Immobilization in external rotation after an initial shoulder dislocation reduces the risk of recurrence compared with that associated with the conventional method of immobilization in internal rotation. This treatment method appears to be particularly beneficial for patients who are thirty years of age or younger.

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Bone morphogenetic protein 4 (BMP4) and growth/differentiation factor 5 (GDF5) are closely related protein family members and regulate early cartilage patterning and differentiation. In this study, we compared the functional outcome of their actions systematically at various stages of chondrogenesis in mouse embryonic limb bud mesenchyme grown in micromass cultures. Overall, both growth factors enhanced cartilage growth and differentiation in these cultures. Uniquely, BMP4 not only accelerated the formation and maturation of cartilaginous nodules, but also induced internodular mesenchymal cells to express cartilage differentiation markers. On the other hand, GDF5 increased the number of prechondrogenic mesenchymal cell condensation and cartilaginous nodules, without altering the overall pattern of differentiation. In addition, GDF5 caused a more sustained elevated expression level of Sox9 relative to that associated with BMP4. BMP4 accelerated chondrocyte maturation throughout the cultures and sustained an elevated level of Col10 expression, whereas GDF5 caused a transient increase in Col10 expression. Taken together, we conclude that BMP4 is instructive to chondrogenesis and induces mesenchymal cells toward the chondrogenic lineage. Furthermore, BMP4 accelerates the progression of cartilage differentiation to maturation. GDF5 enhances cartilage formation by promoting chondroprogenitor cell aggregation, and amplifying the responses of cartilage differentiation markers. These differences may serve to fine-tune the normal cartilage differentiation program, and can be exploited for the molecular manipulation in biomimetics.

Amelogenins, major components of developing enamel, are predominantly involved in the formation of tooth enamel. Although amelogenins are also implicated in cementogenesis, their precise spatial expression pattern and molecular role are not clearly understood. Here, we report for the first time the expression of two alternate splice forms of amelogenins, M180 and the leucine-rich amelogenin peptide (LRAP), in the periodontal region of mouse tooth roots. Lack of M180 and LRAP mRNA expression correlated with cementum defects observed in the amelogenin-null mice. The cementum defects were characterized by an increased presence of multinucleated cells, osteoclasts, and cementicles. These defects were associated with an increased expression of the receptor activator of the nuclear factor-B ligand (RANKL), a critical regulator of osteoclastogenesis. These findings indicate that the amelogenin splice variants, M180 and LRAP, are critical in preventing abnormal resorption of cementum.Ameloblasts synthesize and secrete amelogenins into the dental enamel matrix that undergo systematic proteolysis during enamel mineralization. Numerous mutations were found in the amelogenin coding sequences in patients with the most common genetic disorder affecting enamel, amelogenesis imperfecta (1-5). The targeted disruption of the amelogenin gene locus in mice also showed a hypoplastic enamel phenotype similar to amelogenesis imperfecta, confirming an important role of amelogenins in enamel formation (6).In addition to their role in enamel formation, amelogenins are also believed to play a key role in the formation of root cementum, a mineralized layer on the surface of root dentin (7,8). During cementogenesis, Hertwig's epithelial root sheath dissociates to form cell aggregates (epithelial rests of Malassez) that are located between the alveolar bone and the tooth root. The mesenchyme-derived cementoblasts secrete cementum matrix onto the root surface to form cementum. The presence of amelogenins was detected on the tooth root surface close to the site of acellular cementum (9) and in the epithelial remnants of the root sheath in rat molars (10), indicating their potential role during cementogenesis. Interestingly, amelogenins were also detected in Hertwig's epithelial root sheath cells and the epithelial rests of Malassez (11-13). Therapeutic application of an enamel matrix derivative (EMDOGAIN®, Biora AB, Malmö, Sweden) rich in amelogenins resulted in regeneration of cementum, the surrounding alveolar bone, and periodontal ligament (PDL) 1 in the experimental treatment of periodontitis (14 -17). However, it is not clear from these studies whether the amelogenin or non-amelogenin components of an enamel matrix derivative regulate regeneration of cementum and periodontal tissues.The present study was undertaken to investigate the expression of various alternate splice forms of amelogenins in tooth roots and correlate their expression with the cementum defects observed in amelogenin-null mice teeth. Herein, we report the expression of ...