Augmentation Surgery E-Book

Hendrik Terheyden

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

Seitenzahl: 574

Veröffentlichungsjahr: 2022

Beschreibung

Bone and soft tissue augmentation of the alveolar ridge is fairly unique in medicine, because true biologic regeneration of lost alveolar bone is achievable. With this book, the author makes a fine contribution to knowledge management and clinical judgment in this dynamic field. The book begins with the basics of jaw atrophy, biology of bone regeneration, and wound healing, as well as grafts and materials. Subsequent chapters cover standard augmentation techniques such as bone grafting and soft tissue management, fully explaining available augmentation techniques for even the most demanding surgeons. The final third of the book is dedicated to a clinical decision-making scheme for different situations, challenges in the esthetic region, posterior jaws, and fully edentulous ridges. The chapters are supplemented with step-by-step clinical cases that illustrate the respective topic in a clear and comprehensible way. The book aims to introduce general dentists to the field of bone and soft tissue augmentation. It also offers more experienced colleagues, including oral and maxillofacial surgeons, many practical tips, particularly with regard to complication management.

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Preface

Bone augmentation of the alveolar process is something special for medicine. In addition to the dental prosthetic options, there is the possibility here of true biologic regeneration of the alveolar bone, a restitutio ad integrum. The new bone can be functionally preserved over the long term thanks to dental implants. Bone augmentation is therefore in principle a functionally based medical rehabilitation, the esthetic aspects of which must not be disregarded. As my teacher Prof Dr Dr Franz Härle used to say, “If you get the function right, the esthetics will fall into your lap.”

This book is aimed at dental colleagues as an introduction to the topic of augmentation and is intended to provide experienced colleagues as well as oral and maxillofacial surgeons with many practical tips. There is a relatively wide range of information and training available in the new media; it is even possible to receive surgical training on video portals. In knowledge management, the task is to separate the wheat from the chaff and to distill the relevant information from the mass of it. It takes a lot of judgment to be able to better assess from the abundance of innovations what will prove itself in the future and what is therefore already worth an investment in clinical practice today. Therefore, even in the modern world of technology, there is still a place for a classic scientific textbook. This book aims to contribute to knowledge management and judgment within the practical background of clinical care and practice.

The book includes the topics of basic biology, surgical techniques, and clinical challenges and decision making. The biologic principles are addressed to the extent that they have clinical consequences. Fundamentally, classical dentistry has long been based relatively heavily on material science, and consequently so has academic training. This was consistent because classical conservative and prosthetic dentistry took place outside the ectodermal barrier, essentially outside the body. Today, dental implants mean that dentists are increasingly working invasively inside the body, so that the classical training content needs to be supplemented. Today, among other things, the biology of wound healing, the body’s reaction to antigens and foreign materials, and antibiotics and resistance are coming more to the fore, alongside the medical management of an invasively treated patient and the reaction to complications.

The operational techniques require surgery, unless one specializes in the prosthetic restoration of dental implants. But even then, knowledge of the surgical options is helpful in advising the patient. Even if one does little augmentation oneself at first, one should know the augmentation possibilities, along with their limitations in at-risk patients, in order to be able to properly refer them to a specialist. In general, a certain restraint is advised when teaching surgical techniques via drawings and animations because paper is known to be uncomplaining, which is why this book relies more on clarification through real clinical cases.

Experience and knowledge of the biologic background are essential for overcoming clinical challenges and making decisions, because dentistry is a science-based discipline. Differential indication means the risk-benefit assessment of which procedure offers the highest safety and the best effect for which situation and patient. This book attempts to facilitate this step in the form of a treatment-planning concept based on indications. It is therefore about decision making, preferably in consensus with the patient as shared decision making.

