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Molecular and Cellular Biochemistry

, Volume 436, Issue 1–2, pp 59–69 | Cite as

Increased expression of damage-associated molecular patterns (DAMPs) in osteoarthritis of human knee joint compared to hip joint

  • John H. Rosenberg
  • Vikrant Rai
  • Matthew F. Dilisio
  • Todd D. Sekundiak
  • Devendra K. Agrawal
Article

Abstract

Osteoarthritis (OA) is a degenerative disease characterized by the destruction of cartilage. The greatest risk factors for the development of OA include age and obesity. Recent studies suggest the role of inflammation in the pathogenesis of OA. The two most common locations for OA to occur are in the knee and hip joints. The knee joint experiences more mechanical stress, cartilage degeneration, and inflammation than the hip joint. This could contribute to the increased incidence of OA in the knee joint. Damage-associated molecular patterns (DAMPs), including high-mobility group box-1, receptor for advanced glycation end products, and alarmins (S100A8 and S100A9), are released in the joint in response to stress-mediated chondrocyte and cartilage damage. This facilitates increased cartilage degradation and inflammation in the joint. Studies have documented the role of DAMPs in the pathogenesis of OA; however, the comparison of DAMPs and its influence on OA has not been discussed. In this study, we compared the DAMPs between OA knee and hip joints and found a significant difference in the levels of DAMPs expressed in the knee joint compared to the hip joint. The increased levels of DAMPs suggest a difference in the underlying pathogenesis of OA in the knee and the hip and highlights DAMPs as potential therapeutic targets for OA in the future.

Keywords

Osteoarthritis Hip joint Knee joint HMGB-1 RAGE S100A8 S100A9 

Notes

Funding

This work was supported by research Grants R01 HL112597, R01 HL116042, and R01 HL120659 to DK Agrawal from the National Heart, Lung and Blood Institute, National Institutes of Health, USA. The content of this review article is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Author contribution

Conception and design: VR, MFD, and DKA; contributed reagents/materials/analysis tool: MFD, TDS, and DKA; analysis and interpretation of the data: JHR and VR; drafting of the manuscript: JHR, VR, MFD, TDS, and DKA; critical revision of the article for important intellectual content: VR, MFD, and DKA; final approval of the article: JHR, VR, MFD, TDS, and DKA.

Compliance with ethical standards

Conflict of interest

As the corresponding author, I declare that this manuscript is original, that the article does not infringe upon any copyright or other proprietary rights of any third party, and that neither the text nor the data have been reported or published previously. All the authors have no conflict of interest and have read the journal’s authorship statement.

Supplementary material

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Supplementary material 1 (DOCX 11 kb)
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Supplementary material 2 (TIFF 1464 kb)
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Supplementary material 3 (TIFF 5202 kb)

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Copyright information

© Springer Science+Business Media New York 2017

Authors and Affiliations

  • John H. Rosenberg
    • 1
  • Vikrant Rai
    • 1
  • Matthew F. Dilisio
    • 1
    • 2
  • Todd D. Sekundiak
    • 2
  • Devendra K. Agrawal
    • 1
    • 3
  1. 1.Department of Clinical and Translational ScienceCreighton University School of MedicineOmahaUSA
  2. 2.Orthopedic SurgeryCreighton University School of MedicineOmahaUSA
  3. 3.Department of Clinical and Translational Science, The Peekie Nash Carpenter Endowed Chair in MedicineCreighton University School of MedicineOmahaUSA

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