Joerg Meyle

Peri‐implant diseases: Consensus Report of the Sixth European Workshop on Periodontology

Issues related to peri-implant disease were discussed. It was observed that the most common lesions that occur, i.e. peri-implant mucositis and peri-implantitis are caused by bacteria. While the lesion of peri-implant mucositis resides in the soft tissues, peri-implantitis also affects the supporting bone. Peri-implant mucositis occurs in about 80% of subjects (50% of sites) restored with implants, and peri-implantitis in between 28% and 56% of subjects (12-40% of sites). A number of risk indicators were identified including (i) poor oral hygiene, (ii) a history of periodontitis, (iii) diabetes and (iv) smoking. It was concluded that the treatment of peri-implant disease must include anti-infective measures. With respect to peri-implant mucositis, it appeared that non-surgical mechanical therapy caused the reduction in inflammation (bleeding on probing) but also that the adjunctive use of antimicrobial mouthrinses had a positive effect. It was agreed that the outcome of non-surgical treatment of peri-implantitis was unpredictable. The primary objective of surgical treatment in peri-implantitis is to get access to the implant surface for debridement and decontamination in order to achieve resolution of the inflammatory lesion. There was limited evidence that such treatment with the adjunctive use of systemic antibiotics could resolve a number of peri-implantitis lesions. There was no evidence that so-called regenerative procedures had additional beneficial effects on treatment outcome.

Interleukin‐1β Concentration of Gingival Crevicular Fluid

The concentration of interleukin-1β is elevated in inflamed gingival tissue. Therefore a method for the measurement of interleukin-1β (Il-1β) in gingival crevicular fluid (GCF) using a commercially available Il-1β ELISA was developed. GCF was collected with periopaper strips and 4 protocols of sampling using filter paper strips were tested; the method with a recovery rate of 111.9% (SD: ± 14.5%) was chosen for subsequent analysis of all samples. Il-1β concentration in GCF of periodontitis patients and a healthy control group was determined. Patients (n = 19, mean age: 29.3 years) had not been treated. The healthy control group (n = 14, mean age: 22.8 years) showed, after a hygiene regimen of 2 weeks, no clinical signs of gingival/periodontal inflammation. Probing depth, clinical attachment level, bleeding upon probing, and a modified plaque index were recorded. Il-1β could be detected in all GCF samples. The concentration ranged between 22.8 ng/ml and 150 ng/ml in the healthy control group and between 85.8 ng/ml and 882.2 ng/ml in the periodontitis patients. No sex-related differences were noted. According to our present results the determination of GCF Il-1β concentration is possible using commercially available test kits if the principle of sample preparation is adapted to the specific requirements of GCF analysis. J Periodontol 1994; 65:423-428.

Peri-implant tissue destruction : the Third EAO Consensus Conference 2012

OBJECTIVEnThe task of this working group was to update the existing knowledge base regarding the prevalence of peri-implant tissue destruction, the role of occlusal overload, and the outcome of non-surgical and surgical treatment.nnnMATERIALS AND METHODSnThe literature was systematically searched and critically reviewed. Four manuscripts were presented in key areas deemed to be essential for the current understanding of the magnitude of the clinical entity peri-implantitis. The role of overload as an etiological component was reviewed. Also available data on the results from non-surgical and surgical interventions for the control of tissue destruction were presented.nnnRESULTSnThe consensus statements following plenary session approval, clinical implications, and directions for future research based on the group discussions are presented in this article. The results and conclusions of the systematic review process are presented by the respective authors in the subsequent papers.

