Orthodontic treatment of patients with cleidocranial dysplasia Systematic review of the literature

Lizończyk, Barbara; Pielech, Kinga; M, Panas; Stós, Wojciech

doi:10.5114/for.2020.102228

Cited by 1 publication

(1 citation statement)

References 17 publications

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“…RUNX2 encodes an essential transcription factor for osteoblast differentiation and skeletal development [10]. Due to the dental symptoms, many CCD patients require orthodontic treatment (Figure 1) [11,12].…”

Section: Introductionmentioning

confidence: 99%

Impact of Mechanical Strain and Nicotinamide on RUNX2-Deficient Osteoblast Mimicking Cleidocranial Dysplasia

Schröder,

Örs,

Byeon

et al. 2023

IJMS

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Cleidocranial dysplasia (CCD) is a rare genetic defect caused by a heterozygous mutation of runt-related transcription factor 2 (RUNX2), which is important for osteoblast and skeletal development. RUNX2-deficiency causes extra- and intra-oral malformations that often require orthodontic treatment. Nicotinamide (NAM) affects bone remodelling processes. As these are crucial for orthodontic therapy, NAM could improve orthodontic treatment in CCD patients. This study investigates the effect of NAM in control and RUNX2-deficient osteoblasts under mechanical strain mimicking orthodontic treatment. First, the optimal NAM concentration and the differences in the expression profile of control and RUNX2-deficient osteoblasts were determined. Subsequently, osteoblasts were exposed to tensile and compressive strain with and without NAM, and the expression of genes critically involved in bone remodelling was investigated. NAM increased the expression of bone remodelling genes. RUNX2-deficient osteoblasts expressed more receptor activator of NFkB ligand (RANKL) and interleukin-6 (IL6), but less colony-stimulating factor-1 (CSF1). Most of the positive effects of NAM on bone remodelling genes were impaired by mechanical loading. In conclusion, NAM stimulated osteoblast differentiation by increasing the expression of RUNX2 and regulated the expression of osteoclastogenic factors. However, the positive effects of NAM on bone metabolism were impaired by mechanical loading and RUNX2 deficiency.

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Section: Introductionmentioning

confidence: 99%