Furcation book

Diagnosis and Treatment  

of Furcation‐Involved Teeth

Diagnosis and Treatment  

of Furcation‐Involved Teeth

Edited by Luigi Nibali

Senior Clinical Lecturer

Centre for Immunobiology and Regenerative Medicine

Centre for Oral Clinical Research, Institute of Dentistry

Barts and the London School of Medicine and Dentistry

Queen Mary University of London (QMUL), London, UK
Honorary Associate Professor, University of Hong Kong

This edition first published 2018

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Library of Congress Cataloging‐in‐Publication Data
Names: Nibali, Luigi, 1978– editor.

Title: Diagnosis and treatment of furcation-involved teeth / edited by Luigi Nibali.

Description: Hoboken, NJ : Wiley, [2018] | Includes bibliographical references and index. |

Identifiers: LCCN 2018010570 (print) | LCCN 2018011380 (ebook) | ISBN 9781119270669 (pdf) |  

ISBN 9781119270676 (epub) | ISBN 9781119270652 (hardback)

Subjects: | MESH: Furcation Defects–diagnosis | Furcation Defects–therapy | Models, Animal

Classification: LCC RK450.P4 (ebook) | LCC RK450.P4 (print) | NLM WU 242 | DDC 617.6/32–dc23

LC record available at https://lccn.loc.gov/2018010570
Cover image: (Main, top left and middle images) © Luigi Nibali; (Top right image) © Roberto Rotundo

Cover design: Wiley

Set in 10/12pt Warnock by SPi Global, Pondicherry, India

10 9 8 7 6 5 4 3 2 1

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Page Number: v

v

List of Contributors 

vii

Foreword 

ix

Preface 

xi

About the Companion Website 

xiii

1  Anatomy of Multi‐rooted Teeth and Aetiopathogenesis of the Furcation Defect 

1

Bernadette Pretzl

2  Clinical and Radiographic Diagnosis and Epidemiology of Furcation Involvement 

15

Peter Eickholz and Clemens Walter

3  How Good are We at Cleaning Furcations? Non‐surgical and Surgical Studies 

33

Jia‐Hui Fu and Hom‐Lay Wang

4 

Furcation: The Endodontist’s View 

55

Federica Fonzar and Riccardo Fabian Fonzar

5  Why do We Really Care About Furcations? Long‐term Tooth Loss Data 

91

Luigi Nibali

6  Regenerative Therapy of Furcation Involvements in  

Preclinical Models: What is Feasible? 

105

Nikolaos Donos, Iro Palaska, Elena Calciolari, Yoshinori Shirakata, and Anton Sculean

7  Regenerative Therapy of Furcations in Human Clinical Studies: What has been Achieved 

So Far? 

137

Søren Jepsen and Karin Jepsen

8  Furcation Therapy: Resective Approach and Restorative Options 

161

Roberto Rotundo and Alberto Fonzar

9 

Furcation Tunnelling 

177

Stefan G. Rüdiger

10  Innovative and Adjunctive Furcation Therapy: Evidence of Success  

and Future Perspective 

191

Luigi Nibali and Elena Calciolari

Contents

Contents

vi

11  Furcation: Why Bother? Treat the Tooth or Extract and Place an Implant? 

209

Nikos Mardas and Stephen Barter

12  Is it Worth it? Health Economics of Furcation Involvement 

229

Falk Schwendicke and Christian Graetz

13  Deep Gaps between the Roots of the Molars: A Patient’s Point of View 

249

Luigi Nibali

14  Assessment of Two Example Cases Based on a Review of the Literature 

257

Luigi Nibali

15  Furcations: A Treatment Algorithm 

269

Luigi Nibali

Index 

285

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vii

Dr Stephen Barter

Private practice, Eastbourne, UK

Dr Elena Calciolari

Centre for Immunobiology and Regenerative 

Medicine

Centre for Oral Clinical Research

Institute of Dentistry

Barts and the London School of Medicine 

and Dentistry

Queen Mary University of London (QMUL)

London, UK

Prof. Nikolaos Donos

Centre for Immunobiology and Regenerative 

Medicine

Centre for Oral Clinical Research

Institute of Dentistry

Barts and the London School of Medicine 

and Dentistry

Queen Mary University of London (QMUL)

London, UK

Prof. Peter Eickholz

Poliklinik für Parodontologie

Zentrum der Zahn‐ Mund‐ und 

Kieferheilkunde (Carolinum)

Johann Wolfgang Goethe‐Universität 

Frankfurt

Frankfurt am Main

Germany

Dr Federica Fonzar

Private practice

Udine

Italy

Dr Alberto Fonzar

Private practice

Udine

Italy

Dr Riccardo Fabian Fonzar

Private practice

Udine

Italy

Dr Jia‐Hui Fu

Discipline of Periodontics

Faculty of Dentistry

National University of Singapore

Singapore

Dr Christian Graetz

Clinic for Conservative Dentistry and 

Periodontology

Christian‐Albrechts‐University

Kiel

Germany

Dr Karin Jepsen

Department of Periodontology

Operative and Preventive Dentistry

University of Bonn

Germany

Prof. Søren Jepsen

Department of Periodontology

Operative and Preventive Dentistry

University of Bonn

Germany

Dr Nikos Mardas

Centre for Immunobiology and Regenerative 

Medicine

Centre for Oral Clinical Research

Institute of Dentistry

Barts and the London School of Medicine 

and Dentistry

Queen Mary University of London (QMUL)

London

UK

List of Contributors

List of Contributors

viii

Dr Luigi Nibali

Centre for Immunobiology and Regenerative 

Medicine

Centre for Oral Clinical Research

Institute of Dentistry

Barts and the London School of Medicine

and Dentistry

Queen Mary University of London (QMUL)

London

UK

Dr Iro Palaska

Centre for Immunobiology and Regenerative 

Medicine

Centre for Oral Clinical Research

Institute of Dentistry

Barts and the London School of Medicine 

and Dentistry

Queen Mary University of London (QMUL)

London

UK

Dr Bernadette Pretzl

Section of Periodontology

Department of Operative Dentistry

University Clinic Heidelberg

Heidelberg

Germany

Dr Roberto Rotundo

Periodontology Unit

UCL Eastman Dental Institute

London

UK

Dr Stefan G. Rüdiger

Department of Periodontology

Public Dental Service/Malmö University

Malmö

Sweden

Dr Falk Schwendicke

Department of Operative and Preventive 

Dentistry

Charité‐Universitätsmedizin Berlin

Berlin

Germany

Prof. Anton Sculean

Department of Periodontology

School of Dental Medicine

University of Bern

Bern

Switzerland

Dr Yoshinori Shirakata

Department of Periodontology

Kagoshima

University Graduate School of Medical and 

Dental Sciences

Kagoshima

Japan

Prof. Clemens Walter

Klinik für Parodontologie

Endodontologie und Kariologie

Universitätszahnkliniken,

Universitäres Zentrum für  

Zahnmedizin Basel

Basel

Switzerland

Prof. Hom‐Lay Wang

Department of Periodontics and Oral 

Medicine

School of Dentistry

University of Michigan

Ann Arbor

MI

USA

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 Foreword

The preservation of tissues and structures 

that support the dentition is a major goal of 

conservative dentistry for the benefit of our 

patients. As dental practitioners, we are 

trained to maintain and restore function, 

aesthetics, and phonetics for the promotion 

of oral health. In the development of this 

book, Diagnosis and Treatment of Furcation‐

Involved Teeth, Luigi Nibali and his 

 

co‐authors have assembled an excellent text 

that comprehensively examines the manage-

ment of the most challenging‐to‐treat teeth 

in the jaws – the molar and premolar teeth 

with furcation involvement. It is clear that 

clinicians are continually tested on which are 

the best approaches to handle these clinical 

scenarios that include furcated teeth. The 

education, skill, and training required to 

manage furcations are significant given the 

anatomy, location, and functional biome-

chanical occlusal forces associated with 

 posterior teeth that make for complex  clinical 

decision‐making.

In this text, Dr Nibali has convened inter-

national experts providing chapters ranging 

from the diagnosis of disease to clinical out-

comes from the health policy expert’s, cari-

ologist’s, periodontist’s, and endodontist’s 

perspectives on periodontal‐endodontic‐

restorative dilemmas in patient care. It is 

important to recognize that there is a large 

evidence base that was initiated from the 

‘pre–dental implant era’ on the long‐term 

success in the maintenance of compromised 

teeth affected by extensive restorative care, 

periodontal involvement, and/or pulpal 

pathology. This text not only focuses on 

 diagnosis and treatment, but includes valua-

ble information from a health economics and 

treatment algorithms perspectives on long‐

term tooth preservation.

In the first part of the book, a thorough 

background on the unique anatomy of multi‐

rooted teeth and corresponding diagnostic, 

prognostic, and therapeutic intricacies is 

presented. The next section provides a strong 

rationale regarding the concept of tooth 

preservation from the restorative, periodon-

tal, and endodontic perspectives, which 

highlights the strong evidence base of 

 treatment success of tooth furcations. This 

background is important to examine criti-

cally, since many oral implantologists in the 

field are not adequately versed on the ramifi-

cations of premature tooth removal versus 

those teeth that can be predictably retained 

for the long‐term success of the patient. The 

application in clinical practice by those with-

out adequate training occasionally errs on 

the expedience of tooth extraction, without 

pausing to weigh methodically the advan-

tages and disadvantages of embarking on 

comprehensive therapy for furcated teeth. 

Those without access to this text on the many 

options available to increase the lifespan of 

molar and premolar teeth may not be pre-

pared to treatment plan the complex dental 

patient appropriately for the comprehensive 

assessment of restorative, periodontal, endo-

dontic, functional, and aesthetic needs. 

Given practice trends of more common 

extractions of furcated periodontally and 

endodontically compromised teeth, it sug-

gests that ‘the time is right’ to emphasize the 

­orreorr

x

great potential available in the proper assess-

ment and treatment of furcated teeth. This 

section highlights the long‐term success with 

proper therapy in maintaining furcated teeth.

The next part of the text highlights the many 

different therapeutic modalities that are clini-

cally available to treat multi‐rooted teeth, 

including non‐surgical maintenance, resective 

procedures (including tunnelling, root resec-

tion, and bicuspidization), and reconstructive 

regenerative therapy using biologics or bioma-

terials. Other chapters in the book build on 

our  existing evidence base to examine the 

cases that can genuinely be retained versus 

those teeth too compromised as ‘hopeless’ 

that may benefit from extraction, implant site 

development (bone grafting and alveolar ridge 

preservation), followed by dental implant 

reconstruction. Indeed, dental implant ther-

apy has revolutionized oral care and clinical 

treatment decision‐making paradigms for 

advanced reconstructive procedures. It is also 

crucial for the advanced clinician to under-

stand when and when not to attempt to retain 

advanced disease cases. Large epidemiologi-

cal studies have demonstrated that dental 

implant therapy is not a ‘panacea’ and that, 

given the significant incidence and prevalence 

of peri‐implant biological complications in 

the molar regions, we should re‐examine the 

opportunities for maintaining and treating 

furcated teeth more diligently and more fully. 

The concluding chapters scrutinize the health 

economics opportunities at the patient and 

clinician levels in terms of tooth preservation 

of furcated molars, and in which types of cases 

which treatment planning approach is indi-

cated for such advanced clinical scenarios.

Stimulated by the comprehensive approach 

in this book, this can be a renaissance period 

in reconstructive dentistry when we firmly 

consider the many options available to us as 

clinicians to better preserve the dentition in 

treating furcation‐involved teeth. This text 

lays out a contemporary and exciting oppor-

tunity for us as clinicians to provide our 

patients with state‐of‐the‐art therapy for the 

betterment of oral health!

William V. Giannobile, DDS, MS, DMedSc

Najjar Endowed Professor of Dentistry & 

Biomedical Engineering

Departments of Periodontics and Oral 

Medicine & Biomedical Engineering, 

University of Michigan School of Dentistry and 

College of Engineering, Ann Arbor, MI, USA

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xi

Declare the past, diagnose the present, 

foretell the future.

Hippocrates

Doubt is not a pleasant condition, but 

 certainty is an absurd one.

Voltaire

Young and new to a periodontal clinic, I 

remember looking at cases of extensive peri-

odontal and bone loss in multi‐rooted teeth 

and wondering how the problem could be 

solved, and if and how the tooth could be 

retained. The fascination with the spaces 

 created by inter‐radicular bone resorption, 

called ‘furcations’, and the struggle over how 

to manage them in the clinic, continues to 

occupy large parts of my days and has 

prompted me to write this book. Here, with 

the help of several expert colleagues, I have 

tried to:

 

●

Critically appraise the evidence.

 

●

Present expert opinions.

 

●

Show treated cases.

 

●

Present useful clinical guidelines, step‐by 

step procedures, and treatment algorithms.

The emphasis of the book is to try and 

 maintain molars affected by furcation involve-

ment and regenerate the lost support, when 

possible, accepting that this is not always pos-

sible in the long term. It goes  without saying 

that primary prevention of periodontitis 

remains the best way to prevent tooth loss. 

I hope that periodontists, dental/postgraduate 

students, hygienists, and  

general dentists 

might find this book useful for the treatment 

of molars already affected by periodontitis 

and furcation involvement.

Immense thanks go to all the expert collab-

orators and friends, Will Giannobile, 

Bernadette Pretzl, Peter Eickholz, Clemens 

Walter, Jia‐Hui Fu, Hom‐Lay Wang, Federica, 

Riccardo, and Alberto Fonzar, Roberto 

Rotundo, Stefan Rüdiger, Nikos Donos, Toni 

Sculean, Elena Calciolari, Iro Palaska, 

Yoshinori Shirakata, Søren and Karin Jepsen, 

Nikos Mardas, Steve Barter, Christian Graetz, 

and Falk Schwendicke, who all contributed 

chapters to this book, and to Paul Kletz for 

kindly proofreading some of the chapters and 

for his support throughout my career. Special 

thanks go to the patients who over the years 

have been a big source of inspiration with 

their interest and commitment, and who 

every day make me want to be a better perio-

dontist. I also need to thank my teachers at the 

University of Catania and at the UCL Eastman 

Dental Institute, who have all contributed, 

some with small and some with larger 

 ingredients, to the cauldron of periodontal 

knowledge from which I drew for the plan-

ning and editing of this book. The students 

and staff at Barts and the London School of 

Medicine and Dentistry, Queen Mary 

University of London (QMUL), are gratefully 

acknowledged. But most of all, I would like to 

thank my family, Daniela, Domenico, Lorenzo, 

Delia, and my parents and in‐laws, for their 

 continued support of my work.

Luigi Nibali

Preface

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Page Number: xiii

xiii

Don’t forget to visit the companion website for this book:

www.wiley.com/go/nibali/diagnosis 

There you will find valuable material designed to enhance your learning, including:

 

●

video clips

 

●

additional treated cases

Scan this QR code to visit the companion website

About the Companion Website

Diagnosis and Treatment of Furcation-Involved Teeth, First Edition. Edited by Luigi Nibali. 

© 2018 John Wiley & Sons Ltd. Published 2018 by John Wiley & Sons Ltd. 

Companion website: www.wiley.com/go/nibali/diagnosis

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1

1.1   Introduction:  Why 

Focus on Molars?

Dentists generally agree on three statements 

about molars:

 

●

They play an important role in the 

dentition.

 

●

They are difficult to reach for self‐performed 

as well as professional cleaning due to their 

posterior position in the mouth.

 

●

They pose some challenges due to their 

unique anatomy.

The important role of molar teeth in the den-

tition mainly consists in their contribution to 

mastication, because they carry a considera-

ble part of the occlusal load. Hiiemäe (1967) 

focused on the masticatory function in mam-

mals and molars grinding the food, and in 

1975 Bates et al. reviewed the literature on 

the masticatory cycle in natural and artificial 

dentitions of men, attributing a fundamental 

role to our posterior teeth regarding the 

intake and preparation of nutrition. Thus, a 

focus on molars and the endeavour to retain 

our posterior teeth in a healthy functional 

state seems justified.

This chapter will reveal how the posterior 

position of molars makes them less accessi-

ble for cleaning, whether it may be self‐ 

performed or carried out by a dental 

professional. This fact, combined with the 

unique anatomy of molars, poses a challenge 

for all dentists focusing on molar retention.

1.2   The  ‘Special’  Anatomy 

of Molar Teeth

The essential knowledge of molar root anat-

omy for every periodontist is stressed in a 

review by Al‐Shammari et al. (2001). Due to 

the higher mortality and compromised 

diagnoses of furcation‐involved molars, and 

likewise to the reduced efficacy of perio-

dontal therapy in multi‐rooted teeth, the 

authors suggest a thorough engagement 

with possibly decisive tooth factors such as 

furcation entrance area, (bi)furcation 

ridges, root surface area, root separation, 

and root trunk length, because they may 

critically affect the diagnosis and therapy 

of  multi‐rooted teeth (Leknes 1997; Al‐

Shammari et al. 2001).

For centuries, scientists have concerned 

themselves with the human teeth, their anat-

omy, evolution, function, histology, and 

 histogenesis. Almost 3000 years ago, the 

Etruscans populating the northern and cen-

tral part of what is now Italy from 900 to 100 

bc recognized the importance of teeth and 

fabricated quite delicate dental prostheses, 

which Loevy and Kowitz (1997) compared to 

prostheses from the mid‐twentieth century.

Chapter 1

Anatomy of Multi‐rooted Teeth and Aetiopathogenesis 
of the Furcation Defect

Bernadette Pretzl

Section of Periodontology, Department of Operative Dentistry, University Clinic Heidelberg, Heidelberg, Germany

Chapter 1  

2

The formation and genesis of teeth have 

been studied in more detail during the last 

three and a half centuries, starting with the 

works of the so‐called father of microscopic 

anatomy and histology, Marcello Malpighi 

(1628–1694) from Italy (Rifkin and 

Ackerman 2011), who referred to an ‘invo-

lucrum externum’ describing the outer part 

of the tooth, which is today known as 

enamel. More than a century later the 

 formation of cementum (1798–1801) and 

dentine (1835–1839) was described (e.g. 

Blake 1801; Bell 1835). Written in 1935, 

Meyer’s Normal Histology and Histogenesis 

of the Human Teeth and Associated Parts 

(Churchill 1935) builds the foundation of 

our understanding regarding the anatomy 

of teeth. Orban and Mueller (1929), who 

studied the development of  furcations in 

multi‐rooted teeth, set a focus on molars 

using graphic reconstructions as early as 

1929. Their three‐dimensional illustrations 

allow a detailed impression of the root area 

comparable to those documented by 

Svärdström and Wennström (1988). In later 

years, scientists focused more and more on 

micro‐anatomical and histological research.

Based on the knowledge thus created, the 

sequence of molar development can be 

divided into three phases analogous to the 

development of all teeth (Thesleff and 

Hurmerinta 1981): initiation, morphogene-

sis, and cell differentiation. The evolution of 

more than one root sets molars apart from 

the rest of the dentition: in multi‐rooted 

teeth the enamel organ expands with 

 projections of Hertwig’s root sheath (an epi-

thelial diaphragm). These expansions were 

described as lobular growing inwards 

between the lobes. Depending on the num-

ber of lobes, two to three (in rarer cases four) 

roots develop as soon as the projections have 

fused (Bhussry 1980). In an investigation by 

Bower (1983) of furcation development, 

evolving mandibular molars from 13 foetuses 

between 17 and 38 weeks of gestation were 

fixed, sectioned, and stained, giving a unique 

and detailed impression of furcation devel-

opment. The author measured the base of 

the dental papilla as well as the buccal and 

lingual epithelial elements and described the 

development as follows: The first epithelial 

elements, which later evolve into the bifurca-

tion, appear at the 24‐week stage of gesta-

tional age. At that time, the crown formation 

of the molar is not complete and Hertwig’s 

root sheath has not developed yet (Bhussry 

1980; Bower 1983). Thus, the author suggests 

that the epithelial elements form extensions 

of the epithelium of the developing crown 

rather than the root (Bower 1983). 

Additionally, he detected stellate reticulum 

(which is essential for the formation of 

ameloblasts) in the furcation area. The 

author speculated about a possible mecha-

nism of enamel formation due to the  presence 

of stellate reticulum in the region of the 

 furcation, which develops into ameloblasts, 

for example resulting in cervical projections 

of enamel.

1.3   Anatomical  Factors 

in Molar Teeth

In 1988, Svärdström and Wennström plotted 

three‐dimensional contour maps in order to 

describe the topography of the furcation area 

and compared drawings of maxillary and 

mandibular molars. These show a complex 

area with small ridges, peaks, and pits, and 

the authors summarize that the complexity 

of the furcation topography evidently 

increases the difficulties with respect to 

proper debridement once the periodontal 

pocket reaches the furcation entrance and 

runs into the furcation area. Thus, in addi-

tion to the aforementioned potentially deci-

sive factors  –  furcation entrance area, 

bifurcation ridges, root surface area, and 

root trunk length – it has to be kept in mind 

that the complexity of the furcation area 

itself poses a challenge to the dental practi-

tioner (Svärdström and Wennström 1988). 

Figure 1.1 shows a diagram of a mandibular 

molar, highlighting the main anatomical 

features.

Anatomy of Multi-rooted Teeth  3

1.3.1  Furcation Entrance Area

The furcation entrance area was measured 

by Bower (1979a) in 114 maxillary and 103 

mandibular first molars. The diameter of 

the entrance area was smaller than a curette 

blade in more than 50% of the examined fur-

cations, with the smallest average diameter 

in buccal (b) sites of maxillary as well as 

mandibular first molars. No correlation 

between the size of the tooth and its furca-

tion entrance area could be detected (Bower 

1979a). Hou et  al. (1994) studied 89 

extracted maxillary and 93 extracted man-

dibular first and second molars microscopi-

cally. In their Chinese population sample, 

they concurred with the results presented 

by Bower (1979a) in the maxilla and found a 

larger diameter in mesio‐ (mp) and disto‐

palatal (dp) furcation entrances for first and 

second molars (mp: 1.04 mm and 0.90 mm; 

dp: 0.99 mm and 0.67 mm; b: 0.74 mm and 

0.63 mm, respectively), which was con-

firmed by Svärdström and Wennström 

(1988) and dos Santos et al. (2009).

In mandibular molars the results differed, 

with wider entrance areas in buccal furca-

tions of first and second molars (b: 0.88 mm 

and 0.73 mm; l: 0.81 mm and 0.71 mm, 

respectively). Nonetheless, the furcation 

entrance area was < 1 mm in the majority of 

molars and < 0.75 mm in 58%, 49%, and 52% 

of molars, respectively (Bower 1979a; Chiu 

et al. 1991; Hou et al. 1994). Thus, the stand-

ard width of curettes (0.75–1.0 mm) is 

mostly too large to access, let alone properly 

clean, a furcation entrance. Hou et al. (1994) 

concluded that in order to achieve complete 

debridement of root surfaces within furca-

tions, an appropriate selection and combi-

nation of ultrasonic tips (diameter 0.56 mm) 

and periodontal curettes should be consid-

ered. A recent study by dos Santos et  al. 

Fornix

Divergence

Root trunk

Root complex

Root cone

Crown

Bone loss

Degree of
separation

Figure 1.1 

Drawing of mandibular molar with furcation involvement, showing the main anatomical features, 

including root trunk (part of the root from the cemento‐enamel junction [CEJ] to the furcation entrance) 

and root cones, and pointing at root divergence and degree of separation between roots. The ‘bone loss’ is 

schematically indicated as the distance between the CEJ and the most apical part of the bone. Source: 

Courtesy of Dr Aliye Akcali.

Chapter 1  

4

(2009) analysed 50 maxillary and 50 man-

dibular molars and confirmed the afore-

mentioned findings, concluding that some 

molar furcation entrances could not be 

 adequately instrumented with curettes and 

 

suggesting the use of alternative hand 

instruments. In a review, Matthews and 

Tabesh (2004) stressed the importance of 

the diameter of the furcation entrance in 

order to judge the effect of professional 

cleaning, and thus the probable success of 

periodontal therapy. The challenges of fur-

cation cleaning are discussed by Fu and 

Wang in Chapter 3.

1.3.2  (Bi)furcation Ridges

In early morphological studies of extracted 

first molar teeth, cementum was found in the 

furcation area in a ridge, building the furca-

tion region in mandibular molars, and was 

called an intermediate bifurcation ridge 

(IBR), with a high presence of cementum 

adjacent to the furcation entrance (Everett 

et al. 1958; Bower 1979a, b; see Figure 1.2). 

In  a study on developing first mandibular 

molars sectioned at different gestational 

ages, the lingual element was found to be 

wider in a mesio‐distal dimension comparable 

to studies in extracted molars (Bower 1983, 

1979b). Secondly, the exclusion of ectomes-

enchyme between the lobes described by 

Bhussry (1980) may explain the large quanti-

ties of cementum in the furcation area of the 

mature tooth corresponding to bifurcation 

ridges (Bower 1983). In general, two types of 

bifurcation ridge are known: one in the 

bucco‐lingual direction, the other in the 

mesio‐distal  direction  (intermediate = IBR). 

Everett et al. (1958) detected buccal and lin-

gual ridges, mainly constituting of dentine, in 

63% of mandibular first molars and IBRs, 

mainly composed of cementum, in 73%. The 

findings of Burch and Hulen (1974), Dunlap 

and Gher (1985), and Hou and Tsai (1997a) 

concur, with a prevalence of 76.3%, 70%, and 

67.9%, respectively, in mandibular first 

molars.

Gher and Vernino (1980) suggest a connec-

tion between the presence of an IBR and the 

progression of the furcation defect due to the 

morphology and location of IBRs. Hou and 

Tsai (1997a) confirmed this correlation. 

Additionally, they stated that an even higher 

significant correlation exists between the 

simultaneous presence of IBRs combined 

with cemento‐enamel projections and furca-

tion involvement (FI).

Figure 1.2 

Furcation ridge. Source: Courtesy of Dr Nicola Perrini.

