An improved polymer orthopedic implant and a method for making the same, where a portion of the implant for engagement with a patient's bone has a rough texture for encouraging micro-ingrowth between the bone and the implant. Substantially all remaining non-bone engaging portions of the implant are smooth for discouraging tissue ingrowth with the implant. The non-bone engaging portions of the implant are polished smooth, and are preferably transparent or translucent. The implant may be comprised of a slow reacting polymethylmethacrylate acrylic.

A treatment for bioprosthetic tissue used in implants or for assembled bioprosthetic heart valves to reduce in vivo calcification is disclosed. The method includes preconditioning, pre-stressing, or pre-damaging fixed bioprosthetic tissue in a manner that mimics the damage associated with post-implant use, while, and/or subsequently applying a calcification mitigant such as a capping agent or a linking agent to the damaged tissue. The capping agent suppresses the formation of binding sites in the tissue that are exposed or generated by the damage process (service stress) and otherwise would, upon implant, attract calcium, phosphate, immunogenic factors, or other precursors to calcification. The linking agent will act as an elastic reinforcement or shock-absorbing spring element in the tissue structure at the site of damage from the pre-stressing. In one method, tissue leaflets in assembled bioprosthetic heart valves are preconditioned by simulating actual flow conditions for a predetermined number of cycles, during or after which the valve is exposed to the capping agent.

The present invention relates to methods for inhibiting stenosis, obstruction, or calcification of a valve following implantation of a valve prosthesis or a native valve which develops disease via the Lrp5/Wnt Pathway in the presence of elevated lipids due to elevated Low Density Lipoprotein. This invention involves dispensing a combination of medications to target inflammation and attachment of the target cell and the secondary drugs to inhibit proliferation and calcification on an elastical stent, gortex graft or valve leaflet. The combination therapy inhibits bioprosthesis and native valve calcification with improvement of the longevity of the prosthetic material including the stent, the native valve, and the gortex covering. The valve prosthesis and or gortex graft is mounted on the elastical stent or prosthesis such that the elastical stent is connected to the valve.

The present invention is directed to compositions and methods for the prevention or treatment of treatment of heterotopic ossification, vascular calcification, or pathologic calcification.

A bioprosthetic tissue having a reduced propensity to calcify in vivo, the bioprosthetic tissue. The bioprosthetic tissue comprises an aldehyde cross-linked and stressed bioprosthetic tissue comprising exposed calcium, phosphate or immunogenic binding sites that have been reacted with a calcification mitigant. The bioprosthetic tissue has a reduced propensity to calcify in vivo as compared to aldehyde cross-linked bioprosthetic tissue that has not been stressed and reacted with the calcification mitigant.

The invention is to articles of extracellular matrix. The articles comprise one or more sheets of mammalian extracellular matrix laminated together. A single sheet can be folded over and laminated on 3 sides. Two or more sheets can be laminated to each other at their edges. The sheets can further encase a composition comprising a cell or cells, such as for example, a stem cell. A single sheet can be folded over to encase a composition, or rolled to encase a composition with lamination at either end of the roll, for example. The invention also includes methods of using these articles to regenerate tissue at tissue defects, or heal wounds in damaged tissue.

A tissue prosthesis comprising an extracellular matrix (ECM) composition, the ECM composition comprising decellularized ECM derived from mesothelial tissue and an exogenously added basic fibroblast growth factor (bFGF).

A sheet structure formed from an extracellular matrix (ECM) composition that includes acellular ECM derived from small intestine submucosa (SIS) tissue, gentamicin and vancomycin. The sheet structure is configured to modulate inflammation of damaged biological tissue and induce cell and tissue proliferation, bioremodeling of the damaged biological tissue, and regeneration of new tissue and tissue structures with site-specific structural and functional properties, when the tissue structure is delivered to the damaged biological tissue.

The present invention relates to self-regenerating antioxidant catalysts and methods of using the same.

A bioremodelable encasement structure comprising a pouch formed from at least one sheet of bioremodelable material, the pouch including an internal region that is configured to receive a device therein, the bioremodelable material comprising mesothelial tissue.