Role of dendritic cell-mediated immune response in oral homeostasis: A new mechanism of osteonecrosis of the jaw.
Animals
Bone Density Conservation Agents
/ pharmacology
Bone and Bones
/ drug effects
Cell Differentiation
/ drug effects
Dendritic Cells
/ immunology
Homeostasis
/ drug effects
Imidazoles
/ pharmacology
Jaw Diseases
/ drug therapy
Osteoclasts
/ drug effects
Osteonecrosis
/ drug therapy
Tooth Extraction
/ methods
Wound Healing
/ drug effects
Zoledronic Acid
/ pharmacology
alveolar bone healing
dendritic cells
osteonecrosis
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
19
07
2019
revised:
25
11
2019
accepted:
05
12
2019
pubmed:
11
1
2020
medline:
30
9
2020
entrez:
11
1
2020
Statut:
ppublish
Résumé
Dendritic cells are an important link between innate and adaptive immune response. The role of dendritic cells in bone homeostasis, however, is not understood. Osteoporosis medications that inhibit osteoclasts have been associated with osteonecrosis, a condition limited to the jawbone, thus called medication-related osteonecrosis of the jaw. We propose that disruption of the local immune response renders the oral microenvironment conducive to osteonecrosis. We tested whether zoledronate (Zol) treatment impaired dendritic cell (DC) functions and increased bacterial load in alveolar bone in vivo and whether DC inhibition alone predisposed the animals to osteonecrosis. We also analyzed the role of Zol in impairment of differentiation and function of migratory and tissue-resident DCs, promoting disruption of T-cell activation in vitro. Results demonstrated a Zol induced impairment in DC functions and an increased bacterial load in the oral cavity. DC-deficient mice were predisposed to osteonecrosis following dental extraction. Zol treatment of DCs in vitro caused an impairment in immune functions including differentiation, maturation, migration, antigen presentation, and T-cell activation. We conclude that the mechanism of Zol-induced osteonecrosis of the jaw involves disruption of DC immune functions required to clear bacterial infection and activate T cell effector response.
Identifiants
pubmed: 31919918
doi: 10.1096/fj.201901819RR
pmc: PMC7712496
mid: NIHMS1643124
doi:
Substances chimiques
Bone Density Conservation Agents
0
Imidazoles
0
Zoledronic Acid
6XC1PAD3KF
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
2595-2608Subventions
Organisme : NIH HHS
ID : S10 OD025177
Pays : United States
Organisme : National Institute of Aging
ID : 2P01AG036675-06A1
Pays : International
Organisme : National Institute of Health
ID : 1-S10 OD025177-01
Pays : International
Organisme : NIDCR NIH HHS
ID : 2R15DE025134-02
Pays : United States
Organisme : NIDCR NIH HHS
ID : R15 DE025134
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG036675
Pays : United States
Informations de copyright
© 2020 Federation of American Societies for Experimental Biology.
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