Objectives: Photodynamic therapy has been proven to promote additional clinical and microbiological benefits in the treatment of chronic periodontitis and aggressive periodontitis. The purpose of this study is to assess the effectiveness of the photodynamic therapy for patient with periodontitis. Methods: We searched the eight Korean databases and Ovid-MEDLINE, Ovid-EMBASE, Cochrane Library. Total 300 studies were searched and 13 studies were included in the final assessment. Each of the stages from literature search and extraction of data were carried out independently by 2 researchers. We used tools of Scottish Intercollegiate Guidelines Networks for assessment of the quality of studies. Results: The safety of the photodynamic therapy was assessed by bleeding. The effectiveness of the photodynamic therapy was assessed by the reduction of Probing pocket depth (PPD) and the gain of Clinical attachment level (CAL). The mean difference of PPD was 0.46(95% CI 0.09~0.82), (p=.01).). The mean difference of CAL was ?0.49(95% CI ?1.12~0.14), (p=.13). Conclusion: The additional use of $^{\circ}{\infty}$Antimicrobial Photodynamic Therapy for Periodontitis$^{\circ}{\pm}$ caused hemorrhage to similar extents to conventional treatment modalities, where scaling and root planing are solely performed, in patients with periodontitis who are expected to have a lower degree of treatment response to non-surgical or surgical periodontal therapies (implant or refractory periodontitis) and those where there is a concern for the possible occurrence of antimicrobial side effects or resistance. This indicates that there are no problems with its safety. But there were no consistent reports about the effects of the additional use of photodynamic therapy. This led to a decision that the safety and efficacy of the current technology deserve further studies (Recommendation rating of A, Classification of technology II-a).
The purpose of this study was to evaluate drug-loaded biodegradable membranes for guided tissue regeneration(GTR). The membranes were made by coating mesh of polyglycolic acid(PGA) with polylactic acid(PLA) containing 10% flurbiprofen or tetracycline. The thickness of membrane was $150{\pm}30{\mu}m$, and the pore size of surface was about $8{\mu}m$ in diameter. The release of drugs from the membrane was measured in vitro. Cytotoxity test for the membrane was performed by gingival fibroblast cell culture, and the tissue response was observed after implant of membrane into the dorsal skin of the rat for 8 wks. Ability to guided tissue regeneration of membranes were tested by measuring new bone in the calvarial defects(5mm in diameter) of the rat for 5 weeks. The amount of flurbiprofen and tetracycline released from membrane were about 30-60% during 7 days. Minimal cytotoxity was observed in the membrane except 20% drug containing membrane. In histologic finding of rat dorsal skin, many inflammatory cells were observed around e-PTFE, polyglactin 910 and PLAPGA membrane after 1 or 2 weeks. PLA-PGA membrane was perforated by connective tissue after 4 or 6 weeks, and divided as a segment at 8 weeks. In bone regeneration guiding potential test, tetracycline loaded membrane was most effective (p
The benefits in using controlled delivery approaches include improved pharmacokinetic response, greater ability to localize the drung adjacent to the disease, and more control of local concentration at a lower total dosage. The purpose of this study was to evaluate the efficacy and safety of Minocline strip on chronic marginal periodontitis. Minocline Strip was applied in the periodontal pocket of 94 patients with a clinically diagnosed as a chronic marginal periodontitis, 4 sites for each patients with a 5mm probing pocket depth were selected in split mouth design and were divided into two group, ie., placebo group ($C_1$, $C_2$) and experimental group ($E_1$, $E_2$). Supragingival scaling and oral hygiene instruction were performed 1 week before experiment. Minocline Strip was applied on day 0 and 7, weekly, Clinical and microbiological tests were performed on day 0, 7, 14, 28 and 42. The results were as follows ; 1. Minocline Strip showed significant improvement on Chronic Marginal Periodontitis in 77 patients (82.0%) and improvement rate was more than 66.7% of all investigational items. 2. Only 6 patients complained mild pruritis during the early therapy but not needed discontinuence of the therapy. 3. The availability of Minocline Strip was 72 patients (76.6%) synthetically evaluating efficacy and safety. In conclusion, Minocline Strip appears to be effective and safe for the treatment of Chronic Marginal Periodontitis.
Immune responses of periodontal tissue may be regulated by products of sensory afferent nerve endings such as neuropeptides. Substance P(SP), a tachykinin neuropeptide, has been previously reported to stimulate the activities of T lymphocyte. Therefore, I examined the role of SP in IL-2 production and cell proliferation by using a homogeneous line of T lymphocytes(Jurkat and HuT78). Cell proliferation rate was determined by [$^3H$]-thymidine incorporation test, and IL-2 was quantitated by the growth rate of CD4+ IL-2-dependent T lymphocyte line CTLL-2. SP stimulated cell proliferation of T lymphocytes at the concentration of $10^{-12}$ and $10^{-8}$M in a biphasic bell-shape dose-dependent manner. However, SP alone did not induce IL-2 release at the concentration range of $10^{-6}$ to $10^{-14}$M. The upregulation of IL-2 release was observed when $10^{-12}$M SP was applied together with mitogens such as Con A or PHA+PMA on T cell lines, especially on Jurkat. Con A or PHA+PMA demonstrated to increase the rate of cell proliferation of Jurkat, which had shown to produce much amount of IL-2 indicating that mitogen-induced cell proliferation might be partially influenced by released IL-2. It was concluded that regulatory effects of SP on the immune/inflammatory response could be mediated through the costimulatory upregulation of IL-2 production and increase of cell proliferation of T lymphocyte.
