Ligature Removal Research Articles

Therapeutic Effects of Alpha Lipoic Acid and Vitamin C on Alveolar Bone Resorption After Experimental Periodontitis in Rats: A Biochemical, Histochemical, and Stereologic Study

Alpha lipoic acid (ALA) and vitamin C (Vit-C) are very important and powerful antioxidants that have been used for the treatment of many diseases. The present study aims to investigate the role of ALA and Vit-C substances in the treatment of alveolar bone resorption in periodontal diseases. Thirty-six male Wistar albino rats were randomly divided into four groups as follows: 1) control rats; 2) rats with experimental periodontitis (PED); 3) rats with PED treated with ALA (ALA); and 4) rats with PED treated with ALA+Vit-C (ALA+Vit-C). PED was simulated by placing ligatures around the neck of teeth for 5 weeks. After ligature removal, the PED group was given a single intragastric dose of 1 mL saline, and the ALA and ALA+Vit-C groups were treated with an intragastric dose of 50 mg/kg ALA and ALA+Vit-C for 15 days, respectively. Levels of serum bone alkaline phosphatase (B-ALP) and myeloperoxidase (MPO) activity in gingival tissues were analyzed. To evaluate the osteoclast activation, expression of activated receptor activator nuclear factor-kappa B ligand (RANKL) and bone density index (BDI) were determined stereologically in the bone sections obtained from the mandibles of the rats. The results showed statistically significant differences between the PED group and groups treated with antioxidant according to B-ALP, MPO, RANKL, and BDI values (P <0.05). ALA and ALA+Vit-C treatments showed beneficial effects on the mesial/distal periodontal bone support at the ligature-induced periodontitis tooth areas. This study shows that ALA and Vit-C treatment provides therapeutic effects on inhibition of alveolar bone resorption and periodontal tissue destruction.

Experimental periodontitis and peri‐implantitis in dogs

To analyze the tissue reactions following ligature removal in experimental periodontitis and peri-implantitis in dogs. Four implants with similar geometry and with two different surface characteristics (turned/TiUnite Nobel BioCare AB, Göteborg) were placed pair-wise in a randomized order in the right side of the mandible 3months after tooth extraction in 5 dogs. Experimental peri-implantitis and periodontitis were initiated 3months later by ligature placement around implants and mandibular premolars and plaque formation. The ligatures were removed after 10weeks, and block biopsies were obtained and prepared for histological analysis 6months later. It was demonstrated that the amount of bone loss that occurred during the period following ligature removal was significantly larger at implants with a modified surface than at implants with a turned surface and at teeth. The histological analysis revealed that peri-implantitis sites exhibited inflammatory cell infiltrates that were larger, extended closer to the bone crest and contained larger proportions of neutrophil granulocytes and osteoclasts than in periodontitis. It is suggested that lesions produced in experimental periodontitis, and peri-implantitis are different and that implant surface characteristics influence the inflammatory process in experimental peri-implantitis and the magnitude of the resulting tissue destruction.

Spontaneous progression of experimental peri‐implantitis at implants with different surface characteristics: An experimental study in dogs

To analyse spontaneous progression of ligature-induced peri-implantitis at implants with different surface characteristics. Four implants with similar geometry and with two different surface characteristics (turned/TiUnite; Nobel Biocare AB) were placed pairwise in one side of the mandible in five dogs, 3 months after tooth extraction. Experimental peri-implantitis was initiated by placement of ligatures and plaque formation. The ligatures were removed when about 40% of the supporting bone was lost. After 6 months, block biopsies were obtained and prepared for histological analysis. The amount of bone loss that occurred during the plaque accumulation period after ligature removal was significantly larger at implants with a TiUnite surface than at implants with a turned surface. The histological analysis revealed that the vertical dimensions of the lesion and the pocket epithelium and the apical extension of the biofilm were significantly larger at TiUnite implants than at turned implants. It is suggested that the implant surface characteristics influence progression of peri-implantitis.

