Objectives: To investigate the effect of experimental diabetes and metabolic control on intramembranous bone healing following guided bone regeneration (GBR).
Material And Methods: Ninety-three Wistar rats were allocated to three experimental groups, healthy (H), uncontrolled diabetes (D) and controlled diabetes (CD). Twenty one days following diabetes induction, a standardised 5-mm defect was created at the mid-portion of each parietal bone. In 75 animals (25H, 25D, 25CD), one defect was treated with an intracranial and extracranial membrane according to the GBR principle, and one defect was left empty (control); five animals per group were then randomly sacrificed at 3, 7, 15, 30 and 60 days and processed for decalcified histology. In 18 animals (6H, 6D, 6CD), both defects were treated according to the GBR principle; three animals from each group were then randomly sacrificed at 7 and 15 days of healing and employed for gene expression analysis.
Results: Application of the GBR therapeutic principle led to significant bone regeneration even in the D group. However, at 15 and 30 days, the osteogenesis process was impaired by uncontrolled diabetes, as shown by the significant reduction in terms of defect closure (38-42%) and newly formed bone (54-61%) compared to the healthy group. The comparison of the D vs. H group at 15 days of healing yielded the largest number of genes with significantly differential expression, among which various genes associated with the ossification process (bmp4, ltbp4, thra and cd276) were identified.
Conclusions: Uncontrolled diabetes seems to affect early phases of the bone regeneration following GBR. A misregulation of genes and pathways related to cell division, energy production, inflammation and osteogenesis may account for the impaired regeneration process in D rats. Further studies are warranted to optimise the GBR process in this medically compromised patient population.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/clr.13031 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Exosomes in Oral Diseases: Mechanisms and Therapeutic Applications.
Drug Des Devel Ther
January 2025
Department of Stomatology, China Academy of Chinese Medical Sciences, Xiyuan Hospital, Beijing, 100091, People's Republic of China.
Exosomes, small extracellular vesicles secreted by various cells, play crucial roles in the pathogenesis and treatment of oral diseases. Recent studies have highlighted their involvement in orthodontics, periodontitis, oral squamous cell carcinoma (OSCC), and hand, foot, and mouth disease (HFMD). Exosomes have a positive effect on the inflammatory environment of the oral cavity, remodeling and regeneration of oral tissues, and offer promising therapeutic options for bone and periodontal tissue restoration.
View Article and Find Full Text PDFRational construction of PCL-PEG/CS/AST nanofiber for bone repair and regeneration.
Front Bioeng Biotechnol
January 2025
Department of Sports Medicine, The Second Affiliated Hospital of Fujian University of Traditional Chinese Medicine (FJTCM), Fuzhou, China.
Humerus greater tuberosity (HGT) avulsion fracture is one of the most common types of proximal humerus fractures. The presence of motion and gap lead to the failure of implants, due to the force pulling from the supraspinatus. In this work, electrospinning technology was applied to fabricate PCL-PEG/CS/AST nanofiber with superior biocompatibility and mechanical property.
View Article and Find Full Text PDFGBR assisted Onlay bone grafting for the posterior maxillary horizontal ridge augmentation: a case report and literature review.
Front Bioeng Biotechnol
January 2025
Hospital of Stomatogy, Jilin University, Changchun, China.
The posterior mandible is the primary area for occlusal function. However, long-term tooth loss in the posterior mandible often leads to rapid absorption of both buccal and lingual trabecular bone plates and subsequent atrophy of the alveolar ridge. This ultimately results in horizontal bone deficiencies that complicate achieving an optimal three-dimensional placement for dental implants.
View Article and Find Full Text PDFEnhancing Periodontal Ligament Regeneration via PDLSC Delivery Using Electrospun PCL/Collagen/Cellulose Acetate Scaffolds and Collagen Hydrogel Incorporated with Curcumin-Loaded ZIF-8 Nanoparticles.
Int J Nanomedicine
January 2025
Department of Stomatology, Shanxi Bethune Hospital, Shanxi Academy of Medical Science, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China.
Background: Regenerating periodontal ligament (PDL) tissue is a vital challenge in dentistry that aims to restore periodontal function and aesthetics. This study explores a tissue engineering strategy that combines polycaprolactone (PCL)/collagen/cellulose acetate electrospun scaffolds with collagen hydrogels to deliver curcumin-loaded ZIF-8 nanoparticles fand periodontal ligament stem cells (PDLSCs).
Methods: Scaffolds were fabricated via electrospinningand collagen hydrogels incorporated PDLSCs and curcumin-loaded ZIF-8 nanoparticles (CURZIF-8) were developed using cross-linking.
Biomaterial Cues for Regulation of Osteoclast Differentiation and Function in Bone Regeneration.
Adv Ther (Weinh)
January 2025
Division of Plastic & Reconstructive Surgery, University of California, Los Angeles David Geffen School of Medicine, Los Angeles, CA, 90095, USA.
Tissue regeneration involves dynamic dialogue between and among different cells and their surrounding matrices. Bone regeneration is specifically governed by reciprocity between osteoblasts and osteoclasts within the bone microenvironment. Osteoclast-directed resorption and osteoblast-directed formation of bone are essential to bone remodeling, and the crosstalk between these cells is vital to curating a sequence of events that culminate in the creation of bone tissue.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!