Publisher Correction: Characteristics, Treatment Options, and Outcomes of Chronic Non-Bacterial Osteomyelitis in Childre
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Publisher Correction: Characteristics, Treatment Options, and Outcomes of Chronic Non-Bacterial Osteomyelitis in Children Raphae¨l Kraus* Ronald M. Laxer Address * Hospital for Sick Children, University of Toronto, Toronto, Canada Email: [email protected]
Published online: 5 August 2020 * Springer Nature Switzerland AG 2020
The online version of the original article can be found at https://doi.org/10.1007/s40674-020-00149-8
Publisher Correction: Curr Treat Options in Rheum https://doi.org/10.1007/s40674-020-00149-8 The original version of this article unfortunately contained a mistake in Tables 1 and 2 entries. Some entries of the tables were incorrectly aligned, and the correct presentation of these tables is shown here.
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Publisher Correction
Table 1. Overview of the molecular pathophysiology of chronic non-bacterial osteomyelitis and related therapeutic considerations
Proposed pathophysiologic mechanism
Associated clinical and translational research evidence
Related therapeutic considerations
Imbalanced cytokine expression
Increased pro-inflammatory cytokines (IL-1, IL-6, IL-20, TNF-α) and decreased immune-regulatory cytokines (IL-10 and IL-19) in CNO patients
Corticosteroids: reduce expression of NFκB-mediated pro-inflammatory cytokines, including IL-1, IL-6, and TNF-α
Stimulation of TLR4 by LPS in monocytes from CNO patients ➔ * impaired IL-10 expression and overexpression of IL-6 and TNF-α
Anti-TNF-α agents (e.g., ETN, IFX, ADA): abate effects of overexpression of TNF-α Anti-IL-1 agents (e.g., anakinra, canakinumab): abate effects of overexpression of IL-1
Reduced activation of the MAPK ERK1 and ERK2 ➔ impaired phosphorylation of transcription factor Sp-1 ➔ decreased recruitment of Sp-1 to regulatory elements at IL10 and IL19 promoters ➔ under-expression of IL-10 and IL-19 Increased inflammasome activation
NLRP3 inflammasome activation ➔ production of IL-1β ➔ bone inflammation in IL-10–deficient mice Increased NLRP3 and IL-1 mRNA expression in monocytes from CNO patients
NSAIDs: exert suppressive effect on inflammasomes Anti-IL-1 agents (e.g., anakinra, canakinumab): abate effects of overexpression of IL-1 by inflammasomes
Inflammasome activity and IL-1β secretion from monocytes from CNO patients reversed by co-culture with recombinant IL-10 or IL-19 Familial monogenic disorders associated with CNO (Majeed syndrome [involving LPIN2], DIRA [IL1RN], PAPA [PSTPIP1]) each involve inflammasome activation and increased IL-1 Increased osteoclast activation and differentiation
Imbalanced cytokine expression ➔ enhanced interaction between RANK receptor and its soluble ligand RANKL on osteoclasts ➔ osteoclast differentiation and activation ➔ inflammatory bone loss Mutations in FBLIM1 reported in 2 families with CNO; FLBLIM1 acts as anti-inflammatory molecule via regulation of RANKL activation FBLIM1 regulated by STAT3 and STAT3 activat
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