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Practical Periodontal Diagnosis and Treatment Planning Understand periodontal diseases and their treatment with this practical guide Practical Periodontal Diagnosis and Treatment Planning, Second Edition provides a fully up-to-date guide to the latest techniques, both surgical and non-invasive, for minimizing the impact of periodontal conditions. The Second Edition has been updated to reflect the new periodontal disease classification, thoroughly explaining the staging and grading system, comparing the new system to previous system, and discussing how to use the classification in everyday clinical practice. This essential step-by-step guide to integrating digital technologies in surgical implant therapy and prosthetic rehabilitations offers a thorough understanding of the concept of facial sculpture to complement and enhance intra-oral rehabilitation. The book takes an evidence-based approach to diagnosis and treatment, incorporating significant research and clinical experience to best reflect the needs of both patients and clinicians. Lavishly illustrated and including three new chapters covering novel disease classifications and cutting-edge treatments, this updated reference helps to develop clinical skills. Practical Periodontal Diagnosis and Treatment Planning includes: * Complete information on the new periodontal disease classification * A digital workflow for a smooth intraoral rehabilitation * Practical instructions for periodontal procedures such as osseous resective surgery, regenerative and supportive periodontal therapy, dental implant complication management, and more * Analysis of the use of Botox and dermal fillers as an alternative to surgical treatment and enhancement of appearance concomitant with dental treatments * Discussion of periodontal disease presentations including occlusion, scaling, and root planing Practical Periodontal Diagnosis and Treatment Planning, Second Edition is an essential guide for periodontists, oral surgeons, and advanced students in dentistry, periodontics, and oral hygiene.
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Practical Periodontal Diagnosis and Treatment Planning
Edited by Serge Dibart and Thomas Dietrich
Second Edition
This edition first published 2024
© 2024 John Wiley & Sons, Inc.
Edition History
Blackwell Publishing (1e, 2010)
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Library of Congress Cataloging-in-Publication Data
Names: Dibart, Serge, editor. | Dietrich, Thomas, 1969- editor.
Title: Practical periodontal diagnosis and treatment planning / edited by Serge Dibart, Thomas Dietrich.
Description: Second edition. | Hoboken, NJ : Wiley-Blackwell, 2024. | Includes bibliographical references and index.
Identifiers: LCCN 2023041028 (print) | LCCN 2023041029 (ebook) | ISBN 9781119830313 (hardback) | ISBN 9781119830320 (pdf) | ISBN 9781119830337 (epub) | ISBN 9781119830344 (ebook)
Subjects: MESH: Periodontal Diseases--diagnosis | Periodontal Diseases--therapy | Patient Care Planning | Evidence-Based Dentistry--methods
Classification: LCC RK450.P4 (print) | LCC RK450.P4 (ebook) | NLM WU 241 | DDC 617.6/32--dc23/eng/20231023
LC record available at https://lccn.loc.gov/2023041028
LC ebook record available at https://lccn.loc.gov/2023041029
Cover Image: © Serge Dibart
Cover Design: Wiley
Set in 9.5/12.5pt STIXTwoText by Integra Software Services Pvt. Ltd, Pondicherry, India
Contents
Cover
Title Page
Copyright Page
List of Contributors
Preface
1 The Necessity of an Evidence-based Approach to Diagnosis and Treatment
2 Classification of Periodontal Diseases and Conditions
3 Periodontal Risk Factors and Modification
4 Scaling and Root Planing
5 Occlusion
6 Systemic and Local Drug Delivery of Antimicrobials
7 Periodontal Osseous Resective Surgery
8 Contemporary Periodontal Regenerative Treatment
9 Surgical Versus Nonsurgical Treatment of Periodontitis
10 Supportive Periodontal Therapy
11 Dental Implants Therapy
12 Digital Integration of Implant Surgery Workflow
13 Introduction to Minimally Invasive Facial Aesthetic Procedures
14 Inflammation and Bone Healing around Dental Implants
15 How to Write and Read a Scientific Paper
Index
End User License Agreement
List of Tables
CHAPTER 02
Table 2.1 Diagnostic guideline for...
Table 2.2 Classification of...
Table 2.3 Periodontitis—staging.
Table 2.4 Periodontitis—grading.
Table 2.5 Classification of systemic...
Table 2.6 Classification of periodontal...
Table 2.7 Classification of mucogingival...
Table 2.8 Classification of factors related...
CHAPTER 06
Table 6.1 Evidence-based indications...
Table 6.2 Dental procedures and cardiac...
Table 6.3 Regimens for a dental...
Table 6.4 Antibiotic regimens for...
Table 6.5 Advantages of local delivery...
Table 6.6 Local delivery systems...
CHAPTER 07
Table 7.1 Indications and contraindications...
Table 7.2 Indications and contraindications...
CHAPTER 11
Table 11.1 Comparative long-term survival...
Table 11.2 Failure rate comparison between...
Table 11.3 Correlation of insertion torque...
CHAPTER 13
Table 13.1 Glogau Classification...
Table 13.2 Properties of hyaluronic...
CHAPTER 15
Appendix Table 15.1 Examples of...
Appendix Table 15.2 Common types...
Appendix Table 15.3 Common types...
List of Illustrations
CHAPTER 02
Figure 2.1 Classification of periodontal...
Figure 2.2 Localized gingivitis...
Figure 2.3 Oral-contraceptive-induced...
Figure 2.4 Maxillary generalized...
Figure 2.5 Gingival fibromatosis.
Figure 2.6 Primary herpetic...
Figure 2.7 Lichen-planus-associated...
Figure 2.8 Lingual gingival recessions...
Figure 2.9 Metallic barbell inserted...
Figure 2.10 Radiograph of teeth number...
Figure 2.11 Aspirin-induced chemical...
Figure 2.12 Post-necrotizing ulcerative...
Figure 2.13 Necrotizing periodontitis...
Figure 2.14 Periodontitis with a...
Figure 2.15 Typical bone loss...
Figure 2.16 Bite wing radiographs...
Figure 2.17 One year post therapy...
Figure 2.18 Periapical radiographs...
Figure 2.19 Periapical radiograph...
Figure 2.20 Periapical radiograph...
Figure 2.21 Periodontal abscess...
Figure 2.22 Perio-endo lesion...
Figure 2.23 Based on (Coslet 1977)...
CHAPTER 03
Figure 3.1 Interplay of modifiable...
Figure 3.2 Impaired wound healing...
Figure 3.3 Clinical and radiographic...
Figure 3.4 Necrotizing ulcerative...
Figure 3.5 Oral hygiene...
Figure 3.6 Oral hygiene...
Figure 3.7 Tobacco use...
Figure 3.8 Tobacco use...
Figure 3.9 Tobacco use...
Figure 3.10 Recommendations...
CHAPTER 04
Figure 4.1 One month follow-up...
Figure 4.2 Scaler design. H: handle...
Figure 4.3 Contrast between the...
Figure 4.4 Series of Gracey...
Figure 4.5 Key differences...
Figure 4.6 The smaller tip...
Figure 4.7 Summary of pocket...
CHAPTER 05
Figure 5.1 When the mandible...
Figure 5.2 The current definition...
Figure 5.3 Thirty-degree anatomical...
Figure 5.4 Left, classical balanced...
Figure 5.5 With lingualized occlusion...
