The SIBLING proteins are a family of non-collagenous proteins (NCPs) previously thought to be expressed only in dentin but have been demonstrated in other mineralized and non-mineralized tissues. They are believed to play vital roles in both osteogenesis and dentinogenesis. Since they are tightly regulated lifelong processes and involve a peak of mineralization, three different age groups were investigated.
View Article and Find Full Text PDFClin Adv Periodontics
September 2022
Focused Clinical Question: What is the key clinically controllable preventive measure that may help reduce the incidence of biological complications?
Summary: Implant complications are common, ineffective care, and delay in diagnosis can lead to expensive time-consuming surgical and nonsurgical interventions. Careful selection and placement of implant allow development of adequate emergence design of the implant suprastructure. This helps achieve effective plaque control, adequate maintenance at hygiene visits, accurate follow-up assessments of the peri-implant tissues addressing the key underlying factor impacting biological complications.
Objective: To better understand the potential effects after corticotomy accelerated osteogenic orthodontic treatment (CAOOT).
Setting And Sample Population: Systematic review with meta-analysis.
Materials And Methods: A literature search up to August 2018 was conducted to identify randomized clinical studies (RCTs) on CAOOT reporting periodontal parameters, bone changes, patient-centred and short- and long-term adverse outcomes.
Birth Defects Res A Clin Mol Teratol
September 2013
Background: Mutations in Fibroblastic Growth Factor Receptors (FGFR) have been associated with human craniosynostotic birth defects like Crouzon syndrome. Several anecdotes and case reports have indicated higher incidence of gastrointestinal tract disorders in FGFR-associated craniosynostotic birth defects. Our objective was to characterize esophageal defects in a mouse model of human Crouzon syndrome, with a mutation in codon 290 of FGFR2.
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