Peri‑Implant Soft‑Tissue Integration and Management E-Book

Mario Roccuzzo

• Herausgeber: Quintessence Publishing
• Kategorie: Fachliteratur
• Serie: ITI Treatment Guide Series
• Sprache: Englisch

Seitenzahl: 315

Veröffentlichungsjahr: 2021

Beschreibung

Popular demand for dental implants as a reliable long-term option to replace missing teeth has risen dramatically. However, situations remain that pose challenges to practitioners and the treatment process. Written by renowned clinicians and supported by cases contributed by expert practitioners, the present volume of the ITI Treatment Guide series highlights the integration and management of peri-implant soft tissues. It discusses soft-tissue management before and during implant placement and during supportive peri-implant therapy and addresses the techniques and materials used for peri-implant soft-tissue augmentation and replacement and for the treatment of peri-implant soft-tissue dehiscences. Volume 12 of the ITI Treatment Guides series offers clinicians a comprehensive overview of various evidence-based techniques and treatment approaches for use in daily practice, with a focus on current techniques and materials.

Leseprobe

ITI Treatment Guide Volume 12

Authors: M. Roccuzzo A. Sculean

Volume 12

Peri-Implant Soft-Tissue Integration and Management

German National Library CIP Data

The German National Library has listed this publication in the German National Bibliography. Detailed bibliographical data are available at http://dnb.ddb.de.

© 2021 Quintessenz Verlags-GmbH Ifenpfad 2–4, 12107 Berlin, Germanywww.quintessence-publishing.com

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

Illustrations:Ute Drewes, Basel (CH),

www.drewes.ch

Copyediting:Triacom Dental, Barendorf (DE),

www.triacom.com

Graphic concept:Wirz Corporate AG, Zürich (CH)

Production:Juliane Richter, Janina Kuhn,

Berlin (DE)

ISBN (ebook): 978-3-86867-559-7 ISBN (print): 978-1-78698-101-1

The materials offered in the ITI Treatment Guide are for educational purposes only and intended as a step-by-step guide to the treatment of a particular case and patient situation. These recommendations are based on the conclusions of the ITI Consensus Conferences and, as such, are in line with the ITI treatment philosophy. These recommendations, nevertheless, represent the opinions of the authors. Neither the ITI nor the authors, editors, or publishers make any representation or warranty for the completeness or accuracy of the published materials and as a consequence do not accept any liability for damages (including, without limitation, direct, indirect, special, consequential, or incidental damages or loss of profits) caused by the use of the information contained in the ITI Treatment Guide. The information contained in the ITI Treatment Guide cannot replace an individual assessment by a clinician and its use for the treatment of patients is therefore the sole responsibility of the clinician.

The inclusion of or reference to a particular product, method, technique or material relating to such products, methods, or techniques in the ITI Treatment Guide does not represent a recommendation or an endorsement of the values, features, or claims made by its respective manufacturers.

All rights reserved. In particular, the materials published in the ITI Treatment Guide are protected by copyright. Any reproduction, whether in whole or in part, without the publisher’s prior written consent is prohibited. The information contained in the published materials can itself be protected by other intellectual property rights. Such information may not be used without the prior written consent of the respective intellectual property right owner.

Some of the manufacturer and product names referred to in this publication may be registered trademarks or proprietary names, even though specific reference to this fact is not made. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.

The tooth identification system used in this ITI Treatment Guide is that of the FDI World Dental Federation.

The ITI Mission is …

“… to serve the dental profession by providing a growing global network for life-long learning in implant dentistry through comprehensive quality education and innovative research to the benefit of the patient.”

Preface

The field of implant dentistry has developed significantly in recent years. As a result, practitioners are faced with higher demand as well as expectations from their patients, not only in terms of successful implant treatment but also the long-term esthetics of the final result. At the same time, the growing number of patients with soft-tissue-related problems is an undeniable reality.

This volume therefore provides readers with guidance and reference material for the treatment of patients with mucogingival deformities. Its aim is to reduce the risk of biological and esthetic complications around dental implants, and to ensure predictable and stable long-term treatment outcomes.

As with every ITI Treatment Guide, this volume illustrates clinical approaches to peri-implant soft-tissue integration and management, step by step, in a variety of clinical situations.

We hope this volume provides clinicians support and orientation towards optimal long-term maintenance of peri-implant soft-tissue health and esthetics.

Acknowledgments

The authors would like to express their gratitude to Dr. Kati Benthaus for her excellent support in the preparation and coordination of this Treatment Guide. We would also like to thank Ms. Ute Drewes for the professional illustrations, Ms. Janina Kuhn (Quintessence Publishing) for the typesetting and for the coordination of the production workflow and Mr. Per N. Döhler (Triacom Dental) for the language editing. We also acknowledge Institut Straumann AG, the corporate partner of the ITI, for its continuing support.