Anatomy of Multi-rooted Teeth  5

1.3.3  Root Surface Area

A team of researchers (Hermann et al. 1983; 

Dunlap and Gher 1985; Gher and Dunlap 

1985) focused on the topic of root surface 

area (RSA) in maxillary and mandibular first 

molars. In a meta‐analysis derived of data 

from 22 original articles, Hujoel (1994) com-

puted a total RSA (corresponding to the 

 periodontal surface area) for the complete 

dentition of 65–86 

cm

2

, excluding third 

molars. In maxillary first molars a mean of 

4.5 cm

2

 (second: 4.0 cm

2

) and in mandibular 

first molars a mean of 4.2 cm

2

 (second: 

3.4 cm

2

) were calculated. In molars, it is often 

difficult to judge the extent of FI clinically 

(Bower 1979b) and thus to determine the 

RSA exactly.

1.3.3.1  RSA in the Maxilla

Hermann et  al. (1983) as well as Gher and 

Dunlap (1985) dissected 20 extracted first 

maxillary molars and cross‐sectioned them in 

1 mm increments. Molars with fused roots 

were excluded. They observed that the disto‐

buccal root had a significantly smaller RSA 

than either the mesio‐buccal or palatal root, 

confirming the results of Bower (1979b). The 

root trunk surface area was significantly larger 

than any surface of the three individual roots, 

and averaged 32% of the total RSA of the max-

illary first molar (Hermann et al. 1983). Gher 

and Dunlap (1985) measured a mean root 

length of 13.6 mm (ranging from 10.5 to 

16 mm) and a total RSA of 4.77 cm

2

 (ranging 

from 3.36 to 5.84 cm

2

). Additionally, a ‘bal-

looning’ of the RSA percentage in the furca-

tion area of maxillary molars was described, 

which could not be detected in other teeth. 

Accordingly, the importance of periodontal 

support in the furcation area of maxillary 

molars was stressed, concluding that a rela-

tively small attachment gain or loss may have 

a significant impact on the stability of the 

maxillary first molar (Gher and Dunlap 1985).

1.3.3.2  RSA in the Mandible

For a study on mandibular first molars, 

10 teeth were hemisected and measured by 

Anderson et al. (1983). They concluded that 

the mesial root showed a statistically signifi-

cant greater RSA than the distal root, which 

should be taken into consideration when 

planning treatment, especially regarding 

resective approaches. Dunlap and Gher 

(1985) dissected 20 extracted mandibulary 

first molars and cross‐sectioned them in 

1 mm increments. They too observed that 

the distal root had a significantly smaller 

RSA than the mesial one, but stressed that 

the shapes of the roots (conical for the distal 

one; hour‐glass shaped for the mesial one) 

should be taken into consideration as well. In 

contrast to their findings in the maxilla, the 

root trunk surface area was not larger than 

the surface of the individual roots, and aver-

aged 30.5% of the total RSA of the mandibu-

lary first molar. They found a mean root 

length of 14.4 ± 1.1 mm and a total RSA of 

4.37 ± 0.64 cm

2

. In other studies (Jepsen 1963; 

Anderson et al. 1983), the total RSA varied 

from 4.31 to 4.7 cm

2

.

1.3.4  Root Trunk Length

The portion of multi‐rooted teeth located api-

cal to the cemento‐enamel junction (CEJ) is 

called the ‘root complex’ and is divided into 

root trunk and root cones. The root trunk is 

generally defined as the area of the tooth from 

the CEJ to the furcation fornix. In a study by 

Gher and Dunlap (1985), the distance between 

the CEJ and the furcation entrance in maxil-

lary molars differed considerably between the 

mesial (3.6 ± 0.8 mm) and the distal entrance 

(4.8 ± 0.8 mm), whereas the buccal entrance 

was detected 4.2 ± 1.0 mm apical to the CEJ. 

These findings led to the conclusion that the 

clinician should suspect a through‐and‐

through furcation (degree III according to 

Hamp et al. 1975) in maxillary molars once a 

loss of 6 mm in vertical attachment occurred. 

In more than 50% of the dissected maxillary 

molars, the furcation roof was found coronal 

of the root separations and formed a concave 

dome between the three roots.

It should be emphasized that the dome‐like 

anatomy further complicates therapy and 

Chapter 1  

6

maintenance of maxillary first molars (Gher 

and Dunlap 1985). Hou and Tsai (1997b) 

measured the root trunk in 166 extracted 

first and second maxillary and 200 extracted 

first and second mandibular molars of a 

Taiwanese tooth sample. In the maxilla, short 

root trunks were more commonly found 

buccally, whereas long root trunks were more 

commonly found mesially (Hou and Tsai 

1997b). The authors found generally longer 

root trunks in second molars than in first 

molars in both jaws, and additionally stated 

that long root trunks are associated with 

short root cone length (Hou and Tsai 1997b).

In 134 extracted first and second mandibu-

lar molars, Mandelaris et al. (1998) detected 

longer root trunks in lingual molar surfaces 

when compared to buccal surfaces (mean: 

4.17 mm and 3.14 mm, respectively), confirm-

ing the results of Hou and Tsai (1997b). The 

mean distance between the CEJ and the furca-

tion entrance was 4.0 ± 0.7 mm in mandibular 

molars (4.6 ± 0.6 mm in maxillary first molars; 

Dunlap and Gher 1985; Gher and Dunlap 

1985), whereas no root trunk of > 6 mm could 

be found (Dunlap and Gher 1985; Mandelaris 

et al. 1998). Like in maxillary molars, it can be 

concluded that a through‐and‐through furca-

tion (Hamp et al. 1975) should be expected in 

the mandible once a loss of 6 mm in vertical 

attachment was reached on both sides (buccal 

and lingual). On the other hand, it has to be 

kept in mind that a furcation defect has a 

 horizontal component as well. Santana et al. 

(2004) measured 100 extracted first and sec-

ond mandibular molars and their findings 

suggest that a horizontal attachment loss of 

4.3–6.9 mm is essential in order to allow com-

munication between the buccal and lingual 

furcation entrance. Complete or partial fusion 

of roots is also not unusual in multi‐rooted 

teeth. Some 40% of maxillary premolars are 

two‐rooted and the entrance to the furcation 

is located an average 8 mm from the CEJ, well 

into the middle third of the root complex 

(Bower 1979a).

A clinically evident FI correlates with the 

vertical length and type of the root trunk 

(Carnevale 1995; Hou and Tsai 1997b, 

Al‐Shammari et  al. 2001). Thus, Al‐

Shammari et al. (2001) summarized that the 

root trunk length significantly relates to the 

prognosis and treatment of molars. A short 

root trunk worsens the prognosis with regard 

to a more likely FI, but once periodontal 

destruction has occurred, it improves the 

chances of a successful treatment (Horwitz 

et al. 2004).

1.4   Anatomical  Aetiological 

Factors

1.4.1  Cervical Enamel Projections

Enamel surfaces do not allow for the attach-

ment of connective tissue and represent an 

anatomical abnormality in the root area. 

Thus, cervical enamel projections (CEP) may 

contribute to the development of a furcation 

defect (Al‐Shammari et al. 2001). The first to 

report a possible connection between CEPs 

and periodontal destruction in molars was 

Atkinson in 1949. According to Masters and 

Hoskins (1964), CEPs can be classified in 

three grades (Table 1.1).

Different prevalences of CEPs have been 

documented so far. Masters and Hoskins 

(1964) found CEPs in 29% of mandibular and 

17% of maxillary molars. In Egyptian skulls, 

Bissada and Abdelmalek (1973) detected a 

CEP prevalence of 8.6%. In the 1138 molars 

studied, a higher incidence of CEPs in the 

Table 1.1 

Classification of cervical enamel 

projections.

Grade I

The enamel projection extends from 

the cemento‐enamel junction of the 

tooth towards the furcation entrance 

(<1/3 of the root trunk).

Grade II The enamel projection approaches 

the furcation entrance but does not 

enter it. No horizontal component is 

present (>1/3 of the root trunk).

See Figure 1.3a.

Grade III The enamel projection extends 

horizontally into the furcation.

Compare Figures 1.3b and 1.3c.

Anatomy of Multi-rooted Teeth  7

mandible could be confirmed. A study in 200 

East Indian skulls with 2000 molars reported a 

32.6% incidence rate of CEPs (Swan and Hurt 

1976). They were most often reported in man-

dibular second molars (51.0%), followed by 

maxillary second molars (45.6%), mandibular 

first and maxillary first molars (13.6%). Grade 

I enamel projections (Masters and Hoskins 

1964) were detected most frequently. These 

could not be significantly related to furcation 

involvement, as could grade II and III CEPs 

(Swan and Hurt 1976). An observation in 78 

Taiwanese individuals reported detection of 

CEPs in 49.3% of second and 62.3% of first 

maxillary and 51.2% of second and 73.9% of 

first mandibular molars (Hou and Tsai 1987). 

A study by the same authors in furcation‐

involved mandibular molars reported even 

higher CEP percentages: 71% of second and 

92.9% of first mandibular molars showed 

enamel projections (Hou and Tsai 1997b). 

Mandelaris et al. (1998) documented CEPs in 

66.4% of mandibular molars (61.9% of buccal 

and 50.8% of lingual surfaces) ranging from 

0.98 to 1.33 mm in diameter. Current research 

on CEPs was published in 2013 and 2016. 

Bhusari et  al. (2013) investigated their inci-

dence on the buccal surface of 944 upper and 

lower first, second and third permanent 

molars from 89 Indian dry human skulls, and 

additionally measured FI. Again, it could be 

confirmed that CEPs are found more fre-

quently in the mandible and are significantly 

associated with the occurrence of FI. The 

incidence ranged from 14.7% in mandibular 

second molars to 5.5% in wisdom teeth. The 

most recent study was performed using cone‐

beam computed tomography data in a Korean 

population analysing 982 mandibular molars 

(Lim et  al. 2016) and reported an overall 

 prevalence rate of CEP of 76%. Grade I CEPs 

were the most common, followed by CEPs of 

grades II and III (Lim et al. 2016).

The huge variations can partly be explained 

by different study objects: in human skulls 

healthier periodontal conditions can be 

assumed, while extracted molars most prob-

ably show worse conditions, and Hou and 

Tsai (1987, 1997a) as well as Mandelaris et al. 

(1998) studied furcation‐involved molars in 

periodontal patients. Additionally, a higher 

prevalence of CEPs in Oriental subjects than 

in Caucasians is suspected (Hou and Tsai 

1987; Lim et al. 2016).

Nonetheless, it can be concluded that CEPs 

are a common problem which must be 

addressed by clinicians when treating molar 

teeth. They are more prevalent than enamel 

pearls and prevent connective tissue attach-

ment, thus contributing to the aetiology of 

 furcation defects, possibly resulting in localized 

chronic periodontitis and FI in molars (Leknes 

Figure 1.3a 

Cervical enamel projection grade II (>1/3 of root trunk; Masters and Hoskins 1964) on upper right 

first molar (REM microscope). Source: Eickholz and Hausmann 1998.

Chapter 1  

8

1997; Al‐Shammari et al. 2001; Bhusari et al. 

2013). Additionally, significantly higher plaque 

and gingivitis index values have been reported 

in the presence of CEPs (Carnevale et al. 1995).

1.4.2  Enamel Pearls

Enamel pearls (see Figure  1.4) were first 

described in an article in the American 

Journal of Dental Science in 1841 (Moskow 

Figure 1.3b 

Cervical enamel projection on lower 

left first molar; grade III (reaching furcation 

entrance area; Masters and Hoskins 1964). Source: 

Eickholz 2005.

Figure 1.3c 

Cervical enamel projection on extracted 

lower right first molar; grade III (reaching furcation 

entrance area; Masters and Hoskins 1964). Source: 

Eickholz and Hausmann 1998.

Figure 1.4a 

Macroscopic image of an enamel pearl 

on an extracted molar. Source: Courtesy of Prof. 

Dr. H.-K. Albers.

Figure 1.4b 

Microscopic image of an enamel pearl. 

Source: Courtesy of Prof. Dr. H.-K. Albers.

Anatomy of Multi-rooted Teeth  9

and Canut 1990). They are ectopic globules 

consisting mostly of enamel, often contain-

ing a core of dentine, and they adhere to the 

tooth root surface, with a distinct predilec-

tion for the furcation areas of molar teeth, 

particularly maxillary third and second 

molars. In a review from 1990, an incidence 

of 2.6% (ranging from 1.1 to 9.7%) was 

reported, with differences among racial 

groups and a greater incidence in histological 

studies (Moskow and Canut 1990). Like 

CEPs, enamel projections prevent connec-

tive tissue attachment and thus contribute to 

the aetiology of periodontal destruction. 

They usually occur singularly, but up to four 

enamel pearls have been observed on the 

same tooth (Moskow and Canut 1990).

More recent research demonstrates an 

incidence within the range documented by 

Moskow and Canut (1990). Darwazeh and 

Hamasha (2000) evaluated the presence of 

enamel pearls in a Jordanian patient sample, 

studying 1032 periapical radiographs. An 

incidence of 1.6% of enamel pearls in molars 

and 4.76% per subject with no gender differences 

was reported. Chrcanovic et al. (2010) evalu-

ated the prevalence of enamel pearls in 

45 539 permanent teeth (20 218 molars) from 

a human tooth bank in Brazil. They con-

firmed the predominant presence in the 

maxilla and reported an incidence of 1.71% 

in molars. Akgül et al. (2012) evaluated the 

presence of enamel pearls using cone‐beam 

computed tomography in 15 185 teeth (4334 

molars). An incidence of enamel pearls of 

0.83% in molars and 4.69% per subject with no 

gender differences was reported. Again, the 

incidence was significantly higher in the max-

illa. Colak et al. (2014) studied the prevalence 

of enamel pearls in Turkish dental patients 

and detected them in 0.85% of teeth and 5.1% 

of subjects, with a contradictory higher inci-

dence in the mandible and in male patients.

Although lower in incidence than enamel 

projections, it can be summarized that 

enamel pearls play an important role in the 

aetiology of furcation defects, and it is con-

sidered essential to diagnose enamel pearls 

early on to allow for an adequate prognosis of 

molar retention and probably alter the thera-

peutic approach.

1.5   Periodontal  Aetiological 

Factors in Molar Teeth

Aetiological factors interact with the previ-

ously described anatomical factors and may 

lead to periodontal destruction and attach-

ment loss in molars, and thus result in a fur-

cation defect. According to Al‐Shammari 

et al. (2001), plaque‐associated inflammation, 

Figure 1.4c 

Orthopantomogram showing enamel pearls on upper right and left second molars. Source: 

Eickholz and Hausmann 1998.

Chapter 1  

10

trauma from occlusion, pulpal pathology, 

vertical root fractures, and iatrogenic factors 

need to be taken into consideration.

1.5.1 Plaque‐associated 

Inflammation

The reader of this book will surely be well 

accustomed to plaque formation and the 

inflammatory component of gingivitis and 

periodontitis. What is special about molars 

in this context? In general, it can be stated 

that furcations are more prone to plaque 

adhesion and less likely to stay plaque free. 

The anatomy of the furcation favours reten-

tion of bacterial deposits and renders hygiene 

procedures difficult (Matthews and Tabesh 

2004). In 1987, Nordland et  al. monitored 

2472 sites in 19 periodontal patients for 

24  months after periodontal therapy, and 

reported that furcation sites responded less 

favourably to therapy and were more likely to 

exhibit higher plaque and gingivitis scores. 

Apart from that, it is assumed that furcation 

areas are an extension of periodontal pock-

ets, because unique histological features are 

lacking (Glickman 1950; Al‐Shammari et al. 

2001). Thus, plaque formation follows the 

same process in molars and their furcations 

as in the remaining dentition (Leknes 1997).

1.5.2  Occlusal Trauma

Trauma from occlusion is suspected to 

be  another aetiological factor contributing 

to  periodontal destruction in molars. 

Two groups of researchers, Glickman and 

co‐workers as well as Lindhe and co‐workers, 

focused on this topic in animal studies apply-

ing excessive occlusal forces on molars. In 

their classic studies on beagle dogs, Lindhe 

and Svanberg (1974) and Nyman et al. (1978) 

reported significant alterations in tooth 

mobility combined with angular bony defects 

and loss of periodontal support in artificially 

created, gingivally inflamed multi‐rooted 

teeth carrying splints, compared to teeth 

with inflammation but carrying no addi-

tional occlusal load. Even before that, 

Glickman et al. (1961) compared the effect of 

occlusal force on splinted and non‐splinted 

teeth in rhesus monkeys, and suggested that 

the fibre orientation in the furcation area 

makes multi‐rooted teeth more susceptible 

to increased functional forces. More recently, 

Nakatsu et  al. (2014) confirmed the afore-

mentioned findings in an observation in rats. 

On the other hand, Waerhaug (1980) con-

cluded from his observations of 46 human 

molars (extracted because of advanced peri-

odontal destruction) that increased mobility 

and occlusal trauma are not involved in the 

aetiology of the FI and are instead a late 

symptom of periodontal disease. Thus, the 

impact of occlusal forces in the aetiology of 

periodontitis in general and FI in particular 

remains controversial (Al‐Shammari et  al. 

2001; Reinhardt and Killeen 2015). In a 

review, Harrel (2003) suggest that occlusal 

interferences should be regarded as a poten-

tial risk factor comparable to smoking, rather 

than a causative or aetiological factor.

1.5.3  Vertical Root Fractures

It is generally agreed that vertical root frac-

tures, which can occur in a longitudinal 

direction on any surface of the root, are dif-

ficult to diagnose because they share symp-

toms with other dental conditions (Matthews 

and Tabesh 2004). Additionally, in most cases 

mild pain or a dull discomfort is the only 

clinical symptom of a vertical root fracture 

(Meister at al. 1980). They result in rapid 

localized loss of attachment and bone 

(Walton et  al. 1984) and can lead to FI 

depending on their position. Mostly, a poor 

prognosis is assigned to teeth exhibiting ver-

tical root fractures (Al‐Shammari et al. 2001; 

Matthews and Tabesh 2004).

1.5.4  Endodontic Origin 

and Pulpal Pathology

Accessory canals are quite common in molar 

teeth. A study of 46 extracted molars of both 

Anatomy of Multi-rooted Teeth  11

jaws found accessory canals in 59% of exam-

ined teeth (Lowman et al. 1973). Burch and 

Hulen (1974) reported ‘openings’ in 76% of 

the furcations of maxillary and mandibular 

molars. These canals allow for products of 

pulpal necrosis to enter the furcation area 

and cause an inflammatory lesion (Carnevale 

et al. 1995). Thus, a pulpal pathosis can result 

in FI. Carnevale et  al. (1995) reported that 

proximal and inter‐radicular bone destruc-

tion of endodontic origin is reversible after 

root canal treatment. Periodontal therapy 

only becomes necessary in the case of a 

 persistent lesion after the endodontic treat-

ment. A more detailed description of the 

associations between FI and endodontic 

pathology is provided in Chapter 4.

1.5.5  Iatrogenic Factors

Generally, overhanging dental restorations 

or discrepancies of the subgingival margin in 

any kind of restoration or even orthodontic 

bands allow for adhesion of plaque and show 

detrimental effects on adjacent gingival tis-

sues; additionally, the fit of  prosthetic resto-

rations is mostly less than perfect (Leknes 

1997) and builds a niche, where plaque 

 formation is facilitated and cleansing diffi-

cult. According to a study by Lang et  al. 

(1983) in dental students with healthy gingi-

vae who received proximal inlays with 1 mm 

overhangs, the microbial composition of the 

subgingival biofilm shifted from healthy to a 

composition characteristically found in peri-

odontitis. Thus, the authors concluded that 

the changes observed in the subgingival 

microflora  document a potential mechanism 

for the initiation of periodontal disease asso-

ciated with iatrogenic factors. Wang et  al. 

(1993) focused on molars and assessed the 

correlation between FI and the presence of a 

crown or proximal restoration in 134 perio-

dontal patients during maintenance therapy. 

Their results showed a significant associa-

tion between FI as well as periodontal attach-

ment loss and the presence of a crown or 

restoration.

Additionally, Matthews and Tabesh (2004) 

commented that overhangs not only build a 

plaque retention niche, but also impinge on 

the biological width (between the depth of a 

healthy sulcus and the alveolar crest) and 

thus cause damage. They report ranges of 

overhangs in restored teeth from 18 to 87% 

(Matthews and Tabesh 2004). In general, the 

placement of restorative margins subgingi-

vally results in more plaque, more gingival 

inflammation and deeper periodontal 

pockets.

It can be concluded that special care needs to 

be taken when placing restorations, and over-

hangs need to be diagnosed and removed as 

early as possible. Should a restoration margin 

need to be placed subgingivally, the biological 

width has to be kept in mind and crown length-

ening considered. Thus, a dento‐gingival attach-

ment may be achieved (Herrero et al. 1995).

 Summary  of Evidence

 

●

Numerous anatomical factors like furca-

tion entrance area, bifurcation ridges, 

root surface area, and root trunk length 

need to be considered in the diagnosis and 

periodontal treatment of molars. The 

periodontist should be aware of these fac-

tors because they may have a significant 

impact on the prognosis and therapeutic 

outcome of multi‐rooted teeth.

 

●

Iatrogenic factors should be tackled early 

on (at the beginning of periodontal ther-

apy), thus allowing for improvement of 

gingival and periodontal conditions.

Chapter 1  

12

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Diagnosis and Treatment of Furcation-Involved Teeth, First Edition. Edited by Luigi Nibali. 

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Companion website: www.wiley.com/go/nibali/diagnosis

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15

2.1   Introduction

In single‐rooted teeth, periodontal destruc-

tion proceeds from the cemento‐enamel 

junction (CEJ) apically, predominantly in a 

vertical direction. The vertical attachment 

loss is assessed as vertical probing attach-

ment loss (PAL‐V) from the CEJ, or if the CEJ 

is destroyed by a restoration from the resto-

ration margin (RM) to the bottom of the per-

iodontal pocket. Vertical bone loss is assessed 

radiographically or by vertical probing bone 

level (PBL‐V) from the CEJ or RM to the 

alveolar crest. If periodontitis affects multi‐

rooted teeth, the tissues are not only 

destroyed vertically but also horizontally 

between the roots, creating furcation involve-

ment. This dimension of periodontal 

destruction (horizontal attachment and bone 

loss) may be assessed as horizontal probing 

attachment loss (PAL‐H) or horizontal 

 probing bone level (PBL‐H).

Horizontal probing attachment loss and 

bone loss in the furcation area create a niche 

(furcation involvement), which impedes 

accessibility for individual oral hygiene in the 

molar region (Lang et al. 1973) and profes-

sional root debridement (Fleischer et  al. 

1989). This adds to the factors contributing 

to more severe disease progression in 

 furcation‐involved molars, recurrent perio-

dontal infection, and as a result an inferior 

long‐term prognosis of these teeth (McGuire 

and Nunn 1996; Dannewitz et al. 2006, 2016; 

Pretzl et  al. 2008; Salvi et  al. 2014; Graetz 

et  al. 2015). Furcation‐involved molars 

respond less favourably to periodontal ther-

apy than molars without furcation involve-

ment or single‐rooted teeth, and are at 

greater risk for further attachment loss 

(Nordland et al. 1987; Loos et al. 1989; Wang 

et al. 1994) than other teeth. Addressing this 

issue, Kalkwarf et al. (1988) reported the suc-

cess of different surgical and non‐surgical 

treatment modalities in 158 molars. 

Irrespective of the therapy performed, the 

horizontal defect in the furcation area 

increased during the two‐year follow‐up. 

Thus, reliable diagnosis of incidence and 

extent of furcation involvement is decisive 

for prognosis and treatment planning.

2.2   Clinical  Furcation 

Diagnosis

Furcation involvement can only be found in 

multi‐rooted teeth (Table  2.1). More than 

one root is regularly found in maxillary and 

mandibular molars as well as in first maxillary 

Chapter 2

Clinical and Radiographic Diagnosis and Epidemiology 
of Furcation Involvement

Peter Eickholz

1

 and Clemens Walter 

2

1

 Poliklinik für Parodontologie, Zentrum der Zahn‐ Mund‐ und Kieferheilkunde (Carolinum), Johann Wolfgang Goethe‐Universität 

Frankfurt, Frankfurt am Main, Germany

2

 Klinik für Parodontologie, Endodontologie und Kariologie, Universitätszahnkliniken, Universitäres Zentrum für Zahnmedizin Basel,  

Basel, Switzerland

Chapter 2 

16

premolars (see Chapter  1). However, two‐

rooted variants may be found in second max-

illary premolars and mandibular anteriors. 

Rarely, three‐rooted variants may be found in 

mandibular molars and maxillary premolars 

(Mohammadi et  al. 2013). Those sites at 

which furcation entrances are regularly 

expected have to be examined for furcation 

involvement on a regular basis in the course 

of periodontal examination. Search for and 

scoring of furcation involvement are funda-

mental elements of periodontal examination.

Particularly in untreated periodontal 

patients, furcation entrances do not lie open. 

In most cases they are covered by gingiva. 

Thus, furcation involvement cannot be seen 

simply with the naked eye, but has to be 

probed below the gingival margin. The 

bizarre anatomy of furcations (Schroeder 

and Scherle 1987), their curved course, and 

the fact that the furcation entrances of maxil-

lary premolars and molars open into inter-

proximal spaces require the use of particular 

curved furcation probes in furcation diagno-

sis (e.g. Nabers probe; Figure 2.1). The probe 

is placed onto the tooth surface coronally of 

the gingival margin at the site where a furca-

tion entrance is expected (e.g. lingual of a 

mandibular molar). Then the probe is pushed 

apically, gently displacing the gingiva in 

 zigzag movements until the bottom of the 

sulcus or pocket is reached. If the probe falls 

into a pit horizontally, in most cases furca-

tion involvement has been detected.

Straight rigid periodontal probes (e.g. 

PCPUNC15) are inappropriate for furcation 

Table 2.1 

Regularly multi‐rooted teeth with location of roots and location 

of furcation entrances.

Tooth type

Location of 
roots

Location of furcation 
entrance

Maxillary molars

Mesio‐buccal

Disto‐buccal

Palatal

Buccal

Mesio‐palatal

Disto‐palatal

Maxillary premolars

Buccal

Palatal

Mesial

Distal

Mandibular molars

Mesial

Distal

Buccal

Lingual

Figure 2.1 

Curved furcation probes: Nabers probes (left: without markings; right: marked in 3 mm steps up to 

12 mm).