Figure 5.6 Group function or unilateral...
Figure 5.7 Mutually protected occlusion...
Figure 5.8 Superimposition of tracing...
Figure 5.9 The patient will receive...
Figure 5.10 Occlusal interference on...
Figure 5.11 A, Because of the medial...
Figure 5.12 A, Resorbed maxillary and...
Figure 5.13 Fine motor control of the...
Figure 5.14 A, The implant was placed...
Figure 5.15 Differences in...
Figure 5.16 A shim stock is used to...
Figure 5.17 A finite element analysis...
Figure 5.18 In vitro evidence suggests...
Figure 5.19 An articulator can be...
Figure 5.20 If a semi-adjustable...
Figure 5.21 Balanced articulation...
Figure 5.22 Relatively steep overlap...
Figure 5.23 Maxillary implant-supported...
CHAPTER 07
Figure 7.1 An example of positive...
Figure 7.2 A, Surgical exposure of...
Figure 7.3 Histologic specimen from...
Figure 7.4 Histologic view of a block...
Figure 7.5 A large semi-circumferential...
Figure 7.6 After flap elevation for pocket...
Figure 7.7 A thick buccal bony ledge can...
Figure 7.8 Strategic use of resective...
Figure 7.9 A diamond coarse round bur...
Figure 7.10 A back action...
Figure 7.11 An osseous resective surgery...
Figure 7.12 A, It may be useful to create...
Figure 7.13 Photograph of a dry human mandible...
Figure 7.14 A, Craters and combined infrabony...
Figure 7.15 A, Presurgical probing for crown...
Figure 7.16 If properly outlined, a palatal ...
Figure 7.17 A, Radiograph of a maxillary...
Figure 7.18 Radiographic view of a Class...
Figure 7.19 The furcation is identified...
Figure 7.20 The mesiobuccal root is isolated...
Figure 7.21 A, Two months healing demonstrates...
Figure 7.22 Maxillary first molar with a resected...
Figure 7.23 A, Lower right first molar with...
Figure 7.24 A, A Class II lingual furcation...
Figure 7.25 A, A Class III furcation defect...
Figure 7.26 Caries at the furcation...
CHAPTER 08
Figure 8.10 Baseline clinical...
Figure 8.4 Trans-surgical view at the...
Figure 8.1 Clinical trans-surgical...
Figure 8.2 Radiographic view at...
Figure 8.3 Area was grafted with...
Figure 8.5 Baseline clinical (A) and...
Figure 8.6 Trans surgical view after...
Figure 8.7 A synthetic polylactic acid...
Figure 8.8 Clinical view one year after...
Figure 8.9 Radiographic evaluation performed...
Figure 8.11 Trans surgical view after...
Figure 8.12 Following mechanical...
Figure 8.13 An EMD gel (Emdogain®) was...
Figure 8.14 A particulate bovine xenograft...
Figure 8.15 A new layer of EMD gel was applied...
Figure 8.16 The flap was coronally advanced...
Figure 8.17 Clinical view one year after...
CHAPTER 09
Figure 9.1 Results Overview...
Figure 9.2 37-year-old female...
CHAPTER 12
Figure 12.1 CBCT Thresholding. Different...
Figure 12.3 Superimposition of intraoral...
Figure 12.2 The merging procedure. Reference...
Figure 12.4 From diagnostic wax-up...
Figure 12.5 Immediate implant placement...
Figure 12.6 Merging CBCT with scan...
Figure 12.7 Abutment teeth-borne surgical...
Figure 12.8 Immediate implant placement...
Figure 12.10 Surgical template in...
Figure 12.11 Guided endosteal implant...
Figure 12.9 Restoratively driven...
Figure 12.12 Merged wax-up/terminal...
Figure 12.13 Implant planning in...
Figure 12.14 Bone-supported surgical...
Figure 12.15 Interim prosthesis...
Figure 12.18 Orthopantomographs...
Figure 12.16 Clinical workflow...
Figure 12.17 One week follow-up...
Figure 12.19 Manufacturing devices...
Figure 12.20 Milled and 3D-printed...
Figure 12.21 Implant surgery workflow...
Figure 12.22 Robotically guided...
Figure 12.23 Robotically assisted...
Figure 12.24 Robotically guided...
Figure 12.25 Robotically guided...
Figure 12.26 Guided antrostomy for...
Figure 12.27 Custom Ti-Mesh for...
Figure 12.28 Clinical workflow for...
CHAPTER 13
Figure 13.1 Subcutaneous facial...
Figure 13.2 The glabellar muscle...
Figure 13.13 (A) Serial puncture,...
Figure 13.3 Vertical glabellae...
Figure 13.4 Hyperdynamic orbicularis...
Figure 13.5 Glabellar frown rhytids...
Figure 13.6 Specialized TB syringe...
Figure 13.7 Typical injection sites...
Figure 13.8 The location of each...
Figure 13.9 Injection of the left...
Figure 13.10 Injection of the...
Figure 13.11 Top: 1 week post...
Figure 13.12 (A) Injection spot...
Figure 13.14 (A) Nasolabial folds...
Figure 13.15 Linear injection...
Figure 13.16 A 1.8‐ml syringe...
Figure 13.17 (A) Pre injection with...
CHAPTER 14
Figure 14.1 Contact vs. distance...
Figure 14.2 The inflammatory...
Figure 14.3 Radiographs showing...
CHAPTER 15
Appendix Figure 15.1 Algorithm for the general...
Appendix Figure 15.2 Component questions...
Appendix Figure 15.3 Balance between the...
Appendix Figure 15.4 The generation and...
Appendix Figure 15.5 The evidence pyramid...
Appendix Figure 15.6 Some types of measurements...
Appendix Figure 15.7 Some types of case report...
Appendix Figure 15.8 Presentation of findings...
Guide
Cover
Title Page
Copyright Page
Table of Contents
List of Contributors
Preface
Begin Reading
Index
End User License Agreement
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List of Contributors
Editors:
Serge Dibart, DMD
Professor of Periodontology and Oral Biology Director,Post-Graduate Program and 2nd Floor Specialty ClinicsBoston University School of Dental Medicine100 East Newton Street Boston, MA
Thomas Dietrich, MD, DMD, MPH
Professor and Head of Oral Surgery The School of Dentistry University of Birmingham 5 Mill Pool Way, Birmingham B5 7EG United Kingdom
Contributors:
Massimo Di Battista, DMD, MSD
Private Practice Limited to Periodontology and Implant Dentistry,Montréal, Québec, Canada
Iain L.C. Chapple, DDS, PhDProfessor, Director of Research Institute of ClinicalSciencesInstitute of Clinical SciencesCollege of Medical & Dental SciencesThe University of Birmingham
Sheilesh Dave, DDS, MSD, CAGS, deceasedPractice limited to Periodontology andImplant Dentistry 1333 8th Street SW Calgary,Alberta, Canada
Thomas Van Dyke, DDS, PhDProfessor, Department of Periodontology andOral Biology Director, Clinical Research Center Boston University School of Dental Medicine 100 East NewtonStreet Boston, MA
Paul S. Farsai, DMD, MPH, FACDAssociate Professor, Director of Evidence-based Dentistryand Behavioral Sciences Department of General Dentistry Boston University School of Dental Medicine 72 EastConcord Street—Robinson Room 334, Boston, MA
Jeremy Kernitsky-Barnatan, DDS, MSDClinical Director and Clinical Assistant ProfessorAdvanced Education Program, Department of PeriodontologyHenry M. Goldman School of Dental Medicine635 Albany Street, Suite G-200, Boston, MA
Raman Kohli, DDS, MSc, FRCD(c)Practice limited to Periodontology and Implant Dentistry3155 Harvester Rd., Suite 401 Burlington, Ontario, Canada
Annika Kroeger Dr. med. dent.
