@article{HedrichMorbachReiseretal.2020,
  author    = {Hedrich, Christian M. and Morbach, Henner and Reiser, Christiane and Girschick, Hermann J.},
  title     = {New Insights into Adult and Paediatric Chronic Non-bacterial Osteomyelitis CNO},
  series = {Current Rheumatology Reports},
  volume    = {22},
  journal   = {Current Rheumatology Reports},
  issn      = {1523-3774},
  doi       = {10.1007/s11926-020-00928-1},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-232636},
  year      = {2020},
  abstract  = {Purpose of Review To describe in detail the clinical synopsis and pathophysiology of chronic non-bacterial osteomyelitis and SAPHO syndrome. Recent Findings Chronic non-bacterial osteomyelitis (CNO) has been identified as a disease entity for almost 50 years. This inflammatory bone disorder is characterized by osteolytic as well as hyperostotic/osteosclerotic lesions. It is chronic in nature, but it can present with episodic flairs and phases of remission, which have led to the denomination "chronic recurrent osteomyelitis", with its severe multifocal form "chronic recurrent multifocal osteomyelitis" (CRMO). For almost three decades, an infectious aetiology had been considered, since especially Propionibacterium acnes had been isolated from bone lesions of individual patients. However, this concept has been challenged since long-term antibiotic therapy did not alter the course of disease and modern microbiological techniques (including PCR) failed to confirm bone infection as an underlying cause. Over recent years, a profound dysregulation of cytokine expression profiles has been demonstrated in innate immune cells of CNO patients. A hallmark of monocytes from CNO patients is the failure to produce immune regulatory cytokines interleukin-10 (IL-10) and IL-19, which have been linked with genetic and epigenetic alterations. Subsequently, a significant upregulation of pro-inflammatory, NLRP3 inflammasome-dependent cytokines (IL-1β and TNF-α), has been demonstrated. Summary The current knowledge on CNO, the underlying molecular pathophysiology, and modern imaging strategies are summarized; differential diagnoses, treatment options, outcome measures, as well as quality of life studies are discussed.},
  language  = {en}
}
@article{HofmannBoettgerRangeetal.2017,
  author    = {Hofmann, Sigrun Ruth and B{\"o}ttger, Fanny and Range, Ursula and L{\"u}ck, Christian and Morbach, Henner and Girschick, Hermann Joseph and Suttorp, Meinolf and Hedrich, Christian Michael},
  title     = {Serum interleukin-6 and CCL11/eotaxin may be suitable biomarkers for the diagnosis of chronic nonbacterial osteomyelitis},
  series = {Frontiers in Pediatrics},
  volume    = {5},
  journal   = {Frontiers in Pediatrics},
  doi       = {10.3389/fped.2017.00256},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-172744},
  year      = {2017},
  abstract  = {Objectives: Chronic recurrent multifocal osteomyelitis (CRMO), the most severe form of chronic nonbacterial osteomyelitis (CNO), is an autoinflammatory bone disorder. In the absence of diagnostic criteria or biomarkers, CNO/CRMO remains a diagnosis of exclusion. The aim of this study was to identify biomarkers for diagnosing multifocal disease (CRMO). Study design: Sera from 71 pediatric CRMO patients, 11 patients with osteoarticular infections, 62 patients with juvenile idiopathic arthritis (JIA), 7 patients with para-infectious or reactive arthritis, and 43 patients with acute leukemia or lymphoma, as well as 59 healthy individuals were collected. Multiplex analysis of 18 inflammation- and/or bone remodeling-associated serum proteins was performed. Statistical analysis included univariate ANOVA, discriminant analysis, univariate receiver operating characteristic (ROC) analysis, and logistic regression analyses. Results: For 14 of 18 blood serum proteins, significant differences were determined between CRMO patients, at least one alternative diagnosis, or healthy controls. Multi-component discriminant analysis delivered five biomarkers (IL-6, CCL11/eotaxin, CCL5/RANTES, collagen Iα, sIL-2R) for the diagnosis of CRMO. ROC analysis allowed further reduction to a core set of 2 biomarkers (CCL11/eotaxin, IL-6) that are sufficient to discern between CRMO, healthy controls, and alternative diagnoses. Conclusion: Serum biomarkers CCL11/eotaxin and IL-6 differentiate between patients with CRMO, healthy controls, and alternative diagnoses (leukemia and lymphoma, osteoarticular infections, para-infectious arthritis, and JIA). Easily accessible biomarkers may aid in diagnosing CRMO. Further studies testing biomarkers in larger unrelated cohorts are warranted.},
  language  = {en}
}