@article{WippertFliesserKrause2017,
  author    = {Wippert, Pia-Maria and Fliesser, Michael and Krause, Matthias},
  title     = {Risk and protective factors in the clinical rehabilitation of chronic back pain},
  series = {Journal of pain research},
  volume    = {10},
  journal   = {Journal of pain research},
  publisher = {Dove Medical Press},
  address   = {Albany, Auckland},
  issn      = {1178-7090},
  doi       = {10.2147/JPR.S134976},
  pages     = {1569 -- 1579},
  year      = {2017},
  abstract  = {Objectives: Chronic back pain (CBP) can lead to disability and burden. In addition to its medical causes, its development is influenced by psychosocial risk factors, the so-called flag factors, which are categorized and integrated into many treatment guidelines. Currently, most studies investigate single flag factors, which limit the estimation of individual factor significance in the development of chronic pain. Furthermore, factors concerning patients' lifestyle, biography and treatment history are often neglected. Therefore, the objectives of the present study are to identify commonly neglected factors of CBP and integrate them into an analysis model comparing their significance with established flag factors. Methods: A total of 24 patients and therapists were cross-sectionally interviewed to identify commonly neglected factors of CBP. Subsequently, the impact of these factors was surveyed in a longitudinal study. In two rehabilitation clinics, CBP patients (n = 145) were examined before and 6 months after a 3-week inpatient rehabilitation. Outcome variables, chronification factor pain experience (CF-PE) and chronification factor disability (CF-D), were ascertained with confirmatory factor analysis (CFA) of standardized questionnaires. Predictors were evaluated using stepwise calculations of simple and multiple regression models. Results: Through interviews, medical history, iatrogenic factors, poor compliance, critical life events (LEs), social support (SS) type and effort-reward were identified as commonly neglected factors. However, only the final three held significance in comparison to established factors such as depression and pain-related cognitions. Longitudinally, lifestyle factors found to influence future pain were initial pain, physically demanding work, nicotine consumption, gender and rehabilitation clinic. LEs were unexpectedly found to be a strong predictor of future pain, as were the protective factors, reward at work and perceived SS. Discussion: These findings shed insight regarding often overlooked factors in the development of CBP, suggesting that more detailed operationalization and superordinate frameworks would be beneficial to further research. Conclusion: In particular, LEs should be taken into account in future research. Protective factors should be integrated in therapeutic settings.},
  language  = {en}
}
@article{KellerCatalaLehnenHuebneretal.2014,
  author    = {Keller, Johannes and Catala-Lehnen, Philip and Huebner, Antje K. and Jeschke, Anke and Heckt, Timo and Lueth, Anja and Krause, Matthias and Koehne, Till and Albers, Joachim and Schulze, Jochen and Schilling, Sarah and Haberland, Michael and Denninger, Hannah and Neven, Mona and Hermans-Borgmeyer, Irm and Streichert, Thomas and Breer, Stefan and Barvencik, Florian and Levkau, Bodo and Rathkolb, Birgit and Wolf, Eckhard and Calzada-Wack, Julia and Neff, Frauke and Gailus-Durner, Valerie and Fuchs, Helmut and de Angelis, Martin Hrabe and Klutmann, Susanne and Tsourdi, Elena and Hofbauer, Lorenz C. and Kleuser, Burkhard and Chun, Jerold and Schinke, Thorsten and Amling, Michael},
  title     = {Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts},
  series = {Nature Communications},
  volume    = {5},
  journal   = {Nature Communications},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2041-1723},
  doi       = {10.1038/ncomms6215},
  pages     = {13},
  year      = {2014},
  abstract  = {The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signalling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P(3). Finally, pharmacologic treatment with the nonselective S1P receptor agonist FTY720 causes increased bone formation in wild-type, but not in S1P(3)-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts.},
  language  = {en}
}