Purpose-Growth factors such as platelet-derived growth factor (PDGF) exert potent effects on wound healing including the regeneration of periodontia. Pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) is a well-known biomarker of bone turnover, and as such is a potential indicator of osseous metabolic activity. The objective of this study was to evaluate the release of the ICTP into the periodontal wound fluid (WF) following periodontal reconstructive surgery using local delivery of highly purified recombinant human PDGF (rhPDGF)-BB.Methods-Forty-seven human subjects at five treatment centres possessing chronic severe periodontal disease were monitored longitudinally for 24 weeks following PDGF regenerative surgical treatment. Severe periodontal osseous defects were divided into one of three groups and treated at the time of surgery with either: β-tricalcium phosphate (TCP) osteoconductive scaffold alone (active control), β-TCP+0.3 mg/ml of rhPDGF-BB, or β-TCP+1.0 mg/ml of rhPDGF-BB. WF was harvested and analysed for local ICTP levels by radioimmunoassay. Statistical analysis was performed using analysis of variance and an area under the curve analysis (AUC).Results-The 0.3 and 1.0 mg/ml PDGF-BB treatment groups demonstrated increases in the amount of ICTP released locally for up to 6 weeks. There were statistically significant differences at the week 6 time point between β-TCP carrier alone group versus 0.3 mg/ml PDGF-BB group (p<0.05) and between β-TCP alone versus the 1.0 mg/ml PDGF-BB-treated lesions (p<0.03). The AUC analysis revealed no statistical differences amongst groups.Conclusion-This study corroborates the release of ICTP as a measure of active bone turnover following local delivery of PDGF-BB to periodontal osseous defects. The amount of ICTP released from the WF revealed an early increase for all treatment groups. Data from this study suggests that when PDGF-BB is delivered to promote periodontal tissue engineering of tooth-supporting osseous defects, there is a direct effect on ICTP released from the wound.
The ribosome is an evolutionarily conserved organelle essential for cellular function. Ribosome construction requires assembly of approximately 80 different ribosomal proteins (RPs) and four different species of rRNA. As RPs co-assemble into one multi-subunit complex, mutation of the genes that encode RPs might be expected to give rise to phenocopies, in which the same phenotype is associated with loss-of-function of each individual gene. However, a more complex picture is emerging in which, in addition to a group of shared phenotypes, diverse RP gene-specific phenotypes are observed. Here we report the first two mouse mutations (Rps7Mtu and Rps7Zma) of ribosomal protein S7 (Rps7), a gene that has been implicated in Diamond-Blackfan anemia. Rps7 disruption results in decreased body size, abnormal skeletal morphology, mid-ventral white spotting, and eye malformations. These phenotypes are reported in other murine RP mutants and, as demonstrated for some other RP mutations, are ameliorated by Trp53 deficiency. Interestingly, Rps7 mutants have additional overt malformations of the developing central nervous system and deficits in working memory, phenotypes that are not reported in murine or human RP gene mutants. Conversely, Rps7 mouse mutants show no anemia or hyperpigmentation, phenotypes associated with mutation of human RPS7 and other murine RPs, respectively. We provide two novel RP mouse models and expand the repertoire of potential phenotypes that should be examined in RP mutants to further explore the concept of RP gene-specific phenotypes.
The kinetic influence of an alkyne ligand, hexafluorobut-2-yne (HFB), has been investigated by studying the reactions of phosphines (PR3) with the complexes M(CO)4(η2-HFB) (M = Fe, Ru, Os). The rate of production of M(CO)3(PR3)(η2-HFB) is independent of the nature and concentration of the phosphine in all cases, indicating that the rate-controlling step is CO dissociation. The kinetic parameters, k 1 (s-1, 25 °C), ΔH* (kJ mol-1), and ΔS* (cal mol-1 K-1) are: 9.5, 88.2 ± 2.3, 70 ± 10 (Fe); 1.25 × 10-2, 103.6 ± 2.4, 66 ± 8.6 (Ru); 3.5 × 10-3, 99.5 ± 0.8, 21 ± 2.7 (Os). When the rate constants at 25 °C for M(CO)4(η2-HFB) are compared to those of the parent M(CO)5, the ratios are ∼3 × 1013, 1.8 × 102 and 1 × 107 for M = Fe, Ru, and Os, respectively. Clearly the alkyne increases the substitution lability, and the effect is spectacular with Fe, very large with Os, and substantial but relatively more modest with Ru. The increased lability results mainly from a reduced ΔH* of ∼80, 10, and 33 kJ mol-1 for Fe, Ru, and Os, respectively, and this is attributed largely to stabilization of the transition state by 4-electron donation from the alkyne ligand. Also reported are kinetics of formation of some trans M(CO)2(PR3)2(η2-HFB) complexes and an extension of earlier work on the Os(CO)5/PPh3 system.
As the prevalence of implants has increased, so has the challenge to augment the remaining osseous structure to house those implants. The biggest surgical challenge clinically is to augment lost bone vertically. The purpose of this article is to review currently available techniques for achieving greater vertical dimension before implant placement. A literature search was conducted using MEDLINE to find all articles published between 1970 and 2004 regarding vertical bone augmentation. Following the literature search, all articles were reviewed and summarized in this review article of vertical bone augmentation. The results of the research showed that guided-bone regeneration, monocortical onlay grafting, and distraction osteogenesis have the potential to be applied to augment deficient areas vertically. The expectations of dimensional gain and bone quality are unique to each technique, as well as the potential complications. Distraction osteogenesis has had the greatest potential for vertical gain, while guided-bone regeneration and monocortical onlay grafting achieve similar results. The choice of procedure is to be based upon the patient's existing anatomy, degree of vertical deficiency, and willingness to participate in treatment.
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