The impact of dietary consistency on structural craniofacial components: Temporomandibular joint/condyle, condylar cartilage, alveolar bone and periodontal ligament. A systematic review and meta-analysis in experimental in vivo research.

OBJECTIVE: The aim of this systematic review was to provide a comprehensive synthesis of available evidence evaluating the effect of dietary loading on temporomandibular joint/condyle, condylar cartilage, alveolar bone of the mandible and the periodontal ligament in healthy mice and rats. DESIGN: Medline via PubMed, EMBASE and Open Grey databases were searched for published and unpublished literature. Search terms included "mandiblular condyle", "alveolar bone", "temporomandibular joint", "condylar cartilage", "periodontal ligament", "rat", "mice". After data extraction, risk of bias (SYRCLE) and reporting quality (ARRIVE) were assessed. Random effects meta-analyses were performed for the outcomes of interest where applicable. RESULTS: A total of 33 relevant articles were considered in the systematic review, while only 6 studies were included in the quantitative synthesis. Risk of Bias in all studies was judged to be unclear to high overall, while reporting quality was suboptimal. Comparing soft to hard diet animals, significantly reduced anteroposterior condylar length (4 studies, weighted mean difference: -0.40 mm; 95% CI: -0.47, -0.32; p < 0.001) and width (4 studies, weighted mean difference: -0.043 mm; 95% CI: -0.51, -0.36; p < 0.001) were found in rats. Decreased anteroposterior condylar dimensions were detected for mice as well (2 studies, weighted mean difference: -0.049; 95% CI: -0.56, -0.43; p < 0.001). CONCLUSIONS: Overall, there was strong evidence to suggest a significant effect of soft diet on reduced condylar dimensions in rodents; however, there is need for further high quality experimental studies to inform current knowledge on condylar cartilage, alveolar bone and periodontal ligament related outcomes.

Putative functions of extracellular matrix glycoproteins in secondary palate morphogenesis.

Cleft palate is a common birth defect in humans. Elevation and fusion of paired palatal shelves are coordinated by growth and transcription factors, and mutations in these can cause malformations. Among the effector genes for growth factor signaling are extracellular matrix (ECM) glycoproteins. These provide substrates for cell adhesion (e.g., fibronectin, tenascins), but also regulate growth factor availability (e.g., fibrillins). Cleft palate in Bmp7 null mouse embryos is caused by a delay in palatal shelf elevation. In contrast, palatal shelves of Tgf-ß3 knockout mice elevate normally, but a cleft develops due to their failure to fuse. However, nothing is known about a possible functional interaction between specific ECM proteins and Tgf-ß/Bmp family members in palatogenesis. To start addressing this question, we studied the mRNA and protein distribution of relevant ECM components during secondary palate development, and compared it to growth factor expression in wildtypewild type and mutant mice. We found that fibrillin-2 (but not fibrillin-1) mRNA appeared in the mesenchyme of elevated palatal shelves adjacent to the midline epithelial cells, which were positive for Tgf-ß3 mRNA. Moreover, midline epithelial cells started expressing fibronectin upon contact of the two palatal shelves. These findings support the hypothesis that fibrillin-2 and fibronectin are involved in regulating the activity of Tgf-ß3 at the fusing midline. In addition, we observed that tenascin-W (but not tenascin-C) was misexpressed in palatal shelves of Bmp7-deficient mouse embryos. In contrast to tenascin-C, tenascin-W secretion was strongly induced by Bmp7 in embryonic cranial fibroblasts in vitro. These results are consistent with a putative function for tenascin-W as a target of Bmp7 signaling during palate elevation. Our results indicate that distinct ECM proteins are important for morphogenesis of the secondary palate, both as downstream effectors and as regulators of Tgf-ß/Bmp activity.