Editors and Authors

Editors:

Nikolaos Donos

DDS, MS, FHEA, FDSRC, PhD

Professor, Head and Chair, Periodontology and Implant Dentistry

Head of Clinical Research

Institute of Dentistry, Barts and The London School of Medicine and Dentistry

Queen Mary University of London

Turner Street

London E1 2AD

United Kingdom

[email protected]

Stephen Barter

BDS, MSurgDent, RCS

Specialist in Oral Surgery

Honorary Senior Clinical Lecturer/Consultant Oral Surgeon

Centre for Oral Clinical Research

Institute of Dentistry, Barts and The London School of Medicine and Dentistry

Turner Street

London E1 2AD

United Kingdom

[email protected]

Daniel Wismeijer

Professor, DMD

Oral Implantology and Prosthetic Dentistry

Private Practice

Zutphensestraatweg 26

6955 AH Ellecom

Netherlands

[email protected]

Authors:

Mario Roccuzzo

DMD, Dr med dent

Private practice (periodontology)

Corso Tassoni 14

10143 Torino (TO)

Italy

[email protected]

Anton Sculean

Professor, Dr med dent, Dr h c, MSc

Executive Director and Chairman

Department of Periodontology

University of Bern

School of Dental Medicine

Freiburgstrasse 7

3010 Bern

Switzerland

[email protected]

Contributors

Sofia Aroca

Dr med dent, PhD

Private practice

35, Rue Franklin

78100 Saint Germain en Laye

France

[email protected]

Paolo Casentini

DDS, Dr med dent

Private practice

Via Anco Marzio 2

20123 Milano (MI)

Italy

[email protected]

Raffaele Cavalcanti

DDS, PhD

Adjunct Professor of Periodontology University of Catania, CLMOPD, Via S. Sofia 78, 95123 Catania (CT), Italy

and

Private practice

Studio Odontoiatrico Associato Cavalcanti & Venezia

(periodontology, implantology, oral surgery)

Via Giuseppe Posca 15

70124 Bari (BA)

Italy

[email protected]

Nikolaos Donos

DDS, MS, FHEA, FDSRC, PhD

Professor, Head and Chair, Periodontology and Implant Dentistry

Head of Clinical Research

Institute of Dentistry, Barts and The London School of Medicine and Dentistry Queen Mary University of London

Turner Street

London E1 2AD

United Kingdom

[email protected]

Daniel Etienne

Dr chir dent, MSc

Private practice

1, Avenue Bugeaud

75116 Paris

France

[email protected]

Jason R Gillespie

BS DDS MS

Private prac:ce (Prosthodon:cs)

105 W El Prado Dr

San Antonio, TX 78212-2024

United States of America

[email protected]

Alfonso Gil

DDS, MS, PhD

Resident Physician

Clinic of Reconstructive Dentistry

Center of Dental Medicine

University of Zurich

Plattenstrasse 11

8032 Zurich

Switzerland

[email protected]

Christoph Hämmerle

Professor, Dr med dent, Dr h c

Chair

Clinic of Reconstructive Dentistry

Center of Dental Medicine

University of Zurich

Plattenstrasse 11

8032 Zurich

Switzerland

[email protected]

Vincenzo Iorio-Siciliano

DDS, MS, PhD

Department of Periodontology

University of Naples Federico II

Via Sergio Pansini 5

80131 Napoli (NA)

Italy

[email protected]

Ronald Jung

Professor, Dr med dent, PhD

Head, Oral Implantology

Clinic of Reconstructive Dentistry

Center of Dental Medicine

University of Zurich

Plattenstrasse 11

8032 Zurich

Switzerland

[email protected]

Eduardo Lorenzana

DDS, MSc

Private practice (periodontology)

3519 Paesano’s Parkway

Suite 103

San Antonio, TX 78231-1266

United States of America

[email protected]

Neil MacBeth

BDS, MFGDP, MGDS RCS, MFDS RCS, FFGDP (UK), MSc, FDS RCS (Rest Dent), CDLM, RAF

Consultant in Restorative Dentistry – Defence Primary Health Care

Clinical Senior Lecturer in Periodontology

Institute of Dentistry, Queen Mary University of London

Institute of Dentistry, Barts and The London School of Medicine and Dentistry

Turner Street

London E1 2AD

United Kingdom

[email protected]

Kurt Riewe

DDS

Private practice, Stone Oak Dental

335 E Sonterra Blvd

Suite 150

San Antonio, TX 78258-4295

United States of America

[email protected]

Shakeel Shahdad

BDS, MMedSc, FDS RCSEd, FDS (Rest. Dent.) RCSEd, DDS, FDT FEd

Consultant in Restorative Dentistry

Barts Health NHS Trust

The Royal London Dental Hospital

and

Honorary Clinical Professor in Oral Rehabilitation and Implantology

Barts and The London School of Medicine and Dentistry

Queen Mary University of London

Turner Street

London, E1 1DE

United Kingdom

[email protected]

Daniel Thoma

Professor, Dr med dent

Vice-Chairman

Head, Reconstructive Dentistry

Clinic of Reconstructive Dentistry

Center of Dental Medicine

Vice Chairman, Center for Dental Medicine

University of Zurich

Plattenstrasse 11

8032 Zurich

Switzerland

[email protected]

