Elevated subgingival temperature infers high bacterial pathogen counts in severe periodontitis.

OBJECTIVES: Periodontal inflammation may be assessed by bleeding on probing and subgingival temperature. This pilot study evaluated the intrapatient relationship between subgingival temperature and selected bacterial groups/species in deep periodontal pockets with bleeding on probing. MATERIALS AND METHODS: In each of eight adults, an electronic temperature probe identified three "hot" pockets with elevated subgingival temperature and three "cool" pockets with normal subgingival temperature among premolars/molars with 6‒10 mm probing depths and bleeding on probing. Microbial samples collected separately from the hot and cool periodontal pockets were cultured for selected periodontal pathogens. RESULTS: Hot compared to cool periodontal pockets revealed significantly higher absolute and normalized subgingival temperatures and yielded higher mean proportions of Porphyromonas gingivalis (10.2% for hot vs. 2.5% for cool, p = 0.030) and total red/orange complex periodontal pathogens (48.0% for hot vs. 24.6% for cool, p = 0.012). CONCLUSIONS: Hot versus cool deep periodontal pockets harbored significantly higher levels of major periodontal pathogens. Subgingival temperature measurements may potentially be useful to assess risk of periodontitis progression and the efficacy of periodontal therapy.

Systemic ciprofloxacin treatment of multidrug-resistant Aggregatibacter actinomycetemcomitans in severe periodontitis.

An adult periodontitis patient treated with mechanical/surgical therapy experienced gingival necrosis and granulomas post-treatment. Aggregatibacter actinomycetemcomitans, a tissue-invasive pathogen, was recovered and multidrug-resistant but susceptible to ciprofloxacin. Systemic ciprofloxacin eliminated A. actinomycetemcomitans with marked clinical improvement. Ciprofloxacin may be prescribed for A. actinomycetemcomitans periodontal infection unresponsive to the common amoxicillin-metronidazole treatment.

Aggressive periodontitis in southwestern American Indian adolescents.

BACKGROUND: This study determined the prevalence of aggressive (molar-incisor pattern) (Ag/MI) periodontitis and assessed the associated subgingival bacterial-herpesvirus microbiota in Pueblo Indian adolescents in the southwestern United States. METHODS: The study included 240 Pueblo Indian adolescents, aged 13-20 years old, residing in three Rio Grande River villages in New Mexico and the Hopi Pueblo reservation in Arizona. Adolescents with Ag/MI periodontitis or periodontal health provided subgingival samples for culture of bacterial pathogens and for polymerase chain reaction detection of periodontal herpesviruses. RESULTS: Ag/MI periodontitis was detected in 22 (9.2%) Pueblo Indian adolescents, with 21 exhibiting a localized molar-incisor breakdown pattern. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and other red/orange complex bacterial pathogens predominated in Ag/MI periodontitis, whereas periodontal health yielded mainly viridans streptococci and Actinomyces species. Periodontal herpesviruses demonstrated a 3.5 odds ratio relationship with Ag/MI periodontitis. The only adolescent with generalized Ag/MI periodontitis harbored viral co-infection by cytomegalovirus plus Epstein-Barr virus Type 1, in addition to A. actinomycetemcomitans, P. gingivalis, and several other periodontopathic bacteria. CONCLUSIONS: Pueblo Indian adolescents showed an unusually high prevalence of early-age Ag/MI periodontitis predominated by periodontopathic bacteria and herpesviruses suspected to be major etiologic agents of the disease.

Herpesvirus-Bacteria pathogenic interaction in juvenile (aggressive) periodontitis. A novel etiologic concept of the disease.

Localized juvenile (aggressive) periodontitis starts at puberty in otherwise healthy individuals and involves the proximal surfaces of permanent incisors and first molars. The disease destroys a sizeable amount of periodontal bone within a few months despite minimal dental plaque and gingival tissue inflammation. Cytomegalovirus and Epstein-Barr virus, as well as the two main periodontopathic bacteria Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, are linked to juvenile periodontitis. Juvenile periodontitis-affected teeth show cementum hypoplasia. We hypothesize that an active herpesvirus infection, at the time of root formation, hampers cementum formation and, at puberty, herpesvirus reactivation triggers an upgrowth of bacterial pathogens which produce rapid periodontal destruction on teeth with a defective periodontium. A pathogenic interaction between active herpesviruses and bacterial pathogens can potentially explain the etiology and incisor-first molar destructive pattern of juvenile periodontitis. Effective treatment of juvenile periodontitis may target the herpesvirus-bacteria co-infection.

