ABSTRACT
BACKGROUND@#The casein kinase 2-interacting protein-1 (CKIP-1) is important in the development of osteoblasts and cardiomyocytes. However, the effects of CKIP-1 on osteoblast precursor mesenchymal stem cells (MSCs) remain unclear. This study aimed to determine whether CKIP-1 affects osteogenic differentiation in MSCs and explore the relationship of CKIP-1 and inflammation.@*METHODS@#Bone marrow MSCs of CKIP-1 wild type (WT) and knockout (KO) mice were cultivated in vitro. Cell phenotype was analyzed by flow cytometry, colony formation was detected to study the proliferative ability. Osteogenic and adipogenic induction were performed. The osteogenic ability was explored by alizarin red staining, alkaline phosphatase (ALP) staining and ALP activity detection. Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to determine the mRNA expression levels of osteoblast marker genes. The adipogenic ability was detected by oil red O staining. Content of the bone was analyzed to observe the differences of bone imaging parameters including trabecular bone volume/tissue volume (BV/TV), bone surface area fraction/trabecular BV, trabecular number (Tb.N), and trabecular spacing (Tb.sp). Interleukin (IL)-1β was injected on WT mice of 2 months old and 18 months old, respectively. Difference in CKIP-1 expression was detected by RT-PCR and western blot. The relationship between CKIP-1 and inflammation was explored by RT-PCR and western blot.@*RESULTS@#ALP assays, alizarin red staining, and qRT-PCR showed that MSCs derived from CKIP-1 KO mice exhibited a stronger capability for osteogenesis. Micro-computed tomography detection showed that among 18-month-old mice, CKIP-1 KO mice presented significantly higher bone mass compared with WT mice (P = 0.02). No significant difference was observed in 2-month-old mice. In vivo data showed that expression of CKIP-1 was higher in the bone marrow of aging mice than in young mice (4.3-fold increase at the mRNA level, P = 0.04). Finally, the expression levels of CKIP-1 in bone marrow (3.2-fold increase at the mRNA level, P = 0.03) and cultured MSCs were up-regulated on chronic inflammatory stimulation by IL-1β.@*CONCLUSIONS@#CKIP-1 is responsible for negative regulation of MSC osteogenesis with age-dependent effects. Increasing levels of inflammation with aging may be the primary factor responsible for higher expression levels of CKIP-1 but may not necessarily affect MSC aging.
ABSTRACT
Objective Coralline hydroxyapatite (CHA),in comparison with Bio-Oss bone meal,is a material with extensive resources but no immunogenicity or risk of disease-transmission. The aim of this article was to study the clinical application of CHA in ridge preservation in the maxillary anterior zone. Methods Twenty-six patients underwent extraction of maxillary anterior teeth (n=26) for chronic periodontitis or periapical periodontitis. The patients were randomly assigned into a CHA and a control group of equal number to receive ridge preservation with CHA and Bio-Oss bone meal respectively. Cone beam computed tomography (CBCT) was performed immediately and at 4 months after ridge preservation to compare the vertical and horizontal alterations of the alveolar ridge be-tween the two groups of patients. Results After ridge preservation,both the CHA and control groups showed a reduction in the width ([1.1±0.7] vs [1.3±1.9] mm) and height of the alveolar ridge ([1.3±1.6] vs [1.2±1.4] mm),but with no statistically significant differences between the two groups (P<0.05). Conclusion For ridge preservation in the maxillary anterior zone,CHA has a similar effect to that of Bio-Oss bone meal and therefore is an ideal material for bone graft.
ABSTRACT
<p><b>OBJECTIVE</b>To identify a rare α-thalassemia gene mutation in a family from south China and perform a pedigree analysis and genetic diagnosis of hemoglobin H (HbH) disease caused by this mutation.</p><p><b>METHODS</b>Peripheral blood samples were collected from the family members for analysis of the hematological phenotype and routine test of thalassemia genes. DNA sequencing was carried out for samples that showed genotype and phenotype inconsistency.</p><p><b>RESULTS</b>A rare α-thalassemia *92A>G gene mutation was detected within this family. The proband and his sister were confirmed to have non-deletional HbH disease with α--/αα genotype. The proband's brother was confirmed to have an α-thalassemia trait with the genotype of -α/αα. The proband's father was identified as an α-thalassemia silent carrier with the genotype of αα/αα.</p><p><b>CONCLUSION</b>A rare α-thalassemia *92A>G gene mutation was identified for first time in south China. The description of the basic phenotypic characteristics of α-thalassemia trait and silent carrier caused by this mutation enriches the α-thalassemia gene mutation spectrum in Chinese population and helps in population screening, clinical molecular diagnosis and genetic counseling.</p>