Pietro Venezia

DDS

Adjunct Professor

Department of Prosthodontics

University of Catania (Italy)

and

Private practice

Via G. Posca, 15

70124 Bari (BA)

Italy

[email protected]

Table of Contents

1 Introduction

M. Roccuzzo

2 Importance of the Peri-Implant Soft Tissues

A. Sculean

3 Soft-Tissue Management around Tissue-Level Implants

M. Roccuzzo

3.1 Soft-Tissue Management at Implant Placement

3.2 Soft-Tissue Management Before Implant Placement

3.3 Soft-Tissue Management During Supportive Care

4 Soft-Tissue Grafting After Implant Placement

M. Roccuzzo, A. Sculean

4.1 Increasing the Width of the Keratinized Mucosa

M. Roccuzzo

4.2 Soft-tissue Replacement Materials

A. Sculean

5 Peri-Implant Soft-Tissue Dehiscences

5.1 Indications for Peri-Implant Soft-Tissue Dehiscence Coverage

M. Roccuzzo

5.2 Techniques for Treating Peri-Implant Soft-Tissue Dehiscences

M. Roccuzzo

5.2.1 Tunneling Technique for Treating Peri-Implant Soft-Tissue Dehiscences

A. Sculean

6 Clinical Case Presentations

6.1 Implant Placement in the Esthetic Zone and Coverage of Multiple Gingival Recessions

S. Aroca

6.2 Periodontal Plastic Surgery and Prosthetic Procedures to Treat Peri-Implant Soft-Tissue Dehiscences

P. Casentini

6.3 GBR and Soft-Tissue Augmentation Following Explantation to Rehabilitate a Soft- and Hard-Tissue Defect

R. Cavalcanti, P. Venezia

6.4 Soft-Tissue Volume Augmentation Using a Connective-Tissue Graft Harvested from the Maxillary Tuberosity

D. Etienne

6.5 Connective-Tissue Graft to Increase the Width of the Keratinized Mucosa Around an Osseointegrated Implant

V. Iorio-Siciliano

6.6 Soft- and Hard-Tissue Regeneration and Implant-Supported Restorations to Treat a Complex Anterior Maxillary Case

R. Jung, A. Gil, C. Hämmerle, D. Thoma

6.7 Early Implant Placement, Contour Augmentation, and Autologous Connective-Tissue Graft Using a Tunneling Technique to Replace an Upper Incisor with Generalized Gingival Recession

E. Lorenzana, J. Gillespie

6.8 Connective-Tissue Graft to Augment the Buccal Tissue for a Bone-Level Implant at an Upper Incisor Site

E. Lorenzana, K. Riewe

6.9 Treatment of a Soft-Tissue Fenestration in the Esthetic Zone

N. MacBeth, N. Donos

6.10 Covering a Soft-Tissue Dehiscence at a Mandibular Incisor

M. Roccuzzo

6.11 Soft-Tissue Augmentation Using a Porcine-Derived Collagen Matrix to Correct a Labial Soft-Tissue Defect Following Extraction of a Maxillary Incisor

S. Shahdad

7 Conclusions

M. Roccuzzo

8 References

1 Introduction

M. Roccuzzo

In the earlier days of implant dentistry, osseointegration was considered to be a sufficient condition for long-term successful implant rehabilitation. With time, however, it became evident that soft-tissue integration is of significant importance and that the formation of an early and long-standing effective mucosal barrier, capable of biologically protecting the peri-implant structures, is essential. This soft-tissue barrier is mainly the result of a wound-healing process that results in an effective interface between “living tissues” and a “foreign body” (Rompen and coworkers 2006).

Whether the presence of a minimum amount of keratinized mucosal (KM) is necessary for the long-term maintenance of peri-implant health has been controversial for many years. Several researchers have found that insufficient KM may be correlated with plaque accumulation, bleeding on probing, discomfort when brushing, mucosal recession, and peri-implant mucositis (Bouri and coworkers 2008; Boynueğri and coworkers 2013; Chung and coworkers 2006; Roccuzzo and coworkers 2016). Other researchers were unable to obtain similar findings (Frisch and coworkers 2015), with some even suggesting that KM may not be essential in the presence of scrupulous oral hygiene and rigorous compliance with a professional maintenance regimen (Lim and coworkers 2019).

On the other hand, complete osseointegration and perfect soft-tissue integration are not necessarily correlated with successful esthetic rehabilitation of a missing tooth or teeth. Indeed, success criteria for esthetically sensitive areas must include measurements of the peri-implant mucosa, as well as the restoration and its relationship to the surrounding dentition (Belser and coworkers 2004).

Apart from the prosthetic aspects, sufficient horizontal and vertical volume is also essential for long-term esthetic soft-tissue stability. Where soft-tissue deficiencies exist, appropriate augmentation procedures may be required for comprehensive rehabilitation. Recent advances in implant dentistry have provided clinicians with various treatment options to treat peri-implant soft-tissue defects. At the same time, though, soft-tissue grafting procedures are of moderate to high complexity and may be associated with a significant risk of complications. For this reason, various step-by-step procedures have been outlined and illustrated by individual case descriptions for the reader of this book.