Effect of supragingival air polishing on subgingival periodontitis microbiota.

Background: Supragingival air polishing of teeth effectively removes dental plaque and extrinsic stain on coronal tooth surfaces, but its impact on specific periodontal pathogens in adjacent subgingival biofilms is not known. This study assessed the microbiological effect of supragingival air polishing on the subgingival microbiota of individuals with severe periodontitis. Methods: Supragingival air polishing with a sodium bicarbonatebased powder was performed on 15 adult test subjects, with the nozzle of the air polishing device aimed apically at a 45° angle onto tooth surfaces immediately coronal to the entrance of periodontal pockets. Supragingival prophylaxis paste polishing, using a slow-speed handpiece, was carried out on 13 adult control subjects. Subgingival specimens were collected from a single 5 mm to 7 mm periodontal pocket with bleeding on probing in each of the study participants before and immediately after supragingival polishing procedures. Viable bacterial counts and selected putative periodontal pathogens (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia/nigrescens, Fusobacterium nucleatum, Parvimonas micra, Campylobacter species) were quantified by microbial culture, and motile morphotypes (spirochetes and motile rods) by phase-contrast microscopy. Results: Statistically significant decreases were detected after supragingival air polishing in total viable counts (84.9% decrease), in P. intermedia/nigrescens, F. nucleatum, Campylobacter species, total proportions of red/orange complex periodontal pathogens (82.3% decrease), and in motile morphotypes (85.3% decrease). No statistically significant subgingival microbiological changes occurred with supragingival prophylaxis paste polishing. Conclusion: Supragingival air polishing of teeth, but not supragingival prophylaxis paste polishing, may serve as a useful therapeutic adjunct to disrupt and help remove pathogenic biofilms in deep periodontal pockets.

Contexte: Le polissage à air supragingival des dents élimine efficacement la plaque dentaire et les taches extrinsèques sur les surfaces coronaires des dents, mais on ignore son incidence sur les agents pathogènes parodontaux spécifiques des biofilms sous-gingivaux adjacents. Cette étude a évalué l'effet microbiologique du polissage à air supragingival sur le microbiote sous-gingival de clients ayant une parodontite sévère. Méthodologie: Quinze sujets d'essai adultes ont obtenu un polissage à air supragingival à base de poudre de bicarbonate de sodium avec la buse du dispositif de polissage à air orienté à un angle de 45° sur les surfaces immédiatement coronaires à l'entrée des poches parodontales. Treize sujets témoins adultes ont obtenu un polissage prophylactique supragingival à pâte effectué au moyen d'une pièce à main à vitesse lente. Des échantillons sous-gingivaux ont été prélevés d'une seule poche parodontale de 5 mm à 7 mm présentant un saignement au sondage chez chacun des participants de l'étude avant et immédiatement après les procédures de polissage supragingival. Le nombre de bactéries viables et certains pathogènes parodontaux putatifs (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia/nigrescens, Fusobacterium nucleatum, Parvimonas micra, espèces de Campylobacter) ont été quantifiés par culture microbienne, et les morphotypes mobiles (spirochètes et bâtonnets mobiles) par microscopie à contraste de phase. Résultats: Des réductions statistiquement significatives ont été décelées après le polissage à air supragingival dans le compte total de bactéries viables (diminution de 84,9 %), de P. intermedia/nigrescens, F. nucleatum et des espèces de Campylobacter, dans les proportions totales de pathogènes parodontaux du complexe rouge/orange (diminution de 82,3 %) et dans les morphotypes mobiles (diminution de 85,3 %). Aucun changement microbiologique sous-gingival statistiquement considérable n'a eu lieu avec le polissage prophylactique supragingival à pâte. Conclusion: Le polissage à air supragingival des dents, mais pas le polissage prophylactique supragingival à pâte, peut servir à titre de complément thérapeutique utile pour perturber et aider à éliminer les biofilms pathogènes dans les poches parodontales profondes.