L-arginine suppresses ischemia/reperfusion induced up-regulation of endothelin-1 production in a rat model of acute myocardial injury

To examine the level of endothelin-1 (ET-1) in serum and its expression in myocardium tissue during the development of acute myocardial ischemia/reperfusion (I/R) injury in rat and the effects of L-arginine (L-Arg) administration on these indexes. One hundred and ten Wistar rats were randomly divided into nine groups to receive: (1) sham surgery, (2)ischemia (I, by ligation of anterior descending coronary artery for 30 minutes), (3) I+reperfusion (R, by the removal of the ligature) for 0.5 hour, (4) I+R for 1 hour, (5) I+R for 2 hours; group (6) ~ (9) also received I/R treatment as in group 2 ~ 5 respectively but with L-Arg pretreatment. Blood and myocardium tissue samples were collected by the end of the experiment for the analysis of: serum level of creatine kinase (CK), lactate dehydrogenase [LDH, by enzyme linked immunosorbent assay (ELISA)], ET-1 (radioimmunoassay), and the tissue content of ET-1 mRNA/peptide [by reverse-transcription polymerase chain-reaction (RT-PCR) and Western blotting]. In comparison with the sham treated control animals, the serum levels of CK, LDH, and ET-1 were all significantly higher in the groups treated with I/R (particularly those exposed to reperfusion). The myocardial tissue content of ET-1 mRNA/peptide were also significantly increased in I/R treated groups (particularly the I+R 2 hours group) as compared to control (ET-1 mRNA: 0.775 ± 0.029 vs. 0.310 ± 0.076; ET-1 peptide: 0.773 ± 0.055 vs. 0.340 ± 0.099, both P < 0.05). The i.v. administration of L-Arg significantly suppressed the up-regulation of tissue content of ET-1 mRNA /peptide in I/R treated animals (ET-1 mRNA: 0.340 ± 0.049 vs. 0.775 ± 0.029; ET-1 peptide: 0.390 ± 0.094 vs. 0.773 ± 0.055, both P < 0.05). L-Arg may be tested during certain stage of I/R injury as a therapeutic intervention for the suppression of ET-1 up-regulation.

Topical and intermittent application of parathyroid hormone recovers alveolar bone loss in rat experimental periodontitis

Periodontitis is characterized by periodontal tissue inflammation and alveolar bone loss. The intermittent administration of parathyroid hormone (PTH), a major regulator of bone remodeling, has been demonstrated to stimulate osteoblastic activity. Although the systemic administration of PTH has been reported to protect against periodontitis-associated bone loss, the effect of the topical administration of PTH is unclear. In this study, the effect of intermittent administration of PTH on osteoblastic differentiation was examined in cultured calvaria cells and then the effect of topical and intermittent administration of PTH was determined by measuring the recovery of alveolar bone loss after inducing experimental periodontitis in rats. Alkaline phosphatase activity and bone nodule formation were measured in fetal rat calvaria cells. Experimental periodontitis was induced by placing nylon ligature around rat maxillary molars for 20 d. After ligature removal (day 0), PTH was topically injected into buccal gingiva three times a week for 10 wk. Micro-computed tomography analysis and histological examination were performed on days 35 and 70. Intermittent exposure of PTH in calvaria cells increased alkaline phosphatase activity and bone nodule formation by 1.4- and 2.4-fold, respectively. Ligature procedures induced marked alveolar bone loss around the molars on day 0 and greater bone recovery was observed in the PTH-treated rats on day 70. An increase in osteoid formation on the surface of alveolar bone was detected in the PTH-treated rats. Intermittent treatment with PTH stimulated osteoblastic differentiation in fetal rat calvaria cell cultures, and topical and intermittent administration of PTH recovered alveolar bone loss in rat experimental periodontitis.

Mechanism of Cardioprotective Effect of Adenocine and Non-Glycoside Cardiotonic Drugs during Experimental Chronic Cardiac Insufficiency

The therapeutic action of adenocine during cardiac insufficiency (heart failure) caused by ischemic (stenosis) or reperfusion (removal of ligature) injury to the myocardium prevents depletion of ATP, the major energy source for myocytes in the right and left ventricles, and a drop in NAD/NADH ratio. The development of energy shortage during heart failure cannot be eliminated by β-acetyldigoxin, levosimendan, or milrinone: the content of ATP in the right and left ventricular myocardium remained below the normal level by 28 and 29%, 37 and 33%, 32 and 28%, respectively; the NAD/NADH ratio of the energy supply system in cardiomyocytes did not return to normal. Adenocine increased the content of NAD to the normal level in both the right and left ventricles, while it remained below the normal level after administration of β-acetyldigoxin (by 24 and 19.5%, respectively), levosimendan (by 27 and 29%), and milrinone (by 26 and 24%). In contrast to β-acetyldigoxin, levosimendan, and milrinone, adenocine inhibited activity of poly(ADP-ribose) polymerase in both ventricles. It is concluded that adenocine directly inhibits the key enzyme triggering apoptosis; we also hypothesized that this drug activates the regulatory and signal mechanisms arresting apoptotic alterations in the myocardium during heart failure.