I would like to thank Quintessenz Verlag, especially senior director Dr h.c. Horst-Wolfgang Haase for the invitation and managing director Christian Haase for the publishing realization despite coincidence with the coronavirus crisis. I have been in close contact with Dr rer. biol. hum. Alexander Ammann for years, among other things through his work in the film and book series Visual Biology, and I am also indebted to him for this book for numerous intellectual suggestions. I would like to thank Bryn Grisham and her team, Anita Hattenbach and Viola Lewandowski for editing the book, as well as my son, Immo Terheyden, DDS. The patience and skill in translating my wishes into perfect drawings are worthy of special thanks to Mrs. Christine Rose. For the production I could rely on Mrs. Ina Steinbrück. Last but not least I would like to thank the numerous colleagues in the scientific exchange internationally and nationally. In particular, the participants in my courses and continuing education courses have always stimulated me to further thinking and practice in bone augmentation by asking questions and reporting on the challenges of their practice activities. In particular, I would like to mention the Implantology Curriculum of the German Society for Implantology and the Academy for Practice and Science of the German Society for Dental, Oral and Maxillofacial Medicine, as well as the Master of Science course. Not the least thanks are due to my wife, Dr med Eva Ulrike Terheyden Niemann for her professional suggestions and corrections and support during the time-consuming and not very family-friendly business of book writing. I would like to address the last sentence to you, dear readers, with the request to enter into an exchange with me and to discuss the contents—this is the only way to move our field forward. Thank you very much for your time.

Prof Dr med Dr med dent Hendrik Terheyden, FEBOMFS

Author

Prof Dr med dent Hendrik Terheyden is head physician at the Department of Oral and Maxillofacial Surgery, Helios Hospital in Kassel, Germany.

Hendrik Terheyden studied dentistry from 1983 to 1989 at the University of Kiel. In 1989, he was a staff physician for the Navy in Flensburg. From 1989-1992 he studied human medicine at the University of Kiel. In 1993 he became a specialist in oral surgery and in 1997 a specialist in oral and maxillofacial surgery with the additional title of plastic surgery (1999). In 1999 he completed his PhD (Habilitation) at the University of Kiel. He received the Wassmund Prize of the German Society for Oral and Maxillofacial Surgery (DGMKG). In 2004, he became an adjunct professor at Kiel University. From 2009 to 2012, he was president of the German Society for Implantology, and from 2017 to 2019, he was Chairman of the Oral and Maxillofacial Surgery Working Group of the German Society for Oral and Maxillofacial Surgery (DGZMK). Since 2006, Prof Terheyden has been section editor of the International Journal of Oral & Maxillofacial Surgery, and since 2012 he has been editor in chief of the International Journal of Implant Dentistry. Since 2021, he has served on the board of the Working Group of Senior Hospitalists of the German Society for Oral and Maxillofacial Surgery

