Innovations in Preventive Dentistry E-Book

• Herausgeber: Quintessence Publishing
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 460

Veröffentlichungsjahr: 2021

Beschreibung

Prevention is better than healing ... or treatment. Thus, preventive dentistry is a cross-sectional challenge for all fields in dentistry, and one that has already achieved great success, as shown by the caries decline in many countries. The walls between prevention and treatment have recently fallen in caries and periodontal disease, as well as in orthodontics, where guidance of function and space maintenance are a combination of prevention and treatment. This book discusses new developments and innovations in preventive dentistry, from primary "real" prevention to secondary prevention by inactivating initial lesions, and on to tertiary prevention to avoid subsequent progression and complications of manifest oral disease. This evidence base is then translated into clinical dental practice. The book addresses everyone interested or involved in dentistry, including students, the whole dental practice team, educators, health scientists, and policy makers, who want to gain insight into these up-to-date clinical practices and future developments. It intends to make an impact on teaching and all fields of clinical dentistry – not by giving cookbook recipes, but by pointing out the rationale behind the changes in our routines. Presented by an international group of recognized specialists in their fields, the topics include the new understanding and management of caries and periodontal disease, prevention of orthodontic problems, diagnostic approaches, the role of diet and according recommendations for oral health, routes to better oral hygiene, changes in oral disease patterns and their consequences, non- and minimally invasive caries treatment, current fluoride guidelines including the use of silver fluorides, risk management, a common risk-factor approach, facilitating behavior changes, sealants, and probiotics. This broad spectrum is elucidated for the most relevant dental problems from early childhood to seniors to implement preventively oriented dental practice.

Leseprobe

Christian Splieth (Editor)

Innovations in Preventive Dentistry

A CIP record for this book is available from the British Library.

ISBN: 978-1-78698-099-1

Quintessenz Verlags-GmbH

Ifenpfad 2–4

12107 Berlin

Germany

www.quintessence-publishing.com

© 2021 Quintessenz Verlags-GmbH, Berlin

All rights reserved. This book or any part thereof may not be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, or otherwise, without prior written permission of the publisher.

Editing: Elizabeth Ducker Publishing, UK

Layout and Production: René Kirchner, Quintessenz Verlags-GmbH, Berlin, Germany

Preface

Preventive dentistry is a cross-sectional success story that has produced a 90% caries decline in children and adolescents, as well as caries reductions in adults in many countries. Periodontology and orthodontics also offer great opportunities for prevention … and prevention in all fields of dentistry has grown from primary prevention through maintaining a healthy state to new concepts of secondary prevention, where initial lesions or imbalances are corrected with minimal intervention. In addition, therapy has shifted from repair to tertiary prevention to regain physiologic and healthy balances that ensure long-lasting therapeutic success.

In order to introduce these new developments and innovations into preventive and clinical dentistry for all ages, a group of internationally recognized specialists presents new diagnostic methods and offers options for putting these into practice both for primary prevention and for non- and minimally invasive treatment. With the introduction of a systematic, evidence-based approach in dentistry, new standards for clinical care are being established in all fields of dentistry, stressing prevention-oriented routines. The understanding of caries and periodontal disease has shifted from a focus on invasive treatment to controlling disease activity, and in orthodontics from mechanics to achieving physiologic function. The various chapters highlight this shift, in addition to a clinical view, the overall concept, interaction with general health, and the common risk-factor approach. The authors offer perspectives for tackling dental and medical problems in the vulnerable populations that exhibit most of the dental and medical disease.

Preventive dentistry has changed for epidemiologic, social, and scientific reasons. Professionals should manage this development actively for the benefit of patients in all fields of dentistry and for all ages.

Christian H. Splieth

Editor

Prof Dr Christian H. Splieth

Department for Preventive & Pediatric Dentistry

University of Greifswald

Greifswald, Germany

Contributors

Dr Mohamed H. Abudrya

Department for Preventive & Pediatric Dentistry

University of Greifswald

Greifswald, Germany

OA Priv Doz Dr Mohammad Alkilzy

Department for Preventive & Pediatric Dentistry

University of Greifswald

Greifswald, Germany

Assoc Prof Dr Azam Bakhshandeh

Department of Odontology

University of Copenhagen

Copenhagen, Denmark

Dr Irene Dige

Department of Dentistry and Oral Health

Aarhus University

Aarhus, Denmark

Prof Dr Henrik Dommisch

Department of Periodontology, Oral Medicine and Oral Surgery

Charité – Universitätsmedizin Berlin

Berlin, Germany

Dr Denise Duijster

Department of Social Dentistry

Academic Center for Dentistry Amsterdam Amsterdam, The Netherlands

Prof Dr Kim R. Ekstrand

Department of Odontology

University of Copenhagen

Copenhagen, Denmark

Prof Dr Elena Figuero

Department of Dental Clinical Specialties, Faculty of Dentistry, University Complutense of Madrid

Madrid, Spain

Prof Dr Margherita Fontana

Department of Cariology, Restorative Sciences and Endodontics

University of Michigan School Dentistry

Ann Arbor, MI, USA

Prof Dr Carlos González-Cabezas

Department of Cariology, Restorative Sciences and Endodontics

University of Michigan School Dentistry

Ann Arbor, MI, USA

Dr Daniela Hoedke

Department of Periodontology, Oral Medicine and Oral Surgery

Charité – Universitätsmedizin Berlin

Berlin, Germany

Prof Dr Nicola Innes

School of Dentistry

College of Biomedical and Life Sciences

Cardiff University, Cardiff, UK

Prof Dr Karl-Friedrich Krey

Department for Orthodontics

University of Greifswald

Greifswald, Germany

Dr Line Staun Larsen

Department of Dentistry and Oral Health

Aarhus University

Aarhus, Denmark

Prof Dr Vita Mačiulskienė

Clinic of Dental and Oral Pathology, Faculty of Odontology

Lithuanian University of Health Sciences

Kaunas, Lithuania

Prof Dr Jukka H. Meurman

Department of Oral and Maxillofacial Diseases

University of Helsinki and Helsinki University Hospital

Helsinki, Finland

Dr Mhd Said Mourad

Department for Preventive & Pediatric Dentistry

University of Greifswald

Greifswald, Germany

Prof Dr Branca Heloisa Oliveira

Department of Community and Preventive Dentistry, School of Dentistry

Rio de Janeiro State University

Rio de Janeiro, Brazil

OÄ Dr Anja Ratzmann

Department for Orthodontics

University of Greifswald

Greifswald, Germany

OÄ Dr Ruth M. Santamaría

Department for Preventive & Pediatric Dentistry

University of Greifswald

Greifswald, Germany

Prof Dr Ana Paula P. Santos

Department of Community and Preventive Dentistry, School of Dentistry

Rio de Janeiro State University

Rio de Janeiro, Brazil

OA Dr Julian Schmoeckel

Department for Preventive & Pediatric Dentistry

University of Greifswald

Greifswald, Germany

Prof Dr Falk Schwendicke

CharitéCentrum für Zahn-, Mund- und Kieferheilkunde

Charité – Universitätsmedizin Berlin

Berlin, Germany

Prof Dr Murali Srinivasan

Clinic of General-, Special Care-, & Geriatric Dentistry, Center of Dental Medicine