Clinical and Radiographic Diagnosis and Epidemiology  17

diagnosis because they fail to follow the 

curved course of most furcations. Their use 

bears a high risk of underestimating the 

extent of the furcation involvement (Eickholz 

and Kim 1998).

2.2.1  Classification of Furcation 

Involvement

Besides the simple fact of the existence of a 

 furcation involvement and its location, the 

severity of furcation involvement is of major 

significance. Severity of furcation involve-

ment is assessed by probing the respective 

furcation in a horizontal direction using a 

rigid curved probe (e.g. Nabers probe) and 

measuring the distance from the probe tip to 

a virtual tangent to the root convexities adja-

cent to the furcation (Figure 2.2). Measuring 

this distance allows assessment of different 

degrees of furcation involvement or the 

amount of horizontal attachment loss in mil-

limetres (horizontal probing/clinical attach-

ment level: PAL‐H/CAL‐H; Figures 2.2–2.4). 

Whereas assessment of the continuous vari-

able horizontal attachment loss provides 

information on small changes of inter‐radicular 

tissues (since they are relevant after regener-

ative therapy), the categorical classification 

of inter‐radicular t issue destruction as degree 

(a)

(b)

(c)

(d)

Figure 2.2 

Furcation involvement degree I (Eickholz and Staehle 1994; Table 2.4): horizontal loss of periodontal 

tissue support up to 3 mm: (a) schematic (maxillary molar, buccal furcation entrance): horizontal probing/clinical 

attachment level 2.5 mm; (b) mesial tooth 24 with neighbouring tooth; (c) buccal tooth 46: the probe does not 

penetrate more than 3 mm between the two buccal roots; (d) disto‐palatal tooth 16 with neighbouring tooth.

Chapter 2 

18

of furcation involvement provides suffi-

ciently relevant information for prognosis 

and decision regarding therapy of the respec-

tive multi‐rooted tooth.

The different classifications of furcation 

involvement basically exhibit differences 

only in the details (Tables 2.2–2‐3). The clas-

sification by Glickman (1953) provides some-

what vague criteria to distinguish classes of 

furcation involvement, and also considers 

radiographic information which is known to 

be of low reliability (Table 2.2; Ammons and 

Harrington 2006). The criteria for the Hamp 

et al. (1975) classification are based on meas-

urements  (threshold:  PAL‐H = 3 mm).  The 

colour‐coded version of the Nabers probe, 

marked in 3 mm steps (PQ2N; Figure 2.1), is 

particularly suitable for scoring degrees of 

furcation involvement, according to Hamp 

et  al. (1975; Eickholz and Kim 1998). 

However, there exist also furcation probes 

with 2 mm markings (Zappa probe ZA 2).

The distinction between degrees I and II of 

the Glickman classification is not as clear or 

definite as the distinction between degrees I 

and II according to Hamp et al. (1975); that 

is, horizontal loss of periodontal tissue sup-

port less than 3 mm (degree I) or exceeding 

3 mm (degree II). Degrees III and IV of the 

Glickman classification describe two severity 

grades of the situation where the desmodon-

tal fibres are detached from the furcation 

 fornix/dome throughout the diameter of 

the  tooth; that is, horizontal ‘through‐ 

and‐through’ destruction of the periodontal 

 tissue in the furcation (degree III according 

to Hamp et al. 1975).

The criteria for assigning a degree III 

(Hamp et al. 1975) to a furcation have also 

been modified. For Graetz et al. (2014), it was 

required to see the tip of the furcation probe 

(Nabers) at the opposite furcation opening to 

assign a degree III. For all other cases of deep 

but not completely penetrating horizontal 

probing, a degree II was assigned (Graetz 

et  al. 2014). Walter et  al. (2009) created a 

degree II–III for the situation of horizontal 

probing of more than 6 mm, but not com-

pletely penetrating to the opposite furcation 

entrance (Table  2.3). This at least partially 

(a)

(b)

Figure 2.3 

Furcation involvement degree II (Hamp et al. 1975; Tables 2.3 and 2.4): horizontal loss of support 

exceeding 3 mm, but not encompassing the total width of the furcation area: (a) schematic (maxillary molar, 

buccal furcation entrance): horizontal probing/clinical attachment level 5 mm; (b) tooth 47: the 9 mm marking 

is at the gingival margin. However, the 6 mm marking is at the height of the virtual tangent placed to the roots 

adjacent to the furcation. Source: Eickholz (2010).

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(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

Figure 2.4 

Furcation involvement degree III (Ammons and Harrington 2006): horizontal ‘through‐and‐through’ 

destruction of the periodontal tissue in the furcation: (a) schematic (maxillary molar, buccal to interproximal 

furcation entrance); (b) tooth 46 (occlusal view); (c) lingual view; (d) tooth 14; (e) tooth 16 without 

neighbouring tooth from mesio‐palatal to disto‐palatal; (f) respective radiograph; (g) tooth 46: the interdental 

bone is destroyed, and the soft tissues have receded apically so that the furcation opening is clinically visible. 

A tunnel therefore exists between the roots of such an affected tooth (Glickman degree IV); (h) respective 

radiograph. Source: d and e, Eickholz (2010).

Chapter No.: 1  Title Name: <TITLENAME> 

c02.indd

Comp. by: <USER>  Date: 14 May 2018  Time: 04:18:51 PM  Stage: <STAGE>  WorkFlow:

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Page Number: 20

Table 2.2 

Classification of furcation involvement according to Glickman (1953).

Degree 0

No furcation involvement.

Degree I

Early/incipient stage of furcation involvement.

The pocket is suprabony and primarily affects the soft tissue.

Early bone loss may have occurred with an increase in probing depth.

Radiographic changes are not usually found.

Degree II

Can affect one or more of the furcations of the same tooth.

The furcation lesion is essentially a cul‐de‐sac with a definite horizontal component.

If multiple defects are present, they do not communicate with each other because a portion 

of alveolar bone remains attached to the tooth.

The extent of the horizontal probing of the furcation determines whether the defect is early 

or advanced.

Vertical bone loss may be present and represents a therapeutic complication.

Radiographs may or may not depict the furcation involvement, particularly with maxillary 

molars because of the radiographic overlap of the roots. In some views, however, the 

presence of furcation ‘arrows’ indicates possible furcation involvement.

Degree III

The bone is not attached to the dome of the furcation.

In early degree III involvement, the opening may be filled with soft tissue and may not be 

visible. The clinician may not even be able to pass a periodontal probe completely through 

the furcation because of interference with the bifurcational ridges or facial/lingual bony 

margins. However, if the clinician adds the buccal and lingual probing dimensions and 

obtains a cumulative probing measurement that is equal to or greater than the buccal/

lingual dimension of the tooth at the furcation orifice, the clinician must conclude that a 

degree III furcation exists (Figure 2.5).

Properly exposed and angled radiographs of early degree III furcations display the defect as 

a radiolucent area in the crotch of the tooth.

Degree IV

The interdental bone is destroyed, and the soft tissues have receded apically so that the 

furcation opening is clinically visible.

A tunnel therefore exists between the roots of such an affected tooth.

The periodontal probe passes readily from one aspect of the tooth to another.

Source: A mmons and Harrington (2006).

Table 2.3 

Classification of furcation involvement according to Hamp et al. (1975).

Degree 0

No furcation involvement.

Degree I

Horizontal loss of periodontal tissue support less than 3 mm (Figure 2.2).

Modifications by:

 

●

Eickholz and Staehle (1994): horizontal loss of periodontal tissue support up to 3 mm.

 

●

Carnevale et al. (1995): horizontal loss of periodontal support not exceeding 

one‐third of the width of the tooth.

Degree II

Degree II–III

Horizontal loss of support exceeding 3 mm, but not encompassing the total width of 

the furcation area (Figure 2.3).

Modifications by:

 

●

Carnevale et al. (1995): horizontal loss of periodontal support exceeding one‐

third of the width of the tooth, but not encompassing the total width of the 

furcation area.

 

●

Walter et al. (2009): degree II – horizontal loss of support exceeding 3 mm, but 

no more than 6 mm.

 

●

Walter et al. (2009): horizontal loss of support exceeding 6 mm, but no detectable 

‘through‐and‐through’ destruction.

Degree III

Horizontal ‘through‐and‐through’ destruction of the periodontal tissue in the 

furcation (Figure 2.4).

Modification by:

 

●

Graetz et al. (2014): through‐and‐through furcation (requiring seeing the tip of 

the Nabers probe at the contralateral furcation opening).

Source: Hamp et al. (1975).

Clinical and Radiographic Diagnosis and Epidemiology  21

explains the low validity of detecting degree 

III furcations accurately by clinical probing 

compared to cone‐beam computer tomography 

(CBCT; Walter et  al. 2009) or intrasurgical 

assessments (Graetz et al. 2014).

Svärdström and Wennström (1996) pro-

posed another classification that does not 

count millimetres but estimates horizontal 

probing: degree 0 = the furcation site not pro-

beable; degree 1 = the root trunk coronal to 

the furcation entrance probeable; degree 

2 = the tip of the probe passes horizontally 

into the furcation but does not reach the cen-

tre of the furcation area; degree 3 = the tip of 

the probe reaches to or beyond the centre of 

the furcation area (Svärdström & Wennström 

1996). The definition of degree 3 is quite sim-

ilar to Walter et  al.’s (2009) degree II–III. 

However, this classification does not con-

sider the case of a clearly probeable through‐

and‐through furcation.

2.2.2  Distinction Between Degree II 

and Degree III Furcation Involvement

The distinction between degree II (Hamp 

et  al. 1975; Figure  2.3) and through‐and‐

through furcation (degree III; Figure 2.4) is of 

decisive significance for either prognosis as 

well as choice of therapy:

 

●

Molars with degree III furcation defects 

have a worse long‐term prognosis than 

degree II lesions (McGuire and Nunn 1996; 

Dannewitz et  al. 2006, 2016; Salvi et  al. 

2014; Graetz et al. 2015).

 

●

Whereas buccal and lingual degree II 

lesions at least can be improved by regen-

erative therapy, there is no clinical evidence 

for any benefit of regenerative treatment 

in through‐and‐through  furcations (Sanz 

et al. 2015; see Chapters 6 and 7).

Particularly from interproximally located 

furcation entrances in the presence of 

 adjacent teeth, a furcation probe cannot be 

completely pushed through the whole furca-

tion area involved. Nevertheless, hard and 

soft tissue may be detached from the furca-

tion fornix; that is, furcation involvement 

degree III. In the definition of degree III by 

Graetz et al. (2014), this situation would be 

rated degree II. Walter et  al. (2009) would 

rate this situation degree II–III. In these 

cases, it is recommended to follow Ammons 

and Harrington (2006): in cases where the 

clinician may not even be able to pass a peri-

odontal probe completely through the furca-

tion because of interference with the 

bifurcational ridges or facial/lingual bony 

margins, they may add the buccal and lin-

gual probing dimensions. If a cumulative 

probing measurement is obtained that is 

equal to or greater than the buccal/lingual 

dimension of the tooth at the furcation ori-

fice, the furcation is rated degree III 

Table 2.4 

Recommended classification of furcation involvement.

Degree 0

No furcation involvement.

Degree I

Horizontal loss of periodontal tissue support up to 3 mm (Eickholz and Staehle 1994).

Degree II

Horizontal loss of support exceeding 3 mm, but not encompassing the total width of the 

furcation area (Hamp et al. 1975).

Degree III

Horizontal ‘through‐and‐through’ destruction of the periodontal tissue in the furcation.

In early degree III involvement, the opening may be filled with soft tissue and may not be 

visible. The clinician may not even be able to pass a periodontal probe completely through 

the furcation because of interference with the bifurcational ridges or facial/lingual bony 

margins. However, if the clinician adds the buccal and lingual probing dimensions and 

obtains a cumulative probing measurement that is equal to or greater than the buccal/

lingual dimension of the tooth at the furcation orifice, the clinician must conclude that a 

degree III furcation exists (Ammons and Harrington 2006).

Sources: Hamp et al. (1975); Eickholz and Staehle (1994); Ammons and Harrington (2006).

Chapter 2 

22

(Tables 2.2 and 2.4). Thus, underestimation 

of furcation involvement as observed by 

Walter et al. (2009) and Graetz et al. (2014) 

can be avoided.

2.2.3  The Vertical Dimension 

of Furcation Involvement

The central problem about furcation involve-

ment is the difficult‐to‐access horizontal 

niche between the roots of multi‐rooted 

teeth. Thus, the classifications referred to 

consider mainly the horizontal component of 

attachment/bone loss. However, it is plausi-

ble that in addition to horizontal attachment/

bone loss, vertical attachment/bone loss in 

the furcation area plays a role. It has been 

demonstrated that survival of molars after 

furcation therapy does not only depend on 

baseline furcation involvement, but also on 

baseline bone loss (Dannewitz et  al. 2006; 

Park et  al. 2009). Thus, a subclassification 

has been proposed that measures the probe-

able vertical depth from the roof of the furca-

tion apically. Subclass A indicates a probeable 

vertical depth of 1–3 mm, B 4–6 mm, and C 

7 mm or more of probeable depth from the 

roof of the furcation apically. Furcations 

would thus be classified as IA, IB, IC, IIA, 

IIB, IIC, and IIIA, IIIB, IIIC (Tarnow and 

Fletcher 1984). The more severe the vertical 

component the worse is long-term prognosis 

of molars with degree II furcation involve-

ment (Tonetti et al. 2017). Prognosis also 

depends on the remaining circular attach-

ment of each root (Walter et al. 2009).

2.2.4  Reproducibility and Validity 

of the Assessment of Furcation 

Involvement

Furcation involvement is difficult to access for 

hygiene. How reliably can furcation lesions be 

diagnosed; that is, scored? Whereas for buccal, 

lingual, and mesio‐ lingual scoring of furcation 

degrees excellent intrarater reproducibility is 

reported, disto‐lingual furcation lesions pro-

vide only moderate reproducibility. Similar 

results are reported for PAL‐H measurements 

(excluding degree III furcation involvement). 

Intrarater reproducibility in disto‐lingual 

furcations is significantly worse than for all 

other locations. In mesio‐buccal furcations, a 

neighbouring tooth is associated with higher 

variability (Eickholz and Staehle 1994; Eickholz 

and Kim 1998). Interproximal furcations, in 

particular the disto‐lingual site and in the pres-

ence of a neighbouring tooth, are more difficult 

to access and to measure than the other loca-

tions. This fact has to be kept in mind when 

the clinical examiner scores maxillary molars 

in particular.

How accurately does the clinical measure-

ment assess the intrasurgically measured fur-

cation involvement (PBL‐H)? Disto‐ lingual 

location and a neighbouring tooth are also 

associated with less accuracy. Furthermore, a 

curved rigid furcation probe (Nabers probe) 

demonstrated better accuracy than a straight 

rigid (PCPUNC 15) and flexible plastic (TPS) 

probe (Eickholz and Kim 1998). Interestingly, 

clinical PAL‐H measurements on average 

overestimated intrasurgically measured 

PBL‐H. However, the difference was only sig-

nificant for measurements with a Nabers 

probe in degree I furcation lesions (Eickholz 

1995; Eickholz and Kim 1998).

2.2.5 Documentation 

of Furcation Involvement

As documented in Chapter 5, differentiated 

documentation of furcation involvement 

according to extent (degree) and location is a 

prerequisite for proper prognosis and treat-

ment planning (Figure 2.5). In the meantime, 

many computer programs for dental patient 

charting provide the necessary differentiated 

digital documentation (Florida probe chart; 

Figure 2.6).

2.3   Radiographic  Diagnosis 

of Furcation Involvement

In general, radiographs provide information 

on the translucency to X‐rays of different tis-

sues. The denser a tissue (e.g. compact 

bone) is, the less translucent it is for X‐rays. 

Thus, both two‐ and three‐dimensional radi-

ographic images primarily provide information 

Clinical and Radiographic Diagnosis and Epidemiology  23

on bone in contrast to soft tissue. However, 

furcation involvement is not only a matter of 

bone, but also of connective tissue attach-

ment. Therefore, radiographs tell a substan-

tial part of but not the whole story about 

furcation involvement. This is particularly 

true after regenerative treatment, where 

there may be a new connective tissue attach-

ment without new bone formation within a 

furcation.

Using two‐dimensional radiographic tech-

niques (projection radiography: periapical 

and panoramic radiographs), reliable diagno-

sis of furcation involvement is not provided 

(Topoll et al. 1988). For maxillary premolars, 

the furcation channel is oriented perpendic-

ularly to the central beam. Thus, furcation 

involvement in maxillary premolars cannot 

be visualized using projection radiography. In 

three‐rooted maxillary molars, the furcation 

channel between mesio‐ and disto‐palatal 

furcation entrances also runs parallel to the 

plane of the radiographic film or sensor and 

perpendicular to the central beam. The buc-

cal furcation entrance is in most cases over-

lapped by the palatal root. Thus, in maxillary 

molars inter‐radicular bone can be judged 

only to a very limited extent. Only in man-

dibular molars is the  

furcation channel 

located perpendicularly to the plane of the 

film/sensor and parallel to the central beam. 

Therefore, under conditions of orthoradial 

projection, inter‐radicular bone may be 

assessed in mandibular molars. However, 

radiographs only provide information on 

resorption or density of bone. Reduced bone 

density may be due to periodontal destruc-

tion or reduced bone density caused by loose 

spongeous structure. Thus, conventional 

radiographs may only provide hints for a sus-

picion of furcation involvement; this suspi-

cion has to be confirmed or rejected by 

furcation probing using a curved probe.

Additional to degree of furcation involve-

ment, radiographs may provide information 

to judge whether a buccal or lingual degree II 

furcation may benefit from regenerative 

therapy. In molars with class II furcation 

involvement, a long root trunk, a furcation 

fornix located coronally of the adjacent inter-

proximal alveolar crest, and a wide furcation 

are associated with less favourable horizontal 

attachment gain after regenerative therapy 

(Horwitz et al. 2004).

(a)

(b)

Figure 2.5 

Furcation probing at tooth 16: (a) from mesio‐palatal – probing (PAL‐H)/clinical horizontal 

attachment loss (CAL‐H) = 9 mm; (b) from disto‐palatal – probing (PAL‐H)/clinical horizontal attachment loss 

(CAL‐H) = 6 mm. In tooth 16 the PAL‐H/CAL‐H measurements add up to 15 mm. At the furcation entrances 

tooth 16 has a width less than 15 mm. Thus the furcation is through and through (degree III; Table 2.4). Source: 

Eickholz (2010).

Chapter 2 

24

Figure 2.6 

Differentiated documentation of furcation scores: (a) periodontal chart from the Department of 

Periodontology of the Johann Wolfgang Goethe‐Universität, Frankfurt am Main: tooth 17 – buccal degree I 

furcation; through‐and‐through furcation from mesio‐palatal to disto‐palatal (Grade III); tooth 16 – through‐

and‐through furcation at all furcation entrances; tooth 14 – distal degree I furcation. (b) Florida Probe: tooth 

17 – buccal degree I furcation; through‐and‐through furcation from mesio‐palatal to disto‐palatal (Grade III); 

tooth 16 – through‐and‐through furcation at all furcation entrances; tooth 14 – distal degree I furcation.

(a)

Furkation

b

0

AL

ST/LG

b

0

b

0

(b)

2 2 2

6

3

8

1

1

111

44

3

3

4

4

10

–1

Tooth #

1

GM

GM

3

3

3

3

3

3

3

1

1

3

6

3

7

2

6

0 1

0

2

4

400

0

4

3

5

4

3

5

000

0

3

7

1 3

0

1

Recession

Mobility

Depth

Recession

Right

Depth

2

3

4

5

Clinical and Radiographic Diagnosis and Epidemiology  25

2.3.1  Digital Subtraction 

Radiography

A highly specialized and technically sensitive 

radiographic method may be used to follow 

up changes of inter‐radicular bone in molar 

furcations: digital subtraction radiography 

(DSR; (Eickholz and Hausmann 1997). Two 

consecutively obtained radiographs (e.g. prior 

to and 12 months after therapy) of the same 

tooth are overlapped in such a way that cor-

responding structures are positioned exactly 

over one another. The grey values of the 

 baseline radiograph are inverted (white to 

black, black to white) and added to those of 

the follow‐up radiograph. In two completely 

identical radiographs that overlap perfectly, a 

middle grey value will result. An increase of 

bone density (bony fill) results in lighter grey 

values, a decrease of bone density (bone loss) in 

darker grey values (Eickholz and Hausmann 

1997; Figure 2.7). However, DSR requires strict 

standardization of projection geometry and is 

highly sensitive to misalignment. Thus, the 

technique is rarely applied in clinical practice.

(a)

(b)

(c)

(d)

Figure 2.7 

Follow‐up of inter‐radicular bone at teeth 46 and 47 using digital subtraction radiography (DSR): 

(a) standardized radiograph of teeth 46 and 47 prior to regenerative therapy; (b) intrasurgical view – buccal 

degree II furcation involvement at both teeth; (c) standardized radiograph six months after regenerative 

therapy; (d) subtraction image – increase of bone density within the furcations of 46 and 47. Source: 

Eickholz (2010).

Chapter 2 

26

2.3.2 Three‐dimensional 

Radiography

Since conventional two‐dimensional radio-

graphic imaging may have some clinically rel-

evant drawbacks, it might be useful to analyse 

distinct clinical situations, particularly in 

maxillary molar teeth, with a suitable three‐

dimensional diagnostic approach with appro-

priate exposure to radiation (Laky et al. 2013; 

Walter et  al. 2016). Cone Beam Computed 

Tomography (CBCT) has been validated in 

vivo for the assessment of furcation‐involved 

maxillary molars (Walter et al. 2016). CBCT 

data were found to be accurate in assessing 

the amount of periodontal tissue loss and in 

classifying the degree of furcation involve-

ment in maxillary molars (Walter et al. 2009, 

2010, 2016). In addition, the three‐dimensional 

images revealed several findings, such as the 

surrounding bony support of each maxillary 

molar root, fusion or proximity of roots, 

 periapical lesions, root perforations, and/or 

missing bony walls (Walter et al. 2009). The 

clinical relevance of these radiographic data 

was analysed regarding the decision‐making 

process for resective or non‐resective thera-

pies (Figures  2.8 and 2.9). These treatment 

options were classified according to their 

graduation of invasiveness (GoI), ranging 

from minimally invasive SPT to maximally 

invasive extraction and implant restoration: 

GoI 0 = supportive periodontal treatment 

Figure 2.8 

Diagnosis and treatment planning using cone‐beam computed tomography (CBCT). CBCT images 

with horizontal, sagittal, and transversal sections of first and second left maxillary molars. According to the 

bone loss around the disto‐buccal root and the remaining periodontal attachment around the mesio‐buccal 

and palatal root, it was decided to extract the distobuccal root. Source: Walter et al. (2010).

Clinical and Radiographic Diagnosis and Epidemiology  27

(SPT); GoI 1 = open flap debridement with or 

without gingivectomy or  apically repositioned 

flap and/or tunnelling; GoI 2 = root separa-

tion; GoI 3 = amputation/trisection of one 

root (with or without root separation or tun-

nel preparation; GoI 4 = amputation/trisec-

tion of two roots; and GoI 5 = extraction of 

the entire tooth. Significant discrepancies 

between conventional and CBCT‐based 

treatment approaches were found in most 

situations, which possibly necessitates intras-

urgical changes in the treatment plan in those 

cases where no CBCT is available (Walter 

et al. 2009).

(a)

(b)

(c)

(d)

(e)

Figure 2.9 

Root resection in a maxillary first molar: (a) pre‐surgical view; (b) tri‐section of the distobuccal root; 

(c) the flap is fixed with monofil synthetic sutures 5 × 0; (d) four months post‐operation, the wound healing was 

uneventful; (e) a crown with an extended metal margin is placed and the patient is introduced to meticulous 

oral hygiene.

Chapter 2 

28

However, the findings from a cost-benefit 

analysis indicate the need for a critical 

appraisal of CBCT applications in upper 

molars (Walter et  al. 2012). In most cases 

with clinically based GoI ≤ 1, CBCT imaging 

seems to have no or only minor impact on 

economic benefit and to reduce treatment 

time only slightly, if at all. With more inva-

sive clinically based treatment decisions 

(GoI > 1), however, the benefits of using 

CBCT were greater, probably because the 

indication for tooth extraction is clarified. 

On the one hand, a straightforward tooth 

extraction followed by implant placement 

and restoration is feasible, thereby avoiding 

explorative periodontal surgeries when the 

tooth is not maintainable. On the other 

hand, unnecessary tooth extractions and 

implant placement in sites where teeth 

would be maintainable may be avoided. 

Moreover, root canal treatments in sites 

planned for GoI degrees 2, 3, or 4 may be 

prevented, when CBCT reveals morphologi-

cal variations such as root proximities or 

root fusions, which preclude clinically based 

resective treatment planning.

The main goal of diagnostic radiology is to 

keep the radiation dose as low as reasonably 

achievable (ALARA), and this should also be 

a prerequisite for CBCT application in den-

tistry, since increased radiation in the dental 

office may potentially cause malignancies, 

including thyroid cancer or intracranial 

 meningioma (Hallquist and Näsman 2001; 

Longstreth et  al. 2004; Hujoel et  al. 2006). 

The potential risks associated with additional 

radiation exposure are only justified in single 

cases and have to be evaluated in each indi-

vidual situation.

2.4   Epidemiology  of 

Furcation Involvement

How frequent is furcation involvement? 

There exists only one population‐representative 

study from the USA on the frequency of 

 furcation involvement. Even in periodontitis 

patients, studies reporting the frequency of 

furcation involvement differentiated accord-

ing to degree are rare and relatively small.

For the third National Health and Nutrition 

Examination Survey (NHANES III), 9689 

individuals representative of the US popula-

tion received periodontal examinations 

including furcation scores. Partial furcation 

involvement was scored in sites where the 

explorer was definitely catching into but did 

not pass through the furcation. This repre-

sents degrees I and II of the Hamp et  al. 