Table of Contents

A BIOLOGIC BASICS

1 General Principles of Augmentation Surgery

1.1 Bone as a Success Factor in Implantology

1.2 Aims of Bone Augmentation: Function – Esthetics – Prognosis

1.3 Atrophy of the Alveolar Process

1.4 Classifications of Alveolar Ridge Atrophy

1.5 Alternatives to Alveolar Ridge Augmentation

1.6 Prosthetic Versus Regenerative Approaches to Defects

1.7 Soft Tissue Augmentation and Management

1.8 Risk Management: SAC Classification

1.9 Teamwork

1.10 References

2 Biologic Basis of Bone Regeneration and Wound Healing

2.1 Bone Tissue Structure

2.2 Wound Healing

2.3 Wound Balance: Proinflammatory and Anti-inflammatory Wound Environment

2.4 Bone Remodeling

2.5 Resorption Protection of Bone Grafts

2.6 Osteoconduction and Osteoinduction

2.7 Factors Influencing the Healing Potential of Bone Defects

2.8 Defect Classes and Augmentation Techniques

2.9 Mechanism of Impaired Wound Healing and Wound Dehiscence

2.10 Biofilm as a Triggering Factor of Impaired Wound Healing

2.11 The Race of Bacteria Against Angiogenesis

2.12 Clinical Consequences: Prevention of Wound Dehiscence

2.13 Open Wound Healing

2.14 Increasing Antibiotic Resistance

2.15 References

3 Bone Grafts

3.1 Biologic Effect of Bone Grafts

3.2 Graft Bed

3.3 The Gold Standard: The Autogenous Iliac Bone Graft

3.4 Donor Sites: Quality and Harvest Morbidity of Autogenous Bone Grafts

3.5 References

4 Augmentation Surgery Materials

4.1 Properties of Foreign Materials

4.2 Bone Graft Substitutes

4.3 Dentin as a Bone Graft Substitute

4.4 Bone Products: Allogeneic and Xenogeneic Bone Grafts

4.5 Soft Tissue Replacement Materials

4.6 Clinical Differential Indication of Autogenous Materials Versus Foreign Materials

4.7 Membranes

4.8 Bioactive Materials and Tissue Engineering

4.9 Conclusions on Bioactive Materials and Tissue Engineering

4.10 References

B OPERATING TECHNIQUES

5 Patient Management and Surgery Preparation

5.1 Elective Surgery

5.2 Patient Selection According to Risk Factors

5.3 Informing the Patient

5.4 Realistic Patient Expectations

5.5 Shared Decision Making

5.6 Anti-infective Patient Preparation

5.7 Surgical Preparation, Anesthesia, and Sedation

5.8 Perioperative Medication Including Antibiotics

5.9 Provisional Prosthetic Restoration

5.10 References

6 Bone Grafting: Standards and Surgical Technique

6.1 Conditions for Bone Grafting

6.2 Mixed Bone Grafts

6.3 Resorption Protection of Bone Block Grafts

6.4 Instruments

6.5 Surgical Procedure

6.6 One- or Two-Stage Implant Placement with Bone Grafting

6.7 References

7 Soft Tissue Management and Augmentation

7.1 Dimensions of the Soft Tissue around the Dental Implant

7.2 Access Incision Guidelines

7.3 Flap Types

7.4 Vestibuloplasty and Other Soft Tissue Plastic Surgery

7.5 Flap Tension and Mobilization

7.6 Suture Technique and Material

7.7 Implant Uncovering After Bone Augmentation

7.8 Soft Tissue Augmentation for Widening Keratinized Attached Gingiva on Dental Implants

7.9 Soft Tissue Augmentation to Increase The Mucosal Thickness at Dental Implants

7.10 Soft Tissue Augmentation in Conjunction with Immediate Implant Placement

7.11 Soft Tissue Augmentation Instead of Guided Bone Regeneration

7.12 Soft Tissue Augmentation for Recession Coverage on Dental Implants

7.13 Vascularized Connective Tissue Flap Coverage

7.14 Tunneling Techniques

7.15 Contraindications

7.16 References

8 Standard Surgical Techniques for Augmentation

8.1 Inlay Grafts

8.2 Interpositional Grafts

8.3 Appositional Bone Grafts (Horizontal Augmentation)

8.4 Onlay Bone Grafts (Vertical Augmentation)

8.5 References

