Osteonecrosis

High tibial osteotomy (HTO) is a widely accepted and performed procedure to treat medial knee arthrosis. The aim of this review is to evaluate the different surgical options in medial knee arthrosis, focusing on indications, patient's selection, long-term follow-up and survival analysis of HTO. Comparison and pooling of results are challenging because of different evaluation systems, small cohort number, and different surgical techniques. No differences have been described between opening and closing wedged HTO in terms of outcomes. Excellent early survivorship and good clinical outcomes were reported also with concomitant procedures. Correct indications, preoperative workup/planning, and technique selection are essential in achieving good results. The choice between opening and closing wedge osteotomy, graft selection in opening wedge HTO, comparison between HTO and unicompartmental knee arthroplasty, and the results of revised HTO to total knee replacement are currently under ...

Through a process called perilacunar remodeling, bone-embedded osteocytes dynamically resorb and replace the surrounding perilacunar bone matrix to maintain mineral homeostasis. The vital canalicular networks required for osteocyte nourishment and communication, as well as the exquisitely organized bone extracellular matrix, also depend upon perilacunar remodeling. Nonetheless, many questions remain about the regulation of perilacunar remodeling and its role in skeletal disease. Here, we find that suppression of osteocyte-driven perilacunar remodeling, a fundamental cellular mechanism, plays a critical role in the glucocorticoid-induced osteonecrosis. In glucocorticoid-treated mice, we find that glucocorticoids coordinately suppress expression of several proteases required for perilacunar remodeling while causing degeneration of the osteocyte lacunocanalicular network, collagen disorganization, and matrix hypermineralization; all of which are apparent in human osteonecrotic lesions. Thus, osteocyte-mediated perilacunar remodeling maintains bone homeostasis, is dysregulated in skeletal disease, and may represent an attractive therapeutic target for the treatment of osteonecrosis. Bone remodeling allows the skeleton to functionally adapt to changing mechanical and metabolic demands. Conversely, dysregulation of bone remodeling underlies osteonecrosis and many other skeletal diseases. Following extensive study of remodeling by bone forming osteoblasts and bone resorbing osteoclasts, bone-embedded oste-ocytes (OCYs) have emerged as crucial regulators of osteoblast and osteoclast differentiation and function 1–6. However, until recently, the direct role of OCYs in bone matrix resorption was left largely unexplored 2,7. As early as 1910, OCYs were shown to actively participate in maintaining mineral homeostasis by resorb-ing their surrounding perilacunar bone matrix to release calcium and phosphate during metabolic stress due to rickets, hibernation, or avian egg production 8–12. This cell-intrinsic bone-resorbing ability of OCYs, known as perilacunar remodeling 7,13 , was long overlooked 14. Recent studies shed new light on this cellular mechanism by showing the induction of OCY-mediated perilacunar remodeling in lactating mice 15 , and its essential role in the maintenance of bone quality 16. Furthermore, these studies show that OCY-mediated perilacunar remodeling is not only invoked in metabolic stress, but is also a constitutive homeostatic process 16. Therefore, elucidating the role of perilacunar remodeling is pivotal to understanding the healthy skeleton and skeletal disease. OCYs project dendritic processes through the intricate lacunocanalicular network to interact with one another, with other bone and marrow cells, and with the vasculature in the bone microenvironment 7,17,18. The canalicular network deteriorates in mice deficient in proteases required for perilacunar remodeling, including MMP-2, MMP-13, and MMP-14 16,19,20 , suggesting an essential role for the activity of these enzymes. In addition, deficiency in these enzymes results in a profound collagen disorganization and matrix hypermineralization 16. Not surprisingly, disruption of the mineralized collagen bone matrix compromises the material quality of bone,