The present invention relates to a device for the topical treatment of pain affecting the vulvar area of the female human genital organ, a formulation for use in the device according to the invention, and a kit comprising the device according to the present intention. Additionally, the present invention relates to a method of topical treatment of pain affecting the vulvar area of the female human genital organ, said method using the device according to the present invention. The device is a layered article shaped to be placed in use inside a female undergarment and at least partially in skin contact with the female vulvar area and comprises a topical formulation.

Disclosed herein are implantable and non-implantable devices coated with an anti-TRAP agent. A system is also disclosed comprising an implantable device or a non-implantable device and a tissue-injectable/infusible liquid, oil or gel comprising an anti-TRAP agent. A system incorporating a drug-injecting pen is described. Medical biomaterials that inhibit TRAPs are discussed, as well as air pouch models for analyzing products and materials. Corresponding methods also are described.

The present invention provides a method of promoting local bone growth by administering a therapeutic amount of a Sost antagonist to a mammalian patient in need thereof. Preferably, the Sost antagonist is an antibody or FAB fragment selectively recognizing any one of SEQ ID NOS: 1-23. The Sost antagonist may be coadministered together or sequentially with a matrix conducive to anchoring new bone growth. Orthopedic and Periodontal devices comprising an implantable portion adapted to be permanently implanted within a mammalian body and bearing an external coating of a Sost antagonist are also disclosed, as it a method of increasing bone density by administering to a mammalian patient a therapeutic amount of a Sost antagonist together with an antiresorptive drug.

Medical devices comprising an anti-connexin agent suitable for introduction into a subject.

The invention relates to a method for healing blood vessels by stimulating the formation of a confluent endothelial autologous cell layer in vivo on an implantable metallic stent having a lumen and a luminal surface, and an exterior surface. More specifically, the method includes implanting the stent with a coating in a patient in need of thereof; wherein the coating includes one or more layers of a matrix covalently adherent on said luminal and exterior surface of said stent containing one or more pharmaceutical substances on said exterior surface and a therapeutically effective amount of a single type of antibody, antibody fragments or combinations thereof being compatible to binding selectively to a specific cell surface antigen of circulating autologous endothelial progenitor cells in peripheral blood. In addition, genetically engineered endothelial progenitor cells can be captured on said luminal surface of stent in vivo, to proliferate to form rapidly a confluent endothelium in situ.

The present invention comprises compositions, methods, and devices for delivering angiogenic factors and signaling molecules to a target tissue, and controlling the release of these factors and signaling molecules to spatially and temporally restrict their release and dissemination, for the purpose of promoting angiogenesis in target tissues wherein increased blood supply is needed.

Disclosed herein are compositions comprising a polymer and a metabolic inhibitor, as well as a method of using the composition to modulate an immune response. The composition may be produced in the form of a synthetic tissue for provision in a subject. The composition or synthetic tissue may further comprise additional therapeutic agents.

Systems and methods to eliminate or reduce the foreign body response (FBR) that occurs when a medical device is implanted into a patient. The FBR causes a chronic inflammatory response that leads to the encapsulation of a medical device by a fibrous capsule. Macrophages have been discovered to become persistent as a result of the implanted biomaterial which occurs by an up-regulation in cFLIP. This persistence of macrophages appears to be the primary driver of the FBR. Re-sensitizing macrophages to apoptosis using a small molecule inhibitor (e.g., YM155) of cFLIP will abrogate the formation of the fibrous capsule in the FBR.

Disclosed herein are compositions comprising a polymer and a metabolic inhibitor, as well as a method of using the composition to modulate an immune response. The composition may be produced in the form of a synthetic tissue for provision in a subject. The composition or synthetic tissue may further comprise additional therapeutic agents.

A layered composite for scar treatment and prevention, the layered composite including a backing section; a drug matrix section; and a skin-interfacing section. The drug matrix section may be disposed between the back section and the skin-interfacing section. The drug matrix section may include pirfenidone in an amount of from about 1 to about 20 mg/cm.sup.2. The layered composite may provide greater than about 75% release of the pirfenidone over a period of about 48 to 72 hours. A method for scar treatment and prevention that includes applying a layered composite as described to a burn wound.