(1975) classification (Table 2.3). Total furca-

tion involvement was assigned when the 

explorer could be passed between the roots 

and through the entire furcation. This repre-

sents degree III of the Hamp et  al. (1975) 

classification (Table 2.3). The prevalence of 

furcation involvement for all age groups was 

13.7%, and the extent was 6.8% of posterior 

teeth per person. The prevalence of through‐

and‐through furcation involvement was 0.9% 

(extent: 0.5%). The prevalence of furcation‐

involved teeth (all/through‐and‐through) 

increased with age (60–69 years: 27.6/2.1%; 

70–79: 31.7/3.2%; 80–89: 37.9/3.4%) and was 

higher in males (17.8/1.2%) than in females 

(11.3/0.7%; Albandar et al. 1999).

For a sample of 71 periodontally diseased 

patients in Germany, Dannewitz et al. (2006) 

reported tooth‐based furcation involvement; 

that is, they assigned to each molar the most 

severe furcation involvement that was 

observed within the particular tooth. Using 

this mode, the information relevant for prog-

nosis is given for each molar. However, the 

frequency of less severe furcation degrees is 

underestimated. They observed degree I 

 furcation lesions in 23%, and degree II and III 

furcation lesions in 24% and 13% of all 

molars, respectively. No furcation involve-

ment at all was exhibited in 40% of all molars. 

Premolars were not scored (Dannewitz et al. 

2006).

In a sample of 345 periodontitis patients 

(Eickholz et al. 2016), the degree of furcation 

involvement of all sites was reported (site 

based). This enlarges the proportion of less 

severe furcation lesions in comparison to 

reporting tooth‐based furcation involvement. 

Clinical and Radiographic Diagnosis and Epidemiology  29

There was no furcation involvement in 45% 

of all furcation sites, which approximately 

confirms the frequency reported for molars 

(Dannewitz et al. 2006). The study observed 

degree I furcation lesions in 36%, and degree 

II and III furcation lesions in 13.5% and 5.5% 

of all molars and first maxillary premolars, 

respectively. Considering this and the fact 

that Dannewitz et  al. (2006) did not report 

premolars, the data on frequency of furcation 

lesions roughly confirm the earlier  findings in 

a much larger sample (Eickholz et al. 2016).

In individuals aged 40 years or older, every 

second molar was affected by advanced peri-

odontal destruction (score 2–3) in at least one 

furcation site (Svärdström and Wennström 

1996). Furcation involvement was found 

more frequently in the maxilla than in the 

mandible (Svärdström and Wennström 1996; 

Dannewitz et al. 2006). However, this may be 

due simply to the fact that maxillary molars 

have more sites at risk than mandibular 

molars (maxillary molars with three, man-

dibular with two furcation entrances).

At least in periodontitis patients, furcation 

involvement is a frequent finding. In perio-

dontally diseased patients, roughly one‐third 

of all molars and almost one‐fifth of all 

 furcation sites exhibit degree II and III furca-

tion involvement, which affects prognosis 

and choice of therapy for the respective 

multi‐rooted teeth.

 References

Albandar, J.M., Brunelle, J.A., and Kingman, A. 

(1999). Destructive periodontal disease in 

adults 30 years of age and older in the 

United States, 1988–1994. Journal of 

Periodontology 70, 13–29.

Ammons, W.F., and Harrington G.W. (2006). 

Furcation: Involvement and treatment. In: 

Carranza’s Clinical Periodontology (ed. M.G. 

Newman, H.H. Takei, P.R. Klokkevold, and 

F.A. Carranza), 991–1004. St. Louis, MO: 

Saunders Elsevier.

Carnevale, G., Pontoriero, R., and Hürzeler, 

M.B. (1995) Management of furcation 

involvement. Periodontology 2000 9, 69–89.

Dannewitz, B., Krieger, J.K., Hüsing, J., and 

Eickholz, P. (2006). Loss of molars in 

periodontally treated patients: A 

retrospective analysis five years or more 

after active periodontal treatment. Journal 

of Clinical Periodontology 33, 53–61.

Dannewitz, B., Zeidler, A., Hüsing, J. et al. 

(2016). Loss of molars in periodontally 

 Summary  of Evidence

 

●

Reliable clinical furcation diagnosis 

requires a rigid curved furcation probe 

(e.g. colour‐coded Nabers probe).

 

●

The distinction between degree II (Hamp 

et al. 1975) and through‐and‐through fur-

cation (degree III) is as difficult as it is of 

decisive significance for either prognosis 

as well as choice of therapy.

 

●

A modified classification of furcation 

involvement is recommended.

 

●

Conventional radiographs may only pro-

vide hints for a suspicion of furcation 

involvement. However, this suspicion has 

to be confirmed or rejected by furcation 

probing using a curved probe. CBCT may 

provide additional information for deci-

sion-making particularly in maxillary 

molars if periodontal surgery is required.

 

●

In periodontally diseased patients, roughly 

one‐third of all molars and almost one‐

fifth of all furcation sites exhibit degree II 

and III furcation involvement.

Chapter 2 

30

treated patients: Results ten years and 

more after active periodontal therapy. 

Journal of Clinical Periodontology 43, 

53–62.

Eickholz, P. (1995). Reproducibility and 

validity of furcation measurements as 

related to class of furcation invasion. Journal 

of Periodontology 66, 984–989.

Eickholz, P. (2010). Glossar der Grundbegriffe 

für die Praxis: Parodontologische Diagnostik 

6: Furkationsdiagnostik. Parodontologie 21, 

261–266.

Eickholz, P., and Hausmann, E. (1997). 

Evidence for healing of class II and III 

furcations after GTR‐therapy: Digital 

subtraction and clinical measurements. 

Journal of Periodontology 68, 636–644.

Eickholz, P., and Kim, T.‐S. (1998). 

Reproducibility and validity of the 

assessment of clinical furcation parameters 

as related to different probes. Journal of 

Periodontology 69, 328–336.

Eickholz, P., and Staehle, H.J. (1994). The 

reliability of furcation measurements. 

Journal of Clinical Periodontology 21, 

611–614.

Eickholz, P., Nickles, K., Koch, R. et al. (2016). 

Is furcation class involvement affected by 

adjunctive systemic amoxicillin plus 

metronidazole? A clinical trial’s exploratory 

subanalysis. Journal of Clinical 

Periodontology 43 (10), 839–848.

Fleischer, H.C., Mellonig, J.T., Brayer, W.K. 

et al. (1989). Scaling and root planing 

efficacy in multirooted teeth. Journal of 

Periodontology 60, 402–409.

Glickman, I. (1953). Clinical Periodontology. 

Philadelphia, PA: Saunders.

Graetz, C., Plaumann, A., Wiebe, J.F. et al. 

(2014). Periodontal probing versus 

radiographs for the diagnosis of furcation 

involvement. Journal of Periodontology 85, 

1371–1379.

Graetz, C., Schützhold, S., Plaumann, A. et al. 

(2015). Prognostic factors for the loss of 

molars – an 18‐years retrospective cohort 

study. Journal of Clinical Periodontology 42, 

943–950.

Hallquist, A., and Näsman, A. (2001). Medical 

diagnostic X‐ray radiation: An evaluation 

from medical records and dentist cards in a 

case‐control study of thyroid cancer in the 

northern medical region of Sweden. 

European Journal of Cancer Prevention 10, 

147–152.

Hamp, S.‐E., Nyman, S., and Lindhe, J. (1975). 

Periodontal treatment of multirooted teeth: 

Results after 5 years. Journal of Clinical 

Periodontology 2, 126–135.

Horwitz, J., Machtei, E.E., Reitmeir, P. et al. 

(2004). Radiographic parameters as 

prognostic indicators for healing of class II 

furcation defects. Journal of Clinical 

Periodontology 31, 105–111.

Hujoel, P., Hollender, L., Bollen, A.M. et al. 

(2006). Radiographs associated with one 

episode of orthodontic therapy. Journal of 

Dental Education 70, 1061–1065.

Kalkwarf, K.L., Kaldahl, W.B., and Patil, K.D. 

(1988). Evaluation of furcation region 

response to periodontal therapy. Journal of 

Periodontology 59, 794–804.

Laky, M., Majdalani, S., Kapferer, I., et al. 

(2013). Periodontal probing of dental 

furcations compared with diagnosis by 

low‐dose computed tomography: A case 

series. Journal of Periodontology 84, 

1740–1746.

Lang, N.P., Cumming, B., and Löe, H. (1973). 

Toothbrushing frequency as it relates to 

plaque development and gingival health. 

Journal of Periodontology 44, 396–405.

Longstreth, W.T., Jr, Phillips, L.E., Drangsholt, 

M. et al. (2004). Dental X‐rays and the risk of 

intracranial meningioma: A population‐based 

case‐control study. Cancer 100, 1026–1034.

Loos, B., Nylund, K., Claffey, N., and Egelberg, 

J. (1989). Clinical effects of root 

debridement in molar and non‐molar teeth: 

A 2‐year follow‐up. Journal of Clinical 

Periodontology 16, 498–504.

McGuire, M.K., and Nunn, M.E. (1996). 

Prognosis versus actual outcome. III: The 

effectiveness of clinical parameters in 

developing an accurate prognosis. Journal of 

Periodontology 67, 666–674.

Clinical and Radiographic Diagnosis and Epidemiology  31

Mohammadi, Z., Shalavi, S., and Jafarzadeh, H. 

(2013). Extra roots and root canals in 

premolar and molar teeth: Review of an 

endodontic challenge. Journal of 

Contemporary Dental Practice 14, 980–986.

Nordland, P., Garrett, S., Kriger, R. et al. 

(1987). The effect of plaque control and root 

debridement in molar teeth. Journal of 

Clinical Periodontology 14, 231–236.

Park, S.Y., Shin, S.Y., Yang, S.M., and Kye, S.B. 

(2009). Factors influencing the outcome of 

root‐resection therapy in molars: A 10‐year 

retrospective study. Journal of 

Periodontology 80, 32–40.

Pretzl, B., Kaltschmitt, J., Kim, T.‐S. et al. 

(2008). Tooth loss after active periodontal 

therapy. 2: Tooth‐related factors. Journal of 

Clinical Periodontology 35, 175–182.

Salvi, G.E., Mischler, D.C., Schmidlin, K. et al. 

(2014). Risk factors associated with the 

longevity of multi‐rooted teeth: Long‐term 

outcomes after active and supportive 

periodontal therapy. Journal of Clinical 

Periodontology 41, 701–707.

Sanz, M., Jepsen, K., Eickholz, P., and Jepsen, 

S. (2015). Clinical concepts for regenerative 

therapy in furcations. Periodontology 2000 

68, 308–332.

Schroeder, H.E., and Scherle, W.F. (1987). 

Warum die Furkation menschlicher Zähne 

so unvorhersehbar bizarr gestaltet ist. 

Schweizerische Monatsschrift für 

Zahnmedizin 97, 1495–1508.

Svärdström, G., and Wennström, J.L. (1996). 

Prevalence of furcation involvements in 

patients referred for periodontal treatment. 

Journal of Clinical Periodontology 23, 

1093–1099.

Tarnow, D., and Fletcher, P. (1984). 

Classification of the vertical component of 

furcation involvement. Journal of 

Periodontology 55, 283–284.

Tonetti, M.S., Christiansen A.L., and 

Cortellini, P. (2017). Vertical 

subclassification predicts survival of molars 

with class II furcation involvement during 

supportive periodontal care. J Clin 

Periodontol 44, 1140–1144.

Topoll, H.H., Streletz, E., Hucke, H.P., and 

Lange, D.E. (1988). Furkationsdiagnostik: 

Ein Vergleich der Aussagekraft von OPG, 

Röntgenstatus und intraoperativem Befund. 

Deutsche Zahnärztliche Zeitschrift 43, 

705–708.

Walter, C., Kaner, D., Berndt, D.C. et al. (2009). 

Three‐dimensional imaging as a pre‐

operative tool in decision making for 

furcation surgery. Journal of Clinical 

Periodontology 36, 250–257.

Walter, C., Schmidt, J.C., Dula, K. et al. (2016). 

Cone beam computed tomography (CBCT) 

for diagnosis and treatment planning in 

periodontology: A systematic review. 

Quintessence International 47, 25–37.

Walter, C., Weiger, R., Dietrich, T. et al. (2012). 

Does three‐dimensional imaging offer a 

financial benefit for the treatment of 

maxillary molars with furcation involvement? 

A pilot clinical case series. Clinical Oral 

Implants Research 23, 351–358.

Walter, C., Weiger, R., and Zitzmann, N.U. 

(2010). Accuracy of three‐dimensional 

imaging in assessing maxillary molar 

furcation involvement. Journal of Clinical 

Periodontology 37, 436–441.

Wang, H.L., Burgett, F.G., Shyr, Y., and 

Ramfjord, S. (1994). The influence of molar 

furcation involvement and mobility on 

future clinical periodontal attachment loss. 

Journal of Periodontology 65, 25–29.

Diagnosis and Treatment of Furcation-Involved Teeth, First Edition. Edited by Luigi Nibali. 

© 2018 John Wiley & Sons Ltd. Published 2018 by John Wiley & Sons Ltd. 

Companion website: www.wiley.com/go/nibali/diagnosis

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33

3.1   Introduction

An experimental gingivitis model in humans 

established that microbial plaque is the aetio-

logical factor of gingivitis (Loe et  al. 1965). 

A 26‐year longitudinal study on well‐maintained 

Norwegian males found that sites with per-

sistent plaque‐induced gingival inflamma-

tion had 70% more clinical attachment loss 

(odds ratio [OR] = 3.22) compared to sites 

that were always healthy, thereby supporting 

the concept that gingivitis is a prerequisite 

for the inception of periodontitis (Schatzle 

et  al. 2003). Microbial plaque exists in the 

oral cavity as biofilms, which are consortia of 

micro‐organisms interacting with the sur-

rounding environment in a dynamic manner. 

Subgingival plaque samples from 588 patients 

with chronic periodontitis demonstrated 

that with increasing probing depth, there was 

a significant increase in the ‘orange’ and ‘red 

complex’ microbes (Socransky and Haffajee 

2005). These Gram‐negative bacteria release 

molecules such as lipopolysaccharide and 

extracellular proteolytic enzymes, which 

interact with the innate host inflammatory 

surveillance system to mount an immune 

response against the invading bacteria 

(Darveau et  al. 1997). The inflammatory 

response results in breakdown of the con-

nective tissue attachment and supporting 

bone, leading to established periodontitis 

lesions (Page and Kornman 1997). The 

microbial nature of periodontitis is very 

complex; it is thought that alterations in the 

composition of the subgingival biofilm (dys-

biosis) involving ‘accessory’ and ‘keystone’ 

pathogens and pathobionts drive periodonti-

tis in a susceptible host (Hajishengallis and 

Lamont 2012).

In order to arrest the initiation and pro-

gression of periodontitis, its management is 

predominantly focused on removing micro-

bial plaque and its retentive factors from root 

surfaces and gingival sulci. This is primarily 

achieved by professional supra‐ and subgin-

gival mechanical debridement, with the aim 

of disrupting the microbial biofilm growing 

on the root surface. Subgingival tooth 

debridement has traditionally been referred 

to as ‘scaling and root planing’, although the 

importance of necessarily planing or smooth-

ening the root surface has been questioned 

(Checchi and Pelliccioni 1988; Smart et  al. 

1990). Microbial biofilm disruption leads to a 

reduction of the host response cascade, 

which halts periodontal destruction and thus 

results in improvement of the clinical signs of 

disease. Immediately after scaling and root 

planing, the denuded root surface will be 

partially covered by fibrin and polymorpho-

nuclear leukocytes. The junctional epithelium 

Chapter 3

How Good are We at Cleaning Furcations? Non‐surgical 
and Surgical Studies

Jia‐Hui Fu

1

 and Hom‐Lay Wang

2

1

 Discipline of Periodontics, Faculty of Dentistry, National University of Singapore, Singapore

2

 Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI, USA

Chapter 3 

34

will start to migrate apically towards the per-

iodontal ligament. Granulation tissue will 

form in the transseptal fibre region. By the 

third week, the apical migration of the junc-

tional epithelium will terminate at the apical 

end of the root instrumentation, with the 

periodontal ligament fibres oriented parallel 

to the root surface. Some root resorption or 

even crestal bone loss may occur along the 

root surface at areas that are not covered by 

the long junctional epithelium. As a result, 

the healing after scaling and root planing is 

therefore mainly by periodontal repair, with 

the formation of the long junctional epithe-

lium and gingival recession (Tagge et  al. 

1975; Biagini et al. 1988).

It is relatively straightforward to debride 

single‐rooted teeth; however, in multi‐rooted 

teeth the furcal areas are anatomically chal-

lenging to access because of their configura-

tions. Several anatomical factors related to 

furcations and roots, covered by Pretzl in 

Chapter  1, contribute to the aetiology and 

compromised prognoses of furcation‐

involved teeth. These factors include furca-

tion entrance width, root trunk length, and 

the presence of root concavities, cervical 

enamel projections, bifurcation ridges, and 

enamel pearls. An evaluation of 50 mandibu-

lar molars revealed variations in the furca-

tion area, with 48%, 34%, and 18% having flat, 

convex, and concave domes, respectively 

(Matia et  al. 1986). Therefore, it has been 

reported that complete plaque and calculus 

removal in the furcation is highly unlikely 

(Matia et  al. 1986; Parashis et  al. 1993a, b; 

Kocher et  al. 1998a, b). The imperfect 

debridement can be attributed to the pres-

ence of difficult‐to‐reach root concavities, 

which are commonly found in the furcal 

areas, with an incidence of 100% in maxillary 

premolars, 17–94% in maxillary molars, and 

99–100% in mandibular molars (Bower 

1979a, b; Booker and Loughlin 1985). In 

addition, furcation entrances are generally 

narrower (less than 0.75 mm) than the blade 

of conventional curettes (0.75–1.10 

mm; 

Bower 1979a, b; Chiu et al. 1991; dos Santos 

et al. 2009). Therefore, this chapter attempts 

to provide an overview of the efficacy of 

non‐surgical and surgical debridement of 

furcal areas, using instruments such as 

curettes, ultrasonic scalers, lasers, photody-

namic therapy, and interdental brushes.

3.2   Longitudinal  Studies 

on Management of 

Furcation‐involved Teeth

Ramfjord and colleagues first introduced 

the concept of longitudinal studies in 1968, 

where they compared different treatment 

modalities in a large subject population over 

time using the split‐mouth design. This 

approach allowed clinicians to better appre-

ciate the possible treatment outcomes that 

will arise over time with minimal host varia-

bility. Subsequently, several research groups 

have adopted this approach to evaluate the 

treatment outcomes of non‐surgical and 

 surgical debridement of single‐ and multi‐

rooted teeth. These studies are generally 

described based on geographical locations 

and treatment modalities performed, 

including scaling and root planing, subgingi-

val curettage, modified Widman flap, modi-

fied Kirkland’s flap, pocket elimination, and 

apically positioned flap with and without 

osseous resection. Clinical parameters, such 

as clinical attachment level gain, probing 

depth reduction, bleeding on probing, and 

plaque index, were used to determine the 

outcome of the treatment rendered. Table 3.1 

shows a summary of longitudinal studies that 

reported data on multi‐rooted teeth. The 

results described the treatment outcomes 

specific to multi‐rooted teeth.

Results from the Michigan longitudinal 

studies reported more tooth loss in teeth 

with baseline furcation involvement (FI) 

despite surgical interventions, thus imply-

ing that the quality of surgical debridement 

or post‐surgical home or professional care 

did not deter disease progression in the long 

term (Ramfjord et  al. 1968, 1987; Wang 

et  al. 1994). The authors believed that 

although flap elevation would improve 

access to the furcation areas, complete 

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  Table 3.1   

 Summary of some longitudinal studies that evaluated multi‐rooted teeth. 

Group

 Author/ 
 Year 

Sample 
Size

No. of 
Teeth

Treatment Modalities

Follow‐Up 
Years

SPT Protocol Results    

Michigan  Ramfjord et al.   1968    32

729

 Initial SRP with curettes. 

 Subgingival curettage vs 

gingivectomy/APF with 

osseous resection as needed. 

2

3 months

Baseline FI did not significantly affect CAL in molars in 

the short term.  

 Ramfjord et al.   1987    72

1881

 Initial SRP with curettes. 

 Surgical pocket elimination 

vs MWF vs subgingival 

curettage vs SRP 

5

3 months

 

Out of 17 teeth that were lost due to periodontal reasons:

 

●

  16 had FI at baseline. 

 

●

 15 were treated with surgical interventions and 2 were 

treated with SRP.     

 Wang et al.   1994   

24

165

 Initial SRP with curettes. 

 Surgical pocket elimination 

vs MWF vs subgingival 

curettage vs SRP. 

8

3 months

FI molars had 2.54 times greater risk of being lost.  

Minnesota  Pihlstrom et al.   1984    10

266

SRP alone vs SRP with 

MWF vs subgingival 

curettage vs SRP

6.5

3–4 months   Compared to non‐molars:

 

●

  Molars with baseline PPD 4–6 mm: significantly deeper 

residual PPD (1.05 mm) and greater apical CAL 

(0.54 mm) after SRP alone. 

 

●

 Molars with baseline PPD of 4–6 mm: significantly 

deeper residual PPD (1.02 mm) and greater apical CAL 

(1.27 mm) after SRP with MWF. 

 

●

 Molars with baseline PPD ≥ 7 mm: no significant 

difference in PPD or CAL, for both treatment 

modalities.   

 9/11 teeth lost after completion of treatment were molars.   

Loma Linda   Nordland et al.   1987    19

Initial SRP with curettes 

and ultrasonic scaler

2

3 months   Compared to non‐molar or non‐furcation sites, molar FI 

sites had:

 

●

  More bleeding on probing. 

 

●

 Higher bleeding scores of 60% to 70% and > attachment 

loss (1 out of 5 molars) when PPDs were 7 mm or more. 

 

●

 Lowest post‐treatment reduction was in PPD (1.0 mm). 

 

●

 0.5 mm loss of CAL instead of attachment gain.     

(Continued)

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Table 3.1 

(Continued)

Group

 Author/ 
 Year 

Sample 
Size

No. of 
Teeth

Treatment Modalities

Follow‐Up 
Years

SPT Protocol Results    

 Loos et al.   1988   

11

43

Initial SRP with ultrasonic 

scaler.

1.1

3 months

 

Compared to non‐molar sites, molar FI sites had:

 

●

  Greater tendency to rebound after treatment. 

 

●

 Mean probing attachment level gain of 0.1 mm (0.7 mm 

at non‐molar sites). 

 

●

 Significantly higher microbial count.     

 Loos et al.   1989   

12

1682

Initial SRP with ultrasonic 

or sonic scaler.

2

3 months

 

Molar FI sites:

 

●

  Similar PPD and CAL pre‐ and post‐treatment. 

 

●

 With at least 7.0 mm PPD had lower PPD reduction 

after treatment. 

 

●

 Did not have significant changes in CAL. 

 

●

 Had greater percentage of sites worsening over time 

(38.5%).     

Nebraska   Kalkwarf et al.   1988    82

1394

 Initial scaling with curettes 

and ultrasonic scaler. 

 Coronal scaling only vs SRP 

vs SRP with MWF vs SRP 

with flap and osseous 

resection. 

2

3 months

 

●

  FI sites tended to progress with horizontal probing 

attachment loss irrespective of treatment. 

 

●

 Periodontal breakdown rate was 2.6% for sites that had 

osseous resection, 5.9% for sites that had MWF, 8.4% 

for sites that had SRP, and 8.3% for sites that had 

coronal scaling only.    

North 

Carolina

 Hirschfeld and 

Wasserman   1978   

600

15 666 SRP, gingivectomy, 

gingivoplasty, and APF 

with osseous surgery.

15

4–6 months

 

●

  19.3% of FI molars were lost compared to 1.7% of 

incisors in a well‐maintained population.    

 McFall   1982   

100

2627

SRP, curettage, gingivectomy, 

gingivoplasty, and APF with 

osseous surgery.

15

3–6 months

 

●

  27.3% of FI molars were lost compared to 0.6% of 

incisors in a well‐maintained population.    

 Wood et al.   1989   

63

1607

SRP.

13.6

6–9 months

 

●

  23.2% of FI molars were lost compared to 0.8% of 

incisors in a well‐maintained population.    

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Table 3.1 

(Continued)

Group

 Author/ 
 Year 

Sample 
Size

No. of 
Teeth

Treatment Modalities

Follow‐Up 
Years

SPT Protocol Results    

 Loos et al.   1988   

11

43

Initial SRP with ultrasonic 

scaler.

1.1

3 months

 

Compared to non‐molar sites, molar FI sites had:

 

●

  Greater tendency to rebound after treatment. 

 

●

 Mean probing attachment level gain of 0.1 mm (0.7 mm 

at non‐molar sites). 

 

●

 Significantly higher microbial count.     

 Loos et al.   1989   

12

1682

Initial SRP with ultrasonic 

or sonic scaler.

2

3 months

 

Molar FI sites:

 

●

  Similar PPD and CAL pre‐ and post‐treatment. 

 

●

 With at least 7.0 mm PPD had lower PPD reduction 

after treatment. 

 

●

 Did not have significant changes in CAL. 

 

●

 Had greater percentage of sites worsening over time 

(38.5%).     

Nebraska   Kalkwarf et al.   1988    82

1394

 Initial scaling with curettes 

and ultrasonic scaler. 

 Coronal scaling only vs SRP 

vs SRP with MWF vs SRP 

with flap and osseous 

resection. 

2

3 months

 

●

  FI sites tended to progress with horizontal probing 

attachment loss irrespective of treatment. 

 

●

 Periodontal breakdown rate was 2.6% for sites that had 

osseous resection, 5.9% for sites that had MWF, 8.4% 

for sites that had SRP, and 8.3% for sites that had 

coronal scaling only.    

North 

Carolina

 Hirschfeld and 

Wasserman   1978   

600

15 666 SRP, gingivectomy, 

gingivoplasty, and APF 

with osseous surgery.

15

4–6 months

 

●

  19.3% of FI molars were lost compared to 1.7% of 

incisors in a well‐maintained population.    

 McFall   1982   

100

2627

SRP, curettage, gingivectomy, 

gingivoplasty, and APF with 

osseous surgery.