Molecular aspects of the pathogenesis of periodontitis

The past decade of basic research in periodontology has driven radical changes in our understanding and perceptions of the pathogenic processes that drive periodontal tissue destruction. The core elements of the classical model of disease pathogenesis, developed by Page & Kornman in 1997, remain pertinent today; however, our understanding of the dynamic interactions between the various microbial and host factors has changed significantly. The molecular era has unraveled aspects of genetics, epigenetics, lifestyle and environmental factors that, in combination, influence biofilm composition and the hosts inflammatory immune response, creating a heterogenic biological phenotype that we label as periodontitis. In this volume of Periodontology 2000, experts in their respective fields discuss these emerging concepts, such as a health-promoting biofilm being essential for periodontal stability, involving a true symbiosis between resident microbial species and each other and also with the host response to that biofilm. Rather like the gut microbiome, changes in the local environment, which may include inflammatory response mediators or viruses, conspire to drive dysbiosis and create a biofilm that supports pathogenic species capable of propagating disease. The host response is now recognized as the major contributor to periodontal tissue damage in what becomes a dysfunctional, poorly targeted and nonresolving inflammation that only serves to nourish and sustain the dysbiosis. The role of epithelial cells in signaling to the immune system is becoming clearer, as is the role of dendritic cells as transporters of periodontal pathogens to distant sites within the body, namely metastatic infection. The involvement of nontraditional immune cells, such as natural killer cells, is being recognized, and the simple balance between T-helper 1- and T-helper 2-type T-cell populations has become less clear with the emergence of T-regulatory cells, T-helper 17 cells and follicular helper cells. The dominance of the neutrophil has emerged, not only as a potential destructor when poorly regulated but as an equally unpredictable effector cell for specific B-cell immunity. The latter has emerged, in part, from the realization that neutrophils live for 5.4 days in the circulation, rather than for 24 h, and are also schizophrenic in nature, being powerful synthesizers of proinflammatory cytokines but also responding to prostaglandin signals to trigger a switch to a pro-resolving phenotype that appears capable of regenerating the structure and function of healthy tissue. Key to these outcomes are the molecular signaling pathways that dominate at any one time, but even these are influenced by microRNAs capable of silencing certain inflammatory genes. This volume of Periodontology 2000 tries to draw these complex new learnings into a contemporary model of disease pathogenesis, in which inflammation and dysbiosis impact upon whether the outcome is driven toward acute resolution and stability, chronic resolution and repair, or failed resolution and ongoing periodontal tissue destruction.

Role of microbial biofilms in the maintenance of oral health and in the development of dental caries and periodontal diseases. Consensus report of group 1 of the Joint EFP/ORCA workshop on the boundaries between caries and periodontal disease

BACKGROUND AND AIMSnThe scope of this working group was to review (1) ecological interactions at the dental biofilm in health and disease, (2) the role of microbial communities in the pathogenesis of periodontitis and caries, and (3) the innate host response in caries and periodontal diseases.nnnRESULTS AND CONCLUSIONSnA health-associated biofilm includes genera such as Neisseria, Streptococcus, Actinomyces, Veillonella and Granulicatella. Microorganisms associated with both caries and periodontal diseases are metabolically highly specialized and organized as multispecies microbial biofilms. Progression of these diseases involves multiple microbial interactions driven by different stressors. In caries, the exposure of dental biofilms to dietary sugars and their fermentation to organic acids results in increasing proportions of acidogenic and aciduric species. In gingivitis, plaque accumulation at the gingival margin leads to inflammation and increasing proportions of proteolytic and often obligately anaerobic species. The natural mucosal barriers and saliva are the main innate defence mechanisms against soft tissue bacterial invasion. Similarly, enamel and dentin are important hard tissue barriers to the caries process. Given that the present state of knowledge suggests that the aetiologies of caries and periodontal diseases are mutually independent, the elements of innate immunity that appear to contribute to resistance to both are somewhat coincidental.

Long-term analysis of osseointegrated implants in non-smoker patients with a previous history of periodontitis

AIMnTo evaluate long-term clinical and radiographic parameters of osseointegrated implants in non-smoker patients with a previous history of chronic periodontitis.nnnMATERIALS AND METHODSnFifty-four screw-type implants with a moderately roughened surface and internal hexagonal implant-abutment connection were placed according to a two-phase protocol and 40 reference teeth were analysed at baseline, and after 5 and 10xa0years. Pocket probing depth (PPD), clinical attachment level (CAL) and bleeding on probing were analysed 6x/tooth in all teeth, implants and reference teeth. Radiographic peri-implant bone level was measured on the mesial and distal surfaces. The prevalence of peri-implantitis and the survival rate of the implants were assessed at the patient and implant levels. Data were analysed using descriptive statistics, Mann-Whitney U-test, and Wald Z-test, at αxa0=xa05%.nnnRESULTSnIn implants, the CAL at 5xa0years was 0.3xa0mm higher, and at 10xa0years 1.2xa0mm higher in comparison to baseline. The corresponding data for the reference teeth were 0xa0mm and 0.5xa0mm respectively. Multilevel testing showed statistical difference for PPD between implants and teeth over time. After 10xa0years, the mean mesial bone loss was 0.63xa0±xa00.26xa0mm, and the mean distal bone loss was 0.56xa0±xa00.25. The survival rates were 100% and 92.3% for the implants in the mandible and the implants in the maxilla respectively.nnnCONCLUSIONSnScrew-type implants with internal hexagon placed in patients with a previous history of periodontitis attending a regular maintenance programme demonstrated stable clinical and radiographic results after 5 and 10xa0years.

