Molecular Mechanisms Controlling Bone Formation During Fracture Healing and Distraction Osteogenesis

Fracture healing and distraction osteogenesis have important applications in orthopedic, maxillofacial, and periodontal treatment. In this review, the cellular and molecular mechanisms that regulate fracture repair are contrasted with bone regeneration that occurs during distraction osteogenesis. While both processes have many common features, unique differences are observed in the temporal appearance and expression of specific molecular factors that regulate each. The relative importance of inflammatory cytokines in normal and diabetic healing, the transforming growth factor beta superfamily of bone morphogenetic mediators, and the process of angiogenesis are discussed as they relate to bone repair. A complete summary of biological activities and functions of various bioactive factors may be found at COPE (Cytokines & Cells Online Pathfinder Encyclopedia), http://www.copewithcytokines.de/cope.cgi

Osteopontin : its role during distraction osteogenesis healing

PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact [email protected] (D.Sc.D.)--Boston University, Goldman School of Dental Medicine, 2007 (Orthodontics).Includes bibliography: leaves 96-103.Introduction: Osteopontin (OPN) is a phosphoprotein found in the extracellular matrices of mineralized tissues and is believed to play a role in the remodeling of these matrices. OPN is also one of a limited number of genes that respond to mechanical strain. Distraction osteogenesis (DO) represents a unique in vivo surgical method of applied mechanical tension that induces new bone formation and therefore represents an ideal model to assess the multiple functional roles of osteopontin. Materials and Methods: Tibia distraction osteogenesis was carried out using a monolateral fixator on male transgenic mice lacking osteopontin (OPN[-/-] C57B1/6) and their background strain (C57B1/6). MicroCT was used for quantitative assessment of DO regenerate size, microstructure and mineralization at the early and late consolidation phases. Histology and molecular analyses were used to evaluate cellular functions related to ECM formation, remodeling and bone resorption. Results: In the absence of OPN, knock out mice displayed a reduced total volume of the bone regenerate at the early consolidation stage of tissue formation. However, as healing progressed this deficiency was corrected by the end of the period of consolidation. A comparison of the anabolic versus catabolic activities during distraction osteogenes is demonstrated that OPN[-/-] regenerate possessed larger numbers of osteoclasts per area of bone accompanied by an increased expression of their makers. Messenger RNAs encoding matrix metalloproteinases 2 and 9 that are associated with matrix remodeling were also induced by higher levels at the end of latency and early consolidation phases in the OPN deficient mice relative to the control animals. On the anabolic side OPN[-/-] mice displayed compensatory increase in the levels of collagen type 1 expression accompanied by an altered organization of its fibers whereas other ECM proteins displayed normal levels. Interesting, all three metalloproteinase inhibitors showed elevated expression over time and strain in the OPN[-/-] mice. Conclusion: This study showed that OPN deficiency lead to structural alterations during the early periods of bone healing; however, during the later periods healing recovered and normal union was achieved. These studies suggest that the absence of OPN led to higher activity of both osteoclasts and osteoblasts demonstrating that insufficiencies in the expression of this extracellular matrix component effects both the anabolic and catabolic activities of coupled remodeling. Thus, the earlier increases in perhaps less than optimally functional osteoclasts are coupled with the subsequent elevation in osteoblastic activities

The Effect of Er,Cr:YSGG and Diode Laser Applications on Dental Implant Surfaces Contaminated with Acinetobacter Baumannii and Pseudomonas Aeruginosa

Treatment of peri-implantitis through several implant surface decontamination techniques have been reported, however, some of them can negatively alter the implant surface or enhance more bacterial resistance. The aim of this in vitro study was to evaluate implant surface decontamination by means of Er,Cr:YSGG and diode lasers. Fifty micro-textured (MTX) dental implants were contaminated with Acinetobacter baumannii (n = 25) and with Pseudomonas aeruginosa (n = 25). All implants were then divided into five groups for the decontamination procedure. In group I (GI), decontamination was done with an Er,Cr:YSGG laser (2780 nm), while in group II (GII) decontamination was performed using photodynamic therapy (a 650 nm diode laser). In Group III (GIII) decontamination was performed with photodynamic therapy (an 808 nm diode laser), and in group IV (GIV) decontamination was performed with 0.12% chlorhexidine. Group V (GV) was the control group with no decontamination. After decontamination, colony forming units (CFU) were counted and implants were prepared for SEM analysis. A significant difference (p < 0.001) was observed for GI compared to the other groups, and also for GIV compared to both GII and GIII. The Er,Cr:YSGG laser (GI) showed the best results in decontaminating the implant surface. Chlorhexidine (GIV), proved to be better in decontaminating the implant surface than photodynamic therapy GII and diode laser GIII. No significant difference was found between group GII and GIII. The SEM analysis showed no significant change in the implant surface topography. The results of this study suggest that the Er,Cr:YSGG laser can be considered as an effective technique for reducing bacteria contamination on implant surfaces

Global economic burden of unmet surgical need for appendicitis

Background There is a substantial gap in provision of adequate surgical care in many low- and middle-income countries. This study aimed to identify the economic burden of unmet surgical need for the common condition of appendicitis. Methods Data on the incidence of appendicitis from 170 countries and two different approaches were used to estimate numbers of patients who do not receive surgery: as a fixed proportion of the total unmet surgical need per country (approach 1); and based on country income status (approach 2). Indirect costs with current levels of access and local quality, and those if quality were at the standards of high-income countries, were estimated. A human capital approach was applied, focusing on the economic burden resulting from premature death and absenteeism. Results Excess mortality was 4185 per 100 000 cases of appendicitis using approach 1 and 3448 per 100 000 using approach 2. The economic burden of continuing current levels of access and local quality was US $92 492 million using approach 1 and$73 141 million using approach 2. The economic burden of not providing surgical care to the standards of high-income countries was $95 004 million using approach 1 and$75 666 million using approach 2. The largest share of these costs resulted from premature death (97.7 per cent) and lack of access (97.0 per cent) in contrast to lack of quality. Conclusion For a comparatively non-complex emergency condition such as appendicitis, increasing access to care should be prioritized. Although improving quality of care should not be neglected, increasing provision of care at current standards could reduce societal costs substantially

Global economic burden of unmet surgical need for appendicitis

Background There is a substantial gap in provision of adequate surgical care in many low- and middle-income countries. This study aimed to identify the economic burden of unmet surgical need for the common condition of appendicitis. Methods Data on the incidence of appendicitis from 170 countries and two different approaches were used to estimate numbers of patients who do not receive surgery: as a fixed proportion of the total unmet surgical need per country (approach 1); and based on country income status (approach 2). Indirect costs with current levels of access and local quality, and those if quality were at the standards of high-income countries, were estimated. A human capital approach was applied, focusing on the economic burden resulting from premature death and absenteeism. Results Excess mortality was 4185 per 100 000 cases of appendicitis using approach 1 and 3448 per 100 000 using approach 2. The economic burden of continuing current levels of access and local quality was US $92 492 million using approach 1 and$73 141 million using approach 2. The economic burden of not providing surgical care to the standards of high-income countries was $95 004 million using approach 1 and$75 666 million using approach 2. The largest share of these costs resulted from premature death (97.7 per cent) and lack of access (97.0 per cent) in contrast to lack of quality. Conclusion For a comparatively non-complex emergency condition such as appendicitis, increasing access to care should be prioritized. Although improving quality of care should not be neglected, increasing provision of care at current standards could reduce societal costs substantially