9 Alternatives and Adjuncts to Standard Augmentation

9.1 Titanium Mesh Technology

9.2 Partial Tooth Extractions

9.3 Implant Site Preparation by Condensation, Bone Expansion Screws, Conical Implants, and Bone Spreaders

9.4 Vertical Distraction Osteogenesis of the Alveolar Process

9.5 Bone Ring Technique with Simultaneous Implant Placement

9.6 Extraoral Tent-Pole Technique in the Anterior Mandible and Lower Border Augmentation

9.7 Shell and Tent Techniques

9.8 Ridge Switch Graft for a Narrow Ridge

9.9 Apical U-Shape Splitting Technique

9.10 References

10 Extraction Socket Treatment

10.1 Gentle Tooth Extraction and Surgical Treatment of the Extraction Wound

10.2 Goals of Ridge Preservation

10.3 Socket Grafting in Intact Alveoli

10.4 Socket Grafting with an Alveolar Defect

10.5 Primary Reconstruction of Extraction Socket Walls Using Bone Blocks

10.6 Socket Seal Surgery

10.7 Augmented Immediate Implant Placement

10.8 Socket-Shield Technique

10.9 References

C CLINICAL CHALLENGES AND DECISION MAKING

11 Decision Making According to Defect Stage

11.1 Defect-Oriented Concept for the Differential Indication of Augmentation Procedures

11.2 Defect Stage 1/4

11.3 Defect Stage 2/4

11.4 Defect Stage 3/4

11.5 Defect Stage 4/4

11.6 References

12 Decision Making in the Anterior Esthetic Region

12.1 Special Anatomical Features of the Anterior Maxilla

12.2 Anatomical Features of the Anterior Mandible

12.3 Gingival Biotype

12.4 Gingival Height and Reverse Planning

12.5 Precise Augmentation by Avoiding Resorption

12.6 Implant Positioning

12.7 Augmentation for Dental Agenesis and Adolescents

12.8 Vertical Augmentation to Preserve Adjacent Teeth

12.9 Implant Treatment of Vertical Defects in Periodontally Compromised Dentition

12.10 Treatment of Bone Defects in the Anterior Maxilla

12.11 Treatment of Bone Defects in the Anterior Mandible

12.12 References

13 The Posterior Regions: Free-End Situations

13.1 Clinical Considerations in Free-End Situations

13.2 Comparison of Soft Tissue Healing in Free-End Situations in the Maxilla and Mandible

13.3 General Information on Short Versus Regular Implants

13.4 General Information on Narrow- Versus Regular-Diameter Implants

13.5 Pros and Cons of Vertical Augmentation in the Posterior Mandible

13.6 Pros and Cons of Sinus Elevation in the Posterior Maxilla

13.7 Conclusion on Differential Indication for Augmentation Versus Modified Implants in the Posterior Region

13.8 Differential Indication for Bone Augmentation in the Posterior Mandible

13.9 Differential Indication for Bone Augmentation in the Posterior Maxilla

13.10 References

14 The Atrophic Edentulous Jaw

14.1 Function (Mastication and Speech) and Alveolar Ridge Atrophy

14.2 Nutrition and Alveolar Ridge Atrophy

14.3 Dementia and Alveolar Ridge Atrophy

14.4 Quality of Life and Alveolar Ridge Atrophy

14.5 Facial Esthetics and Alveolar Ridge Atrophy

14.6 Dental Prosthetic Features in Severe Alveola Ridge Atrophy

14.7 Step 1: Differential Indication for Implant-Retained Overdenture Versus Implant-Supported Denture

14.8 Step 2: Differential Indication for Fixed or Removable Implant-Supported Dentures

14.9 Step 3: Differential Indication Based on Pros and Cons of Vertical Augmentation

14.10 Extreme Atrophy

14.11 Differential Indication for Augmentation-Free Restoration and Immediate Loading on Oblique Implants (All-on-Four Methods)

14.12 Differential Indication for Augmentation-Free Restoration of the Maxilla with Zygoma Implants

14.13 Differential Indication for Augmentation-Free Restoration of Cawood Class V to VI Atrophied Mandible with Short Implants

