Cellular biology of fracture healing

The biology of bone healing is a rapidly developing science. Advances in transgenic and gene‐targeted mice have enabled tissue and cell‐specific investigations of skeletal regeneration. As an example, only recently has it been recognized that chondrocytes convert to osteoblasts during healing bone, and only several years prior, seminal publications reported definitively that the primary tissues contributing bone forming cells during regeneration were the periosteum and endosteum. While genetically modified animals offer incredible insights into the temporal and spatial importance of various gene products, the complexity and rapidity of healing—coupled with the heterogeneity of animal models—renders studies of regenerative biology challenging. Herein, cells that play a key role in bone healing will be reviewed and extracellular mediators regulating their behavior discussed. We will focus on recent studies that explore novel roles of inflammation in bone healing, and the origins and fates of various cells in the fracture environment. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop ResAdvances in transgenic and gene‐targeted mice have enabled tissue and cell‐specific investigation of skeletal regeneration. While genetically modified animals offer incredible insights into the temporal and spatial importance of various molecules, the complexity and rapidity of healing renders studies of regenerative biology challenging. Herein, cells and extracellular mediators that play a key role in bone healing are reviewed. We will focus on recent studies that explore the origins and fates of various cells in the fracture environment.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/148261/1/jor24170_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/148261/2/jor24170-sup-0002-SuppTab-S2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/148261/3/jor24170-sup-0001-SuppTab-S1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/148261/4/jor24170.pd

Medial unicompartmental knee arthroplasty in the ACL-deficient knee

Symptomatic osteoarthritis (OA) of the knee develops often in association with anterior cruciate ligament (ACL) deficiency. Two distinct pathologies should be recognised while considering treatment options in patients with end-stage medial compartment OA and ACL deficiency. Patients with primary ACL deficiency (usually traumatic ACL rupture) can develop secondary OA (typically presenting with symptoms of instability and pain) and these patients are typically young and active. Patients with primary end stage medial compartment OA can develop secondary ACL deficiency (usually degenerate ACL rupture) and these patients tend to be older. Treatment options in either of these patient groups include arthroscopic debridement, reconstruction of the ACL, high tibial osteotomy (HTO) with or without ACL reconstruction, unicompartmental knee arthroplasty (UKA) and total knee arthroplasty (TKA). General opinion is that a functionally intact ACL is a fundamental prerequisite to perform a UKA. This is because previous reports showed higher failure rates when ACL was deficient, probably secondary to wear and tibial loosening. Nevertheless in some cases of ACL deficiency with end-stage medial compartment OA, UKA has been performed in isolation and recent papers confirm good short- to mid-term outcome without increased risk of implant failure. Shorter hospital stay, fewer blood transfusions, faster recovery and significantly lower risk of developing major complications like death, myocardial infarction, stroke, deep vein thrombosis (as compared to TKA) make the UKA an attractive option, especially in the older patients. On the other hand, younger patients with higher functional demands are likely to benefit from a simultaneous or staged ACL reconstruction in addition to UKA to regain knee stability. These procedures tend to be technically demanding. The main aim of this review was to provide a synopsis of the existing literature and outline an evidence-based treatment algorithm