Jason L. Dragoo, MD
Academic Appointments
Appointment
Organization
Assistant Professor - Med Center Line
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Curriculum Vitae Doc
Honors & Awards
Title
Organization
Date(s)
InScope Orthopeadic Research Grant
Innovative Scientific Centers of Orthopaedic Excellence Orthopaedic
2005
Investigation of treatments for osteochondral defects in
children-Educational Grant
Shriners Hospital System for Children
2003
Aventis Orthopaedic Research Scholarship
UCLA Department of Orthopaedics
2002
Zimmer Research Award
American Orthopaedic Association
2002
Basic Science Manuscript Award
Smith and Nephew National Research Awards
Conference
Smith and Nephew
2002
12 honors and awards: view full list
Administrative Appointments
Title
Organization
Start Year
End Year
Team Physician
Stanford Men's Football
2007
-
Professional Education
Degree
Awarding Institution
Field of Study
Year of Graduation
MD
Steadman-Hawkins Sports Medicine
Sports Medicine
2005
MD
UCLA
Orthopaedic Surgery
2004
MD
University of Arizona
Medicine
1998
Research Interests
Tissue Engineering
Current laboratory studies will focus on 3 main areas:
1.The ability to harvest stem cells from a patient, induce them into cartilage cells, and place them back into the patient during the same surgical procedure. Current surgical techniques require 1 surgery to harvest the cells, 2-3 weeks of laboratory processing, and another surgery to implant the cells. Needless to say, the implication of this work would revolutionize the use of stem cells in Orthopaedic Surgery.
2.Reconfigure the biologic matrices and processing to allow resurfacing of entire joint surfaces. This process would make current metal joint replacements obsolete and would allow the treatment of arthritis with the patients own stem cells.
3.Decipher the genetic induction code and ideal matrix for meniscal cartilage engineering. This would allow the production of meniscal cartilage grafts from the patients own stem cells.
Anterior Cruciate Ligament
The incidence of anterior cruciate ligament (ACL) rupture in female athletes is two to eight times that in males. Although many anatomical and biomechanical gender differences have been described, evidence is beginning to accumulate that female hormones are responsible for alterations in ligament laxity and strength. The ACL injury rate has been shown to increase during the luteal phase of the menstrual cycle, corresponding to peak relaxin levels in the non-pregnant female. Relaxin is a peptide hormone found in the sera of pregnant and non-pregnant females, yet has never been detected in male serum. This hormone is thought to be responsible for connective tissue remodeling secondary to its collagenolytic effects. This restructuring occurs at the maternal-fetal interface, allowing for elongation of the pubic symphysis during late pregnancy and parturition. Ligamentous laxity of the knee has also been reported in pregnant women who have high relaxin titers. These effects are largely mediated by the release of collagenase, several matrix metalloproteinases, and plasminogen activator, which lead to a marked local decrease in collagen content. Since collagen is the main load-bearing component in ligamentous tissue, alterations in collagen content and organization could lead to changes in ligament integrity.
We have since identified relaxin receptors on the human female ACL. This supports the conclusion that relaxin, a hormone found in some non-pregnant females, may be responsible for the high incidence of ACL rupture in female athletes.
Future studies will involve the administration of relaxin to female guinea pigs to see if ACL laxity occurs. If laxity is found, we will test female intercollegiate athletes for relaxin levels, and monitor them to see if athletes with high relaxin levels are more susceptible to ACL injury. If this hypothesis is proven, we can then develop a blocking antibody to administer to susceptible female athletes to hopefully decrease the ACL injury rate.
Additional research will also be completed to evaluate the damage of articular cartilage during ACL injury. This may explain why certain athletes with ACL injury develop degenerative changes and early arthritis. Identification of cartilage injury patterns will help change treatment protocols to minimize the development of early arthritis in athletes.
Current laboratory studies will focus on 3 main areas:
1.
2.
3.
Anterior Cruciate Ligament
The incidence of anterior cruciate ligament (ACL) rupture in female athletes is two to eight times that in males. Although many anatomical and biomechanical gender differences have been described, evidence is beginning to accumulate that female hormones are responsible for alterations in ligament laxity and strength. The ACL injury rate has been shown to increase during the luteal phase of the menstrual cycle, corresponding to peak relaxin levels in the non-pregnant female. Relaxin is a peptide hormone found in the sera of pregnant and non-pregnant females, yet has never been detected in male serum. This hormone is thought to be responsible for connective tissue remodeling secondary to its collagenolytic effects. This restructuring occurs at the maternal-fetal interface, allowing for elongation of the pubic symphysis during late pregnancy and parturition. Ligamentous laxity of the knee has also been reported in pregnant women who have high relaxin titers. These effects are largely mediated by the release of collagenase, several matrix metalloproteinases, and plasminogen activator, which lead to a marked local decrease in collagen content. Since collagen is the main load-bearing component in ligamentous tissue, alterations in collagen content and organization could lead to changes in ligament integrity.
We have since identified relaxin receptors on the human female ACL. This supports the conclusion that relaxin, a hormone found in some non-pregnant females, may be responsible for the high incidence of ACL rupture in female athletes.
Future studies will involve the administration of relaxin to female guinea pigs to see if ACL laxity occurs. If laxity is found, we will test female intercollegiate athletes for relaxin levels, and monitor them to see if athletes with high relaxin levels are more susceptible to ACL injury. If this hypothesis is proven, we can then develop a blocking antibody to administer to susceptible female athletes to hopefully decrease the ACL injury rate.
Additional research will also be completed to evaluate the damage of articular cartilage during ACL injury. This may explain why certain athletes with ACL injury develop degenerative changes and early arthritis. Identification of cartilage injury patterns will help change treatment protocols to minimize the development of early arthritis in athletes.
Publications
- Dragoo JL, Carlson G, McCormick F, Khan-Farooqi H, Zhu M, Zuk PA, Benhaim P "Healing Full-Thickness Cartilage Defects Using Adipose-Derived Stem Cells." Tissue Eng 2007; More »
- Stevens KJ, Dragoo JL "Anterior Cruciate Ligament Tears and Associated Injuries." Top Magn Reson Imaging 2006; 17: 5: 347-362 More »
- Dragoo JL, Lieberman JR, Lee RS, Deugarte DA, Lee Y, Zuk PA, Hedrick MH, Benhaim P "Tissue-engineered bone from BMP-2-transduced stem cells derived from human fat." Plast Reconstr Surg 2005; 115: 6: 1665-73 More »
- Carlson GA, Dragoo JL, Samimi B, Bruckner DA, Bernard GW, Hedrick M, Benhaim P "Bacteriostatic properties of biomatrices against common orthopaedic pathogens." Biochem Biophys Res Commun 2004; 321: 2: 472-8 More »
- Dragoo JL, Lee RS, Benhaim P, Finerman GA, Hame SL "Relaxin receptors in the human female anterior cruciate ligament." Am J Sports Med 2003 Jul-Aug; 31: 4: 577-84 More »
10 publications: view full list