14.14 Differential Indication for Augmentation-Free Restoration with Subperiosteal Implants

14.15 Recommendations for Augmentative Treatment of Atrophied Edentulous Ridges

14.16 References

15 Reparative Surgery and Complication Management

15.1 Reparative Surgery and Implant Replacement

15.2 Augmentative Treatment of Peri-implantitis

15.3 Infectious Complications of Augmentations

15.4 Preoperative Measures to Prevent Wound Dehiscence in Augmentation Sites

15.5 Intraoperative Measures to Prevent Wound Dehiscence in Augmentation Sites

15.6 Postoperative Measures to Prevent Wound Dehiscence in Augmentation Sites

15.7 Complications and Their Avoidance During Sinus Elevation

15.8 General Complications of Augmentation Surgery

15.9 References

A

BIOLOGIC BASICS

1

General Principles of Augmentation Surgery

Information has never been as widely available as it is today. This is especially true for dental implantology, which is still very much in flux many decades after its establishment. In the dynamic interplay between product developers and clinicians, new biomaterials and augmentation procedures enter the practice almost daily. There are countless publications and tempting continuing education courses on everything. The art of the (dental) practitioner is to correctly classify the amount of innovations and information for the benefit of the patient. What is good and what is bad for my patient? What is risky and what is predictable? What is effective and what is unnecessary? What pays off and what only costs? What is fashionable and what is enduring? The basis of judgment is experience and profound knowledge.

Dentistry has traditionally been strongly influenced by material sciences, because until a few years ago it took place predominantly outside the better ectodermal envelope of the body. Through implantology, among other things, the spectrum of dental treatment has expanded into the interior of our patients’ bodies. This requires better: a broadened theoretical basis for dentistry, which is derived from biology and medicine. The performance of the surgeon in augmentations depends not only of the correct technical execution, but above all the correct therapeutic recommendations under consideration of numerous influencing factors. This book is intended to help the practitioner build self-confidence and critical judgment in making good decisions and to provide some joy when the biology behind one’s clinical observations becomes apparent and sustained success is achieved.

1.1 Bone as a Success Factor in Implantology

The opportunity for functional and biological tissue regeneration is a privilege of dentistry compared to most other branches of medicine. Today, bone regeneration techniques allow dentists to accept almost no deviation in the shape of the jaw bone as a given, whether acquired by accident, tumor, or atrophy of the alveolar ridge after tooth loss or as the result of congenital lack of dentition.

This also applies to corrections of the occlusal relation and vertical dimension of the jaws. The foundations for surgical correction of the bone and the overlying soft tissues in preparation for tooth replacement treatment were largely laid by specialists in preprosthetic surgery in the 1970s and 1980s.1 Bone augmentation is a safe procedure in the long term. Data from prospective 10-year studies exist today for major techniques.

Fig 1-1 The fate of the implant is decided by the first millimeter. Roughened implant parts must not come into contact with the bacteria of the sulcus. Augmentation is required here.

The fate of the implant is decided on the first millimeter2 (Fig 1-1). A circumferential ring of bone covering all roughened portions of the implant on all sides can prevent downgrowth of the junctional epithelium and thus pocket formation3 and supports a good long-term prognosis for lasting implant health.4 Circumferential bone of at least 1-mm but preferably 2-mm thickness supports a good long-term prognosis and the basis for a soft tissue sealing apparatus. Sufficiently thick bone creates a natural gingival color by preventing a discoloration by the dark titanium of the dental implants (Fig 1-2). Bone is generally the basis of esthetics as it defines the height of the gingiva (Fig 1-3) and anchors the facial soft tissues. The alveolar process must be sufficiently wide to accommodate a stable implant with sufficient material thickness that will not deform or even fracture under mastication. In addition, the bone height should be sufficient to avoid long dental crowns and interdental plaque retention. Bone should be present within the prosthetic and functional loading axis of the restoration. This allows the prosthesis to be more delicate and esthetic (Figs 1-4 to 1-6).

Fig 1-2 Photo superimposition. Replacement of the maxillary lateral incisors with titanium implants. A gray discoloration by titanium should be prevented by sufficiently thick bone and soft tissue.

1.2 Aims of Bone Augmentation: Function – Esthetics – Prognosis

The aforementioned guidelines result in the following goals of bone augmentation:

Function

Esthetics

Prognosis

Implantology has masticatory rehabilitation as its primary medical goal. With good function, good esthetics often results automatically. In addition, esthetics is becoming more important as a therapeutic goal. The position of the bone shoulder determines the position of the overlying soft tissue and thus the gingival (pink) esthetics. These relationships are summarized in the English rhyme:

The tissue is the issue,

but the bone sets the tone,

and the clue is the screw. (D. Garber, Atlanta)

Fig 1-3 The soft tissue height (biologic width) is composed of the following elements: connective tissue attachment, junctional epithelium, and sulcus depth or free gingiva. It is the same for teeth and implants, averaging about 3 mm. Because the soft tissue height is a constant, it can be planned in advance by augmenting the bone height.