School of Dentistry, University of Birmingham, UK
Cataldo W. Leone, DMD, DMSc
Professor of Periodontology and Oral Biology AssociateDean for Academic AffairsDiplomate, American Board of Periodontology BostonUniversity Goldman School of DentalMedicine 100 East Newton Street Boston, MA
Luca Landi, MD, DDSPractice limited to Periodontology and Implant DentistryVia della Balduina 114 Roma, Italy
Gail McCausland, DMD, M.Dent.Sci., FICDClinical Professor and Assistant Dean for AcademicAffairs, Boston University Henry M. GoldmanSchool of Dental Medicine, 72 East Concord Street;Robinson Suite B309Boston, MA
Lorenzo Montesani, DDSImplant Fellow, Department of PeriodontologyHenry M. Goldman School of Dental Medicine635 Albany Street, Suite G-200, Boston, MA
Steven M. Morgano, DMDProfessor and Director, Division of PostdoctoralProsthodontics Department of Restorative Sciences andBiomaterials Boston University School of Dental Medicine100 East Newton Street Boston, MA
Christoph A. Ramseier, MASPrivatdozent, Scientific Associate, Periodontist SSO,EFPMaster of Advanced Studies (MAS) in PeriodontologyUniversity of Bernzmk bernSchool of DentalMedicine Department of Periodontology Freiburgstrasse7CH-3010 Bern Switzerland
Dimitra Sakellari, DDS, PhDAssistant Professor Department of Preventive Dentistry,Periodontology, and Implant Dentistry AristotleUniversity of Thessaloniki Dental School 212 A. Vas.Olgas Avenue Thessaloniki, Greece
Carolina Miller Mattos de Santana, DDS, MScD, PhDAssociate ProfessorUniversidade Federal Fluminense, Department ofPeriodontologyRio de Janeiro, Brazil
Ronaldo Barcellos de Santana, DDS, MScD, DScProfessor, Deputy Chair of PeriodontologyDirector of MSc program and Research in PeriodontologyTemple University, Maurice H. Kornberg School ofDentistry, Department of Periodontology and OralBiology, Philadelphia, USA
Praveen Sharma BDS, MFDS (RCS Edin.), FHEA, FDS(Restorative Dentistry) (RCS Edin.), PhDAssociate Professor & Honorary Consultant in RestorativeDentistry University of Birmingham School of DentistryBirmingham, UK
Bradford Towne, DMDRetired, Oral and Maxillofacial Surgery, 3600 GoldenCascade Ln, Indian Land, SC. USA
Mehmet Ilhan Uzel, DMD, DScClinical Associate Professor, Department of PeriodonticsDirector, International Program in Periodontics and Implant Dentistry University of Pennsylvania School ofDental Medicine Robert Schattner Center, Evans Building240 S. 40th Street Philadelphia, PA
Clemens Walter Prof. Dr. med. dent
Charité – Berlin University of Medicine, Department ofPeriodontology, Oral Medicine and Oral SurgeryBerlin, Germany
Preface
Welcome to the second edition of Practical Periodontal Diagnosis and Treatment Planning, skillfully edited by Serge Dibart and Thomas Dietrich. This edition delves into the foundational principles of periodontal and dental implant therapy, with a focus on processes that culminate in accurate diagnoses and well-rounded, pragmatic treatment planning. The methodology embraced is evidence-based, retaining the integrity of the first edition, while also offering a refreshingly practical approach. The reader is guided systematically from risk assessment through minimally invasive therapies to rehabilitation, whether through surgical tissue regeneration or dental implant therapy.
This edition confronts the complexities of the 2017 International Workshop Classification of Periodontal and Peri-implant Diseases and Conditions. It contrasts the new system with the 1999 classification, enlightening readers on the rationale and evolution that led to what is now known as the 2018 Classification. The reader is provided with a hands-on guide to implementation in day-to-day practice, along with comprehensive explanations of the radical changes in thinking that shaped the 2018 classification.
The book features three new and very engaging chapters. The first explores the classification topic mentioned above; the second delves into the rapid emergence of digital systems within dental practice. These systems now form the crux of three-dimensional planning in dento-facial aesthetics, extending beyond mere “in-silico” modeling by interfacing with contemporary recording techniques for dento-facial parameters, and transitioning through to innovative methods of implementation such as dynamic surgery with navigation and robotic placement systems. The final chapter on prosthetic rehabilitation, employing digitized systems, actualizes the initial planning and fulfills the patient care circle.
The third fresh chapter examines a subject of great contemporary relevance: the human pursuit of beauty and the harmonization of facial features. These considerations have increasingly become essential to the well-being and self-confidence of many individuals in the twenty-first century. The chapter delves into the meticulous knowledge and appreciation of applied facial anatomy, risk–benefit assessment, and the critically important concept of informed consent, required for the successful implementation of various facial tissue management strategies. Although the impact of such interventions can be transformative, a clear understanding of the risks, side effects, and psychological effects of facial remodeling is emphasized.
Doctors Dibart and Dietrich have once again orchestrated a harmonious collaboration of experts in their respective fields, updating the first edition of this vital textbook to resonate with the pulse of this rapidly changing and dynamic discipline. The book’s relevance extends to periodontists, periodontal residents, general dentists with a special interest in this rapidly evolving field, oral surgeons, dental hygienists, and dental students alike. With something to offer the entire periodontal team, the evidence-based approach reassures readers that the content is delivered in a manner that is both balanced, state-of-the-art, and eminently practical.
Iain L. C. Chapple
1 The Necessity of an Evidence-based Approach to Diagnosis and Treatment
Paul Farsai and Thomas Van Dyke
Today, the concept of evidence-based healthcare surrounding our clinical practice of dentistry is discussed more than ever. However, many times this term is used to define anything but “evidence-based dentistry” (EBD).
The term “evidence-based” has evolved through certain iterations through the years. Archie Cochrane initiated the discussion of putting into action the concept of science-based medicine when in 1971 he published Effectiveness and Efficiency: Random Reflections of Health Services (Cochrane 1972). In 1992 a clinical epidemiology group at McMaster University in Canada (Evidence Based Medicine Working Group 1992) published a paper on evidence-based healthcare (EBM Working Group 1992). Their article described their challenge to adopt an “evidence-based practice” (EBP) approach since it “de-emphasizes intuition, unsystematic clinical experience and pathophysiological rationale as sufficient grounds for clinical decision making.” The paper was written with the clear intent of placing a greater emphasis on a systematic appraisal of the evidence.
The first well-defined use of the term “evidence-based” in the UK was in a 1996 British Medical Journal article by David Sackett et al. (Sackett et al. 1996) and was defined as the “… conscientious, explicit and judicious use of current best evidence in making decisions about the care of individual patients.”
