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Adult acquired flatfoot deformity becomes permanent with stage III posterior tibialis tendon dysfunction and results in foot pain and difficulty walking and balancing. To prevent progression to stage III posterior tibialis tendon dysfunction when conservative treatment fails, a flexor digitorum longus to posterior tibialis tendon transfer is often conducted. However, since the flexor digitorum longus only has one-third the force-capability of the posterior tibialis, an osteotomy is typically also required. We propose the use of a novel implantable mechanism to replace the direct attachment of the tendon transfer with a sliding pulley to amplify the force transferred from the donor flexor digitorum longus to the foot arch. In this work, we created four OpenSim models of an arched foot, a flatfoot, a flatfoot with traditional tendon transfer, and a flatfoot with implant-modified tendon transfer. Paired with these models, we developed a forward dynamic simulation of the stance phase of gait that reproduces the medial/lateral distribution of vertical ground reaction forces. The simulation couples the use of a fixed tibia, moving ground plane methodology with simultaneous activation of nine extrinsic lower limb muscles. The arched foot and flatfoot models produced vertical ground reaction forces with the characteristic double-peak profile of gait, and the medial/lateral distribution of these forces compared well with the literature. The flatfoot model with implant-modified tendon transfer produced a 94.2% restoration of the medial/lateral distribution of vertical ground reaction forces generated by our arched foot model, which also represents a 2.1X improvement upon our tendon transfer model. This result demonstrates the feasibility of a pulley-like implant to improve functional outcomes for surgical treatment of adult acquired flatfoot deformity with ideal biomechanics in simulation. The real-world efficacy and feasibility of such a device will require further exploration of factors such as surgical variability, soft tissue interactions and healing response. 

Dynamic loading is a shared feature of tendon tissue homeostasis and pathology. Tendon cells have the inherent ability to sense mechanical loads that initiate molecular-level mechanotransduction pathways. While mature tendons require physiological mechanical loading in order to maintain and fine tune their extracellular matrix architecture, pathological loading initiates an inflammatory-mediated tissue repair pathway that may ultimately result in extracellular matrix dysregulation and tendon degeneration. The exact loading and inflammatory mechanisms involved in tendon healing and pathology is unclear although a precise understanding is imperative to improving therapeutic outcomes of tendon pathologies. Thus, various model systems have been designed to help elucidate the underlying mechanisms of tendon mechanobiology via mimicry of the in vivo tendon architecture and biomechanics. Recent development of model systems has focused on identifying mechanoresponses to various mechanical loading platforms. Less effort has been placed on identifying inflammatory pathways involved in tendon pathology etiology, though inflammation has been implicated in the onset of such chronic injuries. The focus of this work is to highlight the latest discoveries in tendon mechanobiology platforms and specifically identify the gaps for future work. An interdisciplinary approach is necessary to reveal the complex molecular interplay that leads to tendon pathologies and will ultimately identify potential regenerative therapeutic targets.