University of Zurich

Zurich, Switzerland

Dr Nadezhda Stancheva

Private Practice

Frauenfeld, Switzerland

Prof Dr Livia M.A. Tenuta

Department of Cariology, Restorative Sciences and Endodontics

University of Michigan School Dentistry

Ann Arbor, MI, USA

Prof emeritus Svante Twetman

Department of Odontology

Faculty of Health and Medical Sciences

University of Copenhagen

Copenhagen, Denmark

Prof (em) Dr Cor van Loveren

Department of Cariology

Academic Center for Dentistry Amsterdam Amsterdam, The Netherlands

Dr J. H. (Erik) Vermaire

Child Health – Oral Health Division

TNO Healthy Living

Leiden, The Netherlands

Prof Dr Egija Zaura

Department of Preventive Dentistry

Academic Centre for Dentistry Amsterdam

Amsterdam, The Netherlands

Prof Dr Stefan Zimmer

Department of Operative and Preventive Dentistry, Dental School

Witten/Herdecke University

Witten, Germany

Abbreviations

AAPD, American Academy of Pediatric Dentistry

ACFP, amorphous calcium fluoride phosphate

ACP, amorphous calcium phosphate

ACPA, anti-citrullinated protein antibody

AD, Alzheimer disease

ART, atraumatic restorative therapy

BL, bone loss

BMI, body mass index

BOP, bleeding on probing

CAL, clinical attachment level

CHALO, Child Health Action to Lower Oral Health and Obesity

CI, confidence interval

CPP, casein phosphopeptide

CRFA, Common Risk Factor Approach

CRP, C-reactive protein

DIFOTI, digital imaging fiber-optic transillumination

DHSW, Dental Health Support Worker

DM, diabetes mellitus

dmfs, decayed, missing, or filled surfaces

DMFT, decayed, missing, or filled teeth

EADPH, European Association of Dental Public Health

ECC, early childhood caries

EHCP, Essential Health Care Program

EPS, extracellular polymeric substances

FOTI, fiber-optic transillumination

GA, general anesthesia

GBR, guided bone regeneration

GER, guided enamel regeneration

GTR, guided tissue regeneration

GWAS, genome-wide association studies

HA, hydroxyapatite

IADR, International Association for Dental Research

ICDAS, International Caries Detection and Assessment System

IgA, immunoglobulin A

IL, interleukin

MFP, monofluorophosphate

MI, motivational interviewing

MIH, molar incisor hypomineralization

NCD, noncommunicable disease

NHS, National Health Service

NNT, number needed to treat

NOCTP, nonoperative caries treatment program

NRCC, nonrestorative cavity control

NSF, nano silver fluoride

OHI, oral hygiene instruction

OHRQoL, oral health-related quality of life

OR, odds ratio

ORCA, European Organisation for Caries Research

OSAS, obstructive sleep apnea syndrome

PAD, peptidylarginine deiminase

PD, probing depth

PISA, periodontal inflamed surface area

PMPR, professional mechanical plaque removal

PSI, Periodontal Screening Index

QLF, quantitative light-induced fluorescence

RME, rapid maxillary expansion

RR, relative risk

RRR, relative risk reduction

SaC, Specific affected Caries Index

SAPM, self-assembling peptide matrix

SDF, silver diammine fluoride

SDG, Sustainable Development Goal

S-ECC, severe early childhood caries

SES, socioeconomic status

SCT, social cognitive theory

SiC, Significant Caries Index

SMART, silver modified atraumatic restorative technique

SNP, single nucleotide polymorphism

SPT, supportive periodontal therapy

SSB, sugar-sweetened beverages

TMD, temporomandibular disorders

TNF, tumor necrosis factor

VAS, visual analog scale

WASH, water, sanitation, and hygiene

WHO, World Health Organization

WIC, Women, Infants, and Children program

Contents

Preface

Editor

Contributors

Abbreviations

Chapter 1 – Understanding caries

Christian H. Splieth, Mhd Said Mourad, Mohammad Alkilzy, Julian Schmoeckel, Ruth M. Santamaría

Caries epidemiology and its consequences

Early childhood caries

Caries diagnostics

Clinical examination

Caries activity

Further diagnostics

Current concepts and treatment approaches in caries management

References

Chapter 2 – Understanding periodontitis

Daniela Hoedke, Henrik Dommisch

Epidemiology

Etiopathogenesis of periodontitis

Periodontitis in relation to systemic diseases

Clinical features and diagnosis

Prevention and therapy of periodontal diseases

Oral hygiene

Preventive and therapeutic aspects in relation to general health

References

Chapter 3 – Fluoride: How much is needed?

Livia M.A. Tenuta, Line Staun Larsen, Branca Heloisa Oliveira, Ana Paula P. Santos, Carlos González-Cabezas

Fluoride: the mode of action and why it is needed

Fluoride toothpaste: how much fluoride is enough?

Professional fluoride use: mechanism and evidence

Using as much fluoride as needed

References

Chapter 4 – Nutrition and caries: Sugar is the enemy, but what solutions are offered by preventive dentistry?

Cor van Loveren

Shape of the dose-response association between sugar intake and caries

Influence of fluoridated toothpaste

Frequency or amount of sugar

Reduction of sugar content in products

Selective taxation for unhealthy and healthy products

Personal advice

References

Chapter 5 – Healthy life, healthy mouth? Interdisciplinary and common risk factor interventions

Denise Duijster, J. H. (Erik) Vermaire

Determinants of childhood dental caries

The rationale for the Common Risk Factor Approach and interdisciplinary action

Interventions using interdisciplinary partnerships for the prevention of dental caries

Integrated interventions to prevent childhood dental caries and obesity

Integrated interventions to prevent childhood dental caries- and hygiene-related diseases

References

Chapter 6 – Oral hygiene: The best route to a healthy mouth?

Elena Figuero, Irene Dige, Vita Mačiulskienė

Definition of the dental biofilm

Nature of the dental biofilm

How to interfere with the dental biofilm

Clinical effect of biofilm control on dental caries

The role of fluoride

The effect of supervised versus individually performed tooth cleaning

Clinical effect of biofilm removal on periodontal and peri-implant diseases

Self-performed mechanical biofilm control

Chemical biofilm control

References

Chapter 7 – Interdental oral hygiene: To floss, or not to floss?

Falk Schwendicke, Christian H. Splieth

The evidence for flossing

The evidence for interdental brushes

Clinical considerations

References

Chapter 8 – Tooth brushing: Myth and science

Stefan Zimmer

Classic criteria of a manual toothbrush

Production of toothbrushes

Evidence-based criteria for manual toothbrushes

Manual toothbrushes for children

Tooth brushing technique

Tooth brushing time

References

Chapter 9 – Guidance for healthy dental and oral behavior: Multilevel prevention of early childhood caries

Julian Schmoeckel

How do we learn: different theories

Ethical considerations in modern patient-doctor relationships

Health literacy and belief in self-efficacy

Evidence of different aspects in counseling for preventing ECC

Access to children: prevention on individual, group, and collective level

References

Chapter 10 – Fissure sealing: Still to be recommended?