Antimicrobial Chemotherapy for Recalcitrant Severe Human Periodontitis.

This study evaluated a combined systemic and topical anti-infective periodontal treatment of 35 adults who had experienced ongoing periodontal breakdown following conventional surgical periodontics. The prescribed anti-infective therapy, based on microbiological testing, consisted of a single course of metronidazole plus ciprofloxacin (23 patients), metronidazole plus amoxicillin/clavulanic acid (10 patients), and metronidazole plus ciprofloxacin followed by metronidazole plus amoxicillin/clavulanic acid (2 patients). In addition, the study patients received 0.1% povidone-iodine subgingival disinfection during non-surgical root debridement and daily patient administered oral irrigation with 0.1% sodium hypochlorite. At 1 and 5 years post-treatment, all study patients showed gains in clinical periodontal attachment with no further attachment loss, and significant decreases in pocket probing depth, bleeding on probing, and subgingival temperature. The greatest disease resolution occurred in patients who at baseline harbored predominantly major periodontal pathogens which post-antibiotics became non-detectable and substituted by non-periodontopathic viridans streptococci. The personalized and minimally invasive anti-infective treatment regimen described here controlled periodontitis disease activity and markedly improved the clinical and microbiological status of the refractory periodontitis patients.

Concise evaluation and therapeutic guidelines for severe periodontitis: A public health perspective.

The main goal of periodontology is to prevent and arrest gingivitis and periodontitis to avoid tooth loss and focal infection of periodontal origin. Periodontal scaling or flap surgery of moderate-to-severe periodontitis have shortcomings, most likely because removal of herpesviruses and bacterial pathogens in deep periodontal lesions and the adjacent inflamed gingiva requires systemic antimicrobial treatment (or gingivectomy). Valacyclovir (1000 mg twice daily on day 1, and 500 mg twice daily on day 2 and on day 3) is a potent anti-herpesvirus agent. Antibiotic combinations against bacterial pathogens include amoxicillin-metronidazole (250 mg of each, thrice daily for 4 days; for systemically healthy adults) and ciprofloxacin-metronidazole (500 mg of each, twice daily for 4 days; for immunosuppressed individuals and patients exposed to contaminated water and poor sanitation). Supportive antiseptic treatment may consist of 0.1%-0.2% sodium hypochlorite (regular household bleach) as cooling spray in ultrasonic scalers, flosser fluid in oral irrigators, and mouthrinse in patient self-care. The anti-infective treatment described here helps control cases of severe periodontitis and constitutes an exceedingly inexpensive alternative to conventional (mechanical) periodontal therapy.

Valacyclovir in Pain Management of Acute Apical Abscesses: A Randomized Placebo-Controlled Double-Blind Pilot Study.

INTRODUCTION: The acute (symptomatic) apical abscess is characterized by pulp necrosis, rapid onset, spontaneous pain, percussion pain, pus formation, and tissue swelling. The etiopathology of acute apical abscesses includes active (lytic) herpesviruses and gram-negative anaerobic bacteria. The present study examined the potential of valacyclovir, an anti-herpesvirus agent, and systemic amoxicillin to manage the pain of acute apical abscesses. METHODS: Twenty emergency patients with moderate to severe apical abscess pain received randomly either amoxicillin (1 g immediate dose followed by 500 mg, 4 times a day, totally 7 days) + valacyclovir (2 g immediate dose followed by 500 mg, twice a day, totally 3 days) ("valacyclovir" group, 10 patients) OR amoxicillin (1 g immediate dose followed by 500 mg, 4 times a day, totally 7 days) + placebo ("placebo" group, 10 patients). Daily telephone calls during the 6-day follow-up period assessed pain level on a numeric rating scale and analgesic intake. The Mann-Whitney and the Friedman statistical tests analyzed the outcome data. RESULTS: At the baseline examination, all 10 valacyclovir and 9 placebo patients exhibited moderate to severe pain and 18 patients needed pain medication. On the first day after baseline, the valacyclovir group showed 2 patients with moderate/severe pain and 1 patient on pain medication, but the placebo group revealed as many as 8 patients with moderate/severe pain and 9 patients on pain medication. The difference in pain level and analgesic usage between the valacyclovir and the placebo group remained statistically significant during the entire post-baseline study period (P < .05). CONCLUSION: The present study points to valacyclovir as a promising adjunctive agent in pain control with acute apical abscesses.

