P Fanning

Paul Fanning, PhD

Research Assistant Professor

Other Affiliations:

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Research Interests


Research Focus

Animal Models of OA - Mechanisms and Drug Testing

The Mechanical Regulation of Biological Mediators of Cartilage and Joint Destruction in Osteoarthritis

Currently in the U.S., musculoskeletal conditions are the leading cause of disability.  Joint diseases account for 50% of all chronic conditions in the elderly.  Worldwide, OA is only the 6th leading cause of years of life lost to ill health.  The burden of musculoskeletal disease, both in terms of human illness and heath care costs is projected to widen significantly by the year 2030.  The aging of the U.S. population is expected to produce an additional 21 million individuals in the 65-and-over age group, representing a 20% increase over current demographics.  Surprisingly, despite the wealth of clinical data on OA, surgical treatment which culminates in total joint replacement, remains the most effective therapy for progressive OA.  Relatively little is known about the basic biology of OA especially how mechanical wear, the major hallmark of OA, influences fundamental biological control mechanisms in chondrocytes, the cells that populate cartilage.
Recently, through the use of specially-designed mechanical compression devices, we have found that chondrocytes respond to increasing mechanical loading signals much as other tissues respond to increasing concentrations of hormones or growth factors by activating 3 distinct MAPK signaling pathways, including the so-called ‘stress-activated’ protein kinase pathways.  This finding not only opens the way for further research into what actions these signaling pathways have on specific genes involved in OA but also provides an opportunity to intervene with pathway-selective MAPK inhibitors in the treatment of OA.

The overall goal of Dr Fanning's projects is to advance the understanding of the molecular mechanisms of osteoarthritis (OA) progression through the novel finding that mechanical force activates critical cellular-signaling pathways in cartilage.  Specific primary goals include:

  • Mechanical Models of Arthritis
  • Mechanical Force and Signaling Pathways in Cartilage
  • Molecular Mechanisms of OA Progression
(Additional information: Link to Fracture Machine specifications )


Recent Publications




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Wixted Wixted JJ, Fanning P, Rothkopf I, Stein GS, Lian JB. Arachidonic acid, eicosanoids, and fracture repair. J Orthop Trauma. 2010 ; 24(9): 539-42.

Wixted JJ, Fanning P, Gaur T, Oconnell SL, Silva JA, Mason-Savas A, Ayers DC, Stein GS, et al. Enhanced fracture repair by leukotriene antagonism is characterized by increased chondrocyte proliferation and early bone formation: a novel role of the cysteinyl LT-1 receptor. J Cell Physiol. 2009 Jun; 221(1): 31-39.
Fitzerald JB, Jin M, Chai DH, Siparsky P, Fanning P, Grodzinsky AJ. Shear-and compression-induced chondrocyte transcription requires MAPK activiation in cartilage explants. J Biol Chem. 2008 Mar; 283: 6735-6743. PMID: 18086670.









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"Role of HtrA1 in the Transition from Cartilage to Bone in Fracture Healing"
Sponsor: Orthopaedic Trauma Association
Paul Fanning, Principal Investigator; Marie Walcott, CO-Principal Investigator; John Wixted, CO-Investigator

"Improving Orthopedic Outcomes Through a National TJR Registry"
Sponsor: NIH-Agency for Healthcare Research and Quality
Patricia Franklin, Principal Investigator; David Ayers, CO-Investigator; Paul Fanning, CO-Investigator; Wenjun Li, CO-Investigator

"Singulair Enhances Fracture Repair: Is there a Dose Response?"
Sponsor: Merck
John Wixted, Principal Investigator; Paul Fanning, CO-Investigator

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