Investigations on the Influencing of the Subgingival Microflora in Chronic Periodontitis

AIM: The aim of the present study was to investigate changes in the subgingival flora in adults with chronic periodontitis undergoing orthodontic fixed appliance therapy. PATIENTS AND METHODS: In seven adult patients who had undergone nonantibiotic periodontal pretreatment, the subgingival bacteria were subjected to microbiological examination and the number of periodontopathogenic organisms was determined before (T1: prior to treatment being started), during (T2: 6 weeks after orthodontic treatment was started) and after the end of orthodontic treatment (T3: 6 weeks after removal of the fixed appliances). RESULTS AND CONCLUSION: During the fixed appliance therapy (metal brackets, NiTi archwires, stainless steel archwires), a marked reduction was observed in the total bacteria count from the subgingival pocket despite the clinical periodontal parameters remaining almost unchanged. However, the total count of some highly pathogenic bacteria rose again slightly after the end of treatment. We attribute the marked improvement in the periodontopathogenic bacteria spectrum under fixed appliance therapy with metal brackets, NiTi archwires and stainless steel archwires to metal corrosion entailing the release of primarily nickel ions, which have a toxic effect on bacteria and thus enable the regeneration of the physiological bacterial flora. In none of the patients was a deterioration of the periodontal status observed during and after fixed appliance therapy.     

Uprighting partially impacted permanent second molars

Impaction of the lower second molar is not a common problem, but it is very challenging for both orthodontist and oral surgeon. Treatment options depend on the degree of tooth inclination, the position of the third molars, and the desired type of movement, which may be surgical and/or orthodontic in nature. A good treatment alternative is surgical uncovering with orthodontically-assisted eruption. A case of successful uprighting using a 0.017 x 0.025-inch titanium molybdenum alloy (TMA) tip-back cantilever is presented. Different aspects of uprighting impacted second molars are discussed in light of the literature. The iatrogenic character of lower second molar impaction is emphasized.     

Inhibition of lesion progression by the penetration of resins in vitro: influence of the application procedure

This study compared the progression of sealed initial enamel lesions penetrated with a fissure sealant (Helioseal, Vivadent) or various adhesives (Heliobond, Excite, Vivadent; Resulcin, Merz; Solobond M, Voco; Prompt L-Pop, 3M-ESPE) after exposure to a demineralizing solution, in vitro. From 27 bovine teeth, 54 enamel specimens were prepared and covered with nail varnish (control), thus obtaining three windows for treatment. After demineralization (pH 5.0; 14 days), two of the windows (A, B) were etched with phosphoric acid (20%; 5 seconds); whereas, the third area served as the control (C). The specimens were divided randomly into six groups (n=9), and the material was applied (90 seconds) either once (A) or twice (B). Light-curing followed each application. Half of the area of each specimen window was then covered with nail varnish, and the samples were again stored in the demineralizing solution (pH 5.0; 14 days). The specimens were cut perpendicular to the surface, and both enamel slabs were studied after infiltration using a fluorescent, low viscous resin (VIRIN) and confocal microscopy (CLSM). Lesion depths were calculated (ImageJ) from the surface to that point in the lesion where the grey values clearly changed to a darker grey. After demineralization, mean lesion depths (SD) (14 days) were measured at 105 (21) microm. The second demineralization led to a mean progression of the lesion depths of 52 (31)%. Adper Prompt L-Pop and Solobond M could not significantly prevent lesion progression after a single application (p > 0.05; t-test); however, the second application of Solobond M significantly decreased lesion progression (p < 0.05; t-test). Helioseal, Heliobond, Resulcin Monobond and Excite showed significantly better inhibition of the demineralization compared to the other materials (p < 0.05; Bonferroni). It can be concluded that the penetration of adhesives into initial lesions inhibited a further demineralization in vitro.     

Stabilizing sodium hypochlorite at high pH: effects on soft tissue and dentin

Introduction

When sodium hypochlorite solutions react with tissue, their pH drops and tissue sorption decreases. We studied whether stabilizing a NaOCl solution at a high pH would increase its soft-tissue dissolution capacity and effects on the dentin matrix compared with a standard NaOCl solution of the same concentration and similar initial pH.

Methods

NaOCl solutions were prepared by mixing (1:1) a 10% stock solution with water (standard) or 2 mol/L NaOH (stabilized). Physiological saline and 1 mol/L NaOH served as the controls. Chlorine content and alkaline capacity of NaOCl solutions were determined. Standardized porcine palatal soft-tissue specimens and human root dentin bars were exposed to test and control solutions. Weight loss percentage was assessed in the soft-tissue dissolution assay. Three-point bending tests were performed on the root dentin bars to determine the modulus of elasticity and flexural strength. Values between groups were compared using one-way analysis of variance with the Bonferroni correction for multiple testing (α < .05).

Results

Both solutions contained 5% NaOCl. One milliliter of the standard and the stabilized solution consumed 4.0 mL and 13.7 mL of a 0.1-mol/L HCl solution before they reached a pH level of 7.5, respectively. The stabilized NaOCl dissolved significantly more soft tissue than the standard solution, and the pH remained high. It also caused a higher loss in elastic modulus and flexure strength (P < .05) than the control solutions, whereas the standard solution did not.

Conclusions

NaOH-stabilized NaOCl solutions have a higher alkaline capacity and are thus more proteolytic than standard counterparts.     

Bleeding and non-bleeding phenotypes in patients with GGCX gene mutations

Functional limitations for the vitamin K cycle, caused either by mutations in gamma-glutamyl carboxylase or vitamin K epoxide reductase genes, result in hereditary deficiency of vitamin K-dependent coagulation factors (VKCFD1 and VKCFD2, respectively). Patients suffering from VKCFD often share several other anatomical irregularities which are not related to haemostasis. Here we report on nine patients, eight of them previously unreported, who presented with VKCFD1. All were examined with special attention to vitamin K-dependent coagulation factors as well as to bone and heart development and to other anatomical signs of embryonal vitamin K deficiency. In total, we detected ten mutations in the gamma-glutamyl carboxylase gene of which seven have not been previously reported. Most interestingly, additional non-bleeding phenotypes were observed in all patients including midfacial hypoplasia, premature osteoporosis, cochlear hearing loss, heart valve defects, pulmonary stenosis, or pseudoxanthoma elasticum-like phenotype. Undercarboxylated matrix Gla protein, osteocalcin, and periostin appear to be responsible for these defects which are also observed in cases of fetal warfarin syndrome.     

Progressive renal decline as the major feature of diabetic nephropathy in type 1 diabetes

Despite almost universal implementation of renoprotective therapies over the past 25 years, the risk of end-stage renal disease (ESRD) in type 1 diabetes (T1D) is not decreasing, and ESRD remains the major cause of excess morbidity and premature mortality [1]. Such a state of affairs prompts a call to action. In this review we re-evaluated the proteinuria-centric model of diabetic nephropathy and showed its deficiencies. On the basis of extensive studies that we have been conducting on the patients attending the Joslin Clinic, we propose that progressive renal decline, not abnormalities in urinary albumin excretion, should be considered as the major feature of disease processes leading to ESRD in T1D. The etiology of diabetic nephropathy should be reconsidered in light of our new findings so our perspective can be broadened regarding new therapeutic targets available for interrupting the progressive renal decline in T1D. Reduction in the loss of glomerular filtration rate, not reduction of albumin excretion rate, should become the measure for evaluating the effectiveness of new therapeutic interventions. We need new accurate methods for early diagnosis of patients at risk of progressive renal decline or, better still, for detecting in advance which patients will have rapid, moderate or minimal rate of progression to ESRD.