Human and herpesvirus microRNAs in periodontal disease.

Periodontitis is a multi-etiologic infection characterized clinically by pathologic loss of the periodontal ligament and alveolar bone. Herpesviruses and specific bacterial species are major periodontal pathogens that cooperate synergistically in producing severe periodontitis. Cellular immunity against herpesviruses and humoral immunity against bacteria are key periodontal host defenses. Genetic, epigenetic, and environmental factors are modifiers of periodontal disease severity. MicroRNAs are a class of noncoding, gene expression-based, posttranscriptional regulatory RNAs of great importance for maintaining tissue homeostasis. Aberrant expression of microRNAs has been associated with several medical diseases. Periodontal tissue cells and herpesviruses elaborate several microRNAs that are of current research interest. This review attempts to conceptualize the role of periodontal microRNAs in the pathogenesis of periodontitis. The diagnostic potential of salivary microRNAs is also addressed. Employment of microRNA technology in periodontics represents an interesting new preventive and therapeutic possibility.

The human oral phageome.

Oral bacteriophages (or phages), especially periodontal ones, constitute a growing area of interest, but research on oral phages is still in its infancy. Phages are bacterial viruses that may persist as intracellular parasitic deoxyribonucleic acid (DNA) or use bacterial metabolism to replicate and cause bacterial lysis. The microbiomes of saliva, oral mucosa, and dental plaque contain active phage virions, bacterial lysogens (ie, carrying dormant prophages), and bacterial strains containing short fragments of phage DNA. In excess of 2000 oral phages have been confirmed or predicted to infect species of the phyla Actinobacteria (>300 phages), Bacteroidetes (>300 phages), Firmicutes (>1000 phages), Fusobacteria (>200 phages), and Proteobacteria (>700 phages) and three additional phyla (few phages only). This article assesses the current knowledge of the diversity of the oral phage population and the mechanisms by which phages may impact the ecology of oral biofilms. The potential use of phage-based therapy to control major periodontal pathogens is also discussed.

A bibliometric analysis of periodontology.

This bibliometric study assessed periodontal/implant articles that were part of the five most-cited dental articles in each of the years 2005-2019. Periodontal/implant articles made up one to four articles in each of 14 years and totaled 40% of the yearly five most-cited dental articles. The three core periodontal journals (Journal of Clinical Periodontology, Journal of Periodontology, and Periodontology 2000) increased ~50%-100% in Journal Impact Factor from 2005 to 2015 and were among the 10 most-cited dental journals in the 2015-2019 period. The Journal of Clinical Periodontology and Periodontology 2000 were in several years assigned the highest Journal Impact Factor in dentistry. In summary, periodontal journals continue to publish high-impact articles that are relevant for both oral health care and medicine.

Life-threatening pathogens in severe/progressive periodontitis: Focal infection risk, future periodontal practice, role of the Periodontology 2000.

Severe/progressive periodontitis is associated with cardiovascular disease, cancer, Alzheimer's disease, and dozens of other serious diseases. Herpesviruses are implicated in severe periodontitis and in specific subsets of each of the above systemic diseases. That both periodontitis and herpesviruses are linked to the same nonoral diseases is consistent with a systemic pathogenic role of periodontal herpesviruses. Effective control of periodontitis-related systemic diseases requires collaboration between dentistry and medicine. Periodontology has emerged as an important preventive medical discipline, and periodontal teaching and practice need to adjust accordingly.

Primer on etiology and treatment of progressive/severe periodontitis: A systemic health perspective.

