Penn Medicine scientists research use of stem cells for meniscus repair, implications for osteogenesis imperfecta: 4 things to know

Biologics

Philadelphia-based University of Pennsylvania Health system researchers at the McKay Orthopaedic Research Laboratory are developing new tissue engineering approaches to improve treatment for meniscus tears, the most common form of orthopedic surgery.

Here is what you need to know:

 

1. Meniscus tear surgery is on the rise, but may not be fully effective, as it removes only the torn part of a meniscus and leaves behind less of it to bear the same body weight as before.

 

2. Penn Medicine professor of orthopedic surgery Robert Mauck, PhD, and Jason Burdick, PhD, a bioengineering professor, are testing an implantable platform for wound healing. They use a microscopic scaffold containing a growth factor to attract stem cells. The scaffold is laced with an enzyme to loosen the matrix, and when they placed it in meniscus tissue from a cow, the matrix loosened, enabling bone stem cells to migrate to the scaffold and initiate the repair process.

 

"The immediate next step is to test this system in a large animal model to see if it can repair a meniscus tear," Dr. Mauck said. "This approach could possibly be in human trials in about five years."

 

3. Assistant professor of orthopedic surgery Joel Boerckel, PhD, along with doctoral student Christopher Kegelman, researches "brother/sister" proteins YAP and TAZ and their role in bone cell development and the matrix. They studied the proteins' individual and combined functions in the bone development of mice engineered to have YAP, TAZ or both deleted in skeletal stem cells. These mice did not complete stem cell differentiation and could not properly mobilize to sites of injury.

 

4. When both YAP and TAZ were deleted, mice showed characteristics similar to the brittle bone disease osteogenesis imperfecta, sustaining spontaneous bone fractures and defective bone matrix quality like human OI patients.

 

"YAP and TAZ regulate the expression of genes whose mutation in people is known to cause OI," said Dr. Boerckel. "We are now exploring whether and how this signaling pathway is involved in patients with OI."

 

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