The aim of this ITI Treatment Guide is to foster awareness of the increasing demands on clinicians to provide treatment for a growing population of patients with soft-tissue related problems. The authors hope that Volume 12 will be a valuable resource and reference work for the treatment of patients with mucogingival deformities to reduce the risk of biological and esthetic complications and to ensure predictable and stable long-term results.

2 Importance of the Peri-Implant Soft Tissues

A. Sculean

Dental implants are anchored in jawbone via direct contact between the bone and the implant, a phenomenon called osseointegration (Albrektsson and coworkers 1981). Emerging evidence indicates that the long-term success and survival of implants does not depend solely on osseointegration, but also on the soft tissues around the transmucosal aspect of the implant that separate the peri-implant bone from the oral cavity. This soft-tissue seal or collar is also called the peri-implant mucosa (Lindhe and coworkers 2008). The attachment of the soft tissue to the implant serves as a biological seal that ensures healthy conditions and prevents the development of peri-implant infections (peri-implant mucositis and peri-implantitis). Consequently, the peri-implant soft tissues play a crucial role for long-term implant survival (Lindhe and coworkers 2008).

The soft tissue around teeth develops during tooth eruption and seals the supporting tissues (the alveolar bone, periodontal ligament, and cementum) against the oral cavity (Bosshardt and Lang 2005). The peri-implant mucosa forms after traumatizing the oral soft and hard tissues to accommodate osseointegrated implants. The following presents a brief description of the most important anatomical features of the periodontal and peri-implant tissues.

Structure of periodontal tissues in health

The periodontium comprises the tissues supporting the teeth: the tooth-facing part of the gingiva, the root cementum, the periodontal ligament, and the part of the alveolar process that lines the tooth socket, termed alveolar bone (Schroeder and Listgarten 1997) (Figs 1 to 5).

Fig 1 Photomicrograph. Tooth with a healthy periodontium. Supporting tissues of the tooth consisting of the root cementum, periodontal ligament, alveolar bone, and gingiva.

Fig 2 Photomicrograph. Supra-alveolar soft tissue consisting of the oral sulcular epithelium, junctional epithelium, and connective-tissue attachment (collagen fibers inserting into the root cementum). The junctional epithelium ends at the cementoenamel junction (CEJ) at the point of the insertion of the collagen fibers into the root cementum.

Fig 3 Higher magnification. Supra-alveolar soft tissue comprising the junctional epithelium and root cementum with inserting collagen fibers. Well-encapsulated minor inflammatory cell infiltrate (arrow) located adjacently to the junctional epithelium.

Fig 4 Higher magnification. Oral sulcular epithelium and junctional epithelium. The apical extension of the junctional epithelium ends at the cementoenamel junction. The well-encapsulated inflammatory cell infiltrate (arrow) is clearly distinguishable next to the junctional epithelium.

Fig 5 Higher magnification. Intact periodontal ligament connecting the root cementum with the alveolar bone. The collagen fibers invest in both root cementum and alveolar bone.

As they develop, the teeth penetrate the epithelial lining of the oral cavity and then persist as transmucosal organs. Their root portion is anchored in the bone, while the crown resides in the oral cavity. The most important function of the gingiva is to protect the underlying soft and hard connective tissues from penetration by microorganisms from the oral cavity. The gingiva terminates coronally at the gingival margin; apically it ends at the mucogingival junction or becomes continuous with the mucosa of the hard palate. The gingival sulcus has an approximate depth of 0.5 mm; however, in a completely healthy situation, it may not be clinically detectable (Schroeder and Listgarten 1997).

The interdental region contains a structure called the gingival papilla. The gingiva consists of two parts, the free gingiva and the attached gingiva. The free gingiva comprises the coronal portion of the gingiva and follows the contour of the cementoenamel junction, varying in width between 1 and 2 mm (Ainamo and Löe 1966). Its apical boundary is accentuated by a stippled line; a gingival groove may also be present. The attached gingiva stretches between the end of the free gingiva and the alveolar mucosa, or the mucosa of the floor of the mouth. Because the palatal mucosa extends to the free gingiva, there is no attached gingiva in the palate. The width of the attached gingiva may range from 1 to 10 mm (Ainamo and Löe 1966).

Junctional epithelium

The junctional epithelium is a non-keratinized epithelium that, due to its unique structural and functional adaptation, plays a critical role in maintaining periodontal health by providing a functional barrier to microbial challenges. Cell division occurs in the basal layer facing the lamina propria, while the innermost cells constitute the epithelial attachment. It consists of the basal lamina and hemidesmosomes that connect the epithelial cells with the tooth surface (Bosshardt and Lang 2005).

Connective tissue of the gingiva

The connective tissue of the gingiva consists mainly of fibroblasts exhibiting phenotypes that differ from those from the periodontal ligament (Bartold and coworkers 2000). They are arranged as groups of collagen fibers with a complex three-dimensional architecture that allows polymorphonuclear neutrophils (PMNs) and mononuclear cells to migrate through the connective tissue until they can pass the basement membrane bordering the junctional epithelium. Even in clinically healthy circumstances, an inflammatory cell infiltrate will be present and can be considered a common (normal) characteristic of the connective tissue adjacent to the junctional epithelium.