Periodontology is an infectious disease-based discipline. The etiopathology of progressive/severe periodontitis includes active herpesviruses, specific bacterial pathogens, and proinflammatory cytokines. Herpesviruses and periodontopathic bacteria may interact synergistically to produce periodontal breakdown, and periodontal herpesviruses may contribute to systemic diseases. The infectious agents of severe periodontitis reside in deep pockets, furcation lesions, and inflamed gingiva, sites inaccessible by conventional (purely mechanical) surgical or nonsurgical therapy but accessible by systemic antibiotic treatment. This brief overview presents an effective anti-infective treatment of severe periodontitis, which includes systemic chemotherapy/antibiotics against herpesviruses (valacyclovir [acyclovir]) and bacterial pathogens (amoxicillin + metronidazole or ciprofloxacin + metronidazole) plus common antiseptics (povidone-iodine and sodium hypochlorite) and select ultrasonic scaling. The proposed treatment can cause a marked reduction or elimination of major periodontal pathogens, is acceptably safe, and can be carried out in minimal time with minimal cost.

Herpesvirus-bacteria synergistic interaction in periodontitis.

The etiopathogenesis of severe periodontitis includes herpesvirus-bacteria coinfection. This article evaluates the pathogenicity of herpesviruses (cytomegalovirus and Epstein-Barr virus) and periodontopathic bacteria (Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis) and coinfection of these infectious agents in the initiation and progression of periodontitis. Cytomegalovirus and A. actinomycetemcomitans/P. gingivalis exercise synergistic pathogenicity in the development of localized ("aggressive") juvenile periodontitis. Cytomegalovirus and Epstein-Barr virus are associated with P. gingivalis in adult types of periodontitis. Periodontal herpesviruses that enter the general circulation may also contribute to disease development in various organ systems. A 2-way interaction is likely to occur between periodontal herpesviruses and periodontopathic bacteria, with herpesviruses promoting bacterial upgrowth, and bacterial factors reactivating latent herpesviruses. Bacterial-induced gingivitis may facilitate herpesvirus colonization of the periodontium, and herpesvirus infections may impede the antibacterial host defense and alter periodontal cells to predispose for bacterial adherence and invasion. Herpesvirus-bacteria synergistic interactions, are likely to comprise an important pathogenic determinant of aggressive periodontitis. However, mechanistic investigations into the molecular and cellular interaction between periodontal herpesviruses and bacteria are still scarce. Herpesvirus-bacteria coinfection studies may yield significant new discoveries of pathogenic determinants, and drug and vaccine targets to minimize or prevent periodontitis and periodontitis-related systemic diseases.

A bibliometric analysis of Periodontology 2000.

The continually high impact factor of Periodontology 2000 (7.861 for 2018), the level of which is unprecedented among dental journals, prompted the present bibliometric analysis of the Journal. Since the inception of Periodontology 2000 in 1993 and until July 2019, the top 100 most-cited articles have received a total of 21,276 (Web of Science), 23,009 (Elsevier's Scopus), and 43,518 (Google Scholar) citations. The citations of the 100 most-cited articles were found to vary from 118 to 827 (Web of Science), 10 to 1069 (Scopus), and 15 to 2028 (Google Scholar). Three articles had more than 600 (Web of Science) citations, 5 had between 400 and 600 citations, 25 had between 200 and 400 citations, and 67 had between 100 and 200 citations. The first authors of the 100 most-cited articles were based in the USA (51%), Switzerland (14%), and Australia (10%). The 5 dental institutions with the most frequently cited articles were The Forsyth Institute, USA (9 articles), The University of Queensland, Australia (8 articles), University of Bern, Switzerland (7), University of Texas Health Science Center at San Antonio, USA (6 articles), and University of Washington, USA, and Temple University School of Dentistry, USA (5 articles each). The likely reason for the high impact factor of Periodontology 2000 is publication of insightful and timely review articles produced by eminent researchers and clinicians from a wide range of dental institutions and countries.

Periodontal herpesvirus morbidity and treatment.

Four billion individuals worldwide have a history of periodontitis, with the poorest people in society most affected. Periodontitis can lead to unsightly drifting of teeth and tooth loss that may interfere with the wellbeing of daily living and has also been linked to at least 57 medical diseases and disabilities. The etiology of severe periodontitis includes active herpesviruses, specific bacterial pathogens, and destructive immune responses, but herpesviruses seem to be the major pathogenic determinant. Periodontal herpesviruses that disseminate via the systemic circulation to nonoral sites may represent a major link between periodontitis and systemic diseases. Current treatment of periodontitis focuses almost exclusively on bacterial biofilm and will require revision. Periodontal therapy that targets both herpesviruses and bacterial pathogens can provide long-term clinical improvement and potentially reduces the risk of systemic diseases. Molecular diagnostic tests for periodontal pathogens may enable early microbial identification and preemptive therapy. This review details an efficient and reliable anti-infective treatment of severe periodontitis that can be carried out in minimal time with minimal cost.