A multi‐centre randomized controlled clinical trial on the treatment of intra‐bony defects with enamel matrix derivatives/synthetic bone graft or enamel matrix derivatives alone: results after 12 months

OBJECTIVESnComparison of the clinical and radiographic outcomes of a combination of enamel matrix derivatives (EMD) and a synthetic bone graft (EMD/SBG) with EMD alone in wide (≥2 mm) and deep (≥4 mm) one- and two- wall intra-bony defects 12 months after treatment.nnnMATERIALS AND METHODSnSeventy-three patients with chronic periodontitis and one wide (≥2 mm) and deep (≥4 mm) intra-bony defect were recruited in five centres in Germany. During surgery, defects were randomly assigned to EMD/SBG (test) or EMD (control). Assessments at baseline, after 6 and 12 months included bone sounding, attachment levels, probing pocket depths, bleeding on probing, and recessions. Changes in defect fill were recorded radiographically.nnnRESULTSnBoth treatment modalities led to significant clinical improvements. In the EMD/SBG group a mean defect fill of 2.7 ± 1.9 mm was calculated, in the EMD group the defect fill was 2.8 ± 1.6 mm. A mean gain in clinical attachment of 1.7 ± 2.1 mm in the test group and 1.9 ± 1.7 mm in the control group after 1 year was observed. Radiographic analysis confirmed for both groups that deeper defects were associated with greater defect fill.nnnCONCLUSIONnThe results show comparable clinical and radiographic outcomes following both treatment modalities 12 months after treatment.

Is progression of periodontitis relevantly influenced by systemic antibiotics? A clinical randomized trial

AIMnWe investigated the long-term impact of adjunctive systemic antibiotics on periodontal disease progression. Periodontal therapy is frequently supplemented by systemic antibiotics, although its impact on the course of disease is still unclear.nnnMATERIAL & METHODSnThis prospective, randomized, double-blind, placebo-controlled multi-centre trial comprising patients suffering from moderate to severe periodontitis evaluated the impact of rational adjunctive use of systemic amoxicillin 500 mg plus metronidazole 400 mg (3x/day, 7 days) on attachment loss. The primary outcome was the percentage of sites showing further attachment loss (PSAL) ≥1.3 mm after the 27.5 months observation period. Standardized therapy comprised mechanical debridement in conjunction with antibiotics or placebo administration, and maintenance therapy at 3 months intervals.nnnRESULTSnFrom 506 participating patients, 406 were included in the intention to treat analysis. Median PSAL observed in placebo group was 7.8% compared to 5.3% in antibiotics group (Q25 4.7%/Q75 14.1%; Q25 3.1%/Q75 9.9%; p < 0.001 respectively).nnnCONCLUSIONSnBoth treatments were effective in preventing disease progression. Compared to placebo, the prescription of empiric adjunctive systemic antibiotics showed a small absolute, although statistically significant, additional reduction in further attachment loss. Therapists should consider the patients overall risk for periodontal disease when deciding for or against adjunctive antibiotics prescription.

A Novel Approach to the Use of Subgingival Controlled-Release Chlorhexidine Delivery in Chronic Periodontitis: A Randomized Clinical Trial

BACKGROUNDnWe aimed to analyze clinical, microbiologic, and serologic effects of chlorhexidine (CHX) chips used as a subgingival controlled-release delivery device before and immediately after scaling and root planing (SRP).nnnMETHODSnTwenty-four patients presenting with ≥12 teeth with probing depth (PD) ≥5 mm and bleeding on probing were assigned in test or control groups. After prophylaxis, CHX chips (test) or placebo chips (control) were placed in pockets with PD ≥5 mm. Ten days later, SRP was performed in all teeth with PD ≥4 mm in a single appointment. Immediately after SRP, new chips were inserted in all pockets with PD ≥5 mm. Parameters were assessed at baseline; beginning of SRP; and 1, 3, and 6 months after treatment. Subgingival samples were obtained at baseline; beginning of SRP; and at 1 month after treatment. Periodontal pathogens Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, and Treponema denticola were analyzed. Serum levels of high sensitive C-reactive and lipopolysaccharide-binding proteins were measured. The changes of the parameters between and within the groups were tested by Mann-Whitney U test (P <0.05).nnnRESULTSnAll clinical and serologic parameters improved in both groups over time. There was a significant difference in clinical attachment level (CAL) gain from baseline to 6 months between groups (1.17 mm in the test group versus 0.79 mm in the placebo group) (P <0.05). The treatment with CHX chips showed a greater reduction of the microorganisms of the red complex after 1 month (P = 0.02).nnnCONCLUSIONnThe use of CHX chips before and immediately after SRP improved CAL and reduced the subgingival microorganisms of the red complex in the treatment of chronic periodontitis.

Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions

Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non-periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non-dental plaque biofilm-induced gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque-induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque-induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or in a currently stable periodontitis patient i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient-centered approach to care, and therefore, creates differences in the way in which a case of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.