Fig 1-4 In implant-retained prosthetic restoration of the maxilla, the implants can be placed intersinusoidally in the anterior region, avoiding sinus floor augmentation. In this case, however, the prosthesis must be an overdenture or otherwise made very solidly to avoid fracture. With augmentation, the support polygon is large, allowing the placement of 6 to 8 implants and the use of a removable prosthesis that can be designed much more delicately because the risk of breakage is low.

Fig 1-5 Maxillary restoration without augmentation. a. Overdenture for the maxilla with intersinusoidally placed implants, avoiding augmentation. b. Lack of salivary irrigation underneath the overdenture leads to reddening of the palate (ie, denture stomatitis, candidiasis) and gingival hyperplasia at the implants with pseudo-pocket formation. The masticatory load-bearing capacity is relatively low due to the lack of abutment spread.

Fig 1-6 Maxillary restoration with augmentation. a. Sinus floor augmentation allowed the placement of more implants, providing a greater number of abutments. b. Panoramic image after sinus floor augmentation on both sides. c. Prosthetic restoration with a delicately crafted removable and prosthesis that allows for irrigation and interdental cleaning (Prof. Dr. M. Kern, Kiel). d. Galvano-telescopic copings. e. Intraoral frontal view of prosthesis. f. Extraoral appearance of the lips with natural esthetics.

1.3 Atrophy of the Alveolar Process

In contrast to the jaw base, the alveolar process in the maxilla and mandible is not embryologically endochondrally preformed. The alveolar process bone is formed via intramembranous ossification alongside the eruption of teeth to the occlusal plane. Accordingly, this bone also disappears after the teeth are lost. Alveolar ridge atrophy therefore is physiologic and not a disease; however, the consequences, ie, loss of masticatory function and the inability to wear dentures, can lead to disease, especially since the atrophy progresses very rapidly in some patients. Resorption of alveolar bone begins at the buccal bone lamella and later involves the oral bone lamella. The resorption of the maxillary alveolar process is also explained by the principle of bundle bone (Fig 1-7). This type of bone consists of the calcified insertions of ligaments. In the alveolar process, these are the insertions of Sharpey fibers (after William Sharpey, anatomist in London). After tooth extraction, the periodontal ligament disappears as does, inevitably, the bundle bone, which can make up the entire facial lamella of the dental compartments. Loss of the alveolar process is accelerated by, among other things, marginal periodontitis, traumatic tooth extraction, unstable overdentures, and generalized osteoporosis. Particularly severe atrophy with formation of a flappy ridge and irritation fibromas is seen in combination syndrome (Fig 1-8) in the anterior maxilla when hard mandibular residual dentition or mandibular dental implants occlude against a maxillary full denture supported only by soft tissues. As atrophy occurs, there is also decreased blood flow to the jaws, which can cause a reverse flow in the mental artery. The risk of fracture increases due to the reduction in the cross-section of the mandible.

Since the teeth and the alveolar process in the maxilla are physiologically inclined buccally and there is a narrow apical base, height reduction of the bone results in a shift of the ridge center inward, ie, centripetal atrophy of the maxilla (Fig 1-9). With a wide apical base and inwardly inclined teeth in the mandible, the opposite occurs in the mandible. The ridge center moves outward with the height reduction of the alveolar process, ie, centrifugal atrophy of the mandible. This effect can lead to a change in the jaw relationship, causing pseudoprognathism and crossbites in the posterior region. The pseudoprognathism is exacerbated because the vertical occlusal dimension usually decreases over the course of life due to tooth attrition, abrasion, tooth extractions, and periodontal tooth migration, among other factors. This causes the mandible to rotate forward in the temporomandibular joint.