The term “current best evidence” is the operative word here, because it implies that our best available evidence should by definition change as we progress through more research findings, to the point that what was true as the best available evidence even as recently as ten years ago in dentistry in some respects is not even true today. Many examples come to mind, such as digital technologies in scanning, designing, milling, or printing restorations and appliances; the newer adhesive systems; newer generations of composites; more nonsurgical and adjunctive periodontal therapies; different dental implant systems, shapes, sizes, components or engineered surfaces; and more procedure-specific use of biomaterials as well as therapies, all due to better applied research results, and so on.
The American Dental Association (ADA) has defined the concept of EBD as:
An approach to oral health care that requires the judicious integration of systematic assessments of clinically relevant scientific evidence, relating to the patient’ s oral and medical condition and history, with the dentist’s clinical expertise and the patient’s treatment needs and preferences.
(Sackett et al. 1996)
EBD has five components. This premise is simply based on the notion that to perform a scientific search for the current best evidence, one must be able to interpret the clinical scenario, translate it into searchable terminology, and then find the best evidence by critically assessing the quality and the appropriateness of the published evidence to address the identified clinical scenario. The five components are:
Translate a clinical problem into a question.
For example: A new patient who is pregnant comes to see you with a chief complaint that she wants a second opinion on her need for periodontal surgery. She has heard periodontal disease may cause low-birth-weight babies and asks, “Do I really need surgery, or could I just have dental cleanings (scaling and root planing) to prevent a low-birth-weight baby?” An easy method to translate a clinical scenario into a searchable format is by using the PICO structure. PICO is an acronym for
P
roblem,
I
ntervention (or Index, i.e., a category or condition),
C
omparison, and
O
utcome. So, by using PICO, one would devise the following structured format for the example described above:
How would I describe the dental Problem or population?
“In pregnant patients …”
Which main Intervention or index am I considering?
“With periodontal disease …”
What is the main Comparison or alternative?
“Compared to pregnant people (patients) without periodontal disease.”
What is the Outcome to be studied?
“Is there a greater risk of “low-birth-weight babies?”
Effectively search for the best evidence. For this component, one must determine which databases to search and then use the appropriate databases and search filters to find the best evidence. The most common database is Medline (accessible via many free Internet portals such as www.pubmed.gov); however, there are many highly specialized databases such as Psychlit for behavioral research, Cancerlit for cancer literature, and NHSEED for economic evaluation research (UK) (see Chapter 4) As a source of high-level study designs, the Cochrane Oral Health Group (OHG), which originated in New England in 1994 and moved to Manchester (UK) in 1996, now has a registry (at the time of print) of 174 reviews, 28 protocols, and 214 subtopics in dentistry (https://oralhealth.cochrane.org). Summaries of the reviews are listed on the OHG website.
The term “filter” refers to the strategy for condensing thousands of articles into a more refined or limited set of relevant data. Filtration could be based on “human” topics, “English” language articles, a certain period of time (certain decade of research and beyond), and so on (many more filtration strategies are available). For the abovementioned example, a search of the best evidence yielded the following number of articles (at the time of print):
199,124 articles that include the word “pregnant”
100,793 articles that include the words “periodontal disease”
716 articles that include the words “pregnant” and “no periodontal disease”
59,888 articles that include the words “low-birth-weight”: Clearly, reading more than 360,000 articles to address our clinical scenario is neither indicated nor necessary. By using just “human” subjects and “English” language as our limits for our filtration strategy, we came up with 198 articles that describe the association (or lack thereof) between periodontal disease in pregnant patients and low-birth-weight babies. A further review of the articles and additional filtration (specificity and sensitivity) yielded 37 articles that describe the potential link between pregnant patients with periodontal disease and the risk for preterm and low-birth-weight babies.
Critically appraise the evidence. One must critically read and evaluate the basis of the articles at hand (all 37 of the articles). This means that for this component level, one must assess at some foundational level the quality of the research methodology, the study design, the statistical analyses, and the conclusions that are published in each research article. It should be noted that the mere fact that an article is published (in a reputable journal or otherwise) does not mean that the study design, the research methods, the statistical analyses, or the conclusions were/are appropriate. Certain clinical or patient-centered questions can be best answered and more scientifically based if they are investigated through specific research designs or methods. For example, randomized control trials are suitable and indicated for the majority of therapeutic interventions, whereas cohort studies are suitable in design to answer questions on prognosis. Critical appraisal skills are evaluative skills that are taught and developed over time with appropriate supervision from knowledgeable and skilled individuals.
For our example, there are 37 studies that show some level of association between low-birth-weight and periodontal disease. The discrepancies come from the use of methods used in conducting the research, the appropriateness of the statistical analyses in interpreting the data, the various study designs compared in the studies, the process by which the data were collected, the criteria used for inclusion or exclusion of risk factors, or the lack of such parameters, and so on. However, care must be taken not to introduce bias, conscious or unconscious, at this step. Filters cannot be arbitrary or be used to eliminate studies that do not seem to support the beliefs of the evaluator of the studies. While the critical review of pertinent studies is intended to eliminate bias, there is that potential every time a decision is made on which studies to include. As a hypothetical example, a filter of studies of at least 9 months duration might be imposed, but the majority of studies are of 6 months duration. It is possible that the majority of studies of 6 months contradict one or two 9-month studies. Eliminating the shorter studies is eliminating valuable information and if only 9-month studies are reported, the outcome is biased.
Apply appraisal results to clinical practice. At this time, if one critically appraises and assesses the quality of the research findings for our abovementioned clinical scenario, the evidence is mounting and suggests a new risk factor—periodontal disease. Pregnant women who have periodontal disease may be seven times more likely to have a baby that is born too early and too small.
More research is certainly needed to confirm how periodontal disease may affect pregnancy outcomes. It appears that periodontal disease triggers increased levels of biological mediators that induce labor. Furthermore, data suggest that women whose periodontal condition worsens during pregnancy have an even higher risk of having a premature baby.
Therefore, by using the most current published clinical evidence available, clinicians in private practice can make the judicious recommendation to their patients that periodontal disease may in fact be a significant risk for a preterm, low-birth-weight baby.
We ask you, the reader, a rhetorical question now: Is this in fact what we are currently telling our patients? If not, then why? More importantly, what is the level of appropriate scientific evidence that supports these communications or recommendations with our patients? Certainly, then, an understanding of the levels of evidence in scientific research becomes necessary for any clinician to judiciously take the research recommendations and translate them to clinical practice (see Chapter 4).
Evaluate application step and outcomes. As with any treatment modality, good science and good patient care must be evaluated once it is rendered. Some therapy or treatment (or preventive care) can be assessed shortly after it has been rendered, and for other occasions, the evaluation of the applied care must be assessed within a much wider time span. Nevertheless, evaluation of outcomes is a necessary component of responsible and appropriate evidence-based healthcare.
From a study design standpoint, identifying whether periodontal disease actually causes preterm, low-birth-weight babies is very difficult to measure with the presence of other variables.
Ethical issues also arise in a clinical trial if periodontal treatment is withheld for an indefinite period from half of the subjects, so technically this question cannot be measured well.
Regardless of whether this association is proven or not, dentists have nothing to lose by encouraging their patients to take care of their teeth.