Kim R. Ekstrand, Azam Bakshandeh, Christian H. Splieth

Caries progression on occlusal surfaces

Preventive and therapeutically placed fissure sealants

Effectiveness of fissure sealants

Clinical application

From science to clinical recommendations

References

Chapter 11 – Prebiotics, probiotics, and synbiotics: A revolution in preventive dentistry?

Svante Twetman, Jukka H. Meurman, Egija Zaura

Oral prebiotics

Oral probiotics

Oral synbiotics

References

Chapter 12 – Silver fluorides: The new magic bullet?

Mohamed H. Abudrya, Christian H. Splieth, Ruth M. Santamaría

Historical background

Composition

Mechanism of action

Indications

Contraindications and side effects

Clinical application

Existing evidence

References

Chapter 13 – Self-assembling peptides: A perfectly engineered preventive and therapeutic tool?

Mohammad Alkilzy, Christian H. Splieth

Self-assembling peptide P11-4

In vitro studies

In vivo and clinical studies

Clinical application of P11-4 for treatment of initial caries

Further clinical implications of SAP

References

Chapter 14 – Nonrestorative cavity control: Can nonoperative “preventive” treatment replace restorations?

Ruth M. Santamaría, Nicola Innes

What is nonrestorative cavity control?

Natural history of dental caries

Prevention as a desirable approach to managing dental caries

Historical management of caries lesions

Is restorative management always necessary or possible?

How to carry out NRCC

What is the aim of NRCC?

For which patients is NRCC indicated?

NRCC technique

What are the main advantages of NRCC?

What are the main disadvantages of NRCC?

Is taking an NRCC approach cost-effective?

Is taking an NRCC approach clinically effective?

References

Chapter 15 – Prevention and prophylaxis in orthodontics: Neglected opportunities for successful prevention

Karl-Friedrich Krey, Anja Ratzmann, Nadezhda Stancheva

Etiology of malocclusion and malfunction as the basis of prevention

Form follows function

The beginning of orthodontic prevention

Breastfeeding, swallowing, and chewing

Habits and malfunctions

Playing musical instruments

Premature loss of primary molars and space maintainers

Canine retention

Unilateral reverse articulation

Anterior reverse articulation and periodontal health

Caries

Sleep disorders and upper airway management

Trauma prevention

Temporomandibular disorders

Third molar removal as prevention of crowding

Orofacial clefts

References

Chapter 16 – Prevention in elderly and medically compromised patients

Murali Srinivasan

Demographics of aging: related effects and retention of natural teeth

Periodontal disease and root caries

Prevention of periodontal disease

Prevention of root caries

References

Chapter 17 – Caries risk or activity: Which should we assess?

Margherita Fontana, Ruth M. Santamaría

Caries risk assessment

Caries activity

References

1

Understanding caries

Christian H. Splieth, Mhd Said Mourad, Mohammad Alkilzy, Julian Schmoeckel, Ruth M. Santamaría

In their new consensus statement on the terminology of dental caries and dental caries management, the European Organisation for Caries Research (ORCA) and the International Association for Dental Research (IADR) define caries as “a biofilm-mediated, diet modulated, multifactorial, noncommunicable, dynamic disease resulting in net mineral loss of dental hard tissues. It is determined by biologic, behavioral, psychosocial and environmental factors. As a consequence of this process, a caries lesion develops.”1 This very modern definition is based on the concept that caries is an imbalance of demineralization and remineralization that results from a dysbiosis of the oral biofilm, the overconsumption of carbohydrates, and insufficient oral hygiene (Fig 1-1).

Thus, the prevention of caries aims to adjust and ensure a healthy balance of the oral microbiome, dietary intake, oral hygiene, and mineral supply to avoid a net loss in enamel and dentin of healthy teeth. Caries therapy can only be successful in the long run if this is achieved when demineralization has already taken place. Therefore, caries prevention and its treatment employ the same concept and are nowadays combined as caries control, management, or care.

Figs 1-1a and b Caries is nowadays understood as an imbalance between de- and remineralizing factors resulting in a net loss of minerals (a). Thus, modern caries management modifies oral hygiene, diet, the biofilm, and the mineral equilibrium, keeping sound tooth surfaces healthy, inactivating existing caries lesions (b), and preventing recurrent demineralization around restorations.

This is also reflected in the ORCA/IADR definition of caries care, management, or control comprising “actions taken to interfere with mineral loss at all stages of the caries disease, including nonoperative and operative interventions/treatment. The terms caries care/management/control may be more appropriate than the term ‘caries prevention’ and because of the continuous de- and remineralization processes, caries control needs to be continued throughout the life course.”1

In consequence, the terms of caries prevention and therapy merge, which is not really surprising as restorative care and accompanying efforts to reduce caries activity have been viewed as secondary and tertiary prevention for a long time. Taking this into account, ORCA/IADR state that caries prevention “traditionally meant inhibition of caries initiation, otherwise called primary prevention. Primary, together with secondary and tertiary prevention, comprising nonoperative and operative treatments, are now summarized under caries care, management, or control.”1

The following chapters regarding caries risk prediction, fluoride use, biofilm and diet control, and promoting oral health are based on this new understanding of caries. As in periodontal disease, the primary goal of all preventive and therapeutic approaches is to achieve a high quality of life by establishing a physiologic, regenerative balance to maintain proper oral health.

Caries epidemiology and its consequences

On a global level, a remarkable caries decline could be achieved for the permanent dentition in children and adolescents in many industrialized regions such as the US, Canada, Europe, or Oceania. Although Germany was not the first country to experience this, consecutive and recent national surveys for all ages allow for a detailed analyses, which reveal trends2,3 that seem to be similar in many countries (Figs 1-2 and 1-3):

Caries prevalence has reduced from ten or more affected permanent teeth in adolescents during the 1970s to a mean of less than one decayed, missing, or filled teeth (DMFT) in 12-year-olds nowadays.

4

About 90% of the caries burden can be prevented and tooth loss is almost eradicated in the permanent dentition in adolescents.

2

,

4

After the caries decline, 80% of the adolescents are caries-free on a DMFT level and this is not much changed by lowering the threshold to initial caries lesions.

3

Thus, the caries distribution is polarized and a so-called high-risk group of about 20% exhibits almost the complete caries burden.

2

,

4

The high-risk group is primarily associated with a low socioeconomic status that leads to less sufficient oral hygiene, fluoride exposure, and often more frequent sugar intake.

2

,

5

In the primary dentition and especially for early childhood caries, the situation is far from satisfactory in many countries.

6

In spite of a less pronounced caries decline in the primary dentition, caries patterns and distribution are equivalent to the situation in adolescents.

7

This is also true for caries in adults.

2

Most likely a further caries decline will also increase the polarization in adults.

Due to the caries distribution after a major caries decline, primary caries prevention needs a dual strategy of maintaining the high levels of oral health in the majority of the population and trying to find intensified measures to improve the situation in the risk group mostly characterized by a low socioeconomic status.

3

There is a realistic perspective that caries levels even in risk groups can be significantly reduced in the future, as the caries decline in this group was proportional to the reductions in the whole population, at least in German adolescents.

4

Figs 1-2a and b Decayed, missing, and filled teeth (dmft/DMFT) in Germany in (a) schoolchildren,3,7 adolescents,3,4 and (b) adults. In many industrialized countries such as Germany, a remarkable caries decline has been recorded for the permanent dentition in adolescents, as well as in adults, and to a lesser extent for the primary dentition in schoolchildren.

