Abstract

Posterior medial meniscus root tears (PMMRTs) make up a relatively notable proportion of all meniscus pathology and have been definitively linked to the progression of osteoarthritis (OA). While known risk factors for development of OA in the knee include abnormal tibial coronal alignment, obesity and female gender, PMMRTs have emerged in recent years as another significant driver of degenerative disease. These injuries lead to an increase in average contact pressure in the medial compartment, along with increases in peak contact pressure and a decrease in contact area relative to the intact state. Loss of the root attachment impairs the function of the entire meniscus and leads to meniscal extrusion, thus impairing the force-dissipating role of the meniscus. Anatomic meniscus root repairs with a transtibial pullout technique have been shown biomechanically to restore mean and peak contact pressures in the medial compartment. However, nonanatomic root repairs have been reported to be ineffective at restoring joint pressures back to normal. Meniscal extrusion is often a consequence of nonanatomic repair and is correlated with progression of OA. In this study, the authors will describe the biomechanical basis of the natural history of medial meniscal root tears and will support the biomechanical studies with a case series including patients that either underwent non-operative treatment (5 patients) or non-anatomic repair of their medial meniscal root tears (6 patients). Using measurements derived from axial MRI, the authors will detail the distance from native root attachment center of the non-anatomic tunnels and discuss the ongoing symptoms of those patients. Imaging and OA progression among patients who were treated nonoperatively before presentation to the authors will be discussed as well. The case series thus presented will illustrate the natural history of meniscal root tears, the consequences of non-anatomic repair, and the findings of symptomatic meniscal extrusion associated with a non-anatomic repair position of the meniscus.

Highlights

  • The meniscus plays a central role in protecting the overall health of the knee, and, while underappreciated in previous years, the maintenance of its integrity has emerged as a key factor in joint preservation (Sims et al, 2009; Yusuf et al, 2011; Driban et al, 2016; Foreman et al, 2020; Willinger et al, 2020)

  • The presence of a complete medial meniscus root tear without end-stage OA was verifiable on prior imaging for most of these patients, and new Magnetic resonance imaging (MRI) were obtained demonstrating the development of chondromalacia, fullthickness cartilage defects, meniscal extrusion, and joint space narrowing

  • We have presented a case series of patients who underwent nonanatomic Posterior medial meniscus root tears (PMMRTs) repairs and patients who presented with OA as a result of neglected medial meniscal root tears

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Summary

INTRODUCTION

The meniscus plays a central role in protecting the overall health of the knee, and, while underappreciated in previous years, the maintenance of its integrity has emerged as a key factor in joint preservation (Sims et al, 2009; Yusuf et al, 2011; Driban et al, 2016; Foreman et al, 2020; Willinger et al, 2020). Root avulsions and radial tears up to 10 mm from the root attachment have been biomechanically validated to be functionally similar, resulting in significantly decreased contact areas at all flexion angles, as well as significantly increased mean and peak contact pressures (Padalecki et al, 2014; LaPrade et al, 2015b) This altered force profile in the knee may lead to meniscal extrusion and subsequent loss of articular cartilage (Athanasiou and SanchezAdams, 2009; Bedi et al, 2010). The presence of a complete medial meniscus root tear without end-stage OA was verifiable on prior imaging for most of these patients, and new MRIs were obtained demonstrating the development of chondromalacia, fullthickness cartilage defects, meniscal extrusion, and joint space narrowing. Clinical evaluation revealed no other probable cause for this rapid progression to OA. (See Figure 12)

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DATA AVAILABILITY STATEMENT
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