Fig 1-7 Bundle bone is the anchorage of tendons and ligaments in the skeleton. The alveolar process consists almost entirely of bundle bone, especially in the maxilla. Alveolar bone is carried alongside the teeth as they erupt to the occlusal plane. When the teeth are lost, the bundle bone also disappears, initially buccally and later lingually and palatally. This effect explains the rapid volume loss of extraction sockets and alveolar ridge atrophy as a physiologic and unavoidable phenomenon unless the bone is physiologically loaded again by dental implants (ie, the bone-protective effect of dental implants).

Due to the shrinkage of their attachment sites on the tooth-bearing alveolar process, the perioral mimic muscles lose their tension. The lips curl in and narrow. Because of the loss of support of the teeth and alveolar processes, the cheeks and lips collapse. As a result of the loss of vertical occlusal dimension, the corners of the mouths tend to turn downward, and lip incontinence may occur, causing drooling and Candida infestation. The mentalis muscle increasingly loses its attachment to the anterior alveolar process, and the chin may droop. All in all, the stigmatizing typical lower face of a toothless old person develops. The decreasing chewing ability often causes a change of diet to diabetogenic food and is statistically correlated with premature onset of dementia,6 without a causal relationship being proven. Thus, severe alveolar ridge atrophy is not a simple sign of aging but a pathological condition with consequences for the whole organism. Masticatory rehabilitation with dental implants becomes a general medical goal.

Fig 1-8 Patient with combination syndrome. a. The panoramic view shows the isolated alveolar ridge atrophy in the anterior maxilla. The hard occlusal force of the mandibular residual dentition meets the soft tissue–supported maxillary full denture, which repeatedly tilts forward, especially under protrusive contacts, thus accelerating the physiologic alveolar ridge atrophy in a localized manner. b. Irritational fibromas in the anterior maxilla caused by ill-fitting full dentures. These pathologies of the vestibular mucosa result particularly when full dentures are advanced anteriorly well beyond the ridge. If they are overloaded anteriorly due to a combination syndrome and the occlusion is not balanced, the prostheses can increasingly tip forward during advancement. In parallel, the corner of the mouth shows candidiasis.

1.4 Classifications of Alveolar Ridge Atrophy

The atrophy of edentulous jaws as a whole is best described by the international classification according to Cawood and Howell (1991)7 (Fig 1-10).

The resorption stage of the individual implant site can be classified by the quarter rule according to Terheyden (2010)8,9 (Fig 1-11). This classification is based on the typical pattern of resorption of the alveolar process after tooth extraction and has the advantage that suitable treatment methods can be assigned to the respective stages (see chapter 12).

Initially, the facial alveolar wall usually resorbs first. If its coronal portion is atrophied, an implant can still be placed with primary stability, but a vestibular dehiscence defect is present (first quarter). With further atrophy, the entire facial wall is resorbed, resulting in a knife egde ridge (second quarter), with the oral wall still standing (corresponding to Cawood class IV). At this stage, there is usually insufficient bone to stabilize an implant, so a staged bone augmentation is necessary. The next stage is a reduction in the height of the ridge as a whole, with the oral wall still partially intact (third quarter), until finally the alveolar process is completely resorbed (fourth quarter; (corresponding to Cawood class V).

This consideration of the cross-section of the individual implant site should be supplemented by an occlusal view of the alveolar bone envelope (Fig 1-12). The term alveolar bone envelope was originally established in the orthodontic and periodontal literature10 and describes the buccal contour line of the alveolar bone in the dental arch. If intact neighboring periodontium is present in a singletooth gap, this is referred to as a contained defect within the envelope (single- or double-tooth gap with intact neighboring periodontium). The situation becomes more difficult with larger gaps or gaps without neighboring periodontium with a poorly defined envelope or in the edentulous jaw with an undefined envelope.