Figs 1-3a to d A large percentage of children are caries-free (80%) (a and b), while a small group of children (20%) (c and d) present with high caries rates (80%). The polarization of the caries distribution especially in children leads to two different preventive approaches: Maintaining the high degree of oral health in the majority group of the population and intensifying measures for the high caries risk group.

In contrast to the general caries decline in many industrialized countries, caries levels in the emerging market economies are still at a high level for most of the population, or even on the rise due to increased wealth and sugar consumption.8 This imposes a great challenge to these countries; in spite of choosing the restorative approach as was done by many Western countries, strengthening primary prevention would be a better choice.

The current epidemiologic situation of a polarized caries distribution calls for two distinctly different approaches to primary caries prevention: For the majority of the population, individual and professional prevention can reduce 90% of the caries burden and keep it at a tolerable very low level.

The so-called caries risk group that accumulates about 80% of the caries defects and the according treatment needs is characterized by a low socioeconomic status. It seems that outreach programs and tailored health regulations are necessary to achieve further health gains in the groups with often low self-efficacy or (oral) health literacy. A common risk factor approach and cooperation with other professionals are useful for risk grouptargeted prevention to strengthen health and probably also educational competencies in these individuals and their families.

Early childhood caries

Early childhood caries (ECC) appears to be a persistent and neglected topic with rather high levels in many countries (Fig 1-4), low treatment rates, and, therefore, severe consequences in many small children that clearly affects their well-being and quality of life.9

Fig 1-4 Global epidemiology of early childhood caries (ECC). ECC or caries in the primary dentition seem to be a persistent problem, with severe consequences for the affected children. Preventive approaches in almost all countries have to be intensified to mirror the success often achieved in the permanent dentition.3,10-16

Only in recent years has research in caries epidemiology focused on early childhood, followed by representative surveys on the prevalence of ECC. Thus, ECC deserves special attention in order to draw conclusions that might deviate from the situation in the permanent dentition.

ORCA and IADR define ECC as “the early onset of caries in young children with often fast progression which can finally result in complete destruction of the primary dentition [Fig 1-1a]. An epidemiologic definition of ECC is the presence of one or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled surfaces, in any primary tooth of a child under [the] age of six.” They also state that the appearance of ECC deviates from the common caries distribution where pits, fissures, and proximal surface dominate.1

“Due to the frequent consumption of carbohydrates, especially sugars, and inadequate to absent oral hygiene in small children, ECC demonstrates an atypical pattern of caries attack, particularly on smooth surfaces of upper anterior teeth.”1 This implies that typical ECC is a type of child neglect, as even minimal and easy preventive oral health measures are omitted for a considerable time. It is amazing that this can be found in so many children in developed and emerging countries.6 It also calls for clearly intensified primary caries-preventive measures from the first tooth on.

The National German Oral Health Survey in Children and Adolescents revealed 14% of 3-year-olds had caries on a dmft level in Germany,3 which is at the lower end of an international comparison. The mean value in the affected children (the newly introduced Specific affected Caries Index [SaC]17) was 3.6 dmft, making pulpal involvement, subsequent toothache, and probably a treatment under general anesthesia (GA) due to the high number of carious teeth as well as the low compliance in these small children likely – or a painful, and potentially traumatic experience when extraction in uncooperative children is performed if GA is not available.3

A closer look reveals that in spite of a very low mean caries prevalence of 0.3 dmft in 2-year-olds, a small risk group of children develops “real” ECC from the first tooth onwards (Table 1-1). Here ECC is caused by infant feeding that provides a high sugar content and/or erosive drinks in combination with insufficient or a complete lack of oral hygiene.18 Regarding the “epidemiologic” definition of ECC, in Germany the prevalence increases to almost 35% at a defect level until school age.3,7 The care index of less than 50% is not satisfactory, and clearly lower than in the permanent dentition.3 The young age of the children and the high burden of the disease in many countries make a primary preventive approach to manage the problem of ECC (see Chapters 5 and 9) more logical than the secondary or tertiary prevention (see Chapters 12 to 14) via, for example, restorations or even extractions.

Caries diagnostics

Analogous to the above-mentioned definition of caries as a net loss of minerals, caries diagnostics would assess the change of minerals over time. As caries is a process, this implies that a one-time diagnosis requires a continuous sampling technique or is even per se impossible.

The ORCA/IADR consensus solves this problem by stating that “caries diagnosis is the clinical judgment integrating available information, including the detection and assessment of caries signs (lesions), to determine presence of the disease.”1 This is especially crucial for secondary or tertiary prevention, with the signs or symptoms of caries already being clearly present in an individual. “The main purpose of clinical caries diagnosis is to achieve the best health outcome for the patient by selecting the best management option for each lesion type, to inform the patient, and to monitor the clinical course of the disease.”1 This is relevant to all levels of prevention, as many teeth and surfaces within one individual often present different stages of the caries process.

It is important to comprehend that the diagnosis of caries as a process or caries activity differs from the diagnosis of past mineral loss or even cavitation, which was traditionally defined as “caries diagnostics.” According to ORCA/IADR, caries activity “is a concept that reflects the mineral balance, in terms of net mineral loss, net mineral gain, or stasis over time.”1 Caries active implies caries initiation or progression; caries inactive implies caries arrest or regression.19 The diagnosis of caries activity can actually be used as the gold standard for the success of preventive measures because they should reduce the net mineral loss to zero or even remineralize existing lesions. The detection of cavitation due to caries is a comparatively crude diagnostic approach.

Clinical examination

A regular, visual-tactile examination of the mouth and teeth is part of the standard routine in dentistry. However, active initial caries lesions, which are the crucial part of the diagnosis, can only be assessed clinically after removal of the dental plaque and drying of the teeth using sufficient lighting. It is important that no force is applied with a pointed probe during the examination of initial lesions, as this can destroy the intact surface and, therefore, reduce the chance of defect-free remineralization.20

The International Caries Detection and Assessment System21 offers a detailed diagnosis of the various caries stages from 0 (healthy) to 6 (deep caries). In daily practice, however, it is usually sufficient in the diagnosis of caries to distinguish between healthy surfaces, initial lesions, moderate stage lesions, and cavitated lesions, as well as their degree of activity.21-23

The clinical caries and activity diagnosis allows a fairly precise therapy decision and selection of the right level of care involving primary, secondary, or tertiary prevention. This makes the traditional concept of caries treatment obsolete. A merely restorative approach to caries would fail, as was often the case, due to the persisting net loss of minerals, leading to “secondary” caries, which is actually the nontreated caries activity that had originally led to the first cavitation.

Caries activity

The degree of caries activity is superior to the assessment of the caries risk (see Chapter 17). While risk refers to the conversion of a healthy state to disease, the diagnosis of caries activity actually uses the knowledge of the disease process to record its early signs, whether heavy plaque in stagnation areas, accompanying gingivitis, or initial caries lesion. These should be carefully viewed after cleaning and drying the teeth (Fig 1-5) and differentiated into a probably active or inactive initial lesion.

