Melanocortin agonism as a viable strategy to control alveolar bone loss induced by oral infection.
Melanocortin agonism as a viable strategy to control alveolar bone loss induced by oral infection.
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黑皮质素激动是控制口腔感染引起的牙槽骨丢失的可行策略。
DOI：
10.1096/fj.201600790r
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Madeira MF
中科院分区：
文献类型：
--
作者：
Madeira MF
牙槽骨丢失是一种与伴放线菌聚集杆菌（Aggregatibacteractinomycetemcomitans，Aa）感染相关的侵袭性牙周病（periodontaldisease，PD）的结果。PD通常与其他全身性炎症性疾病（包括关节炎）一起观察到。黑皮质素肽激活特异性受体发挥抗关节炎特性，避免过度炎症和调节巨噬细胞功能。最近的研究表明，黑皮质素可以控制破骨细胞的发育和功能，但这种保护作用是否发生在感染引起的牙槽骨丢失还没有研究。本研究的目的是评估黑皮质素在Ainduced PD中的作用。小鼠经口感染Aa，并每天用黑皮质素类似物DTrp 8-γMSH或溶剂处理30天。然后，牙周组织收集和分析。经DTrp 8-γMSH处理的Aα感染小鼠表现出比溶剂处理的动物更少的牙槽骨丢失和更低程度的牙周组织中的中性粒细胞浸润;这些作用与牙周组织中TNF-α、IFN-γ和IL-17 A水平的降低有关。体外实验表明，经DTrp 8-γMSH处理后，破骨细胞的形成和吸收活性减弱。因此，黑皮质素激动剂可能代表了一种创新的方式来驯服过度的炎症，同时，保护骨生理学，如感染后所见。马德拉群岛F. M.，Queiroz-Junior，C. M.，蒙特罗-梅伦德斯韦尔内克，S. M. C.的方法，Corrêa，J. D.，Soriani，F. M.，Garlet，G. P.，Souza，D.G.，特谢拉，医学硕士，席尔瓦助教Perretti，M.Melanocortin agonismas是一种控制口腔感染引起的牙槽骨丢失的可行策略。FASEB J.30，4033-4041（2016）。www.fasebj.org
Alveolar bone loss is a result of an aggressive form of periodontal disease (PD) associated withAggregatibacter 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, butwhether 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 Aainduced PD. Mice were orally infected withAaand treated with the melanocortin analog DTrp8‐γMSH or vehicle daily for 30 d. Then, periodontal tissue was collected and analyzed. Aα‐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 vitroexperiments 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 afterAainfection.—Madeira, M. F. M., Queiroz‐Junior, C. M., Montero‐Melendez, T., Werneck, S. M. C., Corrêa, J. D., Soriani, F.M., Garlet, G. P., Souza, D.G., Teixeira, M.M., Silva, T.A., Perretti, M.Melanocortin agonismas a viable strategy to control alveolar bone loss induced by oral infection. FASEB J. 30, 4033–4041 (2016). www.fasebj.org