The purpose of this stuffy was to assess and compare the osseous responses to implanted particles of porous synthetic HA (Interpore $200^{(R)}$, Interpore International, U.S.A.), resorbable natural bovine derived HA (Bio-$oss^{(R)}$, Gestlich Pharma, Switzerland) and calcium carbonate(Biocoral $450^{(R)}$, Inoteb, France) in bone defects. Four calvarial defects of 2.5mm diameter were created in earth of 16 Sprague-Dawley rats. The experimental materials were subsequently implanted hi three defects, leaving the fourth defect for control purpose. Four animals were earth sacrificed at 3 days, 1week, 2weeks and 4 weeks after surgery. The tissue response was evaluated under light microscope. Overall, histologic responses showed that all the particles were well tolerated and caused no aberrent tissue responses. There were difference in the amount of newly formed bone at the experimental sites and control site. There was more new bone formation associated with calcium carbonate site. In addition, the calcium carbonate site displayed multinucleated giant cells surrounding calcium carbonate particles after the 1st week, and osteoid tissue within the particle after the 2nd week. After 4 weeks, calcium carbonate particles were resorbed and replaced with new bone. The healing of the natural bovine derived HA site was similar to that of porous synthetic HA, except that new bone growth between the two particles have progressed more in the former site after the 2nd week. In the natural bovine derived HA site, the particle was surrounded by newly formed bone after the 4th week. After 4 weeks, the control site showed more mature bone than other sites. In conclusion, the grafted site were better in new bone formation than non-grafted sites. In particular the calcium Carbonate site showed the ability of osteoinduction and natural bovine denver HA showed osteoconduction in rat calvarial defects. This suggest that calcium carbonate and natural bovine derived HA could enhance the regenerative potential in periodontal defects.
An oral environment is constantly exposed to environmental factors and microorganisms. The periodontal ligament (PDL) fibroblasts within this environment are subject to bacterial infection and allergic reaction. However, how these condition affect PDL fibroblasts has yet to be elucidated. PDL fibroblasts were isolated from healthy donors. We examined using reverse transcription-polymerase chain reaction and measuring the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$). This study investigated the receptors activated by exogenous bacterial pathogens (Lipopolysaccharide and peptidoglycan) and allergens (German cockroach extract and house dust mite) as well as these pathogenic mediators-induced effects on the intracellular $Ca^{2+}$ signaling in human PDL fibroblasts. Moreover, we evaluated the expression of pro-inflammatory cytokines (interleukin (IL)-$1{\beta}$, IL-6, and IL-8) and bone remodeling mediators (receptor activator of NF-${\kappa}B$ ligand and osteoprotegerin) and intracellular $Ca^{2+}$-involved effect. Bacterial pathogens and allergic mediators induced increased expression of pro-inflammatory cytokines, and these results are dependent on intracellular $Ca^{2+}$. However, bacterial pathogens and allergic mediators did not lead to increased expression of bone remodeling mediators, except lipopolysaccharide-induced effect on receptor activator of NF-${\kappa}B$ ligand expression. These experiments provide evidence that a pathogens and allergens-induced increase in $[Ca^{2+}]_i$ affects the inflammatory response in human PDL fibroblasts.
The surface characteristics of titanium have been shown to have an important role in contact ossseointegration around the implant. Anodizing at high voltage produces microporous structure and increases thickness of surface titanium dioxide layer. The aim of present study was to analyse the response of rat calvarial osteoblast cell to commercially pure titanium and Ti-6A1-4V anodized in 0.06 mol/l ${\beta}$-glycerophosphate and 0.03 mol/l sodium acetate. In this study, rat calvarial osteoblasts were used to assay for cell viability and cell proliferation on the implant surface at 1,2,4,7 days. 1. Surface roughness was 1.256${\mu}m$ at 200V, and 1.745${\mu}m$ at 300V. 2. The thickness of titanium oxide layer was increased 1 ${\mu}m$ with the increase of 50V. 3. The proliferation rate of osteoblastic cells was increased with the increase of the surface roughness and the thickness of titanium oxide layer. 4. There was no difference in cell viability and cell proliferation between commercially pure titanium and Ti-6A1-4V anodized at the same condition. In conclusion, the titanium surface modified by anodizing was biocompatible, produced enhanced osteoblastic response. The reasons of enhanced osteoblast response might be due to reduced metal ion release by thickened and stabilized titanium dioxide layer and microporous rough structures.
