Regeneration of bone and periodontal ligament induced by recombinant amelogenin after periodontitis.

Regeneration of mineralized tissues affected by chronic diseases comprises a major scientific and clinical challenge. Periodontitis, one such prevalent disease, involves destruction of the tooth-supporting tissues, alveolar bone, periodontal-ligament and cementum, often leading to tooth loss. In 1997, it became clear that, in addition to their function in enamel formation, the hydrophobic ectodermal enamel matrix proteins (EMPs) play a role in the regeneration of these periodontal tissues.

Amelogenin expression in long bone and cartilage cells and in bone marrow progenitor cells.

The amelogenin protein is considered as the major molecular marker of developing ectodermal enamel. Recent data suggest other roles for amelogenin beyond structural regulation of enamel mineral crystal growth. Here we describe our novel discovery of amelogenin expression in long bone cells, in cartilage cells, in cells of the epiphyseal growth plate, and in bone marrow stromal cells.

Amelogenin, a major structural protein in mineralizing enamel, is also expressed in soft tissues: brain and cells of the hematopoietic system.

The amelogenin protein is considered as the major molecular marker of developing and mineralizing ectodermal enamel. It regulates the shape, size, and direction of growth of the enamel mineral crystallite. Recent data suggest other roles for amelogenin beyond regulation of enamel mineral crystal growth.

Coverage of Miller class I and II recession defects using enamel matrix proteins versus coronally advanced flap technique: a 2-year report.

Background: The aim of this study was to evaluate a comparison of the coronally advanced flap procedure with or without the use of enamel matrix proteins in the treatment of recession defects.

Methods: This 2-year study was conducted as a blinded, split-mouth, placebo-controlled, and randomized design. Thirty patients from two dental schools with two paired buccal recession defects were chosen.