The street children of Manila are affected by early-in-life periodontal infection: description of a treatment modality: sea salt.

Thousands of street children of Manila are affected by early-in-life oral infection. The aim of the present investigation was to evaluate the effectiveness of a sea-salt mouthrinse solution in street children of Manila affected by mild to severe forms of periodontal disease. These children were all in need of special protection: abandoned, abused, exploited, neglected, orphaned, poor. During 3 oral-health missions in 2003, 2004 and 2005, 617 abandoned children (5 to 13 year-old), received oral examination at a non-sectarian child-caring institution in Metro Manila (Virlanie Foundation) by calibrated examiners. A treatment based on what could be done was proposed: 1. Teaching of a precise tooth brushing technique with sea-salt, controlled and reinforced every two days for one week by calibrated health educators, 2. The application of sea-salt water mouthrinse (2.5 gram in 20 ml). Periodontal measurements were repeated at the end of each mission. All children returned to child-caring institution for the followup examinations. In 2003, 10 male and 11 female (n=21) were diagnosed with aggressive periodontitis. In 2009 and 2010, none was affected by aggressive periodontitis. For all patients, the gingival index decreased from 1.08 at the first mission to 1.04 at the end of the second mission and 0.98 at the end of the third mission. The periodontal index decreased from 1.33 at the first mission to 0.98 at the second mission and 0.92 at the last mission. The present investigation confirms that prevention and early diagnosis can result in success with minimum cost. The provided oral health program empowered street children in the most desperate circumstances to be educated and become self-reliant, independent, and responsible. We propose here an antimicrobial approach which has a high degree of efficacy and tolerability, and can be implemented in virtually all parts of the world using low-cost resources.

Examination of periodontal pathogens in stenotic valve specimens and in whole blood samples in patients affected by aortic valve stenosis and chronic periodontitis.

Periodontitis may be a risk factor for atherosclerosis and coronary heart disease. The influence of periodontal pathogens in cardiovascular diseases needs further investigation. Therefore, the aims of this clinical study are: to test the presence of periodontal bacteria DNA in aortic valves and to assess the concomitant presence of the same periodontal bacteria DNA in whole blood samples in patients affected by aortic valve stenosis and chronic periodontitis. Nineteen consecutive patients (12 males and 7 females, age: 49-85 years) were enrolled in this study after having been subjected to a complete periodontal evaluation to confirm the diagnosis of chronic periodontitis. All patients were scheduled for aortic valve replacement surgery. After clinical and microbial periodontal examination, the aortic valve tissue specimens were obtained by excision during valve replacement surgery and the patients were subjected to the whole blood sampling before the surgery. The polymerase chain reaction technology was used to detect the putative periodontal pathogens Tannerella forshytia, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, Campylobacter rectus, Eikenella corrodens and Treponema denticola. Neither the 19 aortic valve specimens nor the blood samples were positive for the genoma of the selected periodontal pathogens. The selected periodontal pathogens did not colonize the aortic valve of patients affected by stenosis and bacterial genoma was not present in whole blood samples. A high blood pressure at the aortic valve may prevent the adhesion and proliferation of bacterial colonies.

Cytomegalovirus infection in symptomatic periapical pathosis.

AIM: To compare the presence of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) infections in samples from 25 symptomatic and 19 asymptomatic periapical lesions. METHODOLOGY: Periapical samples were collected by sterile curettes in conjunction with apicectomy. cDNA-based HCMV and EBV identification was performed on total mRNAs extracted from peripapical tissues, using primers for genes transcribed during the productive phase of the herpesvirus infection. Statistical analysis was performed using chi-squared test. RESULTS: HCMV was detected in 100% of the symptomatic and in 37% of the asymptomatic study lesions. EBV was identified only in HCMV-infected periapical lesions. The difference in occurrence of HCMV and EBV between symptomatic and asymptomatic periapical lesions was statistically significant (P < 0.0001). CONCLUSIONS: The noteworthy finding of this study was the ubiquitous occurrence of HCMV active infection in symptomatic periapical pathosis. EBV may contribute to periapical pathogenesis in a subset of symptomatic lesions. HCMV and EBV infections may cause periapical pathosis by inducing cytokine and chemokine release from inflammatory or connective tissue cells, or by impairing local host defences resulting in heightened virulence of resident bacterial pathogens. Knowledge about the role of herpesviruses in periapical pathosis seems important to fully delineate the pathogenesis of endodontic infectious diseases. HCMV and probably EBV should be added to the list of putative pathogenic agents in symptomatic periapical disease.

