Evaluation of thin amorphous calcium phosphate coatings on titanium dental implants deposited using magnetron sputtering.

OBJECTIVE: Calcium phosphate is used for dental material because of its biocompatibility and osteoconductivity. Amorphous calcium phosphate (ACP) coatings deposited by magnetron sputtering can control their thickness and absorbability. This study aimed to evaluate and characterize ACP coatings deposited via magnetron sputtering. It was hypothesized that ACP coatings would enhance bone formation and be absorbed rapidly in vivo. METHODS: ACP coatings that are 0.5 µm in thickness were deposited via magnetron sputtering on dental implants. Uncoated implants served as controls. The effect of the ACP coatings in vivo was investigated in New Zealand white rabbit. To evaluate the effect of the ACP coatings on the bone response of the implants, the removal torque, implant stability quotient, and histomorphometric analysis were performed on the implants at 1, 2, and 4 weeks after implantation. RESULTS: Results of the x-ray diffraction analyses confirmed the deposition of ACP coatings. Images from the scanning electron microscopy revealed that the coatings were dense, uniform, and 0.5 µm in thickness and that they were absorbed completely. Mechanical stability and bone formation in the case of the ACP-coated implants were higher than those of control. CONCLUSION: These results suggest that implants coated with thin ACP layers improve implant fixation and accelerate bone response.

Antibodies to proteinase 3 prime human monocytic cells via protease-activated receptor-2 and NF-kappaB for Toll-like receptor- and NOD-dependent activation.

Anti-neutrophil cytoplasmic Abs against proteinase 3 (PR3) have been detected in relation to a wide range of inflammatory conditions, and the interaction of anti-PR3 Abs with leukocytes provokes cell activation, although how is not clear. Flow cytometric analysis revealed an increase in cell-surface CD14, Toll-like receptor (TLR)2, TLR4 and intracellular TLR3, TLR7, TLR8, TLR9, NOD1 and NOD2 expression during anti-PR3 priming in human monocytic THP-1 cells. Anti-RP3 Abs markedly promoted the release of IL-8 induced by chemically synthesized TLR and NOD ligands mimicking bacterial components: TLR2-agonistic lipopeptide (FSL-1), TLR3-agonistic poly I:C, TLR4-agonistic lipid A (LA-15-PP), TLR7/8-agonistic single stranded RNA (ssPolyU), TLR9-agonistic bacterial CpG DNA, NOD1-agonistic FK156/565 and NOD2-agonistic muramyldipeptide (MDP) in THP-1 cells and human peripheral blood mononuclear cells, although sole incubation with anti-PR3 Abs induced only a low level of IL-8. The priming response was evident after 2h of preincubation with anti-PR3 Abs and peaked after 6h. Priming was also observed for the production of TNF-alpha and monocyte chemoattractant protein-1. An RNA interference assay revealed that anti-PR3 Abs activated THP-1 cells in a PR3- and protease-activated receptor-2-dependent manner. Furthermore, the anti-PR3 Ab-mediated cell activation was significantly abolished by RNA interference targeted at PR3 mRNA and by inhibition of phospholipase C and NF-kappaB. These results suggest that anti-PR3 Abs prime human monocytic cells to produce cytokines upon stimulation with various bacterial components by up-regulating the TLR and NOD signaling pathway, and that these mechanisms may actively participate in the inflammatory process.

Risk factors related to aggressive condylar resorption after orthognathic surgery for females: retrospective study.