Are peri‐implantitis lesions different from periodontitis lesions?

To compare histopathological characteristics of peri-implantitis and periodontitis lesions. A search was conducted on publications up to July 2010. Studies carried out on human biopsy material and animal experiments were considered. While comprehensive information exists regarding histopathological characteristics of human periodontitis lesions, few studies evaluated peri-implantitis lesions in human biopsy material. Experimental peri-implantitis lesions were evaluated in 10 studies and three of the studies included comparisons to experimental periodontitis. Human biopsy material: the apical extension of the inflammatory cell infiltrate (ICT) was more pronounced in peri-implantitis than in periodontitis and was in most cases located apical of the pocket epithelium. Plasma cells and lymphocytes dominated among cells in both types of lesions, whereas neutrophil granulocytes and macrophages occurred in larger proportions in peri-implantitis. placement of ligatures together with plaque formation resulted in loss of supporting tissues and large ICTs around implants and teeth. Following ligature removal, a "self-limiting" process occurred in the tissues around teeth with a connective tissue capsule that separated the ICT from bone, while in peri-implant tissues the ICT extended to the bone crest. Despite similarities regarding clinical features and aetiology of peri-implantitis and periodontitis, critical histopathological differences exist between the two lesions.

Short-term induction of thrombocytopenia delays periodontal healing in rats with periodontal disease: participation of endostatin and vascular endothelial growth factor

Platelets contain factors, including VEGF and endostatin, that can modulate the healing process. We evaluated the effects of severe thrombocytopenia on periodontal healing in rats and determined the contribution of VEGF and endostatin to the healing process. Rats were distributed into three test groups and two control groups. Cotton ligatures were placed at the gingival margin level of the lower first molar in the test groups. Sham-operated rats and rats in one of the periodontitis groups were killed 15 days later. Rats in the remaining two periodontitis groups had the ligatures removed in order to study the spontaneous recovery from the periodontal disease 15 days later, and these rats were treated with rabbit antiplatelet serum, in order to induce thrombocytopenia, or normal rabbit serum. An additional group without ligatures received antiplatet serum in the same period. After ligature removal, rats treated with normal rabbit serum showed reduced myeloperoxidase activity, decreased alveolar bone loss and increased numbers of blood vessels. Thrombocytopenia caused a delay in alveolar bone regeneration, a decrease in the number of vessels and a modest decrease in myeloperoxidase activity. In the rats with periodontitis, serum endostatin concentrations were slightly decreased and serum VEGF remained unchanged compared with sham-operated animals. After ligature removal, a significant VEGF increase and endostatin decrease were observed in the rats treated with normal rabbit serum. Thrombocytopenia led to a dramatic fall in both VEGF and endostatin concentrations. Thrombocytopenia leads to a delay of periodontal healing in the situation of experimental periodontitis, which might be mediated in part by a decrease in the serum concentration of VEGF and endostatin derived from the platelets. However, other factors derived from the platelets may also have contributed to a delay of periodontal healing in the rats with thrombocytopenia.

Effect of internal carotid artery reperfusion in combination with Tenecteplase on clinical scores and hemorrhage in a rabbit embolic stroke model

