Melanocortin agonism as a viable strategy to control alveolar bone loss induced by oral infection

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dc.creatorMila Fernandes Moreira Madeira achou
dc.creatorTarcília Aparecida da Silva achou
dc.creatorMauro Perretti
dc.creatorCelso Martins Queiroz-Junior
dc.creatorTrinidad Montero-Melendez
dc.creatorSílvia Maria Cordeiro Werneck
dc.creatorJôice Dias Corrêa
dc.creatorFrederico Marianetti Soriani
dc.creatorGustavo Pompermaier Garlet
dc.creatorSouza Danielle Glória Souza
dc.creatorMauro Martins Teixeira
dc.date.accessioned2025-04-16T16:41:40Z
dc.date.accessioned2025-09-09T00:44:15Z
dc.date.available2025-04-16T16:41:40Z
dc.date.issued2016-12
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1096/fj.201600790r
dc.identifier.issn1530-6860
dc.identifier.urihttps://hdl.handle.net/1843/81668
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofThe FASEB Journal
dc.rightsAcesso Restrito
dc.subjectAggregatibacter actinomycetemcomitans
dc.subjectInflammation
dc.subjectOsteoclasts
dc.subjectPeriodontitis
dc.subjectMelanocortins
dc.subjectEvaluation study
dc.subjectPeriodontal diseases
dc.subjectAlveolar bone loss
dc.subjectTumor necrosis factor-alpha
dc.subjectInterferon-gamma
dc.subjectInterleukin-17
dc.subjectNeutrophil Infiltration
dc.subjectPeriodontium
dc.subjectPhysiology
dc.subjectBone and bones
dc.subject.otherAggregatibacter actinomycetemcomitans
dc.subject.otherDTrp8-γMSH
dc.subject.otherInflammation
dc.subject.otherOsteoclasts
dc.subject.otherPeriodontitis
dc.titleMelanocortin agonism as a viable strategy to control alveolar bone loss induced by oral infection
dc.typeArtigo de periódico
local.citation.epage4041
local.citation.issue12
local.citation.spage4033
local.citation.volume30
local.description.resumoAlveolar bone loss is a result of an aggressive form of periodontal disease (PD) associated with Aggregatibacter actinomycetemcomitans (Aa) infection. PD is often observed with other systemic inflammatory conditions, including arthritis. Melanocortin peptides activate specific receptors to exert antiarthritic properties, avoiding excessing inflammation and modulating macrophage function. Recent work has indicated that melanocortin can control osteoclast development and function, but whether such protection takes place in infection-induced alveolar bone loss has not been investigated. The purpose of this study was to evaluate the role of melanocortin in Aa-induced PD. Mice were orally infected with Aa and treated with the melanocortin analog DTrp8-γMSH or vehicle daily for 30 d. Then, periodontal tissue was collected and analyzed. Aa-infected mice treated with DTrp8-γMSH presented decreased alveolar bone loss and a lower degree of neutrophil infiltration in the periodontium than vehicle-treated animals; these actions were associated with reduced periodontal levels of TNF-α, IFN-γ, and IL-17A. In vitro experiments with cells differentiated into osteoclasts showed that osteoclast formation and resorptive activity were attenuated after treatment with DTrp8-γMSH. Thus, melanocortin agonism could represent an innovative way to tame over exuberant inflammation and, at the same time, preserve bone physiology, as seen after Aa infection.
local.identifier.orcidhttps://orcid.org/0000-0002-1770-9978
local.identifier.orcidhttps://orcid.org/0000-0001-9623-7835
local.identifier.orcidhttps://orcid.org/0000-0002-3563-376X
local.identifier.orcidhttps://orcid.org/0000-0002-5071-8382
local.identifier.orcidhttps://orcid.org/0000-0003-0170-6163
local.identifier.orcidhttps://orcid.org/0000-0003-4720-6746
local.identifier.orcidhttps://orcid.org/0000-0002-6944-3008
local.identifier.orcidhttps://orcid.org/0000-0003-2068-3331
local.publisher.countryBrasil
local.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICA
local.publisher.departmentICB - DEPARTAMENTO DE BIOLOGIA GERAL
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MICROBIOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fj.201600790R

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