Aging, inflammation, stem cells, and bone healing.

Emmanuel Gibon,Stuart B Goodman,Laura Lu

doi:10.1186/s13287-016-0300-9

Abstract

Complex interactions among cells of the monocyte-macrophage-osteoclast lineage and the mesenchymal stem cell-osteoblast lineage play a major role in the pathophysiology of bone healing. Whereas the former lineage directs inflammatory events and bone resorption, the latter represents a source of cells for bone regeneration and immune modulation. Both of these lineages are affected by increasing age, which is associated with higher baseline levels of inflammatory mediators, and a significant reduction in osteogenic capabilities. Given the above, fracture healing, osteoporosis, and other related events in the elderly present numerous challenges, which potentially could be aided by new therapeutic approaches to modulate both inflammation and bone regeneration.

Highlights

Most developed countries are facing an aging population
This review will address the effect of aging on both macrophages and mesenchymal stem cell (MSC) as it relates to bone healing
Increased levels of S-endoglin, a transmembrane glycoprotein associated with inflammatory processes, were associated with decreased macrophage proliferation, decreased survival response to granulocyte macrophage colony-stimulating factor (GM-CSF), increased oxidative stress, and skewed myeloid cell polarization toward an M2 phenotype [32]

Summary

Introduction

Most developed countries are facing an aging population. Currently, persons over 65 years of age represent 13 % of the American population [1], and this number is expected to grow as the “Baby Boomer” generation continues to age beyond 65 [2]. Other studies reported the important role of osteal macrophages in the processes of bone healing [10,11,12]. Beyond pro-inflammatory signals, macrophages secrete many growth factors and chemokines that are critical during the inflammatory phase of bone healing [6, 13].

Results

Conclusion