In the present study, we used a modification of the rabbit small clot embolic stroke model (RSCEM), a multiple infarct ischemia model to achieve reperfusion (REP) through the internal carotid artery (ICA) following small clot embolization. We determined if increasing regional cortical blood flow (RCBF) following an embolic stroke is beneficial to neurological outcome. We compared this to cerebral reperfusion induced by the administration of the thrombolytic Tenecteplase (TNK, 1.5 mg/kg, IV bolus) in the presence or absence of REP. In this study, we also measured the incidence of ICH following REP and thrombolytic treatment. Following embolization, RCBF was reduced to 48–55% of baseline. When REP was induced by removal of a CCA ligature, RCBF initially increased to 185% of baseline. REP (P 50 = 1.18 ± 0.43 mg) had no effect on embolization-induced behavior measured 24 h following embolization compared to control (P 50 = 1.01 ± 0.48 mg). However, TNK treatment (2-hours post-embolization) in the absence or presence of REP (initiated 2 h following embolization) significantly ( p < 0.05) increased the group P 50 to 2.92 ± 0.55 mg and 2.42 ± 0.40 mg, respectively. In addition, ICH was increased in the REP (42%, p < 0.05) and REP-TNK (35%, p > 0.05) group compared to either the control group (5.5%) or TNK group (10%). This study show that reperfusion of ICA can increase RCBF following embolization, but this is not associated with improved neurological outcome measured using quantal analysis. However, TNK administration significantly increased behavioral outcome when given 2 h following embolization; an increase that is not affected by combining TNK with REP.

Spontaneous progression of ligatured induced peri‐implantitis at implants with different surface characteristics. An experimental study in dogs II: histological observations

The aim of the present study was to analyze tissue reactions to plaque formation following ligature removal in experimental peri-implantitis at commercially available implants in dogs. Mandibular premolars and the three anterior premolars in both sides of the maxilla were extracted in six Labrador dogs. After 3 months, four implants representing four different implant systems--groups A (turned), B (TiOblast), C (SLA), D (TiUnite)--were placed in a randomized order in the right side of the mandible. Three months after implant installation, experimental peri-implantitis was initiated by placement of ligatures and plaque formation. The ligatures were removed when about 40-50% of the supporting bone was lost. After the subsequent 24-week period of continued plaque accumulation, block biopsies containing implants and their surrounding tissues were obtained and prepared for histological analysis. All types of implants exhibited extensive inflammatory cell infiltrates and large associated crater-formed osseous defects. The lesions were consistently characterized by insufficient encapsulation of pus and biofilm layers and the inflammatory cell infiltrates extended apical of the pocket epithelium. The presence of numerous osteoclasts indicated active tissue destruction. The vertical dimension and the overall surface area of the infiltrated connective tissue (ICT) were larger at implants of group D than at other implant types. It is suggested that spontaneous progression of peri-implantitis is associated with severe inflammation and tissue destruction.

Spontaneous progression of peri‐implantitis at different types of implants. An experimental study in dogs. I: clinical and radiographic observations

The aim of the present study was to analyze tissue reactions to plaque formation following ligature removal at commercially available implants exposed to experimental peri-implantitis. Six Labrador dogs about 1 year old were used. All mandibular premolars and the three anterior premolars in both sides of the maxilla were extracted. After 3 months four implants representing four different implant systems with different surface characteristics--implant group A (turned), B (TiOblast), C (sandblasted acid-etched; SLA) and D (TiUnite)--were placed in a randomized order in the right side of the mandible. Three months after implant installation experimental peri-implantitis was initiated by placement of ligatures in a submarginal position and plaque accumulation. At week 12, when about 40-50% of the supporting bone was lost, the ligatures were removed. During the subsequent 24-week period plaque accumulation continued. Radiographic and clinical examinations were performed during the 'active breakdown' period (plaque accumulation and ligatures) and the plaque accumulation period after ligature removal. The experiment was terminated at week 36. The bone loss that took place during the 'active breakdown' period varied between 3.5 and 4.6 mm. The additional bone loss that occurred during the plaque accumulation period after ligature removal was 1.84 (A), 1.72 (B), 1.55 (C) and 2.78 mm (D). Spontaneous progression of experimentally induced peri-implantitis occurred at implants with different geometry and surface characteristics. Progression was most pronounced at implants of type D (TiUnite surface).