It is important to note that inactivation is possible at any stage from initial enamel lesion to deep dentinal caries (see Fig 1b),21,23 and it can be achieved by disturbing the dental biofilm (eg, by brushing teeth) and by influencing the de- and remineralization processes (eg, with fluorides). In spite of being classically primary preventive measures, they are “therapeutic” here and can be perceived as nonoperative caries treatment or management, which should result in a net gain of minerals.

Figs 1-5a to c Maxillary anterior teeth: (a) before plaque removal, (b) after staining, and (c) after brushing. Active caries lesions can only be diagnosed on cleaned tooth surfaces, and gingivitis becomes clearer for the patient as a result of bleeding during cleaning.

Further diagnostics

If proximal caries is present or going to be expected, a radiographic examination should be considered since proximal caries rarely occurs in an isolated spot and pulpal involvement can be assessed (Fig 1-6). Bitewing radiographs are still considered to be the gold standard in proximal caries diagnostics.24

Figs 1-6a and b Bitewing radiographs (a) allow a staging of proximal lesions and planning of primary preventive measures (flossing and fluorides, see Chapter 7), secondary prevention such as nonoperative treatment of initial lesions with cleaning and fluorides, proximal sealing or infiltration, and tertiary prevention meaning restorative care. This can be supported by fiber-optic transillumination (FOTI) (b), digital imaging fiber-optic transillumination (DIFOTI), or quantitative light-induced fluorescence (QLF).

Another method to monitor proximal surfaces is fiber-optic transillumination (FOTI), which is particularly suitable for the first examination of “apparently healthy” proximal surfaces,25 especially if a proximal lesion has already been detected on another tooth. In addition, several new caries diagnostic systems such as digital imaging fiber-optic transillumination (DIFOTI) and quantitative light-induced fluorescence (QLF) have been available on the market for several years with the aim of providing reliable results in caries diagnosis. Still, reviews stress that they can be used as adjunct tools, but they should not substitute x-rays completely, and do not overrule the clinical verification.26

Current concepts and treatment approaches in caries management

Primary caries prevention is traditionally considered as the “real” prevention, aiming to maintain the health of sound teeth that are at risk for caries. The concepts of the classical preventive measures are based on a variety of approaches. In several chapters, this book looks at their current evidence base and provides clinical recommendations on how to implement these nowadays, eg for fluorides (see Chapter 3), plaque removal via tooth brushing or flossing (see Chapters 6 and 7), diet control (see Chapter 4), or probiotics (see Chapter 11).

A key issue of primary caries prevention is a change from caries activity to inactivation or, in other words, from predominantly demineralization to remineralization of dental hard tissues, which involves behavior change in the patients or caretaker (see Chapter 9). Especially after the caries decline, oral diseases are concentrated on a minority group, linked to the socioeconomic status.27 Thus, future gains in oral health must have a focus on this group, possibly employing all levels from individualized, group- and population-based prevention, outreach programs, and a common risk factor approach (see Chapter 5).

Secondary caries prevention aims to arrest or even remineralize initial caries lesions with nonoperative or minimally invasive techniques. These techniques involve nonrestorative caries control, which implements primary caries-preventive measures but employs them for initial or even cavitated caries lesions (see Chapter 14). This can be enhanced with silver fluoride products or other fluorides (see Chapters 3 and 12), antimicrobials, or biomimetic remineralization using self-assembling peptides (Curodont Repair, Credentis),28 that work like a magnet for attracting minerals (see Chapter 13).

For management of initial caries lesions with intact macroscopic enamel surfaces, plaque control and fluoridation play a central role in arresting the lesions, promoting remineralization, and consequently avoiding further lesion progression to visible cavitation. It is known that tooth brushing with fluoridated toothpaste is the most cost-effective strategy for controlling caries lesions.29,30

In addition, individualized preventive strategies that take into consideration patient’s caries risk/activity as well as involve parents and other care takers are key factors for successful intervention in caries control. One of the most effective caries prevention strategies is the “Next model.”31,32 These techniques are especially needed in patients with reduced cooperation, such as small children, persons with handicap, chronically ill patients, or elderly patients (see Chapter 16).

As minimally invasive techniques, therapeutic sealants can be used (see Chapter 10), even on proximal surfaces (Fig 1-7a).33 Another option is caries infiltration (Icon, DMG Dental; Fig 1-7b), where a resin-like material is diffused in the porous initial caries lesion.34

Figs 1-7a and b Minimally invasive treatment of approximal initial caries lesions by (a) therapeutic sealants and (b) caries infiltration with Icon (DMG Dental).

“Tertiary” caries prevention tries to prevent progression of the disease and subsequent complication. Traditionally, complete removal of carious tissue with subsequent restorative treatment was regarded as the standard treatment for carious teeth. In recent years, there has been a paradigm shift in caries understanding: Caries is no longer understood as an infectious disease, but as the result of an ecologic imbalance, which is triggered, for instance, by the frequent consumption of fermentable carbohydrates (see above). In the biofilm, among other things, carbohydrates are metabolized to acids, which cause demineralization of the tooth structure. Not only in the field of primary caries prevention is this of fundamental importance, but also for the treatment of cavitated caries lesions, dentin demineralization, and (amount of) removal of carious tissues. For instance certain techniques encourage inactivation of caries lesions without carious tissue removal, such as nonrestorative cavity control,35,36 presented in Chapter 14. Here, also the silver agents37 (see Chapter 12) or sealing techniques with no carious tissue removal using preformed metal crowns like the Hall Technique35 are part of the modern caries management spectrum.

Thus, it is possible to control or arrest caries by disturbing the biofilm and influencing the de- and remineralization processes at any time and stage during lesion development.38,39 For cavitated caries lesions, biologically based techniques such as the selective (to firm, to leathery, to soft dentin) or stepwise carious tissue removal are currently advocated. These techniques are recommended for the management of shallow, moderately deep, and deep lesions in vital teeth in order to prevent pulpal exposure and to preserve the pulp vitality of the carious tooth.40

References

1.Machiulskiene V, Campus G, Carvalho JC, et al. Terminology of dental caries and dental caries management: Consensus Report of a Workshop Organized by ORCA and Cariology Research Group of IADR. Caries Res 2020;54:7–14.

2.IDZ. Fünfte Deutsche Mundgesundheitsstudie – DMS V. Köln, 2016.

3.Team DAJ. Epidemiologische Begleituntersuchungen zur Gruppenprophylaxe 2016. 1st ed. Bonn: Deutsche Arb.-Gemeinsch. f. Jugendzahnpflege, 2017.

4.Splieth CH, Santamaria RM, Basner R, Schüler E, Schmoeckel J. 40-year longitudinal caries development in german adolescents in the light of new caries measures. Caries Res 2019;53:609–616.

5.Schmidt CO, Fahland RA, Franze M, et al. Health-related behaviour, knowledge, attitudes, communication and social status in school children in Eastern Germany. Health Educ Res 2010;25:542–551.

6.Chen KJ, Gao SS, Duangthip D, Lo ECM, Chu CH. Prevalence of early childhood caries among 5-year-old children: a systematic review. J Investig Clin Dent 2019;10:e12376.

7.Santamaria RM, Schmoeckel J, Basner R, Schüler E, Splieth CH. Caries trends in the primary dentition of 6- to 7-year-old schoolchildren in Germany from 1994 to 2016: Results from the German National Oral Health Surveys in Children. Caries Res 2019;53:659–666.

