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. 2017 Jul:10:28-35.
doi: 10.1016/j.jot.2017.04.002. Epub 2017 May 15.

Inflammation, ageing, and bone regeneration

Emmanuel Gibon  1 , Laura Y Lu  1 , Karthik Nathan  1 , Stuart B Goodman  1
Affiliations

Inflammation, ageing, and bone regeneration

Emmanuel Gibon et al. J Orthop Translat. 2017 Jul.

Abstract

Summary: Bone healing involves complex biological pathways and interactions among various cell types and microenvironments. Among them, the monocyte-macrophage-osteoclast line-age and the mesenchymal stem cell-osteoblast lineage are critical, in addition to an initial inflammatory microenvironment. These cellular interactions induce the necessary inflammatory milieu and provide the cells for bone regeneration and immune modulation. Increasing age is accompanied with a rise in the basal state of inflammation, potentially impairing osteogenesis.

The translational potential of this article: Translational research has shown multiple interactions between inflammation, ageing, and bone regeneration. This review presents recent, relevant considerations regarding the effects of inflammation and ageing on bone healing.

Keywords: ageing; bone; inflammation; macrophages; stem cells.

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Conflict of interest statement

Conflicts of interest/Funding The authors have no conflicts of interest relevant to this article.

Figures

Figure 1
Figure 1
The three phases of bone healing. COX-2 = cyclooxygenase-2; IL1,6 = interleukin 1 & 6; M1 = M1 macrophages; M2 = M2 macrophages; MΦ = macrophage; MSCs = mesenchymal stem cells; PGE2 = prostaglandin E2; RANKL = receptor activator of nuclear factor kappa-B ligand.
Figure 2
Figure 2
Factors impairing bone healing. COPD = chronic obstructive pulmonary disease; COX-2 = cyclooxygenase-2; IL 1,6 = interleukin 1 & 6; M1 = M1 macrophage; NSAIDs = nonsteroidal antiinflammatory drugs; PGE2 = prostaglandin E2; RA = rheumatoid arthritis; RANKL = receptor activator of nuclear factor kappa-B ligand; TNF = tumour necrosis factor.
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