Mitogen-activated protein kinase up-regulation and activation during rat parotid gland atrophy and regeneration: role of epidermal growth factor and β2-adrenergic receptors

The rat secretory ductal obstruction model has been widely used to assess salivary gland injury, growth, and differentiation. In this study, a novel ductal obstruction and release procedure was used to explore the signaling pathways leading to salivary gland regeneration. Rats underwent bilateral parotid ductal obstruction in which the duct was occluded against a plastic disk subcutaneously and released by external ligature removal. This ductal obstruction/release procedure was validated to produce glandular atrophy and regeneration with histological analysis and periodic acid-Schiff staining. Immunoblot analysis indicated that during ductal obstruction and the early post-release period (day 7), expression of immunoreactive proliferating cell nuclear antigen and vimentin was increased in the parotid glands compared with sham-operated animals. Immunohistochemical staining and immunoblots revealed up-regulation of the mitogen-activated protein kinases (MAPKs), extracellular signal-regulated receptor kinase (ERK)1/2, and p38 during the atrophic and regeneration phases of ductal obstruction/release. Similarly, increases in activated, i.e., phosphorylated, ERK1/2 (pERK1/2) and p38 (phospho-p38) were demonstrable in both ductal and recovering acinar cells, with pERKs expressed predominantly in the nuclei and phospho-p38 distributed throughout the cells. Furthermore, levels of epidermal growth factor (EGF) receptor and β2-adrenergic receptor (β2-AR) were elevated in the ligated glands and at day 7 post-release; β1-AR levels did not change over the same time period. These results support the view that cell proliferation is involved in duct ligation-induced atrophy of the rat parotid gland and gland recovery upon ligature removal. Up-regulation of ERKs and p38, and the activation of these MAPKs by up-regulated EGF and β2-ARs, may be important signaling components underlying glandular atrophy and subsequent regeneration.

Topical administration of simvastatin recovers alveolar bone loss in rats

Simvastatin, a cholesterol-lowering drug, has been reported to show anabolic effects on bone metabolism. We examined the effects of simvastatin in vitro using cultured rat calvaria cells and in vivo using periodontitis-induced rats. Alkaline phosphatase activity and bone nodule formation were measured in cultured rat calvaria cells. Nylon ligature was placed around the maxillary molars of Fischer male rats for 20 d to induce alveolar bone resorption. After ligature removal, simvastatin was topically injected into the buccal gingivae for 70 d and then microcomputed tomography and histological examinations were performed. Simvastatin maintained high alkaline phosphatase activity and increased bone nodule formation in rat calvaria cells in a dose-dependent manner, showing that simvastatin increased and maintained a high level of osteoblastic function. Microcomputed tomography images revealed that treatment with simvastatin recovered the ligature-induced alveolar bone resorption, showing a 46% reversal of bone height. Histological examination clarified that low-mineralized alveolar bone was formed in simvastatin-treated rats. These findings demonstrate that simvastatin has the potential to stimulate osteoblastic function and that topical administration of simvastatin may be effective for the recovery of alveolar bone loss in rats.

Spontaneous progression of ligature induced peri‐implantitis at implants with different surface roughness: an experimental study in dogs

Peri-implantitis is associated with the presence of submarginal plaque, soft-tissue inflammation and advanced breakdown of the supporting bone. The progression of peri-implantitis following varying periods of continuing plaque accumulation has been studied in animal models. The aim of the current experiment was to study the progression of peri-implantitis around implants with different surface roughness. In five beagle dogs, three implants with either a sandblasted acid-etched surface (SLA) or a polished surface (P) were installed bilaterally in the edentulous premolar regions. After 3 months on a plaque control regimen, experimental peri-implantitis was induced by ligature placement and plaque accumulation was allowed to progress until about 40% of the height of the supporting bone had been lost. After this 4-month period, ligatures were removed and plaque accumulation was continued for an additional 5 months. Radiographs of all implant sites were obtained before and after 'active' experimental peri-implantitis as well as at the end of the experiment. Biopsies were harvested and the tissue samples were prepared for light microscopy. The sections were used for histometric and morphometric examinations. The radiographic examinations indicated that similar amounts of bone loss occurred at SLA and P sites during the active breakdown period, while the progression of bone loss was larger at SLA than at polished sites following ligature removal. The histological examination revealed that both bone loss and the size of the inflammatory lesion in the connective tissue were larger in SLA than in polished implant sites. The area of plaque was also larger at implants with an SLA surface than at implants with a polished surface. It is suggested that the progression of peri-implantitis, if left untreated, is more pronounced at implants with a moderately rough surface than at implants with a polished surface.

