Antibody-induced pain-like behavior and bone erosion: links to subclinical inflammation, osteoclast activity, and acid-sensing ion channel 3-dependent sensitization

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AudienciaPúblico en generales_ES
CoberturaMéxicoes_ES
Fecha de ingreso2026-10-05T16:33:39Z
Fecha de publicación2022-01-01
ResumenSeveral bone conditions, eg, bone cancer, osteoporosis, and rheumatoid arthritis (RA), are associated with a risk of developing persistent pain. Increased osteoclast activity is often the hallmark of these bony pathologies and not only leads to bone remodeling but is also a source of pronociceptive factors that sensitize the bone-innervating nociceptors. Although historically bone loss in RA has been believed to be a consequence of inflammation, both bone erosion and pain can occur years before the symptom onset. Here, we have addressed the disconnection between inflammation, pain, and bone erosion by using a combination of 2 monoclonal antibodies isolated from B cells of patients with RA. We have found that mice injected with B02/B09 monoclonal antibodies (mAbs) developed a long-lasting mechanical hypersensitivity that was accompanied by bone erosion in the absence of joint edema or synovitis. Intriguingly, we have noted a lack of analgesic effect of naproxen and a moderate elevation of few inflammatory factors in the ankle joints suggesting that B02/B09-induced pain-like behavior does not depend on inflammatory processes. By contrast, we found that inhibiting osteoclast activity and acid-sensing ion channel 3 signaling prevented the development of B02/B09-mediated mechanical hypersensitivity. Moreover, we have identified secretory phospholipase A2 and lysophosphatidylcholine 16:0 as critical components of B02/B09-induced pain-like behavior and shown that treatment with a secretory phospholipase A2 inhibitor reversed B02/B09-induced mechanical hypersensitivity and bone erosion. Taken together, our study suggests a potential link between bone erosion and pain in a state of subclinical inflammation and offers a step forward in understanding the mechanisms of bone pain in diseases such as RA.es_ES
Doihttps://doi.org/10.1097/j.pain.0000000000002543es_ES
URIhttps://riuat.uat.edu.mx/handle/123456789/5462
Idiomaenes_ES
EditorialLIPPINCOTT WILLIAMS \& WILKINSes_ES
RelaciónPaines_ES
URL relacionadohttps://doi.org/10.1097/j.pain.0000000000002543es_ES
DerechosAcceso abierto (Metadatos de producción científica)es_ES
Licenciahttp://purl.org/coar/access_right/c_abf2es_ES
FuentePain
Palabra clavePaines_ES
Palabra claveOsteoclastses_ES
Palabra claveBonees_ES
Palabra claveAutoantibodieses_ES
Palabra claveRheumatoid arthritises_ES
Palabra claveASIC3es_ES
Palabra claveLipidses_ES
Palabra claveLPCes_ES
Palabra clavesPLA(2)es_ES
TítuloAntibody-induced pain-like behavior and bone erosion: links to subclinical inflammation, osteoclast activity, and acid-sensing ion channel 3-dependent sensitizationes_ES
TipoArtículoes_ES
ArbitradoHa sido Arbitradoes_ES
AutorJurczak, Alexandra
AutorDelay, Lauriane
AutorBarbier, Julie
AutorSimon, Nils
AutorKrock, Emerson
AutorSandor, Katalin
AutorAgalave, Nilesh M.
AutorRudjito, Resti
AutorWigerblad, Gustaf
AutorRogoz, Katarzyna
AutorBriat, Arnaud
AutorMiot-Noirault, Elisabeth
AutorMartinez-Martinez, Arisai
AutorBromme, Dieter
AutorGronwall, Caroline
AutorMalmstrom, Vivianne
AutorKlareskog, Lars
AutorKhoury, Spiro
AutorFerreira, Thierry
AutorLabrum, Bonnie
AutorDeval, Emmanuel
AutorMiguel Jimenez-Andrade, Juan
AutorMarchand, Fabien
AutorSvensson, I, Camilla
AutorJurczak, Alexandraes_ES
AutorDelay, Laurianees_ES
AutorBarbier, Juliees_ES
AutorSimon, Nilses_ES
AutorKrock, Emersones_ES
AutorSandor, Katalines_ES
AutorAgalave, Nilesh M.es_ES
AutorRudjito, Resties_ES
AutorWigerblad, Gustafes_ES
AutorRogoz, Katarzynaes_ES
AutorBriat, Arnaudes_ES
AutorMiot-Noirault, Elisabethes_ES
AutorMartinez-Martinez, Arisaies_ES
AutorBromme, Dieteres_ES
AutorGronwall, Carolinees_ES
AutorMalmstrom, Viviannees_ES
AutorKlareskog, Larses_ES
AutorKhoury, Spiroes_ES
AutorFerreira, Thierryes_ES
AutorLabrum, Bonniees_ES
AutorDeval, Emmanueles_ES
AutorMiguel Jimenez-Andrade, Juanes_ES
AutorMarchand, Fabienes_ES
AutorSvensson, I, Camillaes_ES
InstituciónUniversidad Autónoma de Tamaulipas
InstituciónUniversidad Autónoma de Tamaulipases_ES
Número8es_ES
Rango de páginas1542-1559es_ES
URL relacionadahttps://doi.org/10.1097/j.pain.0000000000002543
Tipo de artículoIndexado
Tipo de artículoIndexadoes_ES
Volumen163es_ES

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