8.Kassebaum NJ, Bernabé E, Dahiya M, Bhandari B, Murray CJL, Marcenes W. Global burden of untreated caries: a systematic review and metaregression. J Dent Res 2015; 94:650–658.

9.Vollú AL, da Costa MdEPR, Maia LC, Fonseca-Gonçalves A. Evaluation of oral health-related quality of life to assess dental treatment in preschool children with early childhood caries: a preliminary study. J Clic Pediatr Dent 2018;42:37–44.

10.DPHEP. National Dental Epidemiology Programme for England: oral health survey of five-year-old children 2015. London: Public Health England, 2016.

11.Turton B, Chher T, Sabbah W, Durward C, Hak S, Lailou A. Epidemiological survey of early childhood caries in Cambodia. BMC Oral Health 2019;19:107.

12.Slabsinskiene E, Milciuviene S, Narbutaite J, et al. Severe early childhood caries and behavioral risk factors among 3-year-old children in Lithuania. Medicina (Kaunas, Lithuania) 2010;46:135–141.

13.Prakash P, Subramaniam P, Durgesh BH, Konde S. Prevalence of early childhood caries and associated risk factors in preschool children of urban Bangalore, India: a cross-sectional study. Eur J Dent 2012;6:141–152.

14.Livny A, Assali R, Sgan-Cohen HD. Early childhood caries among a Bedouin community residing in the eastern outskirts of Jerusalem. BMC Public Health 2007;7:167.

15.Postma TC, Ayo-Yusuf OA, van Wyk PJ. Socio-demographic correlates of early childhood caries prevalence and severity in a developing country: South Africa. Int Dent J 2008;58:91–97.

16.Colak H, Dülgergil CT, Dalli M, Hamidi MM. Early childhood caries update: a review of causes, diagnoses, and treatments. J Nat Sci Biol Med 2013;4:29–38.

17.Schmoeckel J, Santamaría RM, Basner R, Schüler E, Splieth CH. Introducing a specific term to present caries experience in populations with low caries prevalence: Specific affected Caries index (SaC). Caries Res 2019;53: 527–531.

18.Pine CM, Adair PM, Nicoll AD, et al. International comparisons of health inequalities in childhood dental caries. Community Dent Health 2004;21(1 Suppl):121–130.

19.Fontana M, Gonzalez-Cabezas C. Evidence-based dentistry caries risk assessment and disease management. Dental Clin North Am 2019;63:119–128.

20.Ekstrand K, Qvist V, Thylstrup A. Light microscope study of the effect of probing in occlusal surfaces. Caries Res 1987;21:368–374.

21.ICDAS Foundation. International Caries Classification and Management System (ICCMS). https://www.iccms-web.com/. Accessed 4 September 2019.

22.Nyvad B, Machiulskiene V, Baelum V. Construct and predictive validity of clinical caries diagnostic criteria assessing lesion activity. J Dent Res 2003;82:117–122.

23.Nyvad B, Machiulskiene V, Baelum V. Reliability of a new caries diagnostic system differentiating between active and inactive caries lesions. Caries Res 1999;33:252–260.

24.Bin-Shuwaish M, Dennison JB, Yaman P, Neiva G. Estimation of clinical axial extension of Class II caries lesions with ultraspeed and digital radiographs: an in-vivo study. Oper Dent 2008;33:613–621.

25.Heinrich-Weltzien R, Haak R, Buchalla W, Kühnisch J. Kariesdiagnostik - Eine Herausforderung für den Zahnarzt? DDZ 2008;117:160–168.

26.Winand C, Shetty A, Senior A, et al. Digital imaging capability for caries detection: a meta-analysis. JDR Clin Trans Res 2016;1:112–121.

27.Schwendicke F, Dörfer CE, Schlattmann P, Foster Page L, Thomson WM, Paris S. Socioeconomic inequality and caries: a systematic review and meta-analysis. J Dent Res 2015;94:10–18.

28.Alkilzy M, Santamaria RM, Schmoeckel J, Splieth CH. Treatment of carious lesions using self-assembling peptides. Adv Dent Res 2018;29:42–47.

29.Walsh T, Worthington HV, Glenny A-M, Marinho VC, Jeroncic A. Fluoride toothpastes of different concentrations for preventing dental caries. Cochrane Database Syst Rev 2019;3:CD007868.

30.Twetman S. Prevention of early childhood caries (ECC): review of literature published 1998-2007. Eur Arch Paediatr Dent 2008;9:12–18.

31.Ekstrand KR, Christiansen MEC. Outcomes of a non-operative caries treatment programme for children and adolescents. Caries Res 2005;39:455–467.

32.Ekstrand KR, Christiansen MEC, Qvist V. Influence of different variables on the inter-municipality variation in caries experience in Danish adolescents. Caries Res 2003;37:130–141.

33.Alkilzy M, Berndt C, Meller C, Schidlowski M, Splieth C. Sealing of proximal surfaces with polyurethane tape: a two-year clinical and radiographic feasibility study. J Adhes Dent 2009;11:91–94.

34.Abdullah Z, John J. Minimally invasive treatment of white spot lesions--a systematic review. Oral Health Prev Dent 2016;14:197–205.

35.Santamaría RM, Innes NPT, Machiulskiene V, Schmoeckel J, Alkilzy M, Splieth CH. Alternative caries management options for primary molars: 2.5-year outcomes of a randomised clinical trial. Caries Res 2018;51:605–614.

36.Gruythuysen RJM, van Strijp AJPG, van Palestein Helderman WH, Frankenmolen FW. Niet-restauratieve behandeling van cariës in het melkgebit: doelmatig en kindvriendelijk. Ned Tijdschr Geneeskd 2011;155:A3489.

37.Chibinski AC, Wambier LM, Feltrin J, Loguercio AD, Wambier DS, Reis A. Silver diamine fluoride has efficacy in controlling caries progression in primary teeth: a systematic review and meta-analysis. Caries Res 2017;51:527–541.

38.Fejerskov O, Kidd EAM. Dental Caries: The disease and its clinical management, 2nd ed. Oxford: Blackwell Munksgaard, 2008.

39.Kidd E. The implications of the new paradigm of dental caries. J Dent 2011;39(Suppl 2):S3–S8.

40.Schwendicke F, Frencken JE, Bjørndal L, et al. Managing carious lesions: consensus recommendations on carious tissue removal. Adv Dent Res 2016;28:58–67.

2

Understanding periodontitis

Daniela Hoedke, Henrik Dommisch

Periodontitis is a complex inflammatory human disease. According to the World Health Organization (WHO), periodontitis is considered as a chronic noncommunicable disease (NCD), and it shares social determinants and risk factors with other NCDs such as cardiovascular diseases, diabetes mellitus, cancer, and chronic pulmonary diseases, which account for two-thirds of the worldwide mortality.1 Thus, prevention of periodontal diseases, such as gingivitis and periodontitis, is highly important for each individuum.

This chapter will give an overview on the current knowledge of the epidemiology, etiopathogenesis, diagnosis, and preventive as well as therapeutic considerations in relation to periodontitis.