Kim, Hae-Jin;Son, Mee-Kyoung;Park, Ji-Il;Chung, Hyun-Ju;Kim, Young-Joon
Journal of Periodontal and Implant Science
/
v.38
no.4
/
pp.595-602
/
2008
Purpose: Ti-6Al-4V alloy is widely used as an implant material because of its good biocompatibility and good mechanical property compared with commercial pure titanium. Otherwise, toxicity of aluminum and vanadium in vivo has been reported. Ti-8Ta-3Nb alloy is recently developed in the R&D Center for Ti and Special Alloys and it was reported that this alloy has high mechanical strength, no cytotoxicity and similar biocompatibility to commercial pure titanium, but many studies are needed for its clinical use. In these experiment, we carried out different surface treatment on each Ti-8Ta-3Nb alloy disks, then cultured cell on it and assessed biological response. Materials and Methods: cpTi, Ti-6Al-4V, Ti-8Ta-3Nb alloy disks were prepared and carried out sandblasting and acid etching (SLA) or alkali-heat treatment (AH) on the Ti-8Ta-3Nb alloy disks. We cultured primary rat calvarial cells on each surface and assessed early cell attachment and proliferation by scanning electron microscopy, cell proliferation, alkaline phosphatase activity. Result: The rates of cell proliferation on the cpTi, Ti-8Ta-3Nb AH disks were higher than others (p<0.05) and alkaline phosphatase activity was significantly enhanced on the Ti-STa-8Nb AH disks(p<0.05). Conclusion: Most favorable cell response was shown on the Ti-8Ta-3Nb AH surfaces. It is supposed that alkali-heat treatment of the Ti-8Ta-3Nb alloy could be induced earlier bone healing and osseointegration than smooth surface.
Purpose: The aim of the present study was to evaluate the biological response of alkali- and heat-treated titanium-8tantalum-3niobium surfaces by cell proliferation and alkaline phosphatase (ALP) activity analysis. Methods: Commercial pure titanium (group cp-Ti) and alkali- and heat-treated titanium-8tantalum-3niobium (group AHT) disks were prepared. The surface properties were evaluated using scanning electron microscopy, energy dispersed spectroscopy and X-ray photoelectron spectroscopy (XPS). The surface roughness was evaluated by atomic force microscopy and a profilometer. The contact angle and surface energy were also analyzed. The biological response of fetal rat calvarial cells on group AHT was assessed by cell proliferation and ALP activity. Results: Group AHT showed a flake-like morphology microprofile and dense structure. XPS analysis of group AHT showed an increased amount of oxygen in the basic hydroxyl residue of titanium hydroxide groups compared with group cp-Ti. The surface roughness (Ra) measured by a profilometer showed no significant difference (P>0.05). Group AHT showed a lower contact angle and higher surface energy than group cp-Ti. Cell proliferation on group AHT surfaces was significantly higher than on group cp-Ti surfaces (P<0.05). In comparison to group cp-Ti, group AHT enhanced ALP activity (P<0.05). Conclusions: These results suggest that group AHT stimulates osteoblast differentiation.
Background: Oxidative stress is a known to be associated with in the pathogenesis of many inflammatory diseases, including periodontitis. Ursolic acid is a pentacyclic triterpenoid with has antimicrobial, antioxidative, and anticancer properties. However, the role of ursolic acid in the regulating of osteogenesis remains undetermined. This study was aimed to elucidate the crucial osteogenic effects of ursolic acid and its ability to inhibit oxidative stress by targeting the immediate early response 3 (IER3)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Methods: Cell proliferation was determined using water-soluble tetrazolium salt assay, cell differentiation was evaluated by alkaline phosphatase (ALP) activity, and formation of calcium nodules was detected using alizarin red S stain. Generation of reactive oxygen species (ROS) was determined using by DCFH-DA fluorescence dye in hydrogen peroxide ($H_2O_2$)-treated MG-63 cells. Expression levels of IER3, Nrf2, and heme oxygenase-1 (HO-1) were analyzed using western blot analysis. Results: Our results showed that ursolic acid up-regulated the proliferation of osteoblasts without any cytotoxic effects, and promoted ALP activity and mineralization. $H_2O_2$-induced ROS generation was found to be significantly inhibited on treatment with ursolic acid. Furthermore, in $H_2O_2$-treated cells, the expression of the early response genes: IER3, Nrf2, and Nrf2-related phase II enzyme (HO-1) was enhanced in the presence of ursolic acid. Conclusion: The key findings of the present study elucidate the protective effects of ursolic acid against oxidative stress conditions in osteoblasts via the IER3/Nrf2 pathway. Thus, ursolic acid may be developed as a preventative and therapeutic agent for mineral homeostasis and inflammatory diseases caused due to oxidative injury.
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