Human cytomegalovirus-associated periodontitis in renal transplant patients.

BACKGROUND: Human cytomegalovirus (HCMV) infection is associated with renal transplant failure. Periodontal pockets may be reservoirs for HCMV replication. OBJECTIVES: This study was done to determine active HCMV replication in saliva and gingival crevicular fluid of renal transplant patients affected by periodontitis. METHODS: HCMV pp67-mRNA amplification was analyzed in oral fluids of 38 transplant recipients at 6 months' posttransplantation. Patients received antiviral therapy until 3 months' posttransplantation. The HCMV-positive cell line VR-977 was the positive control, and oral fluids from healthy volunteers served as the negative control. Periodontitis was diagnosed by clinical examination. Serum HCMV IgG and IgM were analyzed to differentiate recent and latent infection. RESULTS: Prevalence of gingival overgrowth was 68.4%. HCMV gene transcripts were detected in the saliva of 21% and the gingival crevicular fluid of 18% of patients. All patients (100%) with HCMV pp67-mRNA detected in saliva demonstrated clinical manifestations of viral infection, as did 86% of patients with HCMV pp67-mRNA detected in the gingival crevicular fluid. Serum IgM was positive in 7.9% of patients and IgG in 65.8%; however, associations with active mRNA replication were not statistically significant. CONCLUSIONS: Renal transplant patients affected by periodontitis are at risk of viral replication within the periodontal tissues despite antiviral therapy. This study suggests that use of HCMV pp67-mRNA detection in saliva and gingival crevicular fluid provides markers of active viral infection, and evidence for a link between HCMV-associated periodontitis and renal transplant complications.

Cytomegalovirus and Epstein-Barr virus active infection in periapical lesions of teeth with intact crowns.

Herpesviruses seem to play an important role in the pathogenesis of aggressive periodontitis and may also contribute to periapical pathosis. This study determined the presence of human cytomegalovirus, Epstein-Barr virus, and herpes simplex virus productive infection in five symptomatic periapical lesions of teeth having intact crowns and calcified necrotic pulps. Periapical samples were collected in conjunction with periapical surgery and kept frozen until virological examination. Reverse transcription-polymerase chain reaction was used in herpesviral identification. RNA was isolated from periapical tissue by a guanidinium isothiocyanate-acid phenol procedure. cDNAs were generated from highly conserved regions of the test viruses using a preamplification kit. Sensitivity and validity of the PCR-primers were determined according to established methods. Amplification products were identified using gel electrophoresis. Human cytomegalovirus and Epstein-Barr virus dual transcription was detected in all five periapical lesions studied. Herpes simplex virus transcript was not identified in any lesion. The present data suggest that human cytomegalovirus or Epstein-Barr virus activation participate in the pathogenesis of symptomatic periapical lesions. We hypothesize that periapical active herpesvirus infection impairs local defenses, thereby inducing overgrowth of endodontopathic bacteria and the clinical flare-up of inflammation.

Cytomegalovirus and Epstein-Barr virus DNA transcription in endodontic symptomatic lesions.

OBJECTIVES: Productive Herpesviridae infections are implicated in the etio-pathogenesis of aggressive periodontitis. However, virtually nothing is known about a possible role of herpesviruses in pulpal and periapical pathosis. This study employed a cDNA analysis to determine transcription of human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV) in 14 recalcitrant periapical lesions and in 2 periapical healthy control sites. METHODS: Periapical samples were collected in conjunction with periapical surgery and kept frozen until virologic examination. RNA was isolated from periapical tissue by using a guanidinium isothiocyanate-acid phenol procedure (TRIZOL LS Reagent, GIBCO BRL, Rockville, MD). cDNAs were amplified by means of oligonucleotides targeting highly conserved regions of the test viruses and the RT-PCR-100 amplification kit (Sigma-Aldrich, St Louis, MO). Standardization of PCR primer sensitivity and validation was carried out according to established methods. Amplification products were identified by agarose gel electrophoresis. RESULTS: HCMV transcript was detected in 12 of 13 symptomatic and in 1 asymptomatic periapical lesion. EBV transcript was demonstrated in 8 of the 13 symptomatic lesions but not in the asymptomatic periapical lesion. HCMV and EBV dual transcription occurred at higher frequency in periapical lesions showing radiographic bone destruction of 5 mm x 7 mm or larger than in smaller size lesions (P = 0.03; Chi-squared test). No HCMV or EBV transcription was identified in the 2 healthy control sites. HSV transcript was not detected in any study site. CONCLUSION: The present data suggest that HCMV or EBV infections participate in the pathogenesis of periapical symptomatic lesions. Herpesviruses may produce periapical pathosis as a direct result of viral infection and replication, or as a consequence of virally induced impairment of the host defense and subsequent increased virulence of resident bacterial pathogens.