15

3–6 months

 

●

  27.3% of FI molars were lost compared to 0.6% of 

incisors in a well‐maintained population.    

 Wood et al.   1989   

63

1607

SRP.

13.6

6–9 months

 

●

  23.2% of FI molars were lost compared to 0.8% of 

incisors in a well‐maintained population.    

Group

 Author/ 
 Year 

Sample 
Size

No. of 
Teeth

Treatment Modalities

Follow‐Up 
Years

SPT Protocol Results    

New 

Jersey

 Ross and 

Thompson   1978   

100

387

Scaling, curettage, 

gingivectomy, gingivoplasty, 

and APF

5–24

–

 

●

   12% of FI maxillary molars were extracted, of which 

22% had been present for at least 6 years and 33% for 

11–18 years. 

 

●

 Changes in bone support of FI maxillary molars at 

5–24 years post‐treatment:

 

–    75% had no significant change. 

 

–   11% had bone loss. 

 

–   2% had slight improvement. 

 

–   12% were extracted.  

     

Sweden

 Lindhe et al.   1982   

15

–

SRP vs MWF.

2

2 weeks for 

6 months, 

followed by 

once every 

3 months

 

●

  Reduction in mean plaque index scores was greater in 

non‐molars. 

 

●

 In surgically treated sites, greater PPD reduction in 

non‐molars, but in non‐surgically treated sites it was 

comparable between non‐molars and molars.    

Germany   Dannewitz 

et al.   2006   

71

505

Initial SRP, followed by OFD, 

GTR, root resection or 

separation, or tunnelling 

procedure.

>5 years

–

 

●

  3.8% of FI molars lost after active therapy. 

 

●

 31.8% of FI molars lost over time after SRP. 

 

●

 34.6% of FI molars lost over time after SRP and flap 

surgery. 

 

●

 Molars with class III FI tended to deteriorate 

significantly over time.    

 Dannewitz 

et al.   2016   

136

–

Initial SRP

13.2

 

●

  Molars with class III furcations had 4.68 times higher 

risk of being lost compared to non‐FI molars.  

  APF = apically positioned flap; CAL = clinical attachment level; FI = furcation involvement; GTR = guided tissue regeneration; MWF = modified Widman flap; OFD = open‐flap 

debridement; PPD = probing pocket depth; SRP = scaling and root planning; SPT = supportive periodontal therapy.  

Chapter 3 

38

debridement was difficult to achieve and 

maintain post‐surgically due to the complex 

configurations of the furcal area; therefore, 

furcation‐involved teeth had a poorer long‐

term prognosis. In addition, it was hard to 

maintain furcated molars, thus they had a 

2.54 times greater susceptibility of being 

lost during the periodontal maintenance 

phase (Wang et  al. 1994). A longitudinal 

study by the Minnesota group demonstrated 

that molars compared to non‐molars had 

significantly greater post‐treatment pocket 

depth and clinical attachment level changes 

at sites with baseline pocket depths of 

4–6 mm, regardless of the treatment ren-

dered. However, at deeper sites (pocket 

depth of 7 mm or more), no significant dif-

ferences were detected between molars and 

non‐molars in the long term. Although the 

authors did not report the severity of FI in 

the molars in their study, 9 out of the 11 

teeth that were extracted at the end of treat-

ment were molars (Pihlstrom et al. 1984).

The Loma Linda group evaluated the 

effectiveness of plaque control and subgin-

gival root debridement of non‐molar, molar 

non‐furcation, and molar furcation sites 

over a two‐year period and found that 

molar furcation sites had persistent inflam-

mation, the poorest response to treatment 

in terms of pocket depth reduction and 

clinical attachment gain, and a significant 

tendency to rebound to baseline status after 

treatment (Nordland et al. 1987; Loos et al. 

1988, 1989). The Nebraska group compared 

coronal scaling alone, complete scaling 

and root planing alone and followed by 

modified Widman flap or osseous‐respec-

tive surgery in the management of molars 

with FI. Their results showed that osseous 

resection had the greatest probing depth 

reduction with the least tendency for fur-

ther breakdown (Kalkwarf et al. 1988). The 

North Carolina group evaluated patients 

over 13–15 years and found that molars 

with FI were lost 10–27 times more fre-

quently compared to  incisors, despite hav-

ing non‐surgical and surgical periodontal 

treatment with regular maintenance 

(Hirschfeld and Wasserman 1978; McFall 

1982; Wood et al. 1989).

A group in New Jersey evaluated 384 

 maxillary molars with varying degrees of FI 

over 5–24 years. They used a combination 

of scaling, curettage, gingivectomy and/or 

gingivoplasty, and apically positioned flap 

to manage the furcation‐involved maxillary 

molars. Their results showed that the ther-

apies rendered were able to maintain maxil-

lary molars with FI over that period, with 

only 12% of molars being lost over time. 

However, the therapies did not have any 

effect on the bone support, as 75% of the 

molars had no significant changes in bone 

levels. On the contrary, 11% had detectable 

bone loss and 12% were extracted (Ross and 

Thompson 1978). A German group evalu-

ated only molars in 136 patients over a 

mean follow‐up period of 13 years. They 

reported that similar percentages of molars 

were lost when treated with both closed‐ 

and open‐flap scaling and root planing 

(Dannewitz et  al. 2006, 2016). A group in 

Sweden too found that reduction in the 

mean plaque index score was greater in 

non‐molars compared to molars (Lindhe 

et al. 1982).

A review of the longitudinal studies seemed 

to show that debridement of the furcation 

areas during root planing or with a surgical 

procedure, for instance apically positioned 

flap with osseous surgery, did not signifi-

cantly improve the long‐term prognosis of 

these teeth. Although furcation‐involved 

teeth might survive in the long term, their 

survival rates were substantially lower than 

single‐rooted teeth such as incisors. The 

authors alluded that the anatomy of the fur-

cation area complicated both professional 

debridement and patient home care, imply-

ing that the quality of debridement might not 

be ideal and thereby indicating that molar 

teeth are tougher to maintain successfully 

over time. A summary on the long‐term sur-

vival of molars with FI is provided in 

Chapter 5.

How Good are We at Cleaning Furcations?  39

3.3   Professional 

Debridement

Conventionally, scaling and root planing are 

carried out using manual instruments, such 

as curettes, sickles, chisels, hoes, and files, or 

power‐driven scalers, for example sonic or 

ultrasonic scalers. These instruments can be 

used in both the non‐surgical and surgical 

phases of periodontal therapy. Curettes, for 

instance universal and Gracey, are double‐

ended instruments with customized cutting 

edges, shank lengths, blade lengths, and 

angulations. Therefore, each one of the nine 

standard Gracey curettes is designed to scale 

and root plane a specific area in the mouth. 

These curettes have a blade width of at least 

0.76 mm and a blade length of 5 mm (Oda 

et al. 2004).

Powered scalers are either sonic or ultra-

sonic. In sonic scalers, compressed air causes 

the working tip to vibrate in an elliptical fash-

ion at frequencies of 2000 to 6000 Hz under a 

water spray. Ultrasonic scalers, on the other 

hand, are subclassified into magnetostrictive 

and piezoelectric scalers. The magnetostric-

tive scalers, such as Cavitron® (Dentsply, 

USA), work by creating a magnetic field 

where an expanding and contracting coil, 

together with an alternating current, results 

in vibrations that are transmitted to the 

working tip. The tip moves in an elliptical 

motion, thus all sides of the tip are active. In 

the piezoelectric scalers, such as Piezon 

Master® (EMS, Switzerland), reactive ceramic 

crystals undergo dimensional changes when 

subjected to an alternating electrical current. 

The expansion and contraction result in 

vibrations that are transmitted to the work-

ing tip, which moves in a linear manner, thus 

only the lateral sides of the tip act as the 

active sides. The average ultrasonic scaler tip 

width is 0.55 mm (Oda et al. 2004).

A comparison between the use of hand 

instruments and ultrasonic scalers showed 

that the latter were better suited for the 

debridement of narrow furcation areas, as 

their tips were narrower than curettes and 

thus could debride the hard‐to‐reach areas 

(Matia et  al. 1986; Sugaya et  al. 2002). In 

addition, they were able to significantly 

reduce the bacterial counts for all degrees of 

FI and were more effective in debriding the 

class II and III furcations compared to 

curettes (Leon and Vogel 1987). A study that 

evaluated the efficacy of four ultrasonic 

sharp tips (Cavitron TFI 10 tip, Cavitron 

EWPP [Probe] tip, Titan‐S Universal tip, and 

Titan‐S Sickle tip) showed that there were no 

significant differences in calculus removal 

when different tips were used (Patterson 

et al. 1989). When sharp tips were compared 

to ball tips, the Titan sonic scaler with uni-

versal tip and Cavitron with ball tip were the 

most efficient at debriding both maxillary 

and mandibular molars, especially the furca-

tion roofs (Takacs et al. 1993). Other similar 

studies evaluated modified sonic tips with 

different angulations, and found that angu-

lated tips provided a more thorough debride-

ment because the tips could better access the 

furcations (Kocher et al. 1996, 1998a, b). In 

addition, some of the sonic tips had an ellip-

soidal terminal end of 0.8 mm in diameter, 

which would provide more intimate contact 

with the root concavities and the furcation 

dome, thus improving the quality of the 

instrumentation. Diamond‐coated ultra-

sonic and sonic scaler tips were found to 

remove calculus 2–3.3 times faster than 

manual curettes, but they were prone to 

remove cementum and dentine during 

debridement (Kocher and Plagmann 1999; 

Scott et al. 1999).

A study that investigated the quality of the 

mechanical and chemical debridement of root 

surfaces on 90 periodontally involved 

extracted teeth found that with unlimited 

access to the root surfaces, all mechanical 

debridement methods – that is, curettes, and 

ultrasonic with regular or diamond‐coated 

P‐10 tip  –  were equally effective. Thus, this 

study suggested that access was the main criti-

cal factor that affected the quality of root sur-

face debridement (Eschler and Rapley 1991). 

In addition, it was reported that interproximal 

Chapter 3 

40

FIs responded less favourably to mechanical 

debridement compared to their buccal and 

lingual counterparts. This phenomenon 

could be due to the increased difficulty in 

accessing the interproximal furcations for 

debridement (Del Peloso Ribeiro et  al. 

2007).

Besides modifying the scaler tips, root 

surface debridement can be performed 

through a non‐surgical (closed) or surgical 

(open) approach. It was reported that sig-

nificantly more residual calculus was found 

in groups that had the closed approach 

(34.1–37.0%) compared to the open 

approach (1.0–2.7%; Matia et  al. 1986). In 

addition, clinical experience and proficiency 

did significantly affect the quality of debride-

ment at the furcations. Less experienced 

residents left significantly more calculus‐

free surfaces with the open approach (43%) 

compared to the closed approach (8%). This 

percentage of only 8% calculus‐free furca-

tion surfaces for less experienced operators 

with a closed approach was particularly 

striking. On the other hand, there was no 

significant difference between the open and 

closed approaches for experienced perio-

dontists (Fleischer et  al. 1989). Using the 

open approach, experienced periodontists 

had 68% calculus‐free furcation surfaces 

compared to 44% with a closed approach. 

Although the percentages were not statisti-

cally significant, they were clinically impor-

tant, because almost a quarter of the root 

surfaces had residual calculus when the 

closed approach was used. However, despite 

the increased visibility with the open 

approach, the use of hand instruments at the 

furcal areas was ineffective (Fleischer et al. 

1989; Wylam et al., 1993).

Figure  3.1 shows an extracted maxillary 

first molar which had received what was 

defined as ‘deep cleaning’ by a general dental 

practitioner. The tooth was extracted, since it 

was deemed hopeless due to bone loss to the 

apex and mobility degree III. The images 

show very extensive deposits of calculus in 

the furcation region.

Table 3.2 shows a summary of the studies 

that evaluated the effectiveness of mechanical 

and chemical debridement at multi‐rooted 

teeth. It is obvious that there is a paucity of 

available literature on the effectiveness of 

mechanical debridement in furcation areas. 

A  systematic review of 13 randomized 

 controlled clinical trials revealed that there 

(a)

(b)

(c)

Figure 3.1 

The upper right maxillary molar (UR6) of a 53‐year‐old female patient affected by generalized 

advanced chronic periodontitis, extracted as deemed hopeless due to bone loss to the apex and mobility 

degree III. This tooth had received what was defined as ‘deep cleaning’ by a general dental practitioner. 

However, the images show very extensive deposits of calculus in the furcation region, testifying to the 

difficulty of achieving good subgingival debridement in furcation regions.

  Table 3.2   

 Summary of studies that evaluated efficacy of mechanical debridement. 

 Author/ 
 Year 

Sample 
Size

No. of Teeth

Study Design

Results    

 Matia et al. 

  1986   

48

50 mandibular 

molars with class II 

or III FI

Curette (closed approach) vs curette 

(open approach) vs ultrasonic (closed 

approach) vs ultrasonic (open approach) 

vs no treatment.

 

●

  Closed approach: ultrasonic scaler and curette had 

37.7% and 34.1% of residual calculus, respectively. 

 

●

 Open approach: ultrasonic scaler and curette had 

1.0% and 2.7% of residual calculus, respectively. 

 

●

 More calculus was removed with the open 

approach. 

 

●

 Ultrasonic scaling removed more calculus in 

narrow furcations (<2.3 mm) compared to curette.    

 Leon and 

Vogel   1987   

6

33 maxillary and 

mandibular molars 

(class I, II, and III FI)

Gracey curettes vs ultrasonic scaler 

(Cavitron® with P‐10 tip) vs no 

treatment.

 

●

  Ultrasonic scaling was significantly more effective 

than curettes in reducing the bacterial counts for all 

degrees of FI. 

 

●

 Ultrasonic scaling was more effective in the class II 

and III FI.    

 Oda and 

Ishikawa 

  1989   

–

120 extracted 

maxillary and 

mandibular molars

Gracey curettes #11/12 and #13/14 vs 

standard tip for ultrasonic scaler (ST‐08) 

vs newly designed spherical tip (0.8 mm 

diameter).

 

●

  Mean % of residual marks that represents calculus: 

15.1%, 50.3%, and 61.1% for newly designed tip, 

conventional ultrasonic scaler tip, and Gracey 

curettes, respectively, in maxillary molars (16.7%, 

44.1%, and 39.5%, respectively, in mandibular molars). 

 

●

 The newly designed tip produced surfaces that 

were as smooth as those produced by the Gracey 

curettes. 

 

●

 The newly designed tip was more effective in 

debriding the furcation area.    

 Patterson 

et al.   1989   

–

24 extracted 

mandibular molars 

mounted on a 

typodont

Cavitron TFI 10 tip vs Cavitron EWPP 

(Probe) tip vs Titan‐S Universal tip vs 

Titan‐S Sickle tip.

 

●

  Mean % of residual calculus: 13 mm 

2

 , 11 mm 

2

 , 

9 mm 

2

 , and 8 mm 

2

  for Cavitron TFI 10 tip, Cavitron 

EWPP (Probe) tip, Titan‐S Universal tip, and 

Titan‐S Sickle tip (no significant differences). 

 

●

 On average 25–30% of calculus remained after 

debridement. 

 

●

 No significant differences between the efficacy of 

the four ultrasonic tips.    

(Continued)

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Table 3.2 

(Continued)

 Author/ 
 Year 

Sample 
Size

No. of Teeth

Study Design

Results    

 Scott et al. 

  1999   

–

60 extracted 

mandibular molars

Cavitron TFI‐10 tip vs Gracey curettes 

vs fine‐ or medium‐grit diamond‐coated 

ultrasonic tips.

 

●

  Ultrasonic scaling was significantly faster than 

hand curettes in calculus removal.    

 Parashis 

et al.   1993b   

23

30 mandibular 

molars (60 

furcations)

SRP with closed approach vs SRP with 

open approach vs SRP with open 

approach + rotary diamond 

instrumentation.

 

●

  The use of the rotary diamond tip significantly 

removed more calculus in the furcation area.    

 Kocher 

et al.   1996   

–

24 acrylic molars

Universal curettes vs sonic scaler vs 

modified sonic scaler with bud‐shaped 

tips and different angulations vs 

modified sonic scaler tips with plastic 

coating.

 

●

  Ultrasonic scaling was more effective than hand 

instrumentation. 

 

●

 Specific angulations of the scaler tips were more 

suited for distal furcations or the root of the 

furcations. 

 

●

 Sonic scaler tips with plastic coatings appeared to 

remove only plaque and thus were not suitable for 

furcation debridement.    

 Kocher 

et al.   1998a   

–

15 extracted 

maxillary and 

mandibular molars 

placed in a dummy 

model

Curettes vs diamond bur and curettes vs 

ultrasonic scaler vs sonic scaler vs 

diamond‐coated sonic scaler tips 

(angulated like Gracey curette #13/14 

with 1.5 mm diameter and 45 microns 

diamond grit size).

 

●

  Ultrasonic and sonic scalers cleaned only 70% of 

the root surfaces compared to the other groups 

(85%). 

 

●

 Only the diamond‐coated sonic scaler managed to 

effectively clean the maxillary molars (85% of the 

root surfaces were clean compared to 75% by 

curettes).    

 Kocher 

et al.   1998b   

–

15 extracted 

maxillary and 

mandibular molars 

placed in a dummy 

model

Curettes vs diamond‐coated sonic scaler 

tips (angulated like Gracey curette 

#13/14 and universal curette, with 1 mm 

diameter and 15 microns diamond grit 

size).

 

●

  Mandibular molars were better debrided compared 

to maxillary molars. 

 

●

 Diamond‐coated sonic scalers do damage the root 

surfaces to the same degree as hand curettes (more 

definitive notches were seen on the palatal roots). 

 

●

 Diamond‐coated sonic scaler tips with varying 

angulations did improve root surface debridement.    

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Table 3.2 

(Continued)

 Author/ 
 Year 

Sample 
Size

No. of Teeth

Study Design

Results    

 Scott et al. 

  1999   

–

60 extracted 

mandibular molars

Cavitron TFI‐10 tip vs Gracey curettes 

vs fine‐ or medium‐grit diamond‐coated 

ultrasonic tips.

 

●

  Ultrasonic scaling was significantly faster than 

hand curettes in calculus removal.    

 Parashis 

et al.   1993b   

23

30 mandibular 

molars (60 

furcations)

SRP with closed approach vs SRP with 

open approach vs SRP with open 

approach + rotary diamond 

instrumentation.

 

●

  The use of the rotary diamond tip significantly 

removed more calculus in the furcation area.    

 Kocher 

et al.   1996   

–

24 acrylic molars

Universal curettes vs sonic scaler vs 

modified sonic scaler with bud‐shaped 

tips and different angulations vs 

modified sonic scaler tips with plastic 

coating.

 

●

  Ultrasonic scaling was more effective than hand 

instrumentation. 

 

●

 Specific angulations of the scaler tips were more 

suited for distal furcations or the root of the 

furcations. 

 

●

 Sonic scaler tips with plastic coatings appeared to 

remove only plaque and thus were not suitable for 

furcation debridement.    

 Kocher 

et al.   1998a   

–

15 extracted 

maxillary and 

mandibular molars 

placed in a dummy 

model

Curettes vs diamond bur and curettes vs 

ultrasonic scaler vs sonic scaler vs 

diamond‐coated sonic scaler tips 

(angulated like Gracey curette #13/14 

with 1.5 mm diameter and 45 microns 

diamond grit size).

 

●

  Ultrasonic and sonic scalers cleaned only 70% of 

the root surfaces compared to the other groups 

(85%). 

 

●

 Only the diamond‐coated sonic scaler managed to 

effectively clean the maxillary molars (85% of the 

root surfaces were clean compared to 75% by 

curettes).    

 Kocher 

et al.   1998b   

–

15 extracted 

maxillary and 

mandibular molars 

placed in a dummy 

model

Curettes vs diamond‐coated sonic scaler 

tips (angulated like Gracey curette 

#13/14 and universal curette, with 1 mm 

diameter and 15 microns diamond grit 

size).

 

●

  Mandibular molars were better debrided compared 

to maxillary molars. 

 

●

 Diamond‐coated sonic scalers do damage the root 

surfaces to the same degree as hand curettes (more 

definitive notches were seen on the palatal roots). 

 

●

 Diamond‐coated sonic scaler tips with varying 

angulations did improve root surface debridement.    

 Author/ 
 Year 

Sample 
Size

No. of Teeth

Study Design

Results    

 Kocher 

and 

Plagmann 

  1999   

15

45 maxillary and 

mandibular molars

OFD with hand curettes (Barnhart 

curette #5/6 and Gracey curettes #7/8, 

#11/12, and #13/14) vs diamond‐coated 

sonic scaler.

 

●

  Diamond‐coated sonic scalers cleaned two times 

faster than hand curettes. 

 

●

 The initial reduction in probing depths at the 

furcations was not maintained over time in both 

groups.    

 Auplish 

et al.   2000   

–

Acrylic molars in 

dummy head

Curettes (Gracey #11/12 and #13/14) vs 

diamond‐coated sonic scaler vs sonic 

scaler.

 

●

  Diamond‐coated sonic scaler took the least time to 

complete the debridement. 

 

●

 Diamond‐coated sonic scaler significantly removed 

more calculus compared to the sonic scalers or 

curettes.    

 Fleischer 

et al.   1989   

36

61

Curette (closed approach) by 

experienced periodontist vs curette 

(open approach) by experienced 

periodontist vs ultrasonic (closed 

approach) by less experienced residents 

vs ultrasonic (open approach) by less 

experienced residents vs no treatment.

 

●

  Experienced periodontists: significantly greater 

calculus‐free area (78%) in open approach vs closed 

approach (36%). 

 

●

 Less experienced residents: significantly greater 

calculus‐free area (45%) in open approach vs closed 

approach (18%). 

 

●

 At the furcal areas, less experienced residents: 

significantly greater calculus‐free surface with open 

approach (43%) vs closed approach (8%). 

 

●

 At the furcal areas, no significant difference 

between the open (68%) and closed (44%) 

approaches for experienced periodontists.    

 Eschler and 

Rapley   1991   

–

90 extracted teeth

Grouping (1) curette (Columbia #13/14) 

vs (2) curette (Columbia #13/14), 

antiformin‐citric acid vs (3) ultrasonic 

with P‐10 tip vs (4) ultrasonic with 

diamond‐coated P‐10 tip vs (5) ultrasonic 

with diamond‐coated P‐10 

tip + antiformin‐citric acid vs (6) 

ultrasonic with diamond‐coated P‐10 tip 

and curette (Columbia #13/14) vs (7) 

ultrasonic with diamond‐coated P‐10 tip 

and curette (Columbia 

#13/14) + antiformin‐citric acid vs (8) 

antiformin‐citric acid vs (9) no treatment.

 

●

  All groups that had mechanical debridement had 

significantly less residual stains compared to groups 

that had no treatment and antiformin‐citric acid 

treatment (chemical root preparation did not 

improve stain removal). 

 

●

 Debridement with ultrasonic with P‐10 tip: 

significantly greater residual stains vs debridement 

with diamond‐coated P‐10 tip and curette. 

 

●

 With unlimited access, all mechanical debridement 

methods appeared to be equally effective.    

(Continued)

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Table 3.2 

(Continued)

 Author/ 
 Year 

Sample 
Size

No. of Teeth

Study Design

Results    

 Takacs 

et al.   1993   

–

100 extracted molars 

with FI

Cavitron® ultrasonic with 0.8 mm ball tip 

vs Cavitron ultrasonic with 

EWP12R/12 L pointed tip vs ENAC 

ultrasonic with furcation 0.8 mm ball tip 

vs EVA contra‐angle reciprocating 

handpiece with Per‐Io‐Tor #1 and #2 tips 

(similar to threaded fissure bur) vs 

Titan‐S sonic scaler with universal tip.

 

●

  On average 74.2% of calculus was left behind at the 

furca roof of mandibular molars after debridement 

(the pointed tip and universal tip removed the most 

calculus). 

 

●

 On average 76.4% of calculus was left behind at the 

furca roof of maxillary molars after debridement 

(Cavitron ball tip and universal tip removed the 

most calculus). 

 

●

 Titan sonic scaler with universal tip and Cavitron 

with ball tip were the most efficient at debriding 

molars.    

 Wylam 

et al.   1993   

26

60 molars with class 

II or III FI

Curettes (closed approach) vs curettes 

(open approach) vs no treatment.

 

●

  Molars after non‐surgical SRP: significantly greater 

residual calculus (54.3%) vs open approach (33.0%). 

 

●

 At the furcal area, molars after non‐surgical SRP: 

slightly greater residual calculus (93.2%) vs open 

approach (91.1%). 

 

●

 Hand instrumentation was unable to effectively 

clean the furcal area.    

 Otero‐

Cagide and 

Lang 

 1997 

–

100 artificial teeth

Curettes (Vision curvettes #11/12 and 

#13/14) vs ultrasonic with EWP‐12 L‐R 

scaler tip.

 

●

  Debridement with curettes had significantly less 

residual calculus compared to ultrasonics.  

  FI = furcation involvement; OFD = open‐flap debridement; SRP = scaling and root planing.  

How Good are We at Cleaning Furcations?  45

was no evidence on the efficacy of powered 

scalers in debriding multi‐rooted teeth. This 

outcome needs to be interpreted with  caution, 

because out of the 13 studies, 7 evaluated 

only single‐rooted teeth, and the remaining 

6  studies focused on patient healing out-

comes. In addition, the instruments used in 

the studies were conventional Gracey and 

Columbia curettes and Cavitron ultrasonic 

tips, which have thicker blade widths than the 

instruments that are available today. The 

 evidence, however, did show that powered 

scalers debride faster than hand curettes 

(Tunkel et al. 2002).

In recent years, advancements in material 

science have allowed curettes and ultrasonic 

tips to be stronger and thinner than in past 

decades. Gracey curettes are available in 

 different angulations, for example Gracey 

curette #17/#18, or blade widths, for instance 

Micro Mini Five® Gracey curettes. The newer 

Micro Mini Five curettes have a shorter blade 

length (2 mm) and thinner blade width 

(0.6 

mm) compared to regular Gracey 

curettes, with a blade length and width of 

5mm and 0.9mm respectively. A study of 100 

artificial teeth used Vision curvettes that had 

50% shorter blades and increased blade cur-

vature to debride the furcation of mandibular 

molars. The authors reported that the modi-

fied blades were more effective than ultra-

sonic scalers in the debridement of the 

furcation area (Otero‐Cagide and Long 

1997). Besides curettes, ultrasonic tips are 

now slimmer with improved angulations. 