Periodontal ligament

The soft connective tissue interposed between the alveolar bone and the root cementum is called the periodontal ligament. Coronal to the alveolar crest, the periodontal ligament merges with the lamina propria of the gingiva, while it is continuous with the dental pulp periapically. The width of the periodontal ligament measures approximately 200 µm, being thinnest in the middle third of the root. Its width decreases with age.

The most important function of the periodontal ligament is to attach the tooth to the surrounding bone. Another important function is the damping of occlusal forces. Additionally, the periodontal ligament serves as an important reservoir for cells that are constantly needed for tissue homeostasis and play a crucial role in periodontal wound healing and regeneration (periodontal fibroblasts, cementoblasts, odontoclasts, osteoblasts and osteoclasts, epithelial cell rests of Malassez, monocytes and macrophages, and undifferentiated mesenchymal progenitor and stem cells).

The fibroblasts of the periodontal ligament synthesize, structure, and remodel the extracellular matrix, which consists of collagen fibers and an amorphous ground substance composed of non-collagenous proteins. Due to its structural configuration, the periodontal ligament provides a flexible attachment of the tooth to the surrounding bone via Sharpey’s fibers into the mineralized tissues (Nanci and Bosshardt 2006).

Root cementum

Root cementum is a mineralized connective tissue coating the roots of teeth, usually extending from the cementoenamel junction to the root apex. Its primary function is to invest and attach the fibers of the periodontal ligament to the root surface (the acellular extrinsic fiber cementum, AEFC, and the cellular mixed stratified cementum, CMSC). However, root cementum also has other important functions, such as adjusting the tooth position to new physiologic requirements and repair of root defects (cellular intrinsic fiber cementum, CIFC) (Nanci and Bosshardt 2006).

Alveolar bone

The teeth are anchored in the alveolar bone, a part of the alveolar process that consists of an outer cortical plate, an inner cortical plate, and a central spongiosa. The alveolar process is continuous with the jawbone and can only develop in the presence of teeth. The inner cortical plate lines the alveolus and is also referred to as the alveolar bone.

In fully erupted and periodontally healthy teeth, the contour of the alveolar crest follows the contour of the cementoenamel junction in a coronoapical direction for approximately 2 mm (Saffar and coworkers 1997). The alveolar bone consists of compact bone characterized by the presence of osteons, the structural unit for cortical bone remodeling. The socket wall exhibits many perforations that connect the periodontal ligament with the endosteal or bone-marrow spaces, thus enabling blood and lymph vessels, and nerve fibers, to pass through these openings.

A characteristic component of the alveolar bone is the bundle bone, which is deposited in successive layers running parallel to the socket wall. Its typical appearance is determined by the Sharpey’s fibers penetrating its layers. The alveolar bone responds to the functional demands placed on it by the processes of resorption and deposition, known as bone remodeling.

Structure of peri-implant tissues in health

During the process of wound healing following the placement of dental implants, the features of the peri-implant mucosa are established (Sculean and coworkers 2014) (Figs 6 to 10).

Fig 6 Photomicrograph. Osseointegrated dental implant with direct bone-to-implant contact and supracrestal soft-tissue implant contact.

Fig 7 Higher magnification- Supracrestal peri-implant soft tissues consisting of oral and sulcular epithelium and connective tissue adhesion to the implant surface.

Fig 8 Higher magnification. Coronal portion of the supracrestal peri-implant soft tissues. The oral and sulcular epithelium are clearly visible. The collagen fibers located apically to the junctional epithelium run parallel to the implant surface. A more diffuse inflammatory infiltrate (arrow) is located immediately adjacent the junctional and sulcular epithelium.

Fig 9 Higher magnification. Supracrestal portion of the peri-implant soft tissues. The collagen fibers located apically to the junctional epithelium run parallel to the implant surface.

Fig 10 Higher magnification. Direct contact between the bone and the implant surface (osseointegrated implant).

Berglundh and coworkers (1991) examined the anatomical and histological features of the peri-implant mucosa in dogs, formed in a two-stage procedure, and compared these with those of the gingiva around teeth. The peri-implant mucosa consisted of a keratinized oral epithelium located at the external surface, connected to a thin barrier epithelium facing the abutment (the equivalent to the junctional epithelium around teeth), the peri-implant junctional epithelium. It terminated 2 mm apical to the coronal soft-tissue margin and 1.0 to 1.5 mm coronal to the peri-implant bone crest. The mean supracrestal soft tissue (including the sulcus depth) measured 3.80 mm around implants and 3.17 mm around teeth. While there was no statistically significant difference in the height of the junctional epithelium and sulcus depth between implants and teeth, the height of the soft connective tissue was statistically significantly greater around implants than around teeth (Fig 11).