Other salient topics with respect to periodontal disease and systemic disease include the suggested link between cardiovascular disease and periodontal inflammation. There is a wealth of cross-sectional studies (which yield limited assessment opportunities) that suggest the association is not random, but longitudinal studies that evaluate outcomes (and allow for multiple assessments) that predict cardiovascular events in people with periodontitis have been lacking. New evidence has been recently reported that independently associates major adverse cardiovascular events (MACE) with periodontal disease activity. Periodontal disease activity is defined as active inflammation of the periodontium, as opposed to a history of periodontal disease that is most often defined by radiographic bone loss. In this study, periodontal inflammation was a significant predictor of MACE. Interestingly, investigation of the mechanism for this observation is consistent with increased periodontal inflammation causing increased arterial inflammation (Van Dyke et al. 2021). While the study and the proposed mechanism seem plausible, it is a single study that has to be repeated in other settings. Thus, advising patients that the association has been proven is still premature. However, advising patients that periodontitis is associated with increased risk for developing cardiovascular disease is supported by literature using evidence-based evaluations (Sanz et al. 2020; Tonetti and Van Dyke 2013).
Problems with Introducing EBD
In the past 20 years, dentists have become more aware of the existence of EBD and generally, the progress from initial skepticism to a more positive attitude of the use of EBD is palpable among the members of the profession. This observation is reflected by the formation of the ADA’s Center for Evidence Based Dentistry, the implementation of EBD concepts in dental school curricula dictated by new ADA Commission on Dental Accreditation (CODA) standards for teaching dental students, and by journals and meetings/conferences all over the world emphasizing EBD concepts.
However, the main barriers to the implementation of EBD into practice have also been identified in many studies (Iqbal and Glenny 2002; Sbaraini et al. 2012; Straub-Morarend et al. 2013). So why are dentists not putting EBD into practice?
Amount of Evidence
There are currently about 500 journals related to dentistry and not all are relevant to all areas of dental practice, nor can a busy practitioner read any more than a small handful of articles routinely.
Quality of Evidence
Because enhancing career prospects in academia is partially tied to the number of publications someone authors, much of the ever-increasing volume of evidence produced is not necessarily to increase the knowledge base, which in essence compromises quality. In addition, a number of publications that are widely read are not subject to peer review, and even when peer review exists, there is always the unfortunate reality of publication bias (defined as the tendency by both researchers and editors to publish positive reviews or results).
Dissemination of Evidence
History has shown that even in the presence of good evidence, the application phase of EBD can take many years to become the norm or standard in practice. Unless good methods of dissemination are available, good evidence can go to waste. Conversely, even with scant or insignificant differences in evidence from the status quo, many new products and procedures have been introduced to the marketplace simply because interest and desire exists to integrate a change in practice.
Practice Based on Authority Rather than on Evidence
Common practice in professional development and continuing education demonstrates that the dental school model, which uses techniques or therapies based on views of authority rather than evidence, may lead to the wrong or outdated treatment being performed.
Advantages of EBD
What Constitutes Evidence?
Personal clinical examination, including specific findings from history and results from tests, constitutes evidence. Research evidence is a manifestation of a much larger scale of interventions and, therefore, becomes a stronger tool for clinical decision making because it extends beyond individual experience. This should not, however, replace individual experience but rather anchor our clinical experience from years of practice. Sound reproducible research outcomes should enable clinicians to recognize gaps and uncertainties in their knowledge rather than wait for the next patient to expose our inadequacies. This implies a marriage between the research process and the clinical application of that process, hence the need for a continuous process of reading, learning, and applying a dynamic field of information.
What Is Good Evidence?
The randomized controlled trial (RCT) study design is the gold standard for evidence for treatment-related questions. An even better level of evidence is a systematic review or a meta-analysis of a series of RCTs. However, this is only true for the clinical question regarding therapeutics. For other clinical questions, a study design hierarchy exists to determine the levels of evidence (see Chapter 4). This means that in the EBD process, no evidence is considered to be bad evidence; there are just levels of applicable good, better, and best evidence.
Finding and Making Sense of Evidence
After finding the evidence, one needs to make sense of it. This appraisal should be critical; after all, no research design is perfect, and the health status of a person is at stake. The Critical Appraisal Skills Program (CASP) at Oxford University has developed a worksheet that can be used while reading and interpreting published articles to make sense of the evidence (https://www.cebm.ox.ac.uk/resources/ebm-tools/critical-appraisal-tools). The aim of the critical appraisal is to systematically consider the validity, results, and relevance to our own clinical practice.
EBD improves the effective use of research evidence in clinical practice. If used judiciously, it favors the early uptake of new and better treatments or results in the early rejection of ineffective treatments. It uses resources more effectively. For example, a systematic review of materials may lead to the earlier adoption of the most effective ones and the subsequent reduction in replacement levels, thereby saving resources.
EBD relies on evidence rather than authority for clinical decision-making. Regular reviewing of currently available literature should develop us as practitioners, so we attain the skills to evaluate evidence for ourselves based on our own experiences rather than have someone interpret the data for us.
To use this approach, we need to develop new interpretive skills for identifying clinical problems, searching literature by using conventional and electronic means, and improving our critical appraisal skills. In the same spirit, this book encompasses practical evidence-based developments in diagnosis and treatment planning for a periodontal patient.
References
Evidence-Based Databases as part of the ADA Library. About EBD.
https://www.ada.org/en/resources/ada-library/evidence-based-databases
(accessed June 2021).
Cochrane, A.L. (1972).
Effectiveness and Efficiency: Random Reflections on Health Services
. London: Nuffield Provincial Hospitals Trust.
https://www.nuffieldtrust.org.uk/research/efectiveness-and-efficiency-random-refections-on-health-services
(accessed June 2021).
EBM Working Group (1992). Evidence based medicine.
JAMA
268: 2420–2425.
Iqbal, A. and Glenny, A.-M. (2002). General dental practitioners’ knowledge of and attitudes towards evidence based practice.
Br. Dent. J
193: 587–591. 18.
Sackett, D.L., Rosenberg, W.M., Gray, J.A. et al. (1996). Evidence based medicine: what it is and what it isn’t.
BMJ
312 (7023): 71–72.
Sanz, M., Del Castillo, A.M., Jepsen, S. et al. (2020 February 3). Periodontitis and cardiovascular diseases. Consensus report.
Glob. Heart
15 (1): 1.
Sbaraini, A., Carter, S.M., and Evans, R.W. (2012). How do dentists understand evidence and adopt it in practice?
Health Educ. J
71: 195–204.
Straub-Morarend, C.L., Marshall, T.A., Holmes, D.C., and Finkelstein, M.W. (2013). Toward defining dentists’ evidence-based practice: influence of decade of dental school graduation and scope of practice on implementation and perceived obstacles.
J. Dent. Educ
77: 137–145. 17.
Tonetti, M.S. and Van Dyke, T.E. (2013 April). working group 1 of the joint EFP/AAP workshop. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on periodontitis and systemic diseases.
J. Periodontol
84 (4 Suppl): S24–S29.
Van Dyke, T.E., Kholy, K.E., Ishai, A. et al. (2021 March). Inflammation of the periodontium associates with risk of future cardiovascular events.
J. Periodontol
92 (3): 348–358.
