Transforming growth factor‐β (TGF‐β) is considered the main inducer of both the α‐smooth muscle actin (α‐SMA) phenotype and collagen synthesis and deposition and plays a significant role in the tissue repair and the development of fibrosis. Since the PRP constitutes an important source of TGF‐β and its efficacy on the craniofacial bone repair remains controversy, the aim of this study was to evaluate the effect of PRP in the presence of levels of TGF‐β on PRP samples, as well as in the presence of collagen III and α‐SMA+ cells, while comparing these results by means of a histomorphometric analysis of the bone matrix and fibrous deposition on the bone repair. Four bone defects of 16 mm² were created on the calvarium of 21 rabbits. The surgical defects were treated with either particulate autograft, particulate autograft mixed with PRP and PRP alone. Animals were euthanized at 15, 30, and 45 days postoperative. Histomorphometric and immunohistochemical analyses were performed to assess repair time, as well as the expression of collagen III, and α‐SMA. The histomorphometric results demonstrated intensive deposition of fibrous tissue while hinder bone deposition occurred in PRP groups. These results coincided with higher values of the TGF‐β on the PRP sample, also larger occurrence of diffuse collagen III deposition and higher presence of α‐SMA+ cells spread among the fibrous tissue. Thus, the higher levels of TGF‐β associated with the both expression of collagen III and α‐SMA on defect treated with PRP suggest that its biomaterial induce an effect that can be considered similarly to a fibroproliferative disorder. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:457–463, 2011

Objective: To evaluate the association of bruxism phenotypes with single nucleotide polymorphisms in FKBP5, DRD2, ANKK1, and COMT. Methods: Clinical oral examination was performed to diagnose bruxism phenotypes in 150 children. DNA was collected from saliva. Logistic univariate regression, Chi-square, and Fisher’s exact tests were performed (p < 0.05). Results: Bruxism was associated with DRD2 (p = 0.02). Tooth grinding while awake was associated with ANKK1 (p < 0.001), and tooth grinding while asleep was associated with DRD2 in the additive (p = 0.030) and dominant (p = 0.008) model. Tooth clenching while awake was associated with ANKK1 in the additive (p = 0.005) and dominant (p = 0.008) models, whereas tooth clenching while asleep was associated with ANKK1 (p < 0.001) and with COMT in the additive (p = 0.001) and dominant (p = 0.003) models. Discussion: Polymorphisms in DRD2, ANKK1, and COMT are associated with bruxism phenotypes.