Periodontitis is one of the most prevalent oral diseases that can be prevented or treated. Figure 2-1 displays a representative image of a patient with periodontitis. In this specific case, the patient experienced tooth movement, tooth mobility, and generalized bleeding on probing. In addition to the resulting gaps between teeth, plaque deposits and discolored swollen gingival tissue are clearly visible in the interdental regions.

Fig 2-1 Representative image of a patient with periodontitis. This image shows the sequelae of periodontal destruction due to periodontitis: tooth movement, tooth mobility, and generalized gingival inflammation. In addition to the resulting gaps between teeth, plaque deposits and discolored swollen gingival tissue are clearly visible in the interdental regions.

Epidemiology

Gingivitis and periodontitis are considered as two entities of the same biofilm-induced inflammatory disease that affects tissues around teeth.2 While gingivitis is a reversible inflammation of the gingiva around teeth without attachment loss, periodontitis comprises an additional nonreversible degradation of the periodontal apparatus, including the alveolar bone. In the worldwide population, approximately 12% exhibit severe forms of periodontitis, whereas approximately 50% show mild to moderate forms of periodontal disease. It is important to note that periodontitis represents the sixth most common human disease.3,4 According to the increasing world population and high numbers of retained teeth, the global burden due to severe periodontitis increased between 1990 and 2013 by 67%.5 This led to a higher economic load to the health care systems.6

With respect to the distribution of periodontal disease in humans, periodontitis is an age-associated but not age-dependent disease, and the prevalence of periodontitis is strongly elevated between the third and fourth decade of life.3,7 Low socioeconomic status is associated with higher risk for periodontitis, and men suffer more from periodontitis compared to women.8,9

Etiopathogenesis of periodontitis

The periodontium is a unique structure in the human body. While body surfaces, such as skin, mucosal tissues, hair, and nails, are constantly renewed, shed, and grow out, respectively, teeth exhibit a nonshedding surface. In addition, the tooth represents a direct connection between bone and the outside microbial environment, only separated by the junctional epithelium and connective tissue fibers. This allows for the dental plaque biofilm to develop and grow along the tooth surface into the gingival crevice, if not disturbed by routine oral hygiene procedures.

Microbial factors

Although periodontitis is a multifactorial disease, the central role to its pathogenesis refers to the interaction between the dental plaque biofilm, mainly consisting of well-organized bacteria adhering to the dental surface, and the immune inflammatory reaction of the host.10

In this context, periodontal health represents a status of homeostasis associated with a symbiotic biofilm and an appropriate immune-inflammatory reaction of the host, including the presence of neutrophils and the expression of antimicrobial peptides.11,12

The immune response to the periodontal bacteria is different for each individuum and impairs the composition of the bacterial biofilm differentiating from a symbiotic into a dysbiotic composition.13 The change of the relative abundance of pathogenic microorganisms when compared to their abundance in a healthy state leads to alterations within the host-microbial interactions that can further accelerate the inflammatory responses.13

The increasing amount of pathogenic periodontal bacteria, including their virulence factors, leads to an elevation of cellular signal transduction, and subsequently, secretion of pro-inflammatory mediators by various periodontal cell types.14-16 Furthermore, the shift within the microbiota activates the complement system.17 In the course of periodontal inflammation, more immune competent cells, such as macrophages, polymorphonuclear neutrophil granulocytes, T-cells, and B-cells, are present. The synthesis of additional pro-inflammatory mediators, such as interleukins, cell stimulating and receptor activating factors, and proteinases leads to changes of the connective tissue and bone metabolism, and therewith, to periodontal attachment loss.18

Initially, a dysbiosis between an altered biofilm in combination with a dysregulation of the immune reaction of a susceptible host leads to an inflammation of the gingiva (Fig 2-1). Gingivitis is a reversible disease that affects epithelium and connective tissue. The ongoing imbalance between the dysbiotic biofilm and the host-related immune reaction can lead to degradation of connective tissue and alveolar bone.10,12,19-22

In the context of the etiopathogenesis of periodontitis, the role of periodontal bacteria has been investigated for decades, and different plaque hypotheses have been developed.23 Several oral bacterial species, eg Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, have been regarded to be pathogenic. Within the periodontal microbiota, a special role is awarded to P gingivalis, a Gram-negative, anaerobic periodontal bacterium. P gingivalis is considered to be a keystone pathogen in the etiopathogenesis of periodontitis. According to its specifications, P gingivalis can influence the course of the periodontal disease by remodeling a health-associated homeostatic biofilm composition into a dysbiotic biofilm composition, even at very low levels of colonization (< 0.01 % of the bacterial count in an animal model).13,24

Within the framework of inflammatory reaction, intercellular connections of periodontal cells disintegrate, and bacteria and their metabolic products can invade into deeper tissue levels, enter the bloodstream, and, eventually, reach the tissues beyond the oral cavity.25,26 Throughout the body, periodontal bacteria may activate immune cells, which then release pro-inflammatory mediators. In this context, periodontal bacteria are able to modify immune-inflammatory reactions in the whole body. Therefore, it seems to be conceivable that periodontitis may also affect other inflammation-driven diseases, such as diabetes mellitus, cardiovascular diseases, and rheumatoid arthritis (see below).

Smoking

Smoking is considered to be one of the most important modifiable risk factors for periodontitis, with a clearly documented dose-response relationship.27-29 In this context, smoking affects the composition of the microorganisms within the dental plaque biofilm leading to a higher proportion of pathogenic periodontal bacteria. Moreover, smoking impairs microcirculation and immune response to the bacteria, such as disturbance of the neutrophil function, increased synthesis of pro-inflammatory mediators, and higher levels of activated T-cells.30,31

In the context of periodontitis, the progression of periodontal break down is highly increased in smokers when compared to nonsmoking individuals with periodontitis.32 The importance of the smoking status has now been integrated into the classification system of periodontal diseases.33

In respect to the progression of periodontitis, smoking represents one of the two modifying factors affecting the grading of periodontitis.33 Smoking cessation has positive effects on periodontal conditions, the treatment of periodontitis, and tooth retention.34-38

Nutrition

Nutrition and malnutrition, respectively, seem to be of importance in relation to periodontal diseases. It is known that nutrient factors influence inflammatory reactions, and malnutrition may lead to depletion of micronutrients which then increases the susceptibility to periodontitis.39 For example, there is an association between periodontal inflammatory responses and vitamin C depletion. Historically, the relationship between the intake of vitamin C-rich vegetables or fruits and periodontal disease has been described. In the 18th century, during maritime trading and exploratory seafaring, sailors often suffered from a condition called scurvy. Scurvy represents a vitamin C deficiency disease associated with gingival bleeding and tooth mobility caused by altered collagen formation, impaired connective tissue barrier formation, and fibroblast growth.40-42 There are a number of different micronutrients associated with periodontal health and disease. For macronutrients, it has been observed that a higher intake of sugar is associated with increased gingival bleeding.43,44 For more detailed information, the authors refer to the relevant literature.39

Obesity

The association between obesity and periodontitis has been described more recently. It was found that central adiposity was associated with an increased risk of developing periodontitis in older adults. However, due to large variability within the available studies, only moderate evidence is currently available.45,46 In addition, there are some indications that periodontal therapy is more ineffective in obese patients with periodontitis. The effect on the therapeutic outcome was similar to the effect of smoking in periodontitis patients.47

In basic science experiments, it has been demonstrated that the differentiation of osteoblasts was altered in the presence of P gingivalis in obese mice.48 Animal experiments have also shown that age and obesity represent risk factors that may result in reduced alveolar bone crest height even in an otherwise healthy periodontium.49 Future research is required in order to gain more robust knowledge of how nutrition is related to periodontitis.