For example, the Cavitron ultrasonic tips 

THINserts® are 47% thinner than the 

Slimline® inserts (diameter 0.5 mm), with an 

additional 9° backbend to gain better access 

to the  subgingival areas. The EMS Piezon 

Master universal ultrasonic tips are 0.6 mm 

in diameter, and are thus able to access most 

furcation areas (<0.75 mm). Certain systems, 

such as Kavo®, have an inbuilt light‐emitting 

diode (LED) to improve visibility in the more 

 posterior areas of the oral cavity. All these 

modifications aim to improve the access 

of  instruments into the furcation area 

(Figures 3.2–3.5).

Other authors have also proposed the use 

of chemotherapeutics, such as chlorhexidine, 

essential oils, locally delivered tetracycline, 

and doxycycline, to facilitate microbial 

 biofilm removal at the furcation areas, with 

contradictory results. A more detailed review 

of this topic is provided in Chapter 10.

Figures  3.6 and 3.7 show two cases of FI 

with pre‐, intra‐, and post‐treatment views, 

showing limitations in non‐surgical debride-

ment of furcation defects and tools used for 

intrasurgical furcation debridement.

3.4   Patient Home Care

It has been shown that poor plaque control 

results in suboptimal treatment outcome 

(Rosling et  al. 1976). The clinician can 

 perform effective instrumentation, but the 

patient must be able to maintain the root 

 surface free of microbial biofilm. Numerous 

tools are available for the patient to clean 

their furcation‐involved multi‐rooted teeth. 

These are manual and powered toothbrushes, 

interspace brushes, interdental brushes, and 

the WaterPik®. A recent Cochrane systematic 

review conducted a meta‐analysis on 51 clini-

cal trials concluded that powered tooth-

brushes, compared to manual ones, were 

more effective in reducing plaque and gingi-

val inflammation in both the short and long 

term (Yaacob et  al. 2014). Powered tooth-

brushes have different modes of action, 

namely side to side, counter‐oscillation, rota-

tion oscillation, multi‐dimensional, and cir-

cular. The rotating oscillating powered 

toothbrushes were found to significantly 

reduce plaque and gingivitis in the short and 

long term, with the greatest benefit at the lin-

gual surfaces (Klukowska et  al. 2014a, b). 

Another Cochrane review evaluated 17 rand-

omized controlled trials comparing the effi-

cacy of powered toothbrushes with different 

modes of action (Deacon et al. 2010). It was 

reported that powered toothbrushes with 

the rotation oscillation motion performed 

better than those with the side‐to‐side action. 

However, limited studies with short follow‐up 

Table 3.2 

(Continued)

 Author/ 
 Year 

Sample 
Size

No. of Teeth

Study Design

Results    

 Takacs 

et al.   1993   

–

100 extracted molars 

with FI

Cavitron® ultrasonic with 0.8 mm ball tip 

vs Cavitron ultrasonic with 

EWP12R/12 L pointed tip vs ENAC 

ultrasonic with furcation 0.8 mm ball tip 

vs EVA contra‐angle reciprocating 

handpiece with Per‐Io‐Tor #1 and #2 tips 

(similar to threaded fissure bur) vs 

Titan‐S sonic scaler with universal tip.

 

●

  On average 74.2% of calculus was left behind at the 

furca roof of mandibular molars after debridement 

(the pointed tip and universal tip removed the most 

calculus). 

 

●

 On average 76.4% of calculus was left behind at the 

furca roof of maxillary molars after debridement 

(Cavitron ball tip and universal tip removed the 

most calculus). 

 

●

 Titan sonic scaler with universal tip and Cavitron 

with ball tip were the most efficient at debriding 

molars.    

 Wylam 

et al.   1993   

26

60 molars with class 

II or III FI

Curettes (closed approach) vs curettes 

(open approach) vs no treatment.

 

●

  Molars after non‐surgical SRP: significantly greater 

residual calculus (54.3%) vs open approach (33.0%). 

 

●

 At the furcal area, molars after non‐surgical SRP: 

slightly greater residual calculus (93.2%) vs open 

approach (91.1%). 

 

●

 Hand instrumentation was unable to effectively 

clean the furcal area.    

 Otero‐

Cagide and 

Lang 

 1997 

–

100 artificial teeth

Curettes (Vision curvettes #11/12 and 

#13/14) vs ultrasonic with EWP‐12 L‐R 

scaler tip.

 

●

  Debridement with curettes had significantly less 

residual calculus compared to ultrasonics.  

  FI = furcation involvement; OFD = open‐flap debridement; SRP = scaling and root planing.  

Chapter 3 

46

periods (three months or less) and unclear 

risk of bias were included. Therefore, the 

results of the review should be interpreted 

with caution.

There is only one study that evaluated the 

efficacy of brushing instruments at the furcal 

areas (Bader and Williams 1997). The authors 

compared a pointed‐end tufted powered brush 

and a small‐head powered toothbrush, and 

found that the former was more effective in 

removing plaque at the furcal area. The pointed 

tip is able to fit into the furcal area to remove 

the plaque. As the end‐tufted brush looks simi-

lar to the interspace brush, it might be inferred 

that the interspace brush will be effective in 

maintaining the furcation area free of biofilm.

Interdental brushes come in various sizes 

and shapes. They can be conical or cylindrical 

in shape, have angled or straight handles, 

have regular nylon bristles or rubber bristles, 

and be of different sizes. They are used to 

(a)

(b)

(c)

Figure 3.2 

(a) Mini Five® Gracey curettes #11/12 and #13/14 with blade width of 0.76 mm; (b) Micro Mini Five® 

Gracey curettes #11/12 and #13/14 with blade width of 0.6 mm; (c) difference in the blade widths of the Micro 

Mini Five Gracey curette #11/12 (left) and Mini Five Gracey curette #11/12 (right).

Figure 3.3 

Traditional piezoelectric ultrasonic scaler 

tips with a diameter of 0.7–0.8 mm.

How Good are We at Cleaning Furcations?  47

clean the interproximal surfaces or furcation 

areas. A comparison between dental floss 

and the interdental brush showed that the 

latter was significantly more effective in 

removing plaque (mean proximal plaque 

score: 1.22 for interdental brush and 1.71 for 

dental floss; Kiger et  al. 1991), hence it is 

 better suited for cleaning proximal surfaces. 

As evidenced by the significantly higher 

bleeding and plaque scores, a short‐term 

study found that conical interdental brushes 

did not clean the lingual proximal surface as 

well as their cylindrical counterparts (Larsen 

et al. 2017). Also, straight brushes can clean 

better than angled ones (Jordan et al. 2014). 

It seemed that rubber‐bristled interdental 

brushes were as effective as regular interden-

tal brushes in terms of plaque removal and 

patients found them more comfortable to use 

(Abouassi et al. 2014). Therefore, in patients 

with periodontitis, and possibly interproxi-

mal FI, interdental brushes remove more 

plaque than flossing or brushing alone 

(Christou et al. 1998).

The WaterPik is an oral irrigator introduced 

in 1962 that uses pulsating hydrodynamic 

force to remove food debris from the tooth 

surface. Its clinical benefits include removal of 

subgingival bacteria, clinical and histological 

reduction in gingival inflammation, down‐

regulation of pro‐inflammatory cytolines, 

reduction of probing depths, improvement of 

clinical attachment loss, being safe for gingival 

tissues, and minimal bacteremia (Jolkovsky 

and Lyle 2015; Cutler et al. 2000). Therefore, 

in patients with less than ideal oral hygiene, 

supragingival irrigation will flush out the sub-

gingival bacteria, reducing gingival inflamma-

tion to a degree greater than toothbrushing 

alone (Research, Science and Therapy 

Committee of the American Academy of 

Periodontology 2001). In comparison to the 

Sonicare Airfloss®, which uses a fluid spray of 

micro‐bubbles to disrupt the plaque, the 

WaterPik may be more effective in terms of 

removing plaque and consequently reducing 

the bleeding score (Goyal et al. 2015).

Evidence on home care of furcations is 

scarce. As such, results from studies that 

assessed interproximal cleaning was used to 

infer the effectiveness of these brushes in 

removing plaque from the tooth surfaces. It 

appears that powered toothbrushes with the 

rotation oscillation action, interspace 

brushes, straight cylindrical interdental 

brushes with rubber or nylon bristles, and 

the WaterPik are effective in cleaning inter-

proximal areas and potentially furcations.

(a)

(b)

(c)

Figure 3.4 

EMS Piezon® Master 

ultrasonic scaler and tips: (a) PL1 tip 

with a diameter of 0.5 mm for 

debridement of hard‐to‐reach 

interproximal areas; (b) PL5 tip with a 

ball end of diameter 0.8 mm for 

debridement of furcations and 

concavities; (c) PS universal tip with a 

diameter of 0.6 mm for debridement of 

deep pockets.

Figure 3.5 

Cavitron® Slimline™ insert with a 

diameter of 0.5 mm.

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Page Number: 48

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

Figure 3.6 

(a) The maxillary right first molar presented with a Grade I cervical enamel projection, 6 mm 

pockets, and a class II furcation. (b) Periapical radiograph showed radiolucency in the furcation area. 

(c) Cervical enamel projection was evident and seen protruding into the furcation. (d) Furcal area was debrided 

with After‐5 Gracey curettes (Hu‐Friedy, USA) and Piezo ultrasonic scalers (EMS, Switzerland). (e) Newmeyer’s 

rotary bur was used to remove the cervical enamel projection and any remaining granulomatous tissue. 

(f) Clinical photo showed the defect after cleaning. (g) Defect was grafted with human cancellous allograft 

(LifeNet, USA). (h) The graft was then protected with a well‐trimmed collagen membrane (2–3 mm beyond the 

defect margin all around). 

How Good are We at Cleaning Furcations?  49

(i)

(j)

(k)

(l)

(m)

Figure 3.6 (Continued) 

(i) The flap was then coronally advanced and sutured. (j) At the two‐year post‐surgery 

follow‐up visit, the probing pocket depth at the furcation area was reduced to 3 mm and (k) radiographic bone fill 

was observed. (l) The furcation area remained stable clinically and (m) radiographically even at the four‐year post‐

surgery follow‐up visit. Further details and indications of furcation regenerative therapy are given in Chapter 7.

Chapter 3 

50

(a)

(b)

(c)

(d)

Figure 3.7 

The mandibular left second molar presented with a grade III cervical enamel projection, 6–8 mm 

pockets, and a class III furcation. (a) Residual calculus observed on flap elevation, reflecting the ineffectiveness 

of non‐surgical debridement. (b) Surgical open‐flap scaling and root planing with fine ultrasonic inserts 

(Cavitron®, Dentsply, USA) and Gracey curettes (Hu‐Friedy, USA) were performed to achieve a smooth root 

surface. The flap was repositioned and sutured apically, exposing the class III furcation involvement. (c) At the 

two‐year post‐surgery follow‐up visit, there was recurrence of the pocket to 5 mm at the midlingual site (d) 

with bleeding on probing, despite the patient using an interdental brush of the appropriate size and being on 

a strict three‐monthly periodontal maintenance regimen. This therefore concurs with the literature that plaque 

removal at the furcation area is unpredictable, even when exposed and visible.

 Summary  of Evidence

 

●

Longitudinal studies show that, compared 

to single‐rooted teeth, furcation‐involved 

teeth respond poorly to non‐surgical and 

surgical treatment. Improvements in the 

furcation area, if any, are also less sustain-

able over time.

 

●

Finer and angulated ultrasonic tips can 

better debride the furcation area than 

hand instruments, e.g. Gracey curettes.

 

●

There is limited evidence on home care of 

furcations, however tools such as pow-

ered toothbrushes, interspace brushes, 

interdental brushes, and the WaterPik 

may be useful in removing plaque from 

the furcation area.

How Good are We at Cleaning Furcations?  51

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jop.1965.36.3.177.

Loos, B., Claffey, N., and Egelberg, J. (1988). 

Clinical and microbiological effects of root 

debridement in periodontal furcation pockets. 

Journal of Clinical Periodontology 15, 453–463.

Loos, B., Nylund, K., Claffey, N., and Egelberg, 

J. (1989). Clinical effects of root 

debridement in molar and non‐molar teeth: 

A 2‐year follow‐up. Journal of Clinical 

Periodontology 16, 498–504.

Matia, J.I., Bissada, N.F., Maybury, J.E., and 

Ricchetti, P. (1986). Efficiency of scaling of the 

molar furcation area with and without surgical 

access. International Journal of Periodontics 

and Restorative Dentitry 6, 24–35.

McFall, W.T., Jr (1982). Tooth loss in 100 

treated patients with periodontal disease: A 

long‐term study. Journal of Periodontology 

53, 539–549. doi: 10.1902/jop.1982.53.9.539.

Nordland, P., Garrett, S., Kiger, R. et al. (1987). 

The effect of plaque control and root 

debridement in molar teeth. Journal of 

Clinical Periodontology 14, 231–236.

Oda, S., and Ishikawa, I. (1989). In vitro 

effectiveness of a newly‐designed ultrasonic 

scaler tip for furcation areas. Journal of 

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jop.1989.60.11.634.

Oda, S., Nitta, H., Setoguchi, T. et al. (2004). 

Current concepts and advances in manual 

and power‐driven instrumentation. 

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Otero‐Cagide, F.J., and Long, B.A. (1997). 

Comparative in vitro effectiveness of closed 

root debridement with fine instruments on 

specific areas of mandibular first molar 

furcations. II. Furcation area. Journal of 

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jop.1997.68.11.1098.

Page, R.C., and Kornman, K.S. (1997). The 

pathogenesis of human periodontitis: An 

introduction. Periodontology 2000 14, 9–11.

Parashis, A.O., Anagnou‐Vareltzides, A., and 

Demetriou, N. (1993a). Calculus removal 

from multirooted teeth with and without 

surgical access. I: Efficacy on external and 

furcation surfaces in relation to probing 

depth. Journal of Clinical Periodontology 20, 

63–68.

Parashis, A.O., Anagnou‐Vareltzides, A., and 

Demetriou, N. (1993b). Calculus removal 

from multirooted teeth with and without 

surgical access. II: Comparison between 

external and furcation surfaces and effect of 

furcation entrance width. Journal of Clinical 

Periodontology 20, 294–298.

Patterson, M., Eick, J.D., Eberhart, A.B. et al. 

(1989). The effectiveness of two sonic and 

two ultrasonic scaler tips in furcations. 

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10.1902/jop.1989.60.6.325.

Pihlstrom, B.L., Oliphant, T.H., and McHugh, 

R.B. (1984). Molar and nonmolar teeth 

compared over 6½ years following two 

methods of periodontal therapy. Journal of 

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jop.1984.55.9.499.

Ramfjord, S.P., Caffesse, R.G., Morrison, E.C. 

et al. (1987). 4 modalities of 

periodontal treatment compared over 5 

years. Journal of Clinical Periodontology 

14, 445–452.

Ramfjord, S.P., Nissle, R.R., Shick, R.A., and 

Cooper, H., Jr (1968). Subgingival curettage 

versus surgical elimination of periodontal 

pockets. Journal of Periodontology 39, 

167–175.

Research, Science and Therapy Committee of 

the American Academy of Periodontology 

(2001). Treatment of plaque‐induced 

gingivitis, chronic periodontitis, and other 

clinical conditions. Journal of Periodontology 

72, 1790–1800. doi: 10.1902/

jop.2001.72.12.1790.

Research, Science and Therapy Committee of 

the American Academy of Periodontology 

(2005). Position paper: The role of supra‐ 

and subgingival irrigation in the treatment 

of periodontal diseases. Journal of 

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Chapter 3 

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Rosling, B., Nyman, S., and Lindhe, J. (1976). 

The effect of systematic plaque control on 

bone regeneration in infrabony pockets. 

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Ross, I.F., and Thompson, R.H., Jr (1978). 

A long term study of root retention in the 

treatment of maxillary molars with furcation 

involvement. Journal of Periodontology 49, 

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Schatzle, M., Loe, H., Burgin, W. et al. (2003). 

Clinical course of chronic periodontitis. 

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Periodontology 30, 887–901.

Scott, J.B., Steed‐Veilands, A.M., and Yukna, 

R.A. (1999). Improved efficacy of calculus 

removal in furcations using ultrasonic 

diamond‐coated inserts. International 

Journal of Periodontics and Restorative 

Dentistry 19, 355–361.

Smart, G.J., Wilson, M., Davies, E.H., and 

Kieser, J.B. (1990). The assessment of 

ultrasonic root surface debridement by 

determination of residual endotoxin levels. 

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174–178.

Socransky, S.S., and Haffajee, A.D. (2005). 

Periodontal microbial ecology. 

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(1975). The clinical and histological 

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D.F. (1993). Efficacy of 5 machining 

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10.1902/jop.1993.64.3.228.

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(2002). A systematic review of efficacy of 

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Ramfjord, S. (1994). The influence of molar 

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(1989). Tooth loss in patients with moderate 

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maintenance care. Journal of Periodontology 

60, 516–520. doi: 10.1902/jop.1989.60.9.516.

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(1993). The clinical effectiveness of open 

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Diagnosis and Treatment of Furcation-Involved Teeth, First Edition. Edited by Luigi Nibali. 

© 2018 John Wiley & Sons Ltd. Published 2018 by John Wiley & Sons Ltd. 

Companion website: www.wiley.com/go/nibali/diagnosis

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55

4.1   Introduction

To avoid contact with the exogenous sub-

stances of the oral cavity, pulp and dentine are 

genetically protected by the overlying enamel 

and cementum. Despite these defensive phys-

ical barriers, the pulp can be threatened by 

manifold insults, such as caries, restorative 

procedures, and mechanical, chemical, and 

thermal trauma. In periodontitis‐affected 

patients, periodontal pathogens can induce 

pulp infection because of the vascular inter-

connections between periodontium and 

endodontium. Through the accessory canals 

or exposed dentinal tubules, bacteria and tox-

ins might gain the access to the pulp. The 

effect is generally atrophy and is comparable 

with ‘pulp aging’. Likewise, endodontic infec-

tions can influence periodontal health. When 

the  noxae of degenerated pulp involve the 

supporting periodontium, rapid inflamma-

tory responses, characterized by bone loss, 

tooth mobility, and/or sinus tract formation, 

might develop. These clinical conditions 

where both endodontium and periodontium 

are simultaneously affected in what appears 

to be a single periodontal lesion are known as 

endodontic‐periodontal lesions.

Despite the topic of the book regarding 

exclusively furcation pathology, the ethi-

opathogenesis of endodontic‐periodontal 

disease cannot be described by merely 

 considering the inter‐radicular space only. 

Therefore, the present chapter aims to com-

prehensively detail the aetiology and devel-

opment of endodontic‐periodontal lesions, 

with particular emphasis on the diagnosis, 

management, and long‐term prognoses of 

the affected teeth, especially when the furca-

tion region is involved.

4.2   Pathways  Between 

Endodontium and 

Periodontium: Anatomical 

Considerations

Because of the anatomical and vascular inter-

connections, periodontium and endodon-

tium can influence each other during 

function and should therefore be considered 

as one biological unit. The main pathways 

involved in the development of endodontic‐

periodontal lesions are the dentinal tubules, 

the lateral and accessory canals, and the 

 apical foramen or foramina (Seltzer et al. 1963).

4.2.1  Dentinal Tubules

Crown and root dentinal tubules, which 

extend from the pulp to the amelodentinal 

and dentinocemental junctions, respectively, 

are permeable structures. Their permeability 

varies with regard to the dentine type, tooth 

Chapter 4

Furcation: The Endodontist’s View

Federica Fonzar and Riccardo Fabian Fonzar

Private practice, Udine, Italy

Chapter 4

56

area, and functional tubular diameter 

(Pashley 1990).

The root dentine is less patent than the 

coronal. The number of tubules generally 

ranges from approximately 42 000/mm

2

 in 

the cervical area to about 8000/mm

2

 in the 

radicular. By the lower permeability, roots 

and furcation dentine act as a real protective 

barrier (Rapp et al. 1992). From the outer to 

the closer surfaces to the pulp, tubules, which 

follow an S‐shaped path, are denser, wider, 

more patent, and therefore greater in flow 

rate (Ghazali 2003). With ageing or as a 

response to continuous low‐grade stimuli, 

diameters and patency might decrease 

through the apposition of highly mineralized 

peritubular dentine.

On healthy teeth, enamel and cementum 

usually prevent the pulpo‐dentinal complex 

from contact with the oral cavity micro‐

organisms. Owing to developmental defects, 

caries, trauma, restorative procedures, or 

periodontal disease, cementum might not 

cover the underlying dentine any longer, and 

the exposed dentinal tubules might serve as 

communication pathways between the endo-

dontium and periodontium (Adriaens et al. 

1988; Love and Jenkinson 2002). Bacteria and 

bacterial products can therefore induce 

 pulpal reactions by migrating towards the 

pulp (Langeland et  al. 1974; Bergenholtz 

1981; Adriaens et al. 1988). By colonizing the 

root dentine tubules of periodontally diseased 

teeth, pathogens might act as a reservoir for 

pocket recolonization after debridement 

(Adriaens et al. 1987). As proof of this, micro-

biological investigations revealed the presence 

of Gram‐negative and Gram‐positive species 

in the root dentine (Adriaens et  al. 1988; 

Guiliana et al. 1997).

While it has been proved that bacteria are 

able to invade radicular dentine from the 

periodontal pocket, it remains unclear 

whether bacteria invade the healthy cemen-

tum before penetrating the dentine, or reach 

the root dentine through breaches in the 

cementum layer (Adriaens et al. 1987, 1988; 

Guiliana et  al. 1997; Love and Jenkinson 

2002). Cementum is a thin, often discontinuous 

layer that commonly shows surface defects, 

for instance in the sites where Sharpey’s 

fibres attach to its matrix (Adriaens et  al. 

1987). Its exposure to crevicular fluid, bacte-

rial enzymes, or acidic metabolites might 

induce physicochemical and structural alter-

ations, such as localized resorptive lacunae 

or demineralization (Daly et  al. 1982; 

Adriaens et  al. 1987). It can be speculated, 

therefore, that cementum might be structur-

ally damaged by physiological, bacterial, and 

environmental factors, and that this altera-

tion might facilitate bacterial penetration 

within the exposed root of periodontally 

 diseased  teeth.

The vitality of the tooth is another variable 

that might play an important role in hinder-

ing bacteria migration towards the pulp. By 

exposing the dentine surface to the oral envi-

ronment for 150 days, bacterial invasion 

occurs faster in non‐vital rather than vital 

teeth (Nagaoka et al. 1995). A possible expla-

nation of this finding might be sought in the 

resistance offered by outward dentinal fluid 

movement and the presence of odontoblast 

processes in the tubules of vital teeth 

(Vongsavan and Matthews 1991, 1992; 

Pashley et al. 2002). In addition, antibodies 

and anti‐microbial components contained 

within the dentinal fluid might also help the 

vital teeth to be more properly defended 

(Hahn and Overton 1997).

4.2.2  Lateral and Accessory 

Canals

An accessory canal is any branch starting 

from the pulp chamber or the main root 

canal that communicates with the external 

surface of the root. When the location is 

the  coronal or middle third of the root, 

and the orientation is horizontal with respect 

to the main canal, accessory canals are named 

lateral canals (American Association of 

Endodontists 2015).

It is estimated that 30–40% of teeth exhibit 

accessory canals, most of which are found in 

the apical third of the root (De Deus 1975). 

Their prevalence might vary within the teeth, 

The Endodontist’s View 57

and was seen to be greater in mandibular 

molars and premolars than in maxillary 

molars and lateral incisors (Kirkham 1975). 

In addition, it can also change according to 

the root third analysed. In fact, De Deus 

(1975) found that 17%, 9%, and less than 2% 

of teeth showed accessory canals in the api-

cal, middle, and coronal third, respectively. 

With regard to the number of accessory 

canals per tooth, 17% and 6% of teeth have 

one or two accessory canals (Kirkham 1975). 

Despite these anatomical considerations, the 

prevalence of periodontal disease associated 

with accessory canals seems to be relatively 

low (Rotstein and Simon 2004).

In multi‐rooted teeth, furcation dentine 

might represent a communication pathway 

between endodontium and periodontium. In 

fact, the vascular system of the pulp is con-

nected to that of periodontium through the 

accessory canals. At the furcation, their 

 prevalence generally ranges from 23 to 76% 

(Lowman et al. 1973; Burch and Hulen 1974; 

Goldberg et al. 1987), but the extension rarely 

covers the entire distance between the pulp 

chamber and the furcation floor (Goldberg 

et al. 1987) and only 30–60% of molars have 

patent canals connecting the main root canal 

system and the periodontal ligament (see 

Figure  4.1). In particular, mandibular molars 

have a higher incidence (56%) than maxillary 

(48%) (Lowman et  al. 1973; Gutmann 1978; 

Vertucci 2005). Because of these interconnec-

tions, pulp inflammation might have  detrimental 

consequences on the furcation by inducing 

inflammatory responses on the inter‐radicular 

periodontal tissues (Seltzer et al. 1963).

4.2.3  Apical Foramen or Foramina

The major connections between periodontal 

and pulp tissues are the apical foramina. The 

(a)

(b)

(c)

(d)

Figure 4.1 

Accessory canal located distally to the mesial root on 4.6 (LR6) (a). Interradicular radiolucency on 

3.6 (LL6) (b). After root canal therapy, the accessory canal located distally to the mesial root was filled with 

cement (c). Complete remineralization after four‐year follow‐up (d).

Chapter 4

58

morphology of the apex might be quite varia-

ble. All the teeth have at least one accessory 

foramen. Generally, there are fewer primary 

dentinal tubules in the apical root third than 

in the coronal dentine. Their direction and 

density might be somewhat irregular, and 

some areas can be completely free of tubules 

(Mjör et al. 2001). Maxillary premolars have 

the most complicated apical morphology with 

the largest accessory foramina, followed by 

maxillary and mandibular molars (Marroquin 

et al. 2004), and this makes the prognosis of 

endodontic therapy in premolars and molars 

more uncertain than for other teeth.