Diabetes Enhances Periodontal Bone Loss through Enhanced Resorption and Diminished Bone Formation

Using a ligature-induced model in type-2 Zucker diabetic fatty (ZDF) rat and normoglycemic littermates, we investigated whether diabetes primarily affects periodontitis by enhancing bone loss or by limiting osseous repair. Diabetes increased the intensity and duration of the inflammatory infiltrate (P < 0.05). The formation of osteoclasts and percent eroded bone after 7 days of ligature placement was similar, while four days after removal of ligatures, the type 2 diabetic group had significantly higher osteoclast numbers and activity (P < 0.05). The amount of new bone formation following resorption was 2.4- to 2.9-fold higher in normoglycemic vs. diabetic rats (P < 0.05). Diabetes also increased apoptosis and decreased the number of bone-lining cells, osteoblasts, and periodontal ligament fibroblasts (P < 0.05). Thus, diabetes caused a more persistent inflammatory response, greater loss of attachment and more alveolar bone resorption, and impaired new bone formation. The latter may be affected by increased apoptosis of bone-lining and PDL cells.

Progression of Experimental Chronic Peri‐Implantitis in Dogs: Clinical and Radiographic Evaluation

The aim of this study was to evaluate the progression of experimental peri-implantitis in dogs using implants with different surface coatings. Thirty-six dental implants with four different surface coatings, commercially pure titanium (cpTi), titanium plasma sprayed (TPS), hydroxyapatite (HA), and acid-etched (AE), were placed in six mongrel dogs. Five months after implantation, peri-implantitis was induced by cotton ligatures to facilitate plaque accumulation for 60 days. After 60 days, the ligatures were removed and supragingival plaque control was initiated for 12 months. Probing depth (PD), clinical attachment level (CAL), vertical bone level (VBL), horizontal bone level (HBL), and mobility were obtained at baseline, and 20, 40, 60 (acute phase), and 425 days (chronic phase) after ligature removal. PD and CAL changed around all implant surfaces after ligature placement (P<0.0001). However, the means of PD and CAL were not statistically significant among the different surfaces (P>0.05). The range of CAL variation, calculated between baseline and 60 days (acute phase) and between 60 and 425 days (chronic phase), decreased (P<0.05). Bone loss increased during the entire experiment (P<0.0001). The HA surface showed the greatest bone loss measurement (5.06+/- 0.38 mm) and the TPS showed the smallest bone loss (4.27+/- 0.62 mm). However, statistical significance was not assessed for different coatings (P>0.05). The clinical data at the initial phase showed rapid and severe peri-implant tissue breakdown. However, removal of ligatures did not convert the acute destructive peri-implant phase to a non-aggressive lesion and the progression of peri-implantitis was observed at chronic phase. The experimental peri-implantitis in dogs may be a useful model to evaluate the progression of peri-implantitis.

Spontaneous progression of experimentally induced periimplantitis.

Periimplantitis represents an inflammatory condition that is associated with the presence of a submarginal biofilm and with advanced breakdown of soft and mineralized tissues surrounding endosseous implants. Animal models have been used to describe mechanisms involved in the pathogenesis and treatment of the soft and hard tissue lesions of periimplantitis. The aim of the present experiment was to study the presence and progression of inflammatory lesions in tissues surrounding implants exposed to "experimental periimplantitis". Five Labrador dogs were used. In each dog, 2 or 3 implants were placed in both the left and right edentulous premolar regions of the mandible. Abutment connection was performed 4 months later and a plaque control regimen was initiated and maintained for 5 months. "Experimental periimplantitis" was subsequently induced by ligature placement and plaque accumulation was allowed to progress until about 40% of the height of the supporting bone had been lost. The ligatures were removed, but plaque formation was allowed to continue for an additional 12 months. Radiographs of all implant sites were obtained before and after active "experimental periimplantitis" as well as at the end of the experiment. Biopsies were harvested from the implant sites in 3 of the dogs. The tissue samples were prepared for light microscopy and the sections were used for histometric and morphometric examinations. One implant was lost during the first 2 months of "experimental periimplantitis" and two implants were lost during the 12 months that followed ligature removal. The radiographic examination indicated that varying amounts of additional bone loss occurred in the majority of the implant sites also following ligature removal. The mucosa of all implant sites harbored inflammatory lesions that extended apically of the pocket epithelium. The lesions were separated from the marginal bone by a zone of apparently normal connective tissue. A remission of the destructive inflammatory lesion in the periimplant tissues was seen in some sites following ligature removal, but in the majority of sites additional loss of supporting bone occurred.

