Gene Therapy of Bone Morphogenetic Protein for Periodontal Tissue Engineering

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141217/1/jper0202.pd

Periostin Is Essential for the Integrity and Function of the Periodontal Ligament During Occlusal Loading in Mice

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141255/1/jper1480.pd

Divergence of the systemic immune response following oral infection with distinct strains of P orphyromonas gingivalis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94514/1/omi12001.pd

3D-Printed Scaffolds and Biomaterials: Review of Alveolar Bone Augmentation and Periodontal Regeneration Applications Farah

To ensure a successful dental implant therapy, the presence of adequate vertical and horizontal alveolar bone is fundamental. However, an insufficient amount of alveolar ridge in both dimensions is often encountered in dental practice due to the consequences of oral diseases and tooth loss. Although postextraction socket preservation has been adopted to lessen the need for such invasive approaches, it utilizes bone grafting materials, which have limitations that could negatively affect the quality of bone formation. To overcome the drawbacks of routinely employed grafting materials, bone graft substitutes such as 3D scaffolds have been recently investigated in the dental field. In this review, we highlight different biomaterials suitable for 3D scaffold fabrication, with a focus on "3D-printed" ones as bone graft substitutes that might be convenient for various applications related to implant therapy. We also briefly discuss their possible adoption for periodontal regeneration

C-Telopeptide Pyridinoline Cross-Links: Sensitive Indicators of Periodontal Tissue Destruction

C-telopeptides and related pyridinoline cross-links of bone Type I collagen are sensitive markers of bone resorption in osteolytic diseases such as osteoporosis and osteoarthritis. We have studied the release of C-telopeptide pyridinoline crosslinks of Type I collagen as measures of bone destruction in periodontal disease. Studies in preclinical animal models and humans have demonstrated the relationship between radiographic bone loss and crevicular fluid C-telopeptide levels. We have recently found that C-telopeptide levels correlate strongly with microbial pathogens associated with periodontitis and around endosseous dental implants. Host-modulation of bone-related collagen breakdown has been shown by studies in humans demonstrating that MMP inhibition blocks tissue destruction and release of C-telopeptides in patients with active periodontal disease.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72598/1/j.1749-6632.1999.tb07698.x.pd

Effect of Systemic Matrix Metalloproteinase Inhibition on Periodontal Wound Repair: A Proof of Concept Trial

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141196/1/jper0441.pd

PDGF-B gene therapy accelerates bone engineering and oral implant osseointegration

Platelet-derived growth factor-BB (PDGF-BB) stimulates repair of healing-impaired chronic wounds such as diabetic ulcers and periodontal lesions. However, limitations in predictability of tissue regeneration occur due, in part, to transient growth factor bioavailability in vivo. Here, we report that gene delivery of PDGF-B stimulates repair of oral implant extraction socket defects. Alveolar ridge defects were created in rats and were treated at the time of titanium implant installation with a collagen matrix containing an adenoviral (Ad) vector encoding PDGF-B (5.5 x 10(8) or 5.5 x 10(9) pfu ml(-1)), Ad encoding luciferase (Ad-Luc; 5.5 x 10(9) pfu ml(-1); control) or recombinant human PDGF-BB protein (rhPDGF-BB, 0.3 mg ml(-1)). Bone repair and osseointegration were measured through backscattered scanning electron microscopy, histomorphometry, micro-computed tomography and biomechanical assessments. Furthermore, a panel of local and systemic safety assessments was performed. Results indicated that bone repair was accelerated by Ad-PDGF-B and rhPDGF-BB delivery compared with Ad-Luc, with the high dose of Ad-PDGF-B more effective than the low dose. No significant dissemination of the vector construct or alteration of systemic parameters was noted. In summary, gene delivery of Ad-PDGF-B shows regenerative and safety capabilities for bone tissue engineering and osseointegration in alveolar bone defects comparable with rhPDGF-BB protein delivery in vivo

Periodontal Therapy Influences DNA Methylation of Inflammatory Genes in Chronic Periodontitis=La terapia parodontale influenza la metilazione del DNA di geni infiammatori nella malattia parodontale cronica

Aim: To evaluate the influence of periodontal therapy on epigenetic modifications in chronic periodontitis patients compared to healthy individuals. Methods: Ten patients with healthy periodontium and ten patients with chronic moderate periodontitis were enrolled. Gingival biopsies were collected at baseline for both groups and at 2 & 8 weeks post-periodontal therapy for the disease group (from normal and periodontitis sites). Random-intercept linear regression models were applied to evaluate methylation levels across groups at baseline and to assess changes in the disease group overtime, separately for normal and periodontitis sites. Results: Periodontal therapy restored methylation levels of TNF-\u3b1, IFN-\u3b3 and COX-2 genes in periodontitis sites after 2 & 8 weeks to levels reported in normal sites. A DNA methylation gradient of COX-2 promoter region was observed at baseline for healthy group and periodontitis group (percentage mean in normal sites = 8.8 \ub1 5.7, p= 0.47 vs healthy; percentage mean in periodontitis sites = 13.2 \ub1 7.3, p = 0.03 vs healthy). Maintenance of high LINE-1 methylation on periodontitis sites was observed throughout all data points, suggesting up-regulation of methyltransferase in chronic disease. Conclusions: Periodontal therapy resets the DNA methylation of inflammatory genes to levels observed in normal sites. Maintenance of high levels of DNA methylation was higher in periodontitis sites, reflecting methyl-transferase up-regulation in chronic disease