4.2.4 Non‐physiological 

Communications

Root perforation, vertical root fracture, and 

inflammatory root resorption are artificial 

pathways between periodontal and pulpal 

tissues.

Iatrogenic root canal perforations are 

 serious complications that originate from 

manual/rotatory instrumentation or post‐

space preparation, and can threaten the 

prognosis of the tooth (Tsesis et  al. 2010; 

Gorni et  al. 2016). The treatment outcome 

depends on several factors that should be 

evaluated early, such as the size and position 

of the root  perforation, the time elapsed 

before making the diagnosis and treatment, 

the degree of periodontal involvement, and 

the sealing ability and biocompatibility of the 

sealant. The faster the sealing, the more con-

trolled the infection. Hence, time elapsed 

before treatment seems to be crucial for 

 

success. Among sealants, reinforced zinc 

oxide‐eugenol cements and bioceramic mate-

rials, such as mineral trioxide aggregate, are 

used most for this purpose (Weldon et  al. 

2002; Parirokh and Torabinejad 2010; 

Haapasalo et al. 2015; Gorni et al. 2016).

Vertical root fractures (see Figures 4.2 and 

4.3) are generally caused by loading trauma 

and occur more frequently in non‐vital teeth 

(Chan et al. 1999; Sugaya et al. 2015). In vital 

teeth, vertical fractures can initiate coronally 

in ‘cracked tooth syndrome’ (Cameron 1964) 

or can involve the root only (Chan et al. 1999; 

Sugaya et al. 2015). While in the past endo-

dontically treated teeth were considered to 

be weaker due to structural changes in den-

tine composition, such as water and collagen 

cross‐linking loss, currently it is believed that 

the greater brittleness is linked to the loss of 

structural integrity. In fact, the extension 

of cavity access might influence the degree of 

cuspal deflection during function, increasing 

the risk of fracture. Furthermore, a history of 

extensive restorations, especially in mandib-

ular posterior teeth, might make the tooth 

even more susceptible to fracture, especially 

in elderly patients (Lewinstein and Grajower 

1981; Huang et al. 1992; Cheron et al. 2011; 

Faria et al. 2011).

Root resorption is a pathological process 

associated with dentine, cementum, and/or 

(a)

(b)

Figure 4.2 

Vertical root fracture starting from the apex on 2.7 (UL7). The lesion resembled an endodontic 

infection (a). Complete failure after two years follow‐up (b). Root resection was not possible due to 

unfavourable anatomy.

The Endodontist’s View 59

bone loss. It can be external or internal, 

depending on whether the origin is the peri-

odontium or the pulp. The aetiopathogenesis 

is far from being completely understood. 

Mechanical and infective factors such as 

orthodontic treatment, trauma, intracoronal 

bleaching, periodontitis, and thermal stimuli 

might be considered as predisposing factors. 

The presence of profuse bleeding on prob-

ing, granulation tissue, and hard cavity 

 bottom might confirm the diagnosis of exter-

nal inflammatory root resorption. Electric 

and cold pulp tests might be positive. 

However, sensitivity tests alone do not differ-

entiate this pathological process from dental 

caries or internal resorption. Radiographic 

evaluation reveals that the canal profile is 

well defined in internal resorption, and 

rather undefined and faded in external. 

External resorption progression (see 

Figure  4.4) can lead to the invasion of the 

pulp space as a last resort. Likewise, untreated 

internal resorption can establish a communi-

cation between endodontium and periodon-

tium by breaking the external root surface 

(Tronstad 1988; Trope 1998; Andreasen and 

Andersson 2007; Patel et al. 2010).

4.3   Bacteria Involved in 

Endodontic‐periodontal Disease

Periodontal diseases are mixed anaerobic 

infections, modulated by a complex interplay 

between local and host factors (Page 1999). 

Similarly, endodontic infection has an anaer-

obic nature. Most of the species found in 

infected root canals are also present in perio-

dontal pockets. However, the endodontic 

 biofilm seems to be less complex than the 

periodontal biofilm (Trope et  al. 1988; 

Kobayashi et  al. 1990; Sundqvist 1994; 

Kurihara et  al. 1995; Zehnder et  al. 2002). 

Root canal infection is a dynamic process, 

and different bacterial species can apparently 

prevail at different stages. The most prevalent 

named species detected in primary endodon-

tic infections, including abscessed cases, 

belong to diverse genera of Gram‐negative 

(Fusobacterium,  Dialister,  Porphyromonas, 

Prevotella, 

Tannerella, 

Treponema, 

Campylobacter, and Veillonella) and Gram‐

positive bacteria (Parvimonas,  Filifactor, 

Pseudoramibacter,  Olsenella,  Actinomyces, 

Peptostreptococcus,  Streptococcus,  Propioni­

bacterium, and Eubacterium). Conversely, 

the microflora changes if endodontic therapy 

fails. Several culture and molecular biology 

studies revealed that Enterococcus faecalis is 

the most frequent species in root canal–

treated teeth, with a prevalence of up to 90% 

of cases and a strong association with persis-

tent infections (Rôças et al. 2004; Mohammadi 

et  al. 2013). Canals that are apparently well 

treated might contain from 1 to 5 bacterial 

species; however, in those not properly 

treated, the number might vary from 10 to 30, 

which is very similar to that of untreated 

canals (Sundqvist et al. 1998; Pinheiro et al. 

2003; Sakamoto et al. 2008).

(a)

(b)

(c)

Figure 4.3 

Vertical fracture of the distal root on 3.6 (LL6) (a). Rizectomy of the distal root (b) and after healing (c).

Chapter 4

60

4.4   Relationship  Between 

Periodontal Disease and 

Histological Pulp Changes

Many controversies still exist about the rela-

tionship between periodontal inflammation 

and pulp health (see Table  4.1). However, it 

seems to be widely accepted that periodontitis 

and periodontal therapy can induce pathologi-

cal changes in the pulp. Periodontal disease 

progression can lead to the exposure and bacte-

rial contamination of the accessory canals, 

more frequent in the apical third of the tooth 

and at the furcation (Seltzer et al. 1963; Rubach 

and Mitchell 1965), or it can reach the root 

apex with subsequent neuro‐vascular bundle 

damage (Langeland et al. 1974; De Deus 1975). 

Cementum removal, resulting from scaling and 

root planing, can expose the dentinal tubules 

and accessory canals (Adriaens et  al. 1988), 

therefore the micro‐organisms can migrate 

towards the pulp, inducing hystological 

changes (Rubach and Mitchell 1965; see 

Figure 4.5). However, the deposition of repara-

tive dentine (Bergenholtz and Lindhe 1978; 

Nilvéus and Selvig 1983; Hattler and Listgarten 

1984), the outward movement of the dentinal 

fluid (Vongsavan and Matthews 1991, 1992; 

Pashley et  al. 2002), the presence of odonto-

blast processes in the tubules (Nagaoka et al. 

1995; Pasley et al. 2002), and the presence of 

antibodies and anti‐microbial components 

within the dentinal fluid (Hahn and Overton 

1997) can act as a defense system, preventing 

the bacteria from reaching the pulp. In refer-

ence to this, we should stress that, as mentioned 

in Chapter 3, subgingival debridement is now 

moving away from the concept of ‘root planing’ 

and ‘removal of all diseased cementum’ (Aleo 

et al. 1974) towards an emphasis on disruption 

of the subgingival biofilm, with minimal altera-

tion to the cementum (Nibali et al. 2015).

Figure 4.4 

Disto‐lingual external progressive root resorption on 4.7 (LR7). Initally, the invisible resorption 

induced pulpitis and root canal therapy was performed.

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Page Number: 61

  Table 4.1   

 Effect of periodontal disease on pulp tissue. 

Do progressive periodontitis and periodontal 
treatment affect the pulp?

Pulp damage

Pulp response    

Progressive 

periodontal 

disease

Yes

  Apex 

 Apical foramen 

 (Langeland et al.   1974  ; 

Harrington et al.   2002  ; 

Sheykhrezaee et al.   2007  ; 

Aguiar et al.   2014  ; Rathod 

et al.   2014  ) 

 Neuro‐vascular 

bundle damage 

 Main canal involved 

Irreversible

 Inflammatory 

 Degenerative 

 (Rubach and Mitchell   1965  ; Zehnder   2001  ; 

Sheykhrezaee et al.   2007  ; Aguiar et al.   2014  ; 

Rathod et al.   2014  ) 

Complete necrosis  

 Apical root third 

 (Rubach and Mitchell   1965  ; 

Adriaens et al.   1988  ; 

Sheykhrezaee et al.   2007  ; 

Zuza et al.   2012  ) 

Bacteria and toxins 

migrate towards the 

pulp through the 

accessory canals

 Irreversible 

 or 

 Reversible 

 Inflammatory 

 Degenerative 

 (Rubach and Mitchell   1965  ; Sheykhrezaee et al. 

  2007  ; Rathod et al.   2014  ) 

 Fibrosis 

 Calcification 

 Inflammation 

 Odontoblast integrity loss 

 Neuro‐vascular alteration 

 Partial/complete necrosis   

 Furcation 

 (Rubach and Mitchell   1965  ; 

Bender and Seltzer   1972  ; 

Adriaens et al.   1988  ; Zuza 

et al.   2012  ) 

 Reparative 

 (Mazur and Massler   1964  ; Bender and Seltzer 

  1972  ; Langeland et al.   1974  ; Lantelme et al. 

  1976  ; Bergenholtz and Lindhe   1978  ; Ross and 

Thompson   1978  ; Czarnecki and Schilder   1979  ; 

Torabinejad and Kiger   1985  ; Cortellini and 

Tonetti   2001  ; Harrington et al.   2002  ; Aguiar 

et al. 2014) 

 Calcification 

 Fibrosis 

 Vascular 

alteration 

 Nerve 

alteration 

≈ pulp ageing  

Periodontal 

treatment 

(scaling and 

root planing)

 Yes 

 (Rubach and Mitchell   1965  ; 

Adriaens et al.   1988  ) 

 Neuro‐vascular 

bundle damage 

 Main canal involved 

Irreversible

 Inflammatory 

 Degenerative 

 (Rubach and Mitchell   1965  ; Sheykhrezaee et al. 

  2007  ; Rathod et al.   2014  ) 

Complete necrosis  

(Continued )

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Page Number: 62

Do progressive periodontitis and periodontal 
treatment affect the pulp?

Pulp damage

Pulp response    

Cementum removal: 

bacteria and toxins 

migrate towards the 

pulp through the 

accessory canals and 

the exposed dentinal 

tubules

 Irreversible 

 or 

 Reversible 

 Inflammatory 

 Degenerative 

 (Rubach and Mitchell   1965  ; Sheykhrezaee et al. 

  2007  ; Rathod et al.   2014  ) 

 Fibrosis 

 Calcification 

 Inflammation 

 Odontoblast integrity loss 

 Vascular alteration 

 Partial/complete necrosis   

 Reparative 

 (Mazur and Massler   1964  ; Bender and Seltzer 

  1972  ; Langeland et al.   1974  ; Lantelme et al.   1976  ; 

Bergenholtz and Lindhe   1978  ; Ross and 

Thompson   1978  ; Czarnecki and Schilder   1979  ; 

Torabinejad and Kiger   1985  ; Cortellini and 

Tonetti   2001  ; Harrington et al.   2002  ; Aguiar et al. 

  2014  ) 

 Calcification 

 Fibrosis 

 Vascular 

alteration 

 Nerve 

alteration 

≈ pulp ageing  

 No 

 (Bergenholtz and Lindhe 

  1978  ; Nilvéus and Selvig 

  1983  ; Hattler and 

Listgarten   1984  ; Nagaoka 

et al.   1995  ; Hahn and 

Overton   1997  ; Pashley 

et al.   2002  ) 

No bacteria and 

toxins migrate 

towards the pulp 

through the 

accessory canals and 

the exposed dentinal 

tubules

Reversible

 Reparative dentine (Bergenholtz and Lindhe   1978  ; Hattler and Listgarten   1984  ; 

Vongsavan and Matthews   1991  ) 

 + 

 Dentinal fluid (Vongsaven and Matthews 1991, 1992; Pashley et al.   2002  ) 

 + 

 Odontoblast processes (Nagaoka et al.   1995  ; Pashley et al.   2002  )   
 Antibodies/antimicrobial components within the dentinal fluids 

 (Hahn and Overton   1997  ) 

Table 4.1 

(Continued)

The Endodontist’s View 63

Pulp response might vary, from normal 

(Mazur and Massler 1964; Smukler and 

Tagger 1976; Czarnecki and Schilder 1979; 

Torabinejad and Kiger 1985) to reparative 

(Mazur and Massler 1964; Langeland et  al. 

1974; Czarnecki and Schilder 1979; 

Torabinejad and Kiger 1985; Harrington 

et  al. 2002) or degenerative (Rubach and 

Mitchell 1965; Sheykhrezaee et  al. 2007; 

Zuza et al. 2012; Aguiar et al. 2014; Rathod 

et al. 2014). Repaired vital pulp is calcificated, 

fibrotic, and has fewer blood vessels and 

nerve fibres (Mazur and Massler 1964; 

Langeland et al. 1974; Czarnecki and Schilder 

1979; Torabinejad and Kiger 1985; Harrington 

et  al. 2002). Conversely, degenerated pulp 

exhibits fibrosis, calcification, inflammation, 

vascular alteration, loss of odontoblast integ-

rity, and partial necrosis (Rubach and 

Mitchell 1965; Aguiar et  al. 2014; Rathod 

et al. 2014). Complete necrosis seems to only 

occur if the apical neuro‐vascular bundle is 

involved (Langeland et  al. 1974; Zehnder 

2001; Harrington et  al. 2002; Sheykhrezaee 

et al. 2007; Aguiar et al. 2014; Rathod et al. 

2014).

The lack of randomized clinical trials with 

test and control groups prevents a clear asso-

ciation between progressive periodontal 

 disease and pulp alterations being established. 

Data have to be carefully interpreted, since 

pulpal alterations might be the result of multi-

ple factors, such as periodontal disease, history 

of caries, physiological pulp ageing, previous 

ignored trauma, or pulp tissue fixation. Indeed, 

pulp fixation is challenging and artifacts result-

ing from improper specimen preparation 

might lead to misjudgements (Harrington 

et al. 2002; Sheykhrezaee et al. 2007).

At the current stage of scientific knowl-

edge, we could summarize that periodontal 

disease might induce reparative or degenera-

tive pulp changes. Pulp necrosis is rather rare 

and occurs when the defect is up to the apical 

third of the tooth and the neuro‐vascular 

bundle is involved. If the blood supply 

through the apical foramen remains intact, 

the pulp is usually able to withstand the 

physiological insults induced by both perio-

dontal disease and therapy.

4.5   Endodontic‐periodontal 

Disease

Because of their anatomical and functional 

interconnection, pulp and periodontium can 

be simultaneously affected in what appears 

to be a single periodontal lesion. This clinical 

scenario, known as ‘endodontic‐periodontal 

lesion’ (Bergenholtz and Hasselgreen 2008) 

was first described by Simring and Goldberg 

in 1964.

4.5.1 Classification

Despite the many attempts to classify endo-

dontic‐periodontal lesions, the Simon, Glick, 

and Frank (1972) classification remains the 

most widely accepted point of reference (see 

Figure 4.5 

Pulp necrosis on 3.6 (LL6) after deep root debridement. Source: Courtesy Dr Cristiano Luciano.

Do progressive periodontitis and periodontal 
treatment affect the pulp?

Pulp damage

Pulp response    

Cementum removal: 

bacteria and toxins 

migrate towards the 

pulp through the 

accessory canals and 

the exposed dentinal 

tubules

 Irreversible 

 or 

 Reversible 

 Inflammatory 

 Degenerative 

 (Rubach and Mitchell   1965  ; Sheykhrezaee et al. 

  2007  ; Rathod et al.   2014  ) 

 Fibrosis 

 Calcification 

 Inflammation 

 Odontoblast integrity loss 

 Vascular alteration 

 Partial/complete necrosis   

 Reparative 

 (Mazur and Massler   1964  ; Bender and Seltzer 

  1972  ; Langeland et al.   1974  ; Lantelme et al.   1976  ; 

Bergenholtz and Lindhe   1978  ; Ross and 

Thompson   1978  ; Czarnecki and Schilder   1979  ; 

Torabinejad and Kiger   1985  ; Cortellini and 

Tonetti   2001  ; Harrington et al.   2002  ; Aguiar et al. 

  2014  ) 

 Calcification 

 Fibrosis 

 Vascular 

alteration 

 Nerve 

alteration 

≈ pulp ageing  

 No 

 (Bergenholtz and Lindhe 

  1978  ; Nilvéus and Selvig 

  1983  ; Hattler and 

Listgarten   1984  ; Nagaoka 

et al.   1995  ; Hahn and 

Overton   1997  ; Pashley 

et al.   2002  ) 

No bacteria and 

toxins migrate 

towards the pulp 

through the 

accessory canals and 

the exposed dentinal 

tubules

Reversible

 Reparative dentine (Bergenholtz and Lindhe   1978  ; Hattler and Listgarten   1984  ; 

Vongsavan and Matthews   1991  ) 

 + 

 Dentinal fluid (Vongsaven and Matthews 1991, 1992; Pashley et al.   2002  ) 

 + 

 Odontoblast processes (Nagaoka et al.   1995  ; Pashley et al.   2002  )   
 Antibodies/antimicrobial components within the dentinal fluids 

 (Hahn and Overton   1997  ) 

Table 4.1 

(Continued)

Chapter 4

64

also Gargiulo 1984; Guldener 1985; Abbott 

and Salgado 2009; Kerns and Glickman 

2011). According to Simon et al., endodon-

tic‐periodontal lesions are classified as:

 

●

Primary endodontic lesion.

 

●

Primary periodontal lesion.

 

●

Primary endodontic lesion with secondary 

periodontal involvement.

 

●

Primary periodontal lesion with secondary 

endodontic involvement.

 

●

True combined lesion.

4.5.1.1  Primary Endodontic Lesion

Primary endodontic lesions (Box  4.1 and 

Table 4.2) mostly involve decayed, restored, or 

traumatized teeth. As a result of the endodon-

tic inflammatory process, bone resorption 

occurs at the apex, along the lateral aspect of 

the root, or at the furcation area when multi‐

rooted teeth are affected (see Figures 4.6 and 4.7). 

Because of the suppurative process, the sinus 

tract can develop through the periodontal lig-

ament space or the cortical bone in accord-

ance with the locus minoris resistentiae (place 

of least resistance) principle. For multi‐rooted 

teeth, the tract can drain off into the furcation 

area, resembling a class III periodontal defect.

Pain, tooth mobility, tenderness to pres-

sure and percussion, and periodontal 

abscess‐like swelling can be the related clini-

cal inflammatory signs.

Sensitivity tests show necrotic pulp, even 

though in multi‐rooted teeth the response 

can be positive because of the partial necrosis. 

As the lesion has an endodontic origin, root 

canal treatment (European Society of 

Endodontology 2006) is mandatory for sinus 

tract resolution without any associated peri-

odontal therapy (Zehnder et  al. 2002; 

Bergenholtz and Hasselgreen 2008; Shenoy 

and Shenoy 2010; Kerns and Glickman 2011). 

Sometimes, a period of up to four or five 

years might be required for the complete 

radiographic healing of the periapical lesion 

(Ng et  al. 2007; Zitzmann et  al. 2009). 

Incongruous root canal treatment or 

untreated canals (i.e. MB2 in first maxillary 

molars or D2 in lower molars) might prevent 

the lesion from healing, because of the 

high  residual bacterial load within the 

endodontium.

4.5.1.2  Primary Periodontal Lesion

Periodontitis (Box 4.2 and Table 4.3) is a pro-

gressive inflammatory process that starts in 

the sulcus and moves towards the apex due 

to the accumulation of plaque and calculus 

on the root surface. The final effect is the loss 

of alveolar bone and supporting tissues 

around the teeth. This process can also be 

accompanied by periodontal abscess in the 

acute phases of the disease (Toto and 

Gargiulo 1970; Hoffman and Gold 1971). 

Clinical examination reveals soft‐tissue 

inflammation, tooth mobility, bleeding on 

probing, and the presence of wide pockets 

(i.e. accessible at different points on the 

Box 4.1  Primary endodontic lesion.

 

●

Tooth history: caries, cracks, extensive restoration, crown or bridge abutment, incongruous 
root canal treatment, dental trauma,* root resorption.**

 

●

Root surface: smooth on probing. No presence of subgingival calculus.

 

●

Pocket conformation: narrow if the pocket is present.

 

●

Sensitivity pulp test response: generally negative. However, it might be positive in multi‐rooted 
teeth.

 

●

Radiographic sign: lateral, apical and/or inter‐radicular radiolucency.

 

●

Treatment: root canal treatment.

* Post‐traumatic pulp healing, especially after luxation injuries, is characterized by temporary loss of sensitivity. 
All sensitivity tests show low reliability right after the trauma (Bastos et al. 2014).
** Root resorption might affect the external surfaces of the tooth (external resorption) or the internal dentine (inter-
nal resorption) after being started in the periodontium or within the pulp space, respectively.

The Endodontist’s View 65

Table 4.2 

Primary endodontic lesions.

Diagnostic Elements

Findings

Clinical Management

Presence of caries/restorations/cracks

+

Anamnesis

Clinical examination

Periodontal probing

Radiographic examination

Sensitivity tests

Endodontic treatment

Re‐evaluation after a few months

Subgingival calculus

−

History of trauma

+/−

Abscess

+*

Narrow deep pocket

+/−

Bleeding on probing

−

Thermal test

−/+**

Electric test

−/+**

Radiolucency

+

Mobility

+/−

Palpation test

+

Percussion test

+

* In the acute phase.

** The test is negative if all the pulp tissue is necrotic, except in case of gases‐related thermal expansion.

The test could be positive in case of partial necrosis.
Differential Diagnosis

Vertical root fractures

Primary periodontal lesions

Favourable Endodontic

Prognostic Factors

Congruous endodontic treatment

No symptoms

No probing within 30 days

Fistular track closure within 30 days

Radiolucency improvement within 6 months

Source: Adapted from AIE – Collana di Monografie Piccin Nuova Libraria S.p.A 2014.

Figure 4.6 

Pulpitis on 3.6 (LL6). Inter‐radicular and periapical radiolucencies due to bacterial toxins. Five‐year 

follow‐up after root canal therapy.

Chapter 4

66

tooth) supported by plaque and calculus 

along the root. It should be noted that perio-

dontal pockets might also originate from 

anomalies in the root development (Rotstein 

and Simon 2004). During the diagnostic 

phase, pulp sensitivity tests generally reveal 

positive responses. However, negative 

responses can also be recorded and do not 

necessarily account for pulp necrosis. Owing 

to dystrophic calcifications, the pulp space 

might be reduced and the tooth might not 

respond to the sensitivity tests despite its 

vitality (Abou‐Rass 1982).

On the basis of the previous considera-

tions, the prognosis would mainly depend on 

the extension of the periodontal disease, the 

outcome of the periodontal therapy, and the 

patient’s ability to comply with potential 

long‐term maintenance (Bergenholtz and 

Hasselgreen 2008; Kerns and Glickman 

2011).

Primary Endodontic Lesion with Secondary 
Periodontal Involvement

Periodontal pathogens might induce perio-

dontitis by migrating apically into the patent 

sinus tract when the endodontic infection is 

not treated or persists after root canal ther-

apy. At the radiographic evaluation, angular 

intrabony or inter‐radicular osseous defects 

are appreciated. Plaque and calculus are 

detected on probing, therefore healing 

requires both endodontic and periodontal 

therapies for necrotic pulp removal and root 

debridement. Since root canal treatment 

resolves only a part of the defect (European 

Society of Endodontology 2006; Shenoy and 

Shenoy 2010), dental prognosis relies on the 

extent and severity of the osseous defect, and 

on the efficacy of the periodontal therapy.

For suppurative processes fistulizing 

through the cortical bone, bacteria from the 

oral cavity might colonize first the fistula and 

Box 4.2  Primary periodontal lesion.

 

●

Tooth history: periodontal pocket, attach-
ment loss, bleeding on probing.

 

●

Root surface: rough on probing because 
of subgingival plaque and calculus.

 

●

Pocket conformation: wide, often multiple 
pockets.

 

●

Sensitivity pulp test response: generally 
positive.

 

●

Radiographic sign: lateral and/or inter‐
radicular radiolucency, apical radiolu-
cency in advanced disease.

 

●

Treatment: oral hygiene instructions (OHI) 
and root debridement.

Figure 4.7 

Primary endodontic lesion with inter‐radicular and apical involvement on 4.6 (LR6). No furcation 

probing after three months and partial healing after one‐year follow‐up.

The Endodontist’s View 67

then the apex, affecting the tooth prognosis. 

Primary endodontic lesion with secondary 

periodontal involvement (Box  4.3 and 

Table 4.4) might also occur in endodontically 

treated teeth because of root perforation 

and/or fracture. Once the communication 

between endodontium and periodontium is 

established, the secondary periodontal lesion 

can develop as a result of the micro‐organ-

isms’ migration from the root canal to the 

periodontium.

The clinical signs may range from local 

periodontal pocket deepening to abscess for-

mation associated with pain, exudate, and 

tooth mobility. In single‐rooted teeth, the 

prognosis is usually poor if the defect is close 

to the apex. In multi‐rooted teeth, the prog-

nosis might be better, since the tooth can be 

maintained by resecting the affected root, if 

the anatomy is indicated for this procedure 

Table 4.3 

Primary periodontal lesions.