Genetic factors

The contribution of genetics to the risk for periodontitis has been estimated as up to 50%. In particular, a strong genetic component is assumed in younger patients with severe periodontitis.50

For several years, the identification of single nucleotide polymorphisms (SNPs) in relation to periodontitis was of high scientific interest.51 SNPs represent the most frequent genetic variation, and an association of this type of variation with disease is, therefore, very likely. Mostly, candidate gene studies have been performed in the past. The evidence, however, for one of the analyzed variations in candidate genes, such as for interleukin-1, is rather weak.52,53 In relation to periodontitis, it is very likely that genetic susceptibility factors for periodontitis will not be found in the genetic sequence of one distinct candidate gene, but rather in a variety of different genes. The technical progress in combination with the publication of the last human chromosome as part of the human genome project (sequencing of the whole human genome) allowed the simultaneous analysis of high numbers of genetic variations (SNPs), with no distinct a priori hypothesis.54 Those genome-wide association studies (GWAS) have been performed with large sets of samples from patients with periodontitis.55-58 To date, a number of different genetic variances in specific genes, such as ANRIL, PLA, SIGLEC5, DEFBA1A3, NPY, and GLT6D1 have been described in periodontitis patients, underlying the hypothesis that there are polygenetic factors that, in a certain but yet unknown combination, alter the susceptibility for periodontitis.57-61 The individual functional characteristics of the identified variations are the subject of current research projects.62

Periodontitis in relation to systemic diseases

Diabetes mellitus

Diabetes mellitus is a metabolic condition with chronic hyperglycemia as the leading symptom. Both diabetes mellitus and periodontitis are chronic, inflammation-driven diseases with mutual influence regarding their impaired immunologic responses.63,64

Diabetes mellitus as well as periodontitis are common, chronic, noncommunicable diseases that exhibit a bidirectional relationship (review65). The relationship between both diseases was first described by Löe in 1993, and periodontitis found as the sixth complication of diabetes mellitus.66 It has been shown that patients with diabetes mellitus exhibit more severe and rapidly progressive forms of periodontitis compared to patients without diabetes mellitus.67-70 It is now widely accepted that diabetes mellitus represents a major risk factor for the development and progression of periodontitis, and thus, diabetes mellitus has now been added as a modifying factor within the grading of periodontitis.29,33

Furthermore, during severe periodontitis, the inflammatory process can have detrimental effects on blood sugar control by influencing the insulin resistance, leading to a poorer glycemic control, increasing the rate of incident prediabetes and type 2 diabetes mellitus.71-74 Here, the periodontal inflammation exhibits a systemic impact along with bacteremia and increased levels of pro-inflammatory mediators detectable in the blood stream, and therewith, blood sugar control and insulin resistance are negatively influenced in patients with periodontitis and diabetes mellitus.65,70,75-77

Diabetes mellitus-related complications, such as cardiovascular, cerebrovascular, renal, retinal, and neuropathic complications, are significantly increased in patients with severe periodontitis and type 2 diabetes mellitus.78-82

Cardiovascular diseases

Cardiovascular diseases also belong to the group of chronic noncommunicable diseases, and it has been shown that there is a clear epidemiologic association with periodontitis.83,84 More precisely, epidemiologic studies have demonstrated that there is a positive association between periodontitis and coronary heart and cerebrovascular disease.84,85

Similar to diabetes mellitus, one of the proposed mechanisms of interaction includes the incidence of bacteremia due to daily routine procedures such as tooth brushing or eating.25 It was found that the magnitude of bacteremia was higher in patients with periodontitis when compared to patients with gingivitis.26 Analyses of atherothrombotic tissues revealed the presence of periodontal bacteria, and patients with periodontitis showed a greater probability for the detection of periodontal pathogenic bacteria in those tissues.86,87

In this context, the influence of periodontitis on the systemic inflammatory status has been recognized as an important mechanism.75,76 When compared to healthy control individuals, patients with periodontitis exhibited elevated levels for C-reactive protein (CRP), interleukin-(IL)-1 beta, IL-6, IL-8, and tumor necrosis factor alpha (TNF-α).88-96

Dyslipidemia is recognized as a risk factor for cardiovascular diseases, and it has been shown that dyslipidemia is present in patients with periodontitis.97,98 Other parameters, such as increased intima media-thickness or alterations in the flow-mediated dilatation of blood vessels, may indicate pathologic cardiovascular alterations. Periodontitis is associated with an increased intima media-thickness, changes in the flow-mediated dilatation, and hypertension.99-103

It is an interesting finding that both periodontitis and cardiovascular diseases seem to share common genetic risk factors.58,59,104 This functional and molecular background is the subject of current research projects.62

Rheumatoid arthritis

Rheumatoid arthritis is a complex autoimmune disease that is characterized by the infiltration of macrophages and T-cells into the synovial membrane of joints leading to cartilage degradation and bone erosion.105 The production of auto-antibodies is typical for rheumatoid arthritis, and the auto-antibody against immune globulin G represents the rheumatoid factor.106,107 Biochemical post-translational processes, such as citrullination and carbamylation, are involved in the mechanisms leading to antibody synthesis.108,109 Citrullination is a post-translational modification of the amino acid arginine to citrulline promoted by an enzyme called peptidylarginine deiminase (PAD). Based on the current knowledge, the link between rheumatoid arthritis and periodontitis could be via the periodontal pathogen P gingivalis, which also expresses a similar enzyme (PPAD).110 The proteins modified by the PPAD from P gingivalis can further promote autoantibody production against citrullinated proteins (anti-citrullinated protein antibodies [ACPAs]), and this may be another stimulus for the development of rheumatoid arthritis.108,110 Current research investigates the hypothesis of periodontitis to be a risk factor for rheumatoid arthritis.111,112

Periodontitis may exhibit a considerable influence on systemic conditions such as diabetes mellitus, cardiovascular disease, and rheumatoid arthritis.

Clinical features and diagnosis

Symptoms, clinical and radiographic features

Periodontitis represents major clinical characteristics including microbial biofilm formation (dental plaque biofilm), inflammation of the gingiva, periodontal attachment loss, and bone loss. The microbial biofilm is visible as dental plaque on tooth surfaces and around the gingival margin, which may calcify and form dental calculus when not routinely removed by daily oral hygiene procedures. In most patients, the amount of plaque formation and calculus is associated with severity of periodontitis. Inflammation of the gingiva around the teeth can be seen by swelling, redness, edema, and bleeding. Pocket formation, bleeding on probing, and gingival recessions combined with periodontal attachment and bone loss are clinical signs of periodontitis. Furthermore, patients with severe periodontitis often suffer from tooth migration, increased tooth mobility, and periodontal abscesses. Clinical periodontal examination comprises the measurements of attachment level, periodontal pocket probing, bleeding on probing, furcation involvement, and tooth mobility. The amount and the type of bone loss (horizontally versus vertically), furcation involvement, and combined periodontal-endodontic lesions are determined by additional radiographic examinations.