2019; 37:1910-1919.
Schlecht SH*, Ramcharan MA, Yang Y, Smith LM, Bigelow EMR, Nolan BT, Moss DE, Devlin MJ, Jepsen KJ. Differential adaptive response of growing bones from two inbred female mouse strains to voluntary cage wheel running. J Bone Miner Res Plus; 2018; 2:143-153.
Schlecht SH*, Smith LM, Ramcharan MA, Bigelow EMR, Nolan BT, Mathis NJ, Cathey A, Manley Jr. E, Nadeau JH, Jepsen KJ. Canalization leads to similar whole bone mechanical function in two inbred strains of mice. J Bone Miner Res; 2017; 32:1002-1013.
Schlecht SH*, Pinto DC, Agnew AM, Stout SD. The effects of disuse on the mechanical properties of bone: what unloading tells us about the adaptive nature of skeletal tissue. Am J Phys Anthrop 2012; 149:599-605.
Schlecht SH*. Understanding entheses: bridging the gap between clinical and anthropological perspectives. Anat Rec 2012; 295:1239-1251.
