Cited by 188Bone Metabolism and DiseasesImmune Response and InflammationOsteomyelitis and Bone Disorders Research

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Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin

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Andreev, Darja, Liu, Mengdan, Weidner, Daniela, Kachler, Katerina, Faas, Maria, Grüneboom, Anika, Schlötzer-Schrehardt, Ursula, Muñoz, Luis E., Steffen, Ulrike, Grötsch, Bettina, Killy, Barbara, Krönke, Gerhard, Luebke, Andreas M., Niemeier, Andreas, Wehrhan, Falk, Lang, Roland, Schett, Georg, Bozec, Aline·2020·Journal of Clinical Investigation

DOI 10.1172/jci134214PMC PMC7456234

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Abstract

Although the control of bone-resorbing osteoclasts through osteocyte-derived RANKL is well defined, little is known about the regulation of osteoclasts by osteocyte death. Indeed, several skeletal diseases, such as bone fracture, osteonecrosis, and inflammation are characterized by excessive osteocyte death. Herein we show that osteoclasts sense damage-associated molecular patterns (DAMPs) released by necrotic osteocytes via macrophage-inducible C-type lectin (Mincle), which induced their differentiation and triggered bone loss. Osteoclasts showed robust Mincle expression upon exposure to necrotic osteocytes in vitro and in vivo. RNA sequencing and metabolic analyses demonstrated that Mincle activation triggers osteoclastogenesis via ITAM-based calcium signaling pathways, skewing osteoclast metabolism toward oxidative phosphorylation. Deletion of Mincle in vivo effectively blocked the activation of osteoclasts after induction of osteocyte death, improved fracture repair, and attenuated inflammation-mediated bone loss. Furthermore, in patients with osteonecrosis, Mincle was highly expressed at skeletal sites of osteocyte death and correlated with strong osteoclastic activity. Taken together, these data point to what we believe is a novel DAMP-mediated process that allows osteoclast activation and bone loss in the context of osteocyte death.

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Background
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Authors: Andreev, D., Liu, M., Weidner, D., Kachler, K., Faas, M., Grüneboom, A., Schlötzer-Schrehardt, U., Muñoz, L. E., Steffen, U., Grötsch, B., Killy, B., Krönke, G., Luebke, A. M., Niemeier, A., Wehrhan, F., Lang, R., Schett, G., & Bozec, A.
Affiliations: Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
University Medical Center Hamburg-Eppendorf (DE)
ORCID: Liu, Mengdan
Weidner, Daniela
Grüneboom, Anika
Schlötzer-Schrehardt, Ursula
Muñoz, Luis E.
Steffen, Ulrike
Grötsch, Bettina
Killy, Barbara
Krönke, Gerhard
Luebke, Andreas M.
Lang, Roland
Schett, Georg
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2020-08-10
Volume: 130
Issue: 9
Pages: 4811-4830
ISSN: 0021-9738 (ISSN-L)
1558-8238
DOI: 10.1172/jci134214
PMC: PMC7456234
OpenAlex: W3047914933
Cited by: 188
References: 68
Citations by year: 2026: 25 · 2025: 38 · 2024: 41 · 2023: 35 · 2022: 24 · 2021: 19 · 2020: 6
FWCI: 6.81
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft (CRC‐1181, FOR 2886 (TP02, FOR2886, BO‐3811/5‐1, BO-3811/6-1)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Health Sciences › Medicine › Rheumatology › Osteomyelitis and Bone Disorders Research
Keywords: osteoclastogenesis, Mincle, damage-associated molecular patterns, bone loss, avascular necrosis, fracture healing, ITAM signaling, calcium signaling, oxidative phosphorylation, RANKL
MeSH terms: RNA-Seq, Animals, Bone Resorption, Membrane Proteins, Necrosis, Osteoclasts, Osteocytes, Mice, Knockout, Lectins, C-Type, Mice

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Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin

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