Fig 11 Schematic drawing. illustrating the structure of clinically healthy supra-alveolar soft tissues adjacent to a tooth or an implant (GM: gingival margin, aJE: apical extent of the junctional epithelium, BC: bone crest).

The peri-implant junctional epithelium and the soft connective tissue adjacent to the abutment appeared to be in direct contact with the implant/abutment surface (Berglundh and coworkers 1991). In summary, the findings of this study showed that the peri-implant mucosa displays comparable anatomical features to those of gingiva around teeth (Berglundh and coworkers 1991).

Subsequent studies provided evidence that a similar mucosal attachment is formed on titanium with different implant systems (Buser and coworkers 1992; Abrahamson and coworkers 1996) and around implants placed using both non-submerged and submerged approaches (Abrahamson and coworkers 1999; Arvidson and coworkers 1996; Weber and coworkers 1996). However, the peri-implant junctional epithelium was significantly longer in implants placed using a submerged approach, where an abutment was connected in a second-stage surgical procedure, than in implants placed using a non-submerged approach (Weber and coworkers 1996).

The biologic width (of the supracrestal soft tissue) was revisited in a further dog experiment, following connection of the abutment to the implant with or without a reduced vertical dimension of the oral mucosa (Berglundh and coworkers 1996). It was found that while the peri-implant junctional epithelium was about 2 mm in depth, the supra-alveolar soft connective compartment had a depth of approximately 1.3 to 1.8 mm.

Interestingly, sites with reduced mucosal thickness consistently revealed marginal bone resorption, thus adjusting the width of the supracrestal soft tissue. Evaluating the biologic width around one- and two-piece titanium implants placed in a non-submerged or submerged approach in the mandibles of dogs, Hermann and coworkers (2001) suggested that the gingival margin is located coronally and the biologic width is more similar to teeth around one-piece non-submerged implants than either two-piece non-submerged or two-piece submerged implants. These findings were later confirmed in a comparably designed dog study with another implant system (Pontes and coworkers 2008).

Several studies evaluated the impact of surface topography (surface roughness measurements) on the peri-implant mucosa. Cochran and coworkers (1997) failed to show any differences in the dimensions of the sulcus depth, peri-implant junctional epithelium, and soft connective tissue in contact with implants with a titanium plasma-sprayed (TPS) surface or a sandblasted and acid-etched surface. Abrahamsson and coworkers (2001, 2002) observed similar epithelial and soft connective tissue components on rough (acid etched) and smooth (turned) titanium surfaces. The biologic width (supracrestal soft tissue) was greater on the rough surfaces, although with no statistically significant difference to that around smooth surfaces.

Findings from two human histologic studies revealed less epithelial downgrowth and a longer soft connective tissue compartment in conjunction with oxidized or acid-etched titanium compared to a machined surface (Glauser and coworkers 2005; Ferreira Borges and Dragoo 2010). In a study in baboons, Watzak and coworkers (2006) showed that implant surface modifications had no significant effect on the biologic width after eighteen months of functional loading. Following a healing period of three months, nanoporous TiO2 coatings of one-piece titanium implants showed similar length of peri-implant soft connective tissue and epithelium than the uncoated, smooth neck portion of the control titanium implants in dogs (Rossi and coworkers 2008). Schwarz and coworkers (2007) have suggested that soft-tissue integration was more influenced by hydrophilicity than by microtopography.

A number of studies revealed that epithelial cells attach to different implant materials in a comparable manner to that in which junctional epithelial cells attach to the tooth surface via hemidesmosomes and a basal lamina (Sculean and coworkers 2014).

Analyzing the intact interface between soft connective tissue and titanium-coated epoxy resin implants, Listgarten confirmed the parallel orientation of collagen fibers to the titanium layer (Listgarten and coworkers 1992, 1996). Since implants lack a cementum layer into which the peri-implant collagen fibers can invest, the attachment of the soft connective tissue to the transmucosal portion of an implant is regarded as being weaker than the soft connective tissue attachment to the surface of a tooth root (Sculean and coworkers 2014). Therefore, improving the quality of the soft tissue-implant interface is of great relevance for maintaining healthy peri-implant tissues (Sculean and coworkers 2014).

The wound-healing sequence leading to the establishment of the soft tissue seal at implants was evaluated by Berglundh and coworkers (2007). Immediately after implant placement, a coagulum occupied the implant-mucosa interface. Numerous neutrophils infiltrated the blood clot, and at four days an initial mucosal seal was established. In the next few days, the number and distribution of leukocytes decreased, becoming confined to the coronal portion, with fibroblasts and collagen dominating the apical part of the implant-tissue interface.

Between one and two weeks of healing, the peri-implant junctional epithelium was located approximately 0.5 mm apical to the mucosal margin. At two weeks, the peri-implant junctional epithelium began to proliferate in an apical direction. After two weeks, the peri-implant mucosa was rich in cells and blood vessels. At four weeks of healing, the peri-implant junctional epithelium migrated further apically and occupied 40% of the total soft-tissue/implant interface. This soft connective tissue was rich in collagen and fibroblasts and was well-organized.