2 Classification of Periodontal Diseases and Conditions
Jeremy Kernitsky and Gail McCausland
Diagnosis and Classification—AAP 2017
History
In 1999 the American Academy of Periodontology assembled an International Workshop for a Classification of Periodontal Diseases and Conditions; this resulted in what became known as the 1999 Armitage Classification. In 2014 an AAP task force looking at the classification determined three areas of concern; attachment level (although clinical attachment level (CAL) is important for research it proved to be overly time consuming in everyday clinical practice); chronic versus aggressive periodontitis; and localized versus generalized periodontitis. In 2017 World Workshop on the Classification of Periodontal Disease and Peri-Implant Conditions was formed to update and standardize the previous 1999 classification and to develop a similar classification for peri-implant diseases and conditions.
Figure 2.1 Classification of periodontal and peri-implant diseases and conditions 2017 (Caton et al., 2018). Adapted from AAP, Journal of Periodontology.
The main differences between the 1999 and the 2017 classifications are: Firstly, different statuses of periodontal and gingival health were described. Secondly, that three forms of periodontitis were identified: necrotizing periodontitis, periodontitis as a manifestation of systemic disease, and periodontitis (comprising the forms of disease previously recognized as “chronic” or “aggressive”). Thirdly, this new classification system encompasses a multidimensional view of periodontitis using a staging and grading system. Fourthly, a change in the classification gingival recessions, and the change of terminology of periodontal biotype for periodontal phenotype. Finally, there was a significant expansion in the descriptions of peri-implant health, peri-implant mucositis, and peri-implantitis.
Periodontal Health, Gingival Diseases and Conditions
Periodontal Health and Gingival Health
The 2017 world workshop for the classification of periodontal diseases (Chapple et al. 2018) defined periodontal health and gingival health into three different entities based on the history of periodontal disease of the patient and presence or absence of clinical attachment level: intact periodontium, reduced periodontium in a non-periodontitis patient, and reduced periodontium in a successfully treated stable periodontitis patient (Table 2.1).
Table 2.1 Diagnostic guideline for periodontal health and gingivitis. Based on 2017 world workshop. Adapted from Chapple et al. 2018.
Intact Periodontium
Health
Gingivitis
Probing attachment loss
No
No
Probing pocket depths
(assuming no pseudo pockets)
≤3 mm
≤3 mm
Bleeding on probing
<10%
Yes (>10%)
Radiological bone loss
No
No
Reduced periodontium
Non-periodontitis patient
Health
Gingivitis
Probing attachment loss
Yes
Yes
Probing pocket depths
(assuming no pseudo pockets)
≤3 mm
≤3 mm
Bleeding on probing
<10%
Yes (>10%)
Radiological bone loss
Possible
Possible
Successfully treated stable periodontitis patient
Health
Gingivitis in a patient with history of periodontitis
Probing attachment loss
Yes
Yes
Probing pocket depths
(assuming no pseudo pockets)
≤4 mm
(no site ≥4 mm with BOP)
≤3 mm
Bleeding on probing
<10%
<10%
Radiological bone loss
Possible
Possible
It is important to mention that there is certain level of tolerance between the definition of periodontal health on an intact periodontium and gingivitis (dental plaque induced) of less than 10% bleeding on probing on all the sites. If there is any presence of loss in the clinical attachment level the correct term to use would be of a reduced periodontium while the differences on bleeding on probing will determine the health status of the periodontium.
Interestingly, patients with a reduced periodontium due to periodontitis successfully treated previously can present with increased probing depths of up to 4 mm, this is due that probing depths of <3 mm are rarely achieved on a 100% of treated sites, therefore it could lead to overtreatment as any non-bleeding site of >3 mm would not be considered “health” and would require further treatment instead of monitoring and supportive care. Yet, in the case of gingivitis patients the maximum allowed probing depth was set to 3 mm irrespective of the previous periodontal history of the patient.
b) Gingivitis: Dental Biofilm-Induced
I) Associated with dental biofilm
alone
As explained before, based on the history of periodontal disease of the patient, there are three possible entities to diagnose dental biofilm-induced gingivitis which can be seen in Table 2.1.
Whether they are associated with hormonal imbalances, mediations, systemic disorders, or malnutrition, these gingival diseases have the following characteristics in common (Mariotti 1999; Trombelli et al. 2018):
The signs and symptoms are confined to the gingiva.
Plaque is the main etiological factor which will initiate or exacerbate the gingival lesions.
Inflammation of the gingival tissues will produce changes in color (transition to a red/bluish-red hue), shape (enlarged gingival contours due to edema or fibrosis), texture, bleeding upon stimulation, and elevated sulcular temperature (
Figure 2.2
).
Figure 2.2 Localized gingivitis, characterized by bleeding upon probing. There is no attachment loss.
There is no alveolar bone loss and pocket depth; clinical attachment levels around teeth are stable.
This is a reversible condition which resolves upon removal of the etiological factors.
Possible role as a precursor to attachment loss around teeth.
Gingivitis primarily induced by dental plaque includes the following disease subdivisions:
Gingivitis associated with dental biofilm only: Signs and symptoms typical of gingivitis can be observed at all ages of dentate populations and this disease has been considered to be the most common form of periodontal disease (Page 1985). The disease can be observed in a child as young as five years of age, progress with a peak during puberty, and remain present throughout life at various extents. Plaque is present at the gingival margin and a positive correlation exists between gingivitis and plaque accumulation.
There is no pathognomonic flora associated with gingivitis, although the dental plaque in gingivitis differs from that present in gingival health (Ranney 1993). Note that gingivitis may also occur on a reduced periodontium (decreased amount of alveolar bone height and connective tissue support around teeth) which was previously surgically treated for a periodontitis. This situation is encountered when there is a recurrence of inflammation of the marginal gingiva on a periodontium with previous attachment loss but without any evidence of progressive attachment loss (no indication of active disease) (Mariotti 1999; Trombelli et al. 2018).
II) Mediated by systemic or local risk factors
Systemic risk factor (modifying factors)
i) Smoking
Smoking is one of the major risk factors for periodontitis, due to its effects upon gingival tissues. Among the effects we can identify: microvascular vasoconstriction and fibrosis. These can mask clinical signs of inflammation, such as bleeding on probing, despite the presence of a significant underlying pathological inflammatory response in the gingival tissues.
ii) Hyperglycemia
Diabetes-mellitus-associated gingivitis: Diabetes mellitus is a complex disease with varying degrees of systemic and oral complications involving abnormalities in insulin production, fat, proteins, and sugar metabolism, and resulting in an impaired vascular and immune system as well as an inadequate inflammatory response. Diabetes mellitus is categorized as Type 1 and Type 2. Type 1 develops due to impaired production of insulin and Type 2 is caused by deficient utilization of insulin. There is evidence to suggest that uncontrolled Type 1 diabetes in children is associated with exaggerated response of the gingival tissues to dental plaque (Lindhe 2003). It is a reversible condition once the diabetes is under control and the dental plaque is removed.
iii) Nutritional factors
Ascorbic acid deficiency gingivitis: Nutritional deficiencies such as ascorbic acid (vitamin C deficiency) can significantly exacerbate the response of the gingiva to plaque bacteria (Mariotti 1999). The clinical description of severe vitamin C deficiency or scurvy consists of bulbous, spongy, hemorrhagic, swollen, and erythematous gingival lesions (Charbeneau et al. 1983). The result of compromised antioxidant micronutrient defenses to oxidative stress and impacts negatively collagen synthesis, resulting in weakened capillary blood vessel walls and consequent enhanced gingival bleeding. This condition is unusually seen in areas of adequate food supply but can potentially affect infants of low socioeconomic families, institutionalized elderly individuals, and alcoholics.
iv) Pharmacological agents (prescription, nonprescription and recreational)
Oral contraceptives: Studies have shown that women taking oral contraceptive drugs have a higher incidence of gingival enlargement in comparison to women who do not take the medications (Kaufman 1969). Pronounced inflammation (change in gingival contour, color, exudate) is seen and is reversible upon removal of medications (
Figure 2.3
).