In vitro kinetic evaluation of titanium alloy biodegradation.

The present controlled in vitro experiment evaluated the dissolution kinetics of titanium (Ti), aluminum (Al) and vanadium (V). Titanium alloy (Ti90Al6V4) dental implants were inserted in 1.8 ml sterile tubes, containing equal volumes of NaCl 0.9% (w/v) and human serum. Metallic elements released by the atomic process of corrosion were measured at pH 7.2 and 37 C by atomic absorption spectrophotometer at 1, 3, 6, 9, 15, 21, 27, 33, 42, 51, 60, 69, 78, 87 and 96 days. Ti dissolution averaged 16+/-5 ng/cm2/day and 1565 ng/cm2 over the experimental period. Al dissolution was stable at 9+/-5 ng/cm2/day and averaged 945 ng/cm2 over the 96-day period. V dissolution was stable at 0.15+/-0.18 ng/cm2/day after the sixth day of incubation and averaged 42 ng/cm2 over the 96-day period. Major disparities in atomic dissolution were detected among implants. No local or systemic reaction to titanium has been documented. In contrast, 4% toxic V and 6% Al may suffice to elicit local and systemic reactions or inhibit cellular proliferation and differentiation.

Esthetic implant dentistry.

Consistency of results, reliability of treatment modalities, and long-term prognosis require scientific approaches to therapeutic procedures. Reliable and unbiased information rooted in academics and research assist the health care professional use current technology to develop the best course of action to restore or enhance the best esthetic outcome for the patient. Without anticipating potential failure, any immediate success is limited to initial satisfaction while ignoring the far greater elements of a future problematic outcome. This article proposes procedures for soft and hard tissue preservation, repair, or reconstruction in esthetic implant dentistry and emphasizes that an essential prerequisite to effective esthetic therapy is the establishment of a complete and accurate diagnosis.

Aggressive periodontitis associated with Fanconi's anemia. A case report.

BACKGROUND: Fanconi's anemia is an autosomal recessive disease associated with chromosomal breakage as well as pancytopenia, skin pigmentation, renal hypoplasia, cardiac defects, microcephaly, congenital malformations of the skeleton, hypogonadism, and increased risk of leukemia. The present report describes the periodontal clinical and microbiological status of an 11-year old male having Fanconi's anemia. METHODS: Polymerase chain reaction analysis to detect human cytomegalovirus (HCMV), Epstein-Barr type 1 virus, and herpes simplex virus (HSV) was performed on paper-point samples pooled from either 3 periodontal sites with advanced attachment loss or 3 gingivitis sites with no clinical attachment loss. Anaerobic bacterial culture examination was performed on the pooled periodontitis sample. RESULTS: The patient suffered from pancytopenia, allergy, asthma, hearing impairment, and mental retardation. Dentition consisted of 7 primary teeth, 11 erupted permanent teeth, and 14 unerupted permanent teeth. Most erupted teeth showed severe gingival inflammation with some gingival overgrowth and various degrees of periodontal attachment loss. Genomes of HCMV and HSV were detected in the pooled periodontitis sample and HCMV in the pooled gingivitis sample. The periodontitis sample but not the gingivitis sample revealed HCMV mRNA of major capsid protein, suggestive of active viral infection. The periodontitis sample also yielded Actinobacillus actinomycetemcomitans (1.1% of total isolates), FusobActerium species (7.9%), Campylobacter species (2.2%), Peptostreptococcus micros (3.4%), and Candida albicans (0.3%). CONCLUSIONS: Oral features of Fanconi's anemia may include increased susceptibility to periodontitis. It is likely that underlying host defense impairment coupled with periodontal infection by HCMV and A. actinomycetemcomitans contribute to the severe type of periodontitis associated with Fanconi's anemia.

Herpesviruses 6, 7 and 8 in HIV- and non-HIV-associated periodontitis.