Focal infection of periodontal origin.

Periodontology has evolved from a predominantly mechanical to a sophisticated infectious disease-based discipline. Research has paved the way for a greater understanding of the periodontal microbiome, improvement in periodontal diagnostics and therapies, and the recognition of periodontitis being associated with more than 50 systemic diseases. The etiopathology of progressive periodontitis includes active herpesviruses, specific bacterial pathogens, and proinflammatory immune responses. This article points to a role of periodontal herpesviruses in the development of systemic diseases and proposes treatment of severe periodontitis not only to avoid tooth loss, but also to reduce the risk for systemic diseases. An efficient, safe, and reliable anti-infective treatment of severe periodontitis is presented, which targets both herpesviruses and bacterial pathogens and which can be carried out in minimal time with minimal cost.

Radiographic alveolar bone morphology and progressive periodontitis.

BACKGROUND: This study evaluated the relationship between radiographic crestal alveolar bone morphology and progressive periodontitis. METHODS: A total of 1,356 posterior interproximal sites in 56 adults treated for chronic periodontitis and receiving systematic 3-month maintenance care were scored for angular or horizontal marginal bone morphology, as well as for alveolar crestal lamina dura, on radiographs obtained at baseline of a 30-month post-treatment period. Semi-annually, the study patients were clinically evaluated for progressive periodontitis. Logistic regression analysis assessed baseline parameters to progressive periodontitis over the 30-month post-treatment period. RESULTS: Progressive periodontitis was detected at 33 (2.4%) posterior interproximal sites in 20 (35.7%) patients. Sites with post-treatment angular bony defects developed progressive periodontitis more frequently (14.7%) than sites with a horizontal bone topography (1.8%). Angular bony defects (odds ratio = 10.6) and periodontal probing depths ≥5 mm (odds ratio = 4.2) were identified as statistically significant independent predictors of progressive periodontitis at posterior interproximal sites. Angular bony and horizontal lesions with intact radiographic lamina dura revealed an absence of progressive periodontitis through 24 months. CONCLUSIONS: Post-treatment presence of angular bone morphology and periodontal probing depths ≥5 mm significantly increased risk of progressive periodontitis at posterior interproximal sites. Sites of all morphology and probing depth that displayed radiographic crestal lamina dura at post-treatment baseline exhibited clinical stability for ≥24 months.

Periodontitis: facts, fallacies and the future.

This volume of Periodontology 2000 represents the 25th anniversary of the Journal, and uses the occasion to assess important advancements in periodontology over the past quarter-century as well as the hurdles that remain. Periodontitis is defined by pathologic loss of the periodontal ligament and alveolar bone. The disease involves complex dynamic interactions among active herpesviruses, specific bacterial pathogens and destructive immune responses. Periodontal diagnostics is currently based on clinical rather than etiologic criteria, and provides limited therapeutic guidance. Periodontal causative treatment consists of scaling, antiseptic rinses and occasionally systemic antibiotics, and surgical intervention has been de-emphasized, except perhaps for the most advanced types of periodontitis. Plastic surgical therapy includes soft-tissue grafting to cover exposed root surfaces and bone grafting to provide support for implants. Dental implants are used to replace severely diseased or missing teeth, but implant overuse is of concern. The utility of laser treatment for periodontitis remains unresolved. Host modulation and risk-factor modification therapies may benefit select patient groups. Patient self-care is a critical part of periodontal health care, and twice-weekly oral rinsing with 0.10-0.25% sodium hypochlorite constitutes a valuable adjunct to conventional anti-plaque and anti-gingivitis treatments. A link between periodontal herpesviruses and systemic diseases is a strong biological plausibility. In summary, research during the past 25 years has significantly changed our concepts of periodontitis pathobiology and has produced more-effective and less-costly therapeutic options.