Figure 2.3 Oral-contraceptive-induced gingivitis in a female patient. Notice the “red patch” in the lower left quadrant. Courtesy of Iain Chapple.
Other. In general any drug that may alter the salivary flow, impact endocrine function, and/or produce gingival enlargement (Trombelli et al. 2018).
v) Sex steroid hormones
Puberty
Puberty-associated gingivitis: A rise in gingival inflammation and gingival volume is noted during puberty in both sexes without necessarily seeing a rise in the quantity of plaque (Sutcliffe 1972). The incidence of the severity of gingivitis in adolescence is not only related to the rise in steroid hormones but is also influenced by a variety of factors such as dental caries, mouth breathing, teeth crowding, and tooth eruption (Stamm 1986). These changes are reversible after puberty. More specifically, hyperplastic gingivitis often seen during the adolescence period can be associated with:
— Orthodontic treatment: Note that fibrotic tissue tends to recur if surgical removal is attempted during orthodontic treatment. It is recommended to wait until orthodontic appliances are removed before surgically removing excess tissue (
Figure 2.4
).
Figure 2.4 Maxillary generalized gingivitis following the placement of braces. Notice the difference with the mandibular arch, which does not have braces.
— Mouth breathing: Mouth breathing, which often accompanies Angle’s classification 2 division 1 malocclusion, is considered to be an exacerbating factor to gingivitis (Lindhe 2003). Gingival hyperplasia tends to affect mostly the anterior superior region and is also prone to recurrence if surgical removal is performed without any correction of the actual mouth breathing through orthodontic treatment or cessation of habit.
Menstrual cycle
Menstrual-cycle-associated gingivitis: The most common sign is a minor gingival inflammation during ovulation; gingival exudate has been shown to increase at least 20% in 75% of women (Hugoson 1971). This situation is reversible after ovulation.
Note: Hormonal gingivitis or postmenopausal gingivitis can be seen in women taking hormone replacement therapy. Signs and symptoms may involve atrophic, thin, erythematous gingival tissues, and patient complaints of gingival sensitivity to spicy foods and acidic beverages. Palliative treatment is suggested.
Pregnancy
Gingivitis: A combination of pregnancy hormones and dental plaque may increase the severity of gingivitis in women sensitive to local irritants. In addition to the typical gingivitis signs, severe inflammation can develop in the presence of relatively low amounts of dental plaque (Hugoson 1971). It will usually affect pregnant women in their second or third trimester, and is reversible after child delivery.
Pyogenic granuloma: This refers to a mass of hyperplastic gingival tissue principally found in the interdental maxillary regions. It is not a tumor but an exaggerated inflammatory response to irritation resulting in a solitary polyploid capillary hemangioma which can easily bleed upon mild provocation (Sills et al. 1996). Pregnancy-associated pyogenic granuloma presents clinically as a painless protuberant exophytic mass attached by a sessile or pedunculated base from the gingival margin. It has been reported to occur in 0.5–5% of pregnancies and can develop as early as the first trimester (Mariotti 1999). It usually regresses or completely disappears following parturition. If needed, surgical excision can be performed postpartum. The treatment for pregnancy-associated gingivitis and pyogenic granuloma during pregnancy is an impeccable control of the etiological factors (scaling, prophylaxis, and chlorhexidine rinses). This condition can also be classified under Epulides in the Reactive processes of non-dental plaque associated gingival conditions (Holmstrup et al. 2018).
Oral contraceptives
iv) Hematological conditions
Leukemia-associated gingivitis: Leukemia is a progressive malignant hematological disease characterized by the development of abnormal leukocytes and leukocytes precursors in the blood and bone marrow. Leukemia is classified according to disease progression (acute or chronic), cell types involved (myeloid or lymphoid), and cell numbers in blood (leukemic or aleukemic). The oral manifestations are acute, consisting of cervical adenopathies, petechia, gingival enlargements, and mucous ulcers. Dental plaque can exacerbate the gingival inflammatory changes which include swelling, redness/blueness, sponginess, and glazed appearance of the gingiva which is infiltrated with leukemic cells (Lindhe 2003). Persistent and unexplained gingival bleeding may indicate an underlying thrombocytopenia associated with the leukemic condition. Lesions are often found in the acute monocytic type, and consist of a modified gingival volume and bleeding of gingiva upon touch. Symptoms lessen when antiseptic mouthwashes are used and plaque volume is reduced.
Other
b) Local risk factors
i) Dental plaque biofilm retention factors
ii) Oral dryness
iii) Drug-influenced gingival enlargement
Drug-induced gingival enlargement: Three commonly used classes of medications create these lesions:
Anti-convulsant drug used for treatment of epilepsy: Dilantin (Phenytoin sodium), 50% incidence (Angelopoulos et al. 1972)
Immunosuppressant drug used to avoid host rejection of grafted tissues: Cyclosporine A, 25–30% incidence (Over time, this drug is tapered and the gingival enlargements become easier to control.) (Romito et al. 2004)
Calcium channels blocking agents used as hypertensive drugs: Nifedipine, Verapamil, Diltiazem, 15–20% incidence (Barclay et al. 1992)
Over the years more medications have been described to induce gingival enlargement, such as (Bharti et al. 2013):
Anticonvulsants
- Ethosuximide
- Ethotoin
- Mephenytoin
- Methsuximide
- Phenobarbital
- Phenytoin
- Primidone
- Sodium valproate
- Vigabatrin
Immunosuppressants
- Cyclosporine
- Sirolimus
- Tacrolimus
Calcium channel blockers
- Amlodipine
- Diltiazem
- Felodipine
- Manidipine
- Nicardipine
- Nifedipine
- Nimodipine
- Nisoldipine
- Nitrendipine
- Verapamil
Individuals taking these medications may develop gingival enlargements leading to pseudopockets. Characteristics of drug-influenced gingival enlargement include (Mariotti 1999):
Predilection of anterior gingiva; starts interproximally and expands
Higher prevalence in children
Onset within the first three months of taking the drug
Enlargement of the gingival contours appears
Stippling is present in the gingiva
Pronounced inflammatory response in relation to the plaque volume
Not associated with attachment loss but can be found in periodonitums with and without bone loss
Treatment consists of control of etiological factors followed by full mouth gingivectomy. Gingivectomy (full mouth or local) may need to be performed annually. If possible, the drugs can also be changed or dosages adjusted to improve the oral condition.
c) Gingival Diseases: Non-Dental Biofilm-Induced
Although these gingival lesions are not produced by plaque and do not disappear when plaque is removed, it should be noted that the severity of the clinical manifestation can often be related to the presence of bacterial plaque (Holmstrup et al. 2018).