OBJECTIVE: The aim of the present study was to identify the risk factors for aggressive condylar resorption (ACR) after orthognathic surgery. METHODS: A total of 25 female patients with osteoarthritis (OA) scheduled for orthognathic surgery were divided into two groups: those who exhibited ACR (ACR (+), n = 8) and those who did not exhibit ACR (ACR (-), n = 17) after surgery. Clinical indices were used to determine the extent of mandibular advancement, the presence of temporomandibular disorder (TMD), and relevant medical treatment histories (including the use of oral contraceptive (OC) medication. TMJ dysfunction was clinically evaluated in terms of pain, the presence of sounds (clicks or crepitus), and disc displacement, joint effusion (JE), and synovial hyperplasia (SH); these were further investigated with the aid of magnetic resonance imaging (MRI). The cephalographic findings were compared with the normal profiles of Japanese subjects. RESULTS: The mean (with SD) extent of mandibular advancement was 11.4 mm (2.4) in ACR (+) and 4.1 mm (1.8) in ACR (-). The TMD medical history of ACR (+) was much more extensive than that of ACR (-); all patients in ACR (+) had a history of OC use. More patients in ACR (+) than in ACR (-) had TMJ dysfunction and disc displacement, JE, and SH on MRI. Preoperative cephalograms showed that ACR (+) patients exhibited counterclockwise rotation of the mandible and retrognathism that was attributable to a small sella-nasion-B (SNB) angle, a wide mandibular plane angle, and a negative inclination of the ramus. CONCLUSIONS: The present findings suggest that the development of ACR after orthognathic surgery to treat mandibular retrognathism may be associated with coexisting TMJ pathologic abnormality.

The Effect of Decortication for Periosteal Expansion Osteogenesis Using Shape Memory Alloy Mesh Device.

BACKGROUND: In conventional bone grafting technique, decortication procedure enhances the healing process and bone regeneration to reach the grafted site more readily. PURPOSE: This study evaluates to improve periosteal expansion osteogenesis (PEO) using a shape memory alloy mesh (SMA) device with decortication in a rabbit model. MATERIALS AND METHODS: The SMA device was inserted under the periosteum at the forehead and pushed, bent, and attached to the bone surface and fixed with a titanium screw. Twelve rabbits were divided into two groups: PEO without decortication (P group) and with decortication (D group). After 2 weeks, the screw was removed, and the mesh was activated by its own elasticity. Rabbits were sacrificed 5 (P1/D1) and 8 (P2/D2) weeks after operation and histologically and radiographically evaluated. RESULTS: The mean activation height was 2.9 ± 0.5 mm. The ratio of new bone volume in the elevated volume was 17.6% in P1, 59.8% in D1 33.4% in P2, and 65.1% in D2. D group had a statistically higher volume of new bone than P group during each period (p < .05). CONCLUSION: PEO with decortication appears to be a promising clinical alternative for bone augmentation and introduces the new concept of "dynamic graft and guided bone regeneration (GBR)."

PR3-ANCA in Wegener's granulomatosis prime human mononuclear cells for enhanced activation via TLRs and NOD1/2.

BACKGROUND: Anti-neutrophil cytoplasmic antibodies (ANCA) is autoantibodies characteristic of vasculitis diseases. A connection between ANCA and Wegener's granulomatosis was well established. The interaction of both ANCA phenotypes (PR3-ANCA and MPO-ANCA) with leukocytes provoked cell activation, which might be involved in the pathogenesis of ANCA-related Wegener's granulomatosis. METHODS: In this study, we examined whether PR3-ANCA sera and purified immunoglobulins from patients with Wegener's granulomatosis prime human monocytic cells for enhanced responses to microbial components in terms of production of proinflammatory cytokines. RESULTS: Flow cytometry demonstrated that stimulation with antibodies to proteinase 3 enhanced the expression of TLR2, 3, 4, 7, and 9, NOD1, and NOD2 in human mononuclear cells. The sera and purified immunoglobulins significantly primed human mononuclear cells to secrete interleukin-8 in response to microbial components via TLRs and NODs. Priming effects were also observed for the production of interleukin-6, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha. On the other hand, PR3-ANCA-negative sera from patients with polyarteritis nodosa which possibly related to MPO-ANCA and aortitis syndrome as well as control sera from a healthy volunteer did not have any priming effects on PBMCs. CONCLUSION: In conclusion, PR3-ANCA prime human mononuclear cells to produce cytokines upon stimulation with various microbial components by up-regulating the TLR and NOD signaling pathway, and these mechanisms may partially participate in the inflammatory process in Wegener's granulomatosis.