Cartilage and bone repair and regeneration using postpartum-derived cells

Abstract

Cells derived from postpartum tissue and methods for their isolation and induction to differentiate to cells of a chondrogenic or osteogenic phenotype are provided by the invention. The invention further provides cultures and compositions of the postpartum-derived cells and products related thereto. The postpartum-derived cells of the invention and products related thereto have a plethora of uses, including but not limited to research, diagnostic, and therapeutic applications, for example, in the treatment of bone and cartilage conditions.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS [0001] This claims benefit of U.S. Provisional Application Ser. No. 60 / 483,264, filed Jun. 27, 2003, the entire contents of which are incorporated by reference herein. Other related applications include the following commonly-owned, co-pending applications, the entire contents of each of which are incorporated by reference herein: U.S. application No. [ETH-5073 NP1], filed Jun. 25, 2004, U.S. application No. [ETH-5073 NP2], filed Jun. 25, 2004, U.S. application No. [ETH-5073 NP3], filed Jun. 25, 2004, U.S. application No. [ETH-5073 NP4], filed Jun. 25, 2004, U.S. application No. [ETH-5073 NP5], filed Jun. 25, 2004, U.S. application No. [ETH-5073 NP7], filed Jun. 25, 2004, and U.S. Provisional Application No. 60 / 555,908 [ETH 5127], filed Mar. 24, 2004. [ETH 5127], filed Mar. 24, 2004.FIELD OF THE INVENTION [0002] This invention relates to the field of mammalian cell biology and cell culture. In particular, the invention relates to cells derived...

AI Technical Summary

Problems solved by technology

Since the subchondral bone tissue is both innervated and vascularized, damage to this tissue is often painful.

The repair reaction induced by damage to the subchondral bone usually results in the formation of fibrocartilage at the site of the full-thickness defect.

Fibrocartilage, however, lacks the biomechanical properties of articular cartilage and fails to persist in the joint on a long term basis.

Partial-thickness defects are caused by mechanical arrangements of the joint which in turn induce wearing of the cartilage tissue within the joint.

In the absence of innervation and vasculature, partial-thickness defects do not elicit repair responses and therefore tend not to heal.

Although painless, partial-thickness defects often degenerate into full-thickness defects.

Cartilage may develop abnormally or may be damaged by disease, such as rheumatoid arthritis or osteoarthritis, or by trauma, each of which can lead to physical deformity and debilitation.

Whether cartilage is damaged from trauma or congenital anomalies, its successful clinical regeneration is often poor at best, as reviewed by Howell, et al.