Release of S100B Differs During Ischemia and Reperfusion of the Liver, the Gut, and the Kidney in Rats

S100B, an acknowledged marker of brain damage, is increased post-traumatically in plasma. The aim of this study was to investigate the diagnostic value of S100B release in experimental local extracranial ischemia and reperfusion. Anesthetized rats underwent laparotomy and ligation of the afferent blood vessels to the liver, gut, or kidney to achieve local ischemia in each organ separately. After 60 min of ischemia, ligatures were removed and resuscitation was performed for 3 h. S100B was determined in plasma by immunoluminometric assay 55, 65, and 240 min after the onset of ischemia (5 min before reperfusion and 5 min and 3 h after the onset of reperfusion). During ischemia of the liver, S100B increased before ligature removal and reperfusion, reaching significance early after the onset of reperfusion and remaining almost unchanged throughout reperfusion. In contrast, S100B did not increase during ischemia of the gut or kidney before ligature removal or during early reperfusion but increased significantly to similar levels as during reperfusion of the liver 240 min after the onset of ischemia (after 3 h of reperfusion). Our findings show for the first time that S100B increases during local extracranial ischemia and reperfusion. These experimental findings support the concept that brain damage is not necessarily the cause of increased S100B. Although S100B has been an acknowledged marker of brain damage for years, our experimental clinically relevant data indicate that S100B is, in fact, not specific as a marker of brain damage in the setting of local ischemia and reperfusion of the liver, gut, and kidney because local ischemia and reperfusion of these organs cause an S100B increase per se.

Lethal photosensitization in microbiological treatment of ligature-induced peri-implantitis: a preliminary study in dogs.

This pilot study evaluated, by culture testing, the effectiveness of lethal photosensitization for the microbiological treatment of peri-implantitis in dogs. Experimental peri-implantitis was induced by ligature placement for 2 months. Following ligature removal, plaque control was instituted by scrubbing with 0.12% chlorhexidine daily for 12 months. Subsequently, mucoperiosteal flaps were elevated for scaling the implant surface. Microbial samples were obtained with paper points before and after treatment of implant surfaces by means of 100 microg/ml toluidine blue O (TBO,) and were exposed, for 80 s, to light with a wavelength of 685 nm from a 50 mW GaAlAs diode laser. The mean initial and final bacterial counts were 7.22 +/- 0.20 and 6.84 +/- 0.44 CFU/ml, respectively for TVC (P < 0.0001); 6.19 +/- 0.45 and 3.14 +/- 3.29 CFU/ml for P. intermedia/nigrescens (P = 0.001); 5.98 +/- 0.38 and 1.69 +/- 2.90 CFU/ml for Fusobacterium spp. (P = 0.001); and 6.07 +/- 0.22 to 1.69 +/- 2.94 CFU/ml for beta-hemolytic Streptococcus (P = 0.0039). It may be concluded that lethal photosensitization resulted in a reduction of the bacterial count. Complete elimination of bacteria was achieved in some samples.

Management of ureteric injuries during gynecological operations: 10 years experience

Objective( s): To present our 10 years experience in the management of ureteric injuries occurring during gynecological surgery. Study design: Seventy-six patients had a variety of injuries. In 29 cases, the ureteric damage was diagnosed intraoperatively. Management of early-diagnosed injuries included suturing, ligature removal, end-to-end anastomosis, and reimplantation of the ureter. In 47 cases, the injury was diagnosed postoperatively. Ureteric catheterization was attempted in all cases presenting with obstruction. Catheterization failures were managed with ureterolysis, and reimplantation. Small ureteric fistula were managed with catheterization, and large communications with reimplantation. Two cases with urinomas were treated with surgical evacuation and anastomoses. Results: Management of early-diagnosed injuries was relatively easy in most cases. Postoperatively-diagnosed injuries were more difficult to treat. Catheterization failed in 28/44 (65.9%) ureters and surgical re-exploration was necessary. Long-term morbidity was minimal and no relapses occurred. Conclusion( s): Early recognition of a ureteric injury is the key to a complications-free repair. Unrecognized injuries cause prolonged morbidity, and their management can be difficult. Treatment of these injuries by experienced teams may minimize long-term consequences.