Human herpesviruses, especially cytomegalovirus and Epstein Barr virus type-1, occur with higher frequency in subgingival specimens from periodontitis lesions than from healthy/gingivitis sites. Little or no information is available on the relationship between herpesvirus 6 (HHV-6), herpesvirus 7 (HHV-7) and herpesvirus 8 (HHV-8) and periodontal disease. This study determined the periodontal occurrence of HHV-6, HHV-7 and HHV-8 in 21 HIV-seropositive and 14 HIV-negative adults affected by periodontitis. Gingival biopsy specimens and paper-point samples of subgingival plaque were collected from sites showing 5 mm or more in probing depth. Nested polymerase chain reaction methodology was employed in herpesvirus identification. In the HIV-seropositive periodontitis group, 90% of gingival biopsies and 62% of subgingival plaque samples revealed at least one of the test viruses. HHV-6 occurred in 71%, HHV-7 in 67% and HHV-8 in 24% of gingival biopsies. In the HIV-negative adult periodontitis group, 43% of gingival biopsies showed at least 1 of the test viruses, with HHV-6 present in 21% and H HV-7 in 29% of gingival biopsies and with no detection of HHV-8. The combined occurrence of the 3 test herpesviruses was significantly higher in HIV-seropositive than in HIV-negative adult periodontitis patients (p = 0.008). The human periodontium might constitute a site of infection or reservoir for HHV-6, -7, -8.

Herpesviruses and periodontopathic bacteria in Trisomy 21 periodontitis.

BACKGROUND: Little is known about the etiology and pathogenesis of periodontal disease in Trisomy 21 patients. This study determined the occurrence of herpesviruses and putative periodontopathic bacteria in Trisomy 21 periodontitis. METHODS: Nineteen Trisomy 21 patients (17 to 37 years of age) contributed subgingival samples from molar and bicuspid teeth presenting interproximal periodontitis lesions (probing depths, 5 to 8 mm) and from shallow periodontal sites (probing depths, 1 to 3 mm). Samples were obtained at baseline, and at 1 and 4 weeks after subgingival debridement by means of hand instruments and ultrasonic scalers. Epstein-Barr virus type 1 and 2 (EBV-1 and EBV-2), human cytomegalovirus (HCMV), and herpes simplex virus (HSV) were identified by sensitive and specific nested polymerase chain reaction. Putative periodontopathic bacteria were identified by means of non-selective and selective culture. RESULTS: Of 19 Trisomy 21 periodontitis lesions, 6 (32%) were positive for EBV-1, 5 (26%) were positive for HCMV, 3 (16%) were positive for HSV, and 2 (11%) showed viral co-infection. Of 19 shallow periodontal sites, only one revealed HCMV. Prevotella intermedia, Bacteroides forsythus, and Capnocytophaga species were detected in higher proportions in deep than in shallow periodontal pockets (P = 0.02). Subgingival debridement did not reduce genomic herpesvirus presence but caused a decrease in proportions of Porphyromonas gingivalis and Capnocytophaga species. CONCLUSIONS: Periodontal herpesvirus-bacteria coinfections may play important roles in the pathogenesis of destructive periodontal disease in Trisomy 21 patients. Herpesviruses may reduce the periodontal defense and promote growth of subgingival bacteria capable of causing periodontal breakdown.

Herpesviruses in periodontal pocket and gingival tissue specimens.

Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in crevicular fluid of deep periodontal pockets, but little or no information is available on occurrence of herpesviruses in gingival tissue. This investigation studied the presence of herpesviruses in periodontal pockets and the corresponding gingival tissues from 11 periodontally healthy and 14 periodontitis sites. A nested-polymerase chain reaction was employed to identify the presence of HCMV, EBV-1, EBV-2, herpes simplex virus, human herpesvirus (HHV)-6, HHV-7 and HHV-8 in each test sample. In healthy periodontal sites, HCMV was detected in 1 (9%) and EBV-1 in 2 (18%) pocket samples, and HCMV was detected in 2 (18%) and EBV-1 in 3 (27%) gingival tissue samples. In periodontitis lesions, HCMV was detected in 9 (64%) pocket samples and in 12 (86%) gingival tissue samples, and EBV-1 was detected in 6 (43%) pocket samples and in 11 (79%) gingival tissue samples. HHV-6 and HHV-8 were detected exclusively in gingival tissue samples. The present findings confirm the frequent presence of HCMV and EBV-1 in periodontitis lesions and suggest using gingival tissue specimens for detecting periodontal HHV-6, HHV-7 and HHV-8.

Clinical and microbiologic study of periodontal surgery by means of apically positioned flaps with and without osseous recontouring.

