Quantification and comparison of the regional acceleratory phenomenon in bone following piezosurgery or bur osteotomy: A pilot study in rats.

Background/objective: The Regional Acceleratory Phenomenon (RAP) can be induced surgically via decortication (selective cortical penetrations) of bone to accelerate orthodontic tooth movement. Few studies have compared the impact and efficiency of different decortication methods to induce the RAP. The aim of this study was to determine if there is a significant difference in the intensity of the RAP induced by a surgical defect created either using a piezoelectric knife or a rotary bur.

Corticotomy depth and regional acceleratory phenomenon intensity.

Objectives: To determine if the depth of corticotomy done with the piezoelectric knife could play a role in the intensity of the regional acceleratory phenomenon (RAP).

Materials And Methods: Eighteen Sprague-Dawley rats were divided into two groups: untreated (3 rats) and treatment (15 rats). In the treatment group, a split-model design was used.

Strategic Use of Ultrasonic Frequencies for Targeted Bone Biomodification Following Piezoelectric Bone Surgery in Rats. Part II: Late Phase.

Piezoelectric surgery utilizes ultrasonic vibrations to cut bone more precisely and less traumatically than conventional methods. The regional acceleratory phenomenon following bone injury has a demineralization phase followed by a remineralization phase. Part I of this study on rats assessed the biologic modifications following bone injuries with the piezoelectric knife at 10-Hz and 30-Hz modulation frequencies.

Strategic Use of Ultrasonic Frequencies for Targeted Bone Biomodification Following Piezoelectric Bone Surgery in Rats. Part I: Early Phase.

Piezocision can set in motion a cascade of physiologic events that lead to accelerated orthodontics, but do all ultrasonic frequencies generate the same effects on bone? Two different Piezotome modulation frequencies (10 and 30 Hz) were tested on the rat maxilla. The animals were sacrificed at days 1, 3, 7, 14, 28, and 70, and MRI, histologic, and biochemical analyses were performed. The results indicated that at 30 Hz, the demineralization process started at day 1 and peaked at day 7, and was initiated by osteocyte apoptosis.

Resolvin E1 receptor activation signals phosphorylation and phagocytosis.

Resolvins are endogenous lipid mediators that actively regulate the resolution of acute inflammation. Resolvin E1 (RvE1; (5S,12R,18R)-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid) is an endogenous anti-inflammatory and pro-resolving mediator derived from eicosapentaenoic acid that regulates leukocyte migration and enhances macrophage phagocytosis of apoptotic neutrophils to resolve inflammation. In the inflammatory milieu, RvE1 mediates counter-regulatory actions initiated via specific G protein-coupled receptors.

Priming of neutrophil oxidative burst in diabetes requires preassembly of the NADPH oxidase.

Hyperglycemia associated with diabetes mellitus results in the priming of neutrophils leading to oxidative stress that is, in part, responsible for diabetic complications. p47phox, a NADPH oxidase cytosolic subunit, is a key protein in the assembly of the NADPH oxidase leading to superoxide generation. Little is known about the priming mechanism of oxidative pathways in neutrophils of people with diabetes.

Resolvin E1 selectively interacts with leukotriene B4 receptor BLT1 and ChemR23 to regulate inflammation.

Resolvin E1 (RvE1) is a potent anti-inflammatory and proresolving mediator derived from omega-3 eicosapentaenoic acid generated during the resolution phase of inflammation. RvE1 possesses a unique structure and counterregulatory actions that stop human polymorphonuclear leukocyte (PMN) transendothelial migration and PMN infiltration in several murine inflammatory models. To examine the mechanism(s) underlying anti-inflammatory actions on PMNs, we prepared [(3)H]RvE1 and characterized its interactions with human PMN.

Regulation of the NADPH-oxidase complex of phagocytic leukocytes. Recent insights from structural biology, molecular genetics, and microscopy.

The NADPH-oxidase complex is a multisubunit enzyme complex that catalyzes the formation of superoxide (O2-) by phagocytic leukocytes. This paper reviews some of the major advances in understanding the assembly and regulation of this enzyme system that have occurred during the past decade. For example, novel domains/motifs have been identified in p47-phox (PX and super SH3 domains) and p67-phox (tetratricopeptide repeat motifs).

A stable aspirin-triggered lipoxin A4 analog blocks phosphorylation of leukocyte-specific protein 1 in human neutrophils.

Lipoxins and their aspirin-triggered 15-epimers are endogenous anti-inflammatory agents that block neutrophil chemotaxis in vitro and inhibit neutrophil influx in several models of acute inflammation. In this study, we examined the effects of 15-epi-16-(p-fluoro)-phenoxy-lipoxin A(4) methyl ester, an aspirin-triggered lipoxin A(4)-stable analog (ATLa), on the protein phosphorylation pattern of human neutrophils. Neutrophils stimulated with the chemoattractant fMLP were found to exhibit intense phosphorylation of a 55-kDa protein that was blocked by ATLa (10-50 nM).

Protein phosphorylation in neutrophils monitored with phosphospecific antibodies.

Protein phosphorylation in neutrophils was monitored with two phosphospecific antibodies (pAbs) [termed pPKC(S1) Ab and pPKC(S2) Ab] that recognize products of protein kinase C (PKC) and other Arg/Lys-directed Ser/Thr protein kinases. The pPKC(S1) Ab bound preferentially to p-Ser/p-Thr residues with Arg or Lys in the -3 and -5 positions or the -2 and -3 positions, whereas the pPKC(S2) Ab bound preferentially to p-Ser with Arg or Lys in the -2 and +2 positions and with a hydrophobic residue at the +1 position. Phosphorylated pleckstrin, myristoylated alanine-rich C-kinase substrate (MARCKS), the 47-kDa subunit of the phagocyte oxidase (p47-phox) and numerous unidentified proteins that underwent phosphorylation during neutrophil stimulation were readily detected with these pAbs.

p21-activated kinase 2 in neutrophils can be regulated by phosphorylation at multiple sites and by a variety of protein phosphatases.

The p21-activated kinase(Pak) 2 undergoes rapid autophosphorylation/activation in neutrophils stimulated with a variety of chemoattractants (e.g., fMLP).

Unique genes induced by mechanical stress in periodontal ligament cells.

Objectives: The aim of this study is to isolate mechanical stress-induced genes (MSGens) from human periodontal ligament (PDL) cells and to analyze profiles of the mRNA expression of these genes.

Background: Differential expression of genes in PDL cells under physiological stress such as occlusal force is thought to be orchestrated not only for the remodeling of PDL itself but also for the repair and regeneration of periodontal tissues. However, little is known about the genes expressed in PDL cells under mechanical stress.