Diagnostic Elements

Findings

Clinical Management

Presence of caries/restorations/cracks

+/−

Anamnesis

Clinical examination

Periodontal probing

Radiographic examination

Sensitivity tests

Splinting of mobile teeth (if needed)

Oral hygiene instructions and periodontal 

non‐surgical therapy

Periodontal re‐evaluation after a few months

Periodontal surgical therapy (if needed)

Subgingival calculus

+

History of trauma

+/−

Abscess

+*

Wide, not isolated, deep pocket/furcation

+

Bleeding on probing

+

Thermal test

+

Electric test

+

Lateral/interradicular radiolucency

+

Mobility

+

Palpation test

+*

Percussion test

+*

* In the acute phase.
Differential Diagnosis

Endodontic‐periodontal lesions

Favourable

Prognostic Factors

No symptoms

Pulpal vitality

No bleeding on probing

Probing pocket depth reduction

Mobility reduction

Radiographic bone remineralization in the apical part 

of the defect

Source: Adapted from AIE – Collana di Monografie Piccin Nuova Libraria S.p.A 2014.

Box 4.3  Primary endodontic lesion 
with secondary periodontal involvement.

 

●

Tooth history: caries, cracks, extensive 
 restoration, crown or bridge abutment, 
incongruous root canal treatment, dental 
trauma.

 

●

Root surface: rough on probing because 
of subgingival plaque and calculus.

 

●

Pocket conformation: narrow to wide, 
depending on the exposition time 
of  the sinus tract to periodontal 
pathogens.

 

●

Sensitivity pulp test response: negative.

 

●

Radiographic sign: lateral, apical, and/or 
inter‐radicular radiolucency.

 

●

Treatment: root canal treatment, oral 
hygiene instructions (OHI), and root 
debridement.

Chapter 4

68

(Cameron 1964; Chan et  al. 1999; Zehnder 

et  al. 2002; Sunitha et  al. 2008; Kerns and 

Glickman 2011; Sugaya et al. 2015; see also 

Chapter 8).

Primary Periodontal Lesion with Secondary 
Endodontic Involvement

Primary periodontal lesion with secondary 

endodontic involvement (Box  4.4 and 

Table  4.5) differs from primary endodontic 

lesion with secondary periodontal involve-

ment only in the temporal sequence of the 

disease processes. If periodontitis remains 

untreated, periodontal pathogens can reach 

the pulp through the accessory canals or 

Table 4.4 

Primary endodontic lesions with secondary periodontal involvement.

Diagnostic Elements

Findings

Clinical Management

Presence of caries/restorations/cracks

+

Anamnesis

Clinical examination

Periodontal probing

Radiographic examination

Sensitivity tests

Splinting of mobile teeth (if 

needed)

Oral hygiene instructions and 

non‐surgical periodontal therapy

§

Endodontic treatment

Re‐evaluation after a few months

Surgical periodontal therapy (if 

needed)

Subgingival calculus

+

History of trauma

+/−

Abscess

+*

Narrow to wide deep pocket

+

Bleeding on probing

+

Thermal test

−

Electric test

−

Radiolucency

+

Mobility

+

Palpation test

+

Percussion test

+

* In the acute phase

§

 Deep Root Debridement Should Be Avoided Before Determining The Endodontic 

Component Of The Defect (See Section 4.5.3)

Differential Diagnosis

Primary periodontal lesion with secondary endodontic 

involvement

Vertical root fracture

Root/furcation perforation in endodontically treated 

teeth

Favourable Endodontic

Prognostic Factors

Congruous endodontic treatment

No symptoms

Partial probing depth reduction within 30 days

Fistular track closure within 30 days

Mobility reduction

Partial radiolucency improvement within 6 months

Source: Adapted from AIE – Collana di Monografie Piccin Nuova Libraria S.p.A 2014.

Box 4.4  Primary periodontal lesion with 
secondary endodontic involvement.

 

●

Tooth history: probing pocket depth 
deepening, bleeding on probing.

 

●

Root surface: rough on probing because 
of subgingival plaque and calculus.

 

●

Pocket conformation: wide, often multiple 
pockets.

 

●

Sensitivity pulp test response: generally 
negative.

 

●

Radiographic sign: lateral, apical, and/or 
inter‐radicular radiolucency.

 

●

Treatment: root canal treatment, oral hygiene 
instructions (OHI), and root debridement.

The Endodontist’s View 69

 apical foramina. Pulp necrosis occurs and an 

endodontic‐periodontal lesion develops 

(Rubach and Mitchell 1965; Aguiar et  al. 

2014). Periodontal therapy can also lead to 

secondary pulp involvement. By exposing 

lateral canals and dentine during scaling and 

root planing or surgical flap procedures, 

blood supply might be interrupted and 

micro‐organisms might penetrate into the 

tubules, resulting in pulp inflammation and/

or necrosis (Adriaens et al. 1988).

To differentiate between endodontic‐ 

periodontal lesions with primary periodontal 

and endodontic origin, anamnesis and 

 clinical examination have to be exhaustively 

performed (see Figure  4.8). A history of 

 generalized periodontitis might suggest a 

primary periodontal origin. The number and 

conformation of pockets can help in the 

diagnosis. Wider or narrower defects gener-

ally suggest a periodontal or endodontic 

 origin of the lesions, respectively (Zehnder 

et  al. 2002; Sunitha et  al. 2008; Kerns and 

Glickman 2011). In addition, periodontal 

probing may reveal the presence of calculus 

on the root surface. Pulp sensitivity tests are 

generally negative when the endodontium is 

involved, whereas the radiographic evalua-

tion does not prove the primary origin of the 

lesion.

Once the endodontic therapy is properly per-

formed (European Society of Endodontology 

Table 4.5 

Primary periodontal lesions with secondary endodontic involvement.

Diagnostic Elements

Findings

Clinical Management

Presence of caries/restorations/cracks

+/−

Anamnesis

Clinical examination

Periodontal probing

Radiographic examination

Sensitivity tests

Splinting of mobile teeth (if 

needed)

Oral hygiene instructions and 

non‐surgical periodontal therapy

§

Endodontic treatment

Periodontal re‐evaluation after a 

few months

Surgical periodontal therapy (if 

needed)

Subgingival calculus

+

History of trauma

+/−

Abscess

+*

Not isolated, wide deep pocket/furcation

+

Bleeding on probing

+

Thermal test

−**

Electric test

−**

Lateral/apical/inter‐radicular radiolucency

+

Mobility

+

Palpation test

+

Percussion test

+

* In the acute phase.

** The test is negative if all the pulp tissue is necrotic, except in case of gases‐related thermal expansion.

The test could be positive in the case of partial necrosis.

§

 Deep Root Debridement Should Be Avoided Before Determining The Endodontic Component of 

The Defect (See Section 4.5.3)
Differential Diagnosis

Primary endodontic lesions with secondary periodontal 

involvement

Favourable Endodontic

Prognostic Factors

Congruous endodontic treatment

No symptoms

Partial probing depth reduction within 30 days

Fistular track closure within 30 days

Mobility reduction

Partial radiolucency improvement within 6 months

Source: Adapted from AIE – Collana di Monografie Piccin Nuova Libraria S.p.A 2014.

Chapter 4

70

2006; Shenoy and Shenoy 2010), clinical  success 

basically depends on the outcome of the 

 periodontal therapy and the patient’s ability to 

comply with potential long‐term maintenance. 

As previously mentioned, multi‐rooted teeth 

might have a better prognosis than single‐

rooted teeth, since root resection represents an 

alternative for tooth survival.

True Combined Lesion

A true combined lesion (Box  4.5 and 

Table  4.6) means that the endodontic and 

periodontal infections simultaneously exist 

as independent, separated, or merging 

lesions. When the periodontal pocket deep-

ens up to the periapical lesion, the endodon-

tic and periodontal components of the defect 

are unidentifiable. Symptoms are similar to 

Figure 4.8 

Degree III furcation involvement on 4.6 (LR6) with progressive deepening of the defect and 

secondary pulp necrosis after 14 years. Root canal therapy led to resolution of the endodontic component of 

the defect. Besides scaling and root planing and oral hygiene instructions, no further periodontal treatment 

was performed.

Box 4.5  True combined lesions.

 

●

Tooth history: caries, cracks, extensive 
 restoration, crown or bridge abutment, 
incongruous root canal treatment, dental 
trauma, probing pocket depth deepen-
ing, bleeding on probing.

 

●

Root surface: rough on probing because 
of subgingival plaque and calculus.

 

●

Pocket conformation: wide and conical 
pocket.

 

●

Sensitivity pulp test response: negative.

 

●

Radiographic signs: communicating or 
non‐communicating extensive apical, lat-
eral, and/or inter‐radicular radiolucencies.

 

●

Treatment: root canal treatment, oral hygiene 
instructions (OHI), and root debridement.

The Endodontist’s View 71

those previously mentioned for the com-

bined lesions with primary endodontic or 

periodontal origin. The radiographic evalua-

tion shows extensive osseous radiolucencies, 

communicating or not, similar to those of 

vertically fractured teeth. Indeed, pulp space 

invasion through vertical root fracture might 

also be considered as a true combined lesion.

Prior to endodontic therapy, mobile teeth 

should be splinted and carefully debrided. 

Once the root canal treatment is properly per-

formed (European Society of Endodontology 

2006), the endodontic component of the 

defect is expected to heal within a couple of 

months (Shenoy and Shenoy 2010; see 

Figure  4.9). Tooth prognosis would entirely 

depend on both the periodontal pocket depth 

and the related periodontal therapy. Uncertain 

prognosis concerns more single‐rooted that 

multi‐rooted teeth, since root resection might 

be a treatment option if not all the roots are 

severely involved and tooth anatomy is indica-

tive for this procedure (Zehnder et al. 2002; 

Rotstein and Simon 2004; Sunitha et al. 2008).

4.5.2  Diagnosis of Endodontic‐

periodontal Disease

Diagnosis of endodontic‐periodontal lesions 

can be easily performed when the patient has 

been monitored over time. Similar clinical 

and radiographic findings might make the 

differential diagnosis somewhat challenging. 

To avoid any misinterpretation, comprehen-

sive information can be obtained through 

detailed anamnesis and clinical examination, 

and by the use of specific tests aimed to assess 

the vitality of the pulp. Primary endodontic 

Table 4.6 

True periodontal‐endodontic combined lesions.

Diagnostic Elements

Findings

Clinical Management

Presence of caries/restorations/cracks

+

Anamnesis

Clinical examination

Periodontal probing

Radiographic examination

Sensitivity tests

Splinting of mobile teeth (if needed)

Oral hygiene instructions and 

non‐surgical periodontal therapy

§

Endodontic treatment

Periodontal re‐evaluation after a 

few months

Surgical periodontal therapy (if 

needed)

Subgingival calculus

+

History of trauma

+/−

Abscess

+*

Not isolated, wide deep pocket/furcation

+

Bleeding on probing

+

Thermal test

−

Electric test

−

Lateral/apical/inter‐radicular radiolucency

+

Mobility

+

Palpation test

+

Percussion test

+

* It depends on whether the phase is acute or chronic.

§

 Deep Root Debridement Should Be Avoided Before Determining The Endodontic 

Component Of The Defect (see Section 4.5.3)

Differential Diagnosis

Vertical root fracture

Favourable Endodontic

Prognostic Factors

Congruous endodontic treatment

No symptoms

Partial probing depth reduction within 30 days

Fistular track closure within 30 days

Mobility reduction

Partial radiolucency improvement within 6 months

Source: Adapted from AIE – Collana di Monografie Piccin Nuova Libraria S.p.A 2014.

Chapter 4

72

lesions generally originate from infected and 

non‐vital pulp, whereas vital teeth are more 

characteristic of primary periodontal disease 

(Rotstein and Simon 2004; Bergenholtz and 

Hasselgreen 2008; Sunitha et al. 2008; Parolia 

et al. 2013).

4.5.2.1  Clinical Examination

Pulpal and periodontal diseases might have 

many clinical signs in common, such as gin-

gival swelling, pus discharge, probing, tooth 

mobility, and tenderness to percussion. Teeth 

have to be evaluated for caries, incongruous 

under‐ or over‐contoured restorations, loss 

of marginal seal, erosions, abrasions, cracks, 

and fractures. All these situations are more 

related to endodontic disease.

4.5.2.2 Palpation

Palpation is performed by applying firm dig-

ital pressure in correspondence with the 

root and the apex, with the index finger 

pressing the mucosa against the underlying 

cortical bone. A positive response might 

indicate an active periradicular inflamma-

tory process. However, this test does not 

indicate whether the origin is endodontic or 

periodontal. The test should be compared to 

control teeth.

4.5.2.3 Percussion

This test indicates the presence of periradic-

ular inflammation without revealing the 

 status of the pulp. An abnormal positive 

response shows inflammation of the perio-

dontal ligament, but it does not indicate 

whether the origin is endodontic or perio-

dontal. The test should be compared to 

 control  teeth.

4.5.2.4  Bite Test

This test does not disclose the condition of 

the pulp. However, it might be positive in 

vital teeth affected by cracked tooth syn-

drome (Cameron 1964) and in non‐vital 

teeth with periradicular inflammation.

4.5.2.5 Mobility

This clinical sign does not prove whether the 

origin of the lesion is primarily periodontal 

or endodontic. It might be speculated that its 

primary cause is periodontitis. In fact, tooth 

mobility depends on the amount and inflam-

mation of the residual supporting tissues. 

The greater the bone loss, the higher the 

mobility. However, periradicular oedema or 

trauma, with or without tooth fracture, can 

also lead to similar mobility (Biancu et  al. 

1995; Séguier et al. 2000).

Figure 4.9 

Class 3 inter‐radicular defect and concomitant decay of the furcation roof on 4.7 (LR7). The caries 

progression led to pulp necrosis. Tunnelling spontaneously occurred after non‐surgical periodontal treatment. 

One‐year follow‐up after root canal therapy.

The Endodontist’s View 73

4.5.2.6  Fistula Tracking

Endodontic and periodontal diseases can 

lead to the formation of a fistulous sinus 

track. Following a minor resistance path, 

inflammatory exudate drains off into the oral 

mucosa through the attached buccal gingiva 

or the vestibule. The track is generally more 

representative of the endodontic infection 

rather than the periodontal disease, which 

often drains through the periodontal pocket 

without any fistulous sinus track formation. 

Fistula tracking is performed by inserting a 

semirigid radiopaque material, commonly a 

gutta‐percha cone, into the sinus track until 

resistance is met (see Figure 4.10). A radio-

graph is taken to identify the course of the 

sinus tract and, therefore, the tooth involved.

4.5.2.7  Cracked Tooth Testing

Cracked teeth (Cameron 1964) or vertical 

root fractures can be diagnosed through the 

observation of incomplete or complete 

cracks by transillumination. The fibre‐optic 

light source is directly placed on the cleaned 

tooth. Cracks can be appreciated with a mag-

nification source by evaluating the disrup-

tion of the light transmission (Liewehr 2001; 

Liewehr et  al. 2010). Unlike a vertical root 

fracture with a ‘tear‐shaped’ radiographic 

radiolucency, cracked teeth do not generally 

show any pathognomonic radiographic signs.

4.5.2.8 Radiographs

Despite the benefits of radiographs, consist-

ing in the detection of caries, over‐ or 

 

under‐ 

contoured restorations, pulp caps, 

periradicular radiolucencies, periodontal 

ligament widening, calculus, alveolar bone 

loss, and root fractures, this examination 

alone does not indicate whether the radiolu-

cency has an endodontic, periodontal, or any 

additional origin. It is important to consider 

that some other pathologies, such as cysts 

and neoplasia, can resemble periodontal or 

endodontic lesions in radiographic 

appearance.

Occlusal trauma may also lead to radio-

graphic radiolucencies on the lateral, apical, 

or inter‐radicular aspect of the root. In 

 periodontally involved teeth suffering from 

occlusal trauma, the amount of deminerali-

zation is not quantitatively reflected in the 

probing pocket depth, which is less deep 

than could be guessed radiographically. 

Occlusal adjustment might be necessary and 

must always precede any endodontic or 

 

periodontal therapy. Demineralization 

resolves within a few months when the 

occlusal interferences and the mobility are 

eliminated by grinding and splinting, respec-

tively [75,81,96,97] (Bergenholtz and 

Hasselgreen 2008; Carnevale et  al. 2008; 

Lindhe et al. 2008; Kerns and Glickman 2011; 

see Figures 4.11 and 4.12).

4.5.2.9  Pocket Probing

To assess whether the origin of the lesion is 

endodontic or periodontal, probing can be 

crucial in the diagnosis (Harrington and 

Steiner 2002). Defects are evaluated for 

(a)

(b)

Figure 4.10 

Fistulous sinus track between 1.6 (UR6) and 1.7 (UR7) (a). Fistula tracking revealed the origin of the 

endodontic infection on 1.7 (b).

Chapter 4

74

extent, severity, and shape by means of a 

 calibrated periodontal probe. The presence 

of plaque and calculus, detected by sounding 

the root surface with the tip of the probe, 

explains the periodontal involvement, 

although this may not be necessarily easy to 

detect. Primary periodontal lesions are fre-

quently characterized by wide calculus‐

induced defects in patients with further 

periodontal pockets, whereas primary endo-

dontic lesions typically show narrow solitary 

calculus‐free defects. Inter‐radicular involve-

ment without further signs of periodontal 

disease might indicate the endodontic origin 

of the lesion.

Periodontal probing can be considered as a 

prognostic indicator in the short term. In 

fact, early fistulous sinus track resolution 

after root canal therapy (Shenoy and Shenoy 

2010) might confirm the endodontic origin 

of the defect without any further concomi-

tant causes, such as vertical root fracture or 

periodontal involvement. On the contrary, a 

persisting sinus track might imply periodon-

tal involvement or unsolved endodontic 

infection (Harrington and Steiner 2002; 

Walton and Torabinejad 2002; Rotstein and 

Simon 2004).

4.5.2.10  Pulp Vitality Tests

Pulp vitality tests are very important to eval-

uate whether the lesion has an endodontic or 

periodontal origin (Walton and Torabinejad 

2002). The sensitivity rather than the vitality 

of the pulp is assessed through sensory nerve 

stimulation. Two different stimuli, electric 

and/or thermal (cold or hot), can be applied, 

and complaints and painful sensations are 

recorded. Figure 4.13 summarizes the diag-

nostic tests for pulp health assessment, and 

(a)

(b)

Figure 4.11 

Radiographic radiolucency on 3.6 (LL6) affected by secondary occlusal trauma without furcation 

involvement (a). Six‐month follow‐up after root debridement and occlusal adjustment (b). Source: AIE—Collana 

di Monografie Piccin Nuova Libraria S.p.A 2014, p. 139.

Figure 4.12 

Degree II furcation defect (lingual) on 3.6 (LL6) affected by secondary occlusal trauma. Being the 

possible result of jiggling movements, the apical radiolucency present on the mesial root disappeared after 

the occlusal adjustment. Twenty‐year follow‐up after non‐surgical periodontal therapy and oral hygiene 

instructions. Source: AIE—Collana di Monografie Piccin Nuova Libraria S.p.A 2014, p. 140.

The Endodontist’s View 75

Box 4.6 considers how sensitivity tests might 

be misinterpreted.

Vital teeth react to cold and hot stimuli by 

exhibiting short‐lasting sharp pain or mild 

heat sensation, respectively. Intense and 

long‐lasting painful reactions might indicate 

irreversible pulp changes. In molars, tissue 

degeneration might be limited to part of the 

pulp only (see Figure 4.14) and the reliability 

of the tests might be questioned, as false 

 negatives can be wrongly recorded (Abou‐

Rass 1982; Mejàre et al. 2012; Levin 2013). A 

lack of response is often associated with pulp 

necrosis (Rowe and Pitt Ford 1990; Peters 

et al. 1994).

Vital teeth react to an electric test by exhib-

iting tingling, slight discomfort, or a burning 

sensation. Scored values per se do not mean 

the presence or absence of pathology, since 

no general threshold for pulpal disease has 

been established so far. As a general rule, the 

higher the scored values, the higher the prob-

ability of irreversible pulpal alterations. To 

better assess the response, healthy teeth 

should be taken as controls. By comparing the 

values obtained at different follow‐up stages, 

more clinical information is provided for the 

diagnosis. However, false negatives and posi-

tives might make clinical evaluation some-

what challenging (Rotstein and Simon 2004; 

Gopikrishna et  al. 2007; Chen and Abbott 

2009; Jafarzadeh and Abbott 2010; Mejàre 

et al. 2012; Alghaithy and Qualtrough 2017).

Figure 4.13 

Diagnostic tests for pulp health assessment. Source: AIE—Collana di Monografie Piccin Nuova 

Libraria S.p.A 2014, pp. 266–268, 271.

Box 4.6  Clinical situations where pulp 
response to sensitivity tests might be 
misinterpreted.

 

●

Teeth with calcified root canals.

 

●

Multi‐rooted teeth with partially affected 
pulp.

 

●

Teeth with partial‐ or full‐coverage 
restorations.

 

●

Traumatized teeth.

 

●

Endodontically treated teeth with untreated 
canals.

Chapter 4

76

While a lack of response can be associated 

with pulp necrosis, exaggerated or misleading 

responses following cold or electric tests can 

be the result of pulpitis, patient anxiety, 

 dentinal hypersensitivity, trauma, or enamel‐

to‐dentine cracks (Abou‐Rass 1982; Eli 1993; 

Peters et al. 1994; Bastos et al. 2014). Cold and 

hot stimuli can respectively mitigate or exacer-

bate the symptoms in partially necrotic teeth.

Vital teeth with a history of deep caries, 

periodontitis, bruxism, or trauma may not 

respond to thermal or electrical stimuli 

because of the reparative changes in the pulp 

tissues (Bastos et  al. 2014). Partial‐ or full‐

coverage restorations can also act as a barrier 

to thermal and, to a lesser degree, electrical 

stimuli, preventing the pulp from being 

properly evaluated (Rowe and Pitt Ford 1990; 

Peters et  al. 1994; Myers 1998; Petersson 

et al. 1999).

The vitality rather than the sensitivity of 

the pulp can be assessed by measuring the 

pulp blood flow through laser doppler flow-

metry or similar procedures. Many investiga-

tions have been conducted to validate the 

efficacy of these tests. However, their clinical 

applicability is still questioned (Gopikrishna 

et al. 2007; Mejàre et al. 2012; Alghaithy and 

Qualtrough 2017).

4.5.2.11  Cavity Test

By drilling the cavity without anaesthetic, the 

pulp status can be objectively evaluated 

through patient‐referred symptoms. The so‐

called cavity test can be performed when all 

the aforementioned tests have failed to give 

comprehensive information about the  vitality 

of the pulp. Positive and negative responses 

indicate vital and necrotic pulp, respectively. 

If no symptoms are reported by extending 

the cavity towards the pulp chamber, partial 

or complete pulp necrosis is confirmed and 

the endodontic treatment can be started 

(Kerns and Glickman 2011).

Figure 4.14 

Pulp necrosis limited to the distal root on 4.6 (LR6) and result after root canal therapy.

The Endodontist’s View 77

4.5.2.12  Selective Anaesthesia Test

To determine the origin of pain, teeth might 

be selectively anaesthetized by carefully 

injecting the anaesthetic through the perio-

dontal ligament. Periodontal intraligament 

injection is limited to a single tooth without 

involving the adjacent teeth. The test is use-

ful to identify the origin of pulpitis‐related 

radiating pain (D’Souza et al. 1987; Rotstein 

and Simon 2004).

4.5.3  Management of 

Endodontic‐periodontal Disease

To properly manage endodontic‐periodontal 

pathology (Box 4.7; Berner and Graber 2008), 

prognosis and treatment decision‐making 

should be based on scrupulous diagnosis. 

The pulp should be assessed for sensitivity, 

whereas bone defects should be assessed for 

severity, extension, and shape.

Primary endodontic disease is character-

ized by necrotic pulp and narrower calculus‐

free defect, thus the prognosis would mainly 

depend on the outcome of root canal therapy. 

Once calculus‐related pockets are excluded 

and root canal treatment is properly per-

formed, the diagnosis of primary endodontic 

lesions is confirmed by the disappearance of 

symptoms, physiological values on soft tissue 

probing, and bony remineralization on recall 

radiographs.

Primary periodontal lesions show vital 

pulp and a wide calculus‐associated pocket. 

In this case, the prognosis depends on peri-

odontal disease severity, treatment execu-

tion, and patient response, motivation, and 

compliance.

Despite the similar clinical and radio-

graphic findings, the presence of plaque and 

calculus is crucial for the diagnosis and prog-

nosis of combined or true endodontic‐ 

periodontal lesions. From a treatment 

viewpoint, the calculus, if present, might be 

useful to detect the limit between the perio-

dontal (rough surfaces due to calculus) and 

endodontic component of the defect (smooth 

surfaces without calculus). When this differ-

ential diagnosis is not possible, deep and 

heavy debridement should be avoided before 

root canal therapy, since healthy cementum 

might be wrongly removed, and a second re‐

evaluation of the site should be made two to 

three months after the endodontic treatment 

(Zehnder 2001; Parolia et al. 2013; Paul and 

Hutter 1997). This time is required for the 

initial bone remineralization, thus the extent 

of the periodontal component can be more 

precisely assessed.

Tooth maintainability should be deeply 

questioned once the extent of the defect is 

seen to depend more on periodontal than 

endodontic disease. The prognosis depends 

on periodontal disease severity, overall treat-

ment execution, and patient response, 

 motivation, and compliance. Cases of true 

combined disease might have more a guarded 

prognosis than the combined endodontic‐

periodontal lesions (Paul and Hutter 1997; 

Rotstein and Simon 2004; Bergenholtz and 

Hasselgreen 2008; Kerns and Glickman 2011; 

Schmidt et al. 2014).

4.5.4  Endodontic‐periodontal Disease 

in Endodontically Treated Teeth

Sensitivity tests cannot be used for diagnostic 

purposes in endodontically treated teeth. 

Improper root canal treatment (see Figure 4.15) 

or iatrogenic injuries (see Figure 4.16), such as 

stripping or perforation, should be radio-

graphically detected to determine whether the 

origin of the lesion is endodontic, particularly 

if there are no signs of periodontal disease. The 

diagnostic dilemma can only be solved through 

proper endodontic retreatment. By controlling 

the infection, clinical and radiographic healing 

Box 4.7  Proper management of 
endodontic‐periodontal pathology.

 

●

Collect all the information referred to by 
the patient (i.e. previous trauma, pulp 
capping).

 

●

Perform all the tests mentioned.

 

●

Match and interprete the data collected.