Genetic/developmental disorders
Hereditary gingival fibromatosis
This gingival hyperplasia (gingival overgrowth) is an uncommon condition of genetic origin. Of idiopathic etiology, this condition develops irrespective of effective plaque removal. Hereditary gingival fibromatosis can be an isolated condition or part of a syndrome or systemic condition (Gorlin et al. 1990) (Figure 2.5).
Figure 2.5 Gingival fibromatosis.
b) Specific infections
i) Bacterial origin
These types of gingivitis and stomatitis can be found in immunocompromised and immunocompetent individuals. They occur when the microorganisms surpass innate host resistance. Clinical signs may range from painful, edematous ulcerations to asymptomatic cancers, mucosal patches, or atypical non-ulcerated inflamed gingiva. Lesions elsewhere on the body may also be present. Gingival lesions may occur due to infections with Neisseria gonorrhea, Treponema pallidum, streptococci, or other organisms.
Neisseria gonorrhoeae (Gonorrhea)
Gonorrhea is a sexually transmitted disease which can affect the oropharyngeal region in approximately 20% of infected individuals (Neville 2002). Diffuse erythema, small erosive pustules, and edema can be seen in this region as well as on tonsils and uvula. Gingivitis and stomatitis, as well as a sore throat and a cervical or submandibular lymphadenopathy, may also be present.
2) Treponema pallidum (Syphilis)
Syphilis is a chronic infection produced by Treponema pallidum. The primary modes of transmission are sexual contact or mother to fetus. The infection undergoes a characteristic evolution that classically proceeds through three stages: In primary syphilis, an asymptomatic contagious chancre appears three to four weeks post contact at the site of inoculation. When affecting the oral cavity, it can affect the lips, gingiva, tonsils, tongue, and palate. It leaves a scar and heals spontaneously. In secondary syphilis, whitish mucous patches as well as maculopalular cutaneous rashes are often present and are still contagious at this point. In tertiary syphilis, a noncontagious granulomatous inflammation (gumma) reaction appears which can often cause necrosis and perforation of the tongue or palate. Serious systemic conditions are involved (Neville et al. 2002).
3) Mycobacterium tuberculosis (Tuberculosis)
4) Streptococcal gingivitis
An upper respiratory tract infection usually causes fever and accompanies a diffuse gingivitis, tonsillitis, pharyngitis, and ulceration of the oral mucosa. One of the most common species involved is the group A, β-hemolytic streptococci (Neville et al. 2002).
ii) Viral origin
Several viral infections are known to cause gingivitis. Most of them enter the body during childhood and may give rise to the disease followed by periods of latency.
Coxsackie virus (Hand-Foot-Mouth disease)
Herpes simplex I and II (primary or recurrent)
– Primary herpetic gingigostomatitis: Herpes simplex virus type 1 (and occasionally type 2) is responsible for causing the primary infection which involves painful severe gingivitis with ulcerations (on keratinized and non-keratinized tissues) and edema followed by stomatitis. High fever and malaise is generally present. Vesicles on lips can produce a crusty lips appearance after rupturing (Miller 1992) (
Figure 2.6
).
Figure 2.6 Primary herpetic gingivostomatitis in a child. Notice the characteristic lesions on the lower lip. Courtesy of Iain Chapple.
– Palliative treatment only is required. The infection lasts approximately 10 days. During this period, the patient must be well hydrated with liquids and topical application of anesthetic agents is also indicated. Chlorhexidine and an antibiotic may be needed to prevent a super-infection. In the adult infection, antiviral drugs such as Zovirax, #70, 200 mg, 1 tabqid, for 2 weeks can be prescribed.
– Recurrent oral herpes: Reactivation of the virus resulting in recurrent infections occurs in 20–40% of individuals with the primary infection (Greenberg 1996). These lesions (vesicles which become ulcers) usually only affect the keratinized tissues and are usually present unilaterally or locally. The treatment, if any, can consist of topical antiviral ointment or tablets.
3) Varicella zoster (chickenpox—Shingles—V nerve)
Varicella-zoster virus causes varicella (chickenpox) as the primary self-limiting infection. The virus then remains latent and can be reactivated resulting in the herpes zoster infection. This painful unilateral infection is often seen in older individuals and is accompanied by cutaneous lesions of the affected nervous territory (Miller 1996).
4) Molluscum contagiosum
5) Human papilloma virus (squamous cell papilloma, condyloma acuminatum, verruca vulgaris, focal epithelial hyperplasia)
iii) Fungal origin
The most frequent oral fungal infections consist of candidosis and histoplasmosis.
Candidosis
Candida-species infections: C. albicans is one of the most frequent candida species affecting the oral cavity. It is considered an opportunistic infection occurring when the host resistance is diminished. Most subtypes of candidosis can be treated with antifungal medications (Ketoconazole 200 mg, 1 tab/day, 10 days, or Fluconazole 100 mg, 1 tab/ day, 14 days).
Generalized gingival candidosis include:
Acute types:
Pseudomembranous candidosis: This type of infection produces soft white patches disseminated throughout the oral mucosa. These patches can be removed with an instrument leaving behind an erythematous mucosal surface.
Atrophic or erythematous candidosis: This type of infection produces red lesions spreading all over the oral mucosa. They are associated with severe pain and discomfort.
Chronic types:
Hyperplasic candidosis: Typically, the lesion is longstanding and presents itself as a thick white patch which cannot be rubbed off (leukoplakia correlation).
Mucocutaneous: This type of candidosis mostly affects the skin, scalp, and nails; much more rarely it affects the gingiva.
Prosthetic stomatitis (types 1,2,3)
Linear gingival erythema: This disease was initially termed “HIV-related gingivitis.” It mostly affects immunocompromised individuals or HIV patients. The unusual pattern of inflammation appears as a distinctive linear band of erythema which involves 2–3 mm of marginal gingival (Neville et al. 2002). Redness can be circumscribed or diffused and can spread until it passes the mucogingival junction. It is often generalized in the oral cavity, but can be localized to just a few teeth. The main characteristic is that it does not respond to conventional treatment (SRP and plaque control).
Note: the HIV patient is also more prone to:
Hyperplasic candidosis
Pseudomembranous candidosis
Cheilitis
Ulcerative necrotizing gingivitis, ulcerative necrotizing periodontitis
Hairy leukoplakia
Kaposi’s sarcoma
2) Other mycoses (Histoplasmosis; Aspergillosis)
Histoplasmosis is a granulomatous disease caused by Histoplasma capsulatum and represents one of the most frequent systemic mycoses in the United States. The frequently seen subclinical development of infection usually includes either a pulmonary chronic histoplasmosis (30% have oral manifestations) or a disseminated form found primarily in HIV patients (60% have oral manifestations). Oral findings can consist of painful granulomatous ulcerations (Holmstrup 1999).
c) Inflammatory and immune conditions
Hypersensitivity reactions
1) Contact allergy
Contact allergy is a rare condition, but it is an inflammatory reaction of the gingival tissue mostly to dental restorative materials, dentifrices, mouthwashes, and foods. Their presentation is associated to a type IV hypersensitivity reaction.
2) Plasma cell gingivitis
