Hofmann Sigrun R, Schnabel Anja, Rösen-Wolff Angela, Morbach Henner, Girschick Hermann J, Hedrich Christian M
From the Pediatric Rheumatology and Immunology, Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Dresden; Department of Pediatrics, University of Würzburg, Würzburg; Children's Hospital, Vivantes Klinikum-Friedrichshain, Berlin, Germany.
S.R. Hofmann, MD, PhD, Pediatric Rheumatology and Immunology, Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden; A. Schnabel, MD, Pediatric Rheumatology and Immunology, Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden; A. Rösen-Wolff, MD, PhD, Pediatric Rheumatology and Immunology, Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden; H. Morbach, MD, PhD, Department of Pediatrics, University of Würzburg; H.J. Girschick, MD, PhD, Children's Hospital, Vivantes Klinikum-Friedrichshain; C.M. Hedrich, MD, PhD, Pediatric Rheumatology and Immunology, Department of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden.
J Rheumatol. 2016 Nov;43(11):1956-1964. doi: 10.3899/jrheum.160256. Epub 2016 Sep 1.
Chronic nonbacterial osteomyelitis (CNO) is an autoinflammatory bone disorder, covering a clinical spectrum with asymptomatic inflammation of single bones at the one end, and chronic recurrent multifocal osteomyelitis (CRMO) at the other end. The exact molecular pathophysiology of CNO remains largely unknown. Provided familial clusters and the association with inflammatory disorders of the skin and intestine suggest a genetic predisposition. Recently, profound dysregulation of cytokine responses was demonstrated in CRMO. Failure to produce antiinflammatory cytokines interleukin (IL)-10 and IL-19 contributes to activation of inflammasomes and subsequent IL-1β release. In IL-10-deficient and in CNO-prone chronic multifocal osteomyelitis mice, IL-1β was linked to bone inflammation. Further, alterations to the gut microbiome were suggested in contributing to IL-1β release from innate immune cells in mice, offering an interesting target in the search for molecular mechanisms in CNO. Here, we summarize clinical presentation and treatment options in CNO/CRMO, current pathophysiological concepts, available mouse models, and promising future scientific directions.
慢性非细菌性骨髓炎(CNO)是一种自身炎症性骨病,涵盖了一系列临床症状,一端是单骨无症状炎症,另一端是慢性复发性多灶性骨髓炎(CRMO)。CNO的确切分子病理生理学在很大程度上仍不清楚。家族聚集现象以及与皮肤和肠道炎症性疾病的关联提示存在遗传易感性。最近,在CRMO中发现了细胞因子反应的严重失调。无法产生抗炎细胞因子白细胞介素(IL)-10和IL-19会导致炎性小体激活及随后IL-1β的释放。在IL-10缺陷型和易患CNO的慢性多灶性骨髓炎小鼠中,IL-1β与骨炎症有关。此外,肠道微生物群的改变被认为有助于小鼠固有免疫细胞释放IL-1β,这为寻找CNO的分子机制提供了一个有趣的靶点。在此,我们总结了CNO/CRMO的临床表现和治疗选择、当前的病理生理概念、现有的小鼠模型以及未来有前景的科学方向。