In periodontitis lesions with interproximal craters, periodontal flap surgery with osseous recontouring allows more apical positioning of the soft periodontal tissue than flap surgery without osseous recontouring. The present study determined the clinical and microbiologic responses to periodontal surgery with and without osseous recontouring in adult periodontitis lesions with interproximal craters. In 7 osseous surgery patients, osteoplasty and ostectomy were performed from the lingual/palatal aspect to eliminate interproximal osseous defects and to partly mimic the original alveolar bony transition to neighboring teeth. In 7 nonosseous surgery patients, the surgical flap was adapted to the preexisting osseous level. Clinical monitoring included periodontal probing depth, Plaque Index, gingival bleeding index, and radiographic examination. Samples of the subgingival microbiota were examined. In sites treated with osseous surgery, mean pocket depth was 5.5 mm at baseline, 1.9 mm at 1 month, 2.0 mm at 3 months, and 2.1 mm at 6 months. In sites not receiving osseous recontouring surgery, the corresponding pocket depths were 5.9 mm, 3.1 mm, 3.8 mm, and 4.1 mm. At baseline in the osseous surgery group, Actinobacillus actinomycetemcomitans was recovered from one patient and Porphyromonas gingivalis from 5 patients; posttreatment, these microbiota were not detected in any patient. In the nonosseous surgery group, the presence of A actinomycetemcomitans increased posttreatment, and levels of P gingivalis remained essentially unchanged after therapy. This study suggests that in patients not receiving adjunctive antibiotic therapy, apically positioned flap surgery with osseous recontouring is more effective than apically positioned flap surgery without osseous recontouring in reducing periodontal pocket depth and levels of major periodontal pathogens.

Herpesvirus infection of inflammatory cells in human periodontitis.

Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in human periodontitis lesions. However, no information is available on the types of gingival cells infected by herpesviruses. The present study determined the presence of herpesviruses in polymorphonuclear neutrophils, monocytes, macrophages and T and B lymphocytes in biopsies of periodontitis lesions from 20 adults. A nested polymerase chain reaction method was employed to detect HCMV, EBV-1, EBV-2, human herpes virus-6 and herpes simplex virus (HSV) in periodontal tissue biopsy and in gingival cell fractions separated by immunomagnetic cell sorting. Tissue specimens from 18 (90%) and cell fractions from 14 (70%) patients demonstrated herpesviruses. Periodontitis-derived monocytes and macrophages revealed HCMV in cell fractions from 11 (55%) patients and HSV in cells from 1 (5%) patient. T lymphocytes harbored HCMV in cell fractions from 4 (20%) patients and HSV in cell fractions from 4 (20%) patients. B lymphocytes showed EBV-1 in cell fractions from 9 (45%) patients. Periodontal polymorphonuclear neutrophils demonstrated no herpesviruses. This study suggests that HCMV mainly infects periodontal monocytes, macrophages and less frequently T lymphocytes and that EBV-1 infects periodontal B lymphocytes. The possible etio-pathologic significance of periodontal herpesvirus infection is discussed.

Tetracycline-coated polytetrafluoroethylene barrier membranes in the treatment of intraosseous periodontal lesions.

BACKGROUND: Periodontal pathogens are detrimental to periodontal healing in barrier membrane-assisted periodontal therapy. Tetracycline-coating of barrier membranes may reduce levels of infecting pathogens. This study evaluated the clinical and microbiological effects of tetracycline-coated expanded polytetrafluoroethylene (T-ePTFE) barrier membranes in the treatment of 2- to 3-wall intraosseous periodontal lesions around mandibular molars. METHODS: Eleven patients received non-coated barrier membranes (ePTFE) and 11 patients received T-ePTFE barrier membranes. Tetracycline coating was performed by placing ePTFE membranes first in a 5% tridodecylmethylammonium chloride solution and then in a basic 3% tetracycline solution. Microbiological examination included conventional culture and DNA probe analyses. Barrier membranes were removed 6 weeks after insertion. RESULTS: At baseline, the periodontal lesion depth averaged 8.0 mm in the ePTFE treated group and 7.4 mm in the T-ePTFE group. At 1 year post-treatment, the mean gain of probing attachment was 1.9 mm in the ePTFE group and 3.3 mm in the T-ePTFE group (P = 0.02). At 3 minutes after membrane placement, suspected periodontal pathogens were detected in several ePTFE membranes but only in one T-ePTFE membrane. At 6 weeks, all membranes showed periodontal pathogens, including Porphyromonas gingivalis, Fusobacterium species, Peptostreptococcus micros, Bacteroides forsythus, and motile rods. CONCLUSIONS: This study suggests that the use of tetracycline-coated ePTFE barrier membranes can result in additional gain of clinical periodontal attachment, most likely due to the antimicrobial properties of tetracycline during initial healing.