The apical migration of the peri-implant junctional epithelium was completed between six and eight weeks, and the fibroblasts formed a dense layer over the titanium surface at that time. From six to twelve weeks, maturation of the soft connective tissue had occurred; the peri-implant junctional epithelium occupied about 60% of the entire implant/soft-tissue interface. Further away from the implant surface, the number of blood vessels was low; fibroblasts were located between thin collagen fibers, running mainly parallel to the implant surface.

These findings indicate that the soft-tissue attachment to transmucosal (non-submerged) implants made of commercially pure titanium with a polished surface in the neck portion requires at least six weeks (Berglundh and coworkers 2007). These findings from animal experiments were corroborated in human studies by Tomasi and coworkers (2013), indicating that a soft-tissue barrier adjacent to titanium implants may form completely within eight weeks. Further studies have provided evidence indicating that in dogs, the dimensions of the soft-tissue seal (the biologic width or supracrestal soft tissue) around implants are stable for at least twelve (Cochran and coworkers 1997; Assenza and coworkers 2003) or fifteen months, respectively (Hermann and coworkers 2000).

The role of keratinized mucosa in maintaining peri-implant tissue health

It is generally accepted that the assessment of peri-implant health is based on clinical and radiographic parameters bleeding on probing (BOP), probing depth (PD), and marginal peri-implant bone level (Salvi and coworkers 2012; Jepsen and coworkers 2015).

The influence of the presence or absence and the thickness of keratinized or attached mucosa (KAM) on peri-implant tissue health and stability is controversial (Bengazi and coworkers 1996; Schou and coworkers 1992; Strub and coworkers 1991; Wennström and coworkers 1994).

On one hand, a number of clinical studies have failed to show a correlation between the presence of an “adequate” band (2 mm or more) of KAM and implant stability, as assessed by peri-implant bone level or probing depths (Bengazi and coworkers 1996; Wennström and coworkers 1994; Chung and coworkers 2006; Bouri and coworkers 2008; Boynueğri and coworkers 2013). These results were also supported by findings from an animal study indicating that the presence of an “adequate” width of KAM does not significantly influence peri-implant tissue conditions (Strub and coworkers 1991).

However, other clinical studies have suggested that an inadequate (2 mm or less) width of KAM is related to a higher risk of peri-implant inflammation and loss of soft and hard tissue (Warrer and coworkers 1995; Block and coworkers 1996; Zarb and coworkers 1990). A number of other studies have reported statistically significant associations between a peri-implant KAM width of less than 2 mm and higher bleeding scores (Zigdon and coworkers 2008; Adibrad and coworkers 2009; Schrott and coworkers 2009; Lin and coworkers 2013), greater plaque accumulation (Chung and coworkers 2006: Bouri and coworkers 2008; Boynueğri and coworkers 2013; Adibrad and coworkers 2009; Schrott and coworkers 2009; Crespi and coworkers 2010), and more mucosal inflammation (Chung and coworkers 2006; Bouri and coworkers 2008; Boynueğri and coworkers 2013; Adibrad and coworkers 2009; Crespi and coworkers 2010), compared to sites with adequate KAM width (2 mm or more).

Conversely, results from a retrospective study reported low rates of peri-implant diseases in patients enrolled in a maintenance program irrespective of the width of the KAM (Frisch and coworkers 2015). The authors of this study suggest that maintaining an optimal level of plaque control seems to be more important for ensuring peri-implant tissue health than the presence of an adequate width of KAM. Schou and coworkers (1992) showed that peri-implant health can be ensured in the absence of keratinized mucosa, provided adequate oral hygiene is established.

These findings were later confirmed in systematic reviews that concluded that the lack of an adequate zone of keratinized attached tissue may not be mandatory for maintaining soft-tissue health around dental implants, as long as an optimal level of oral hygiene is ensured (Wennström and Derks 2012; Gobbato and coworkers 2013; Lin and coworkers 2013). However, preclinical and clinical data indicate that in the absence of stable keratinized attached mucosa, plaque control is more difficult, which in turn may lead to peri-implant soft-tissue inflammation and, eventually, bone loss (Warrer and coworkers 1995; Wennström and Derks 2012; Gobbato and coworkers 2013; Lin and coworkers 2013).

Roccuzzo and coworkers (2016) evaluated the clinical conditions around dental implants placed in the posterior mandible of healthy or moderately periodontally compromised patients as a function of the presence or absence of keratinized attached mucosa (KAM). The results showed that the absence of KAM was associated with higher plaque accumulation, greater soft-tissue recession (REC), and a higher number of sites that required additional surgical or antibiotic treatment, indicating that implants not surrounded by KAM are more prone to plaque accumulation and to developing soft-tissue recessions despite adequate oral hygiene and supportive periodontal therapy. These findings are in line with the results of three recent reviews, which concluded that the presence of an adequate width of KAM around dental implants is associated with better soft and hard tissue stability, less plaque accumulation, soft-tissue recession, and a lower incidence of peri-implant mucositis (Sculean and coworkers 2017; Chackartchi and coworkers 2019).

Taken together, the by far greater part of the available evidence indicates that the lack of an adequate width of KAM around dental implants is associated with more plaque accumulation, inflammation, soft-tissue recession, and attachment loss (Warrer and coworkers 1995; Wennström and Derks 2012; Gobbato and coworkers 2013; Lin and coworkers 2013; Sculean and coworkers 2017; Chackartchi and coworkers 2019; Iorio-Siciliano and coworkers 2019).

A recent systematic review evaluated the effects of soft-tissue augmentation procedures on peri-implant health or disease in partially and fully edentulous patients (Thoma and coworkers 2018a), using soft-tissue grafting procedures to increase the width of the KAM or the thickness of the peri-implant mucosa. The findings indicated that soft-tissue grafting by means of autologous grafts may favor peri-implant health through a gain of KAM, improved bleeding scores, and less marginal bone loss.

In the esthetic zone, autologous connective-tissue grafts resulted in increased mucosal thickness around implants and were associated with statistically significantly less marginal bone loss over time. However, the data failed to reveal statistically significant changes in terms of bleeding on probing, probing depths, or plaque scores at grafted sites compared to sites without grafting. Nevertheless, the authors concluded that based on the available evidence, it is generally accepted that soft-tissue augmentation is beneficial to establishing and maintaining peri-implant health (Thoma and coworkers 2018a).

Regarding the thickness of the peri-implant mucosa, findings of preclinical and clinical studies suggest a threshold value of 2 mm for establishing a natural appearance of the peri-implant mucosa and minimal soft-tissue discoloration at implant-supported prosthetic reconstructions (Jung and coworkers 2007; Cosgarea and coworkers 2015; Ioannidis and coworkers 2017; Thoma and coworkers 2016). Moreover, an adequate mucosal thickness was associated with a decreased risk of mucosal recessions in immediate-placement protocols or in specific anatomic situations (e.g., minimal or no facial bony wall, orofacial implant malposition, various angles of the implant fixtures) (Buser and coworkers 2004; Evans and coworkers 2008; Sculean and coworkers 2017).

In summary, despite the fact that the available evidence is still inconclusive, there is reason to suggest that the presence of KAM favors peri-implant health through facilitating oral hygiene measures, with a consequent reduction in both inflammation (lower bleeding scores) and marginal bone loss. Furthermore, its presence or absence also plays a key role in ensuring esthetics.

Acknowledgments

Photography

Professor Dieter D. Bosshardt – Bern, Switzerland

3 Soft-Tissue Management Around Tissue-Level Implants

M. Roccuzzo

3.1 Soft-Tissue Management at Implant Placement

From the biological point of view, the apicocoronal positioning of an implant, particularly those of tissue-level design, should follow the principle of “as shallow as possible, as deep as necessary” (Buser and coworkers 2004) in order to avoid deep peri-implant probing depths, taking into account the prosthetic and esthetic factors in the area.

This concept has recently been confirmed in a case-control study on 19 patients that evaluated the modifying effect of a deep mucosal tunnel (DMT, ≥ 3 mm) on the induction and resolution phases of experimental peri-implant mucositis (Chan and coworkers 2019). All patients, each with a properly placed tissue-level implant, were assigned either to the test group (DMT, depth ≥ 3 mm) or to the control group (shallow mucosal tunnel, SMT, ≤ 1 mm). The subjects underwent a standard experimental peri-implant mucositis protocol, characterized by an oral-hygiene optimization phase, a three-week induction phase using an acrylic stent to prevent self-performed oral hygiene at the experimental implant, and a three-plus-two-week resolution phase.

The modified plaque index (mPI), gingival index (mGI), and IL-1β concentrations in the peri-implant sulcus fluid were determined over time. Both the mPI and the mGI increased during the induction phase. After normal oral hygiene had resumed, the mPI and mGI resolved towards baseline values in the SMT group, while they diverged in the DMT group. Although plaque accumulation was resolved in the DMT group, the resolution of inflammation was delayed and found to be of smaller magnitude during the first three weeks after resumption of oral hygiene. IL-1β Concentrations were significantly higher in the DMT group at the end of induction and during the resolution phase, corroborating the clinical findings. Removal of the crown and submucosal professional cleaning were needed to revert mGI to baseline values in the DMT group.

The fact that the depth of the peri-implant sulcus influenced the resolution of experimental mucositis raised doubts as to the efficacy of self-performed oral hygiene in scenarios where implants are placed too deeply. Therefore, since the risk of mucositis evolving into peri-implantitis appears to be higher in such clinical situations, clinicians should make every effort to place implants properly—not only for esthetic, but also for biological reasons (Berglundh and coworkers 2018).

It should be noted that, from a clinical point of view, this may be more easily achievable for implants without adjacent teeth, but more challenging if the implant has to be placed between two teeth, particularly if these teeth are periodontally compromised. Figures 1a-b show examples of correct implant positioning. Figures 2a-b show examples of incorrect implant positioning.

Fig 1a The implant was carefully selected and positioned in a periodontally compromised patient so as to present minimal probing depth (time of crown cementation).

Fig 1b