Fig 1-9 Effects on alveolar bone atrophy. a. Alveolar ridge atrophy has resulted in maxillary retroposition due to the oblique position of the superior alveolar process and the narrow apical base of the maxilla (left image). The reduced vertical occlusal dimension due to alveolar ridge atrophy has resulted in counterclockwise rotation of the mandible at the pivot point of the temporomandibular joint. This has caused pseudoprognathism. Alveolar bone augmentation (eg, by LeFort I interposition in the maxilla and sandwich interposition in the mandible) leads to forward and downward movement of the upper alveolar process in the direction of the red arrows. The goal is to create the conditions present with a full dentition (right image) through dental implants. b. Due to alveolar ridge atrophy, the perioral mimic muscles have lost their bony attachment point. The lips become narrower and inverted, and especially the mentalis muscle loses its upper attachment point at the level of the roots of the mandibular incisors. As a result, the chin sags. Passive relining of the lips by a dental prosthesis does not improve the muscle attachments or traction. Bony regeneration of the alveolar processes can restore a condition similar to that before tooth loss. c. In contrast to conventional complete dentures, implant-supported dentures can achieve better pretension of the facial muscles because they do not dislocate as easily as conventional complete dentures when the lips are pulling back. If the alveolar processes are also reconstructed by bone augmentation, the mimic muscles regain their correct attachment points. In addition, stretching of the lower face and retraction of the chin can be achieved by increasing the vertical occlusal dimension, so that the nasolabial and supramental folds are smoothed. The goal is a relaxed and younger facial expression as a side effect of masticatory rehabilitation. (Adapted from Cawood.5)

Fig 1-10 The classification of alveolar process atrophy of the edentulous maxilla according to Cawood and Howell.7 (Adapted from Cawood.5)

Fig 1-11 Classification of the implant site following the natural resorption stages in quarters, according to Terheyden.8

Fig 1-12 a. The position within the envelope (contour line of the dental arch) is important for the prospective success of a localized augmentation. Also, it is favorable for success if a defect is enclosed by bony walls (ie, a contained defect). b. The chances of success of a localized augmentation increase if the augmentation volume is within the envelope. Therefore, the implant should usually be placed against the palatal/ lingual wall and should not be too large in diameter.

1.5 Alternatives to Alveolar Ridge Augmentation

Augmentation surgery always comes at a price, in terms of surgical burden, discomfort, and cost for the patient; surgical complexity for dentists and their teams; and increased possibility of complications. The risks and benefits of augmentation surgery should always be well communicated and weighed. Many efforts are underway to reduce the surgical burden of bone augmentation through alternatives and minimally invasive techniques.

Overall, the development of implantology, supported by new materials, is showing that good masticatory function can be achieved even without augmentation measures. This is particularly relevant for patients undergoing antiresorptive therapies, which do not allow bone augmentation surgery at all. Furthermore, the success of therapy is made less dependent on the individual skill of a clinician, which is a general trend in medicine. Examples of augmentationfree implant surgery are zygoma implants or the renaissance of the subperiosteal-implants in severe alveolar ridge atrophy (see chapter 14).

1.6 Prosthetic Versus Regenerative Approaches to Defects

In the defect prosthetic approach, missing tissue and function is replaced by foreign material, ie, a prosthesis made of plastic, ceramic, and metal, similar to a prosthesis for missing limbs. In this therapeutic approach, the dental implant is a retaining anchor for the prosthesis. Because the implant is also a risk factor due to the risk of biologic complications, as few implants as possible are planned, sometimes as few as only one. The rationale is that the patient can concentrate their hygiene efforts on a few posts, and that fewer implants equate to lower costs.

Fig 1-13 Prosthetic versus regenerative approaches to defect treatment.

The replacement of missing body parts with a prosthesis is the conventional procedure in many medical fields; the regenerative approach of augmentation is seen as the future.11 This approach has broader goals than mere prosthesis retention, including a functionally and biologically complete regeneration of the missing tissue by the body’s own material and a long-term, if not lifelong, prognosis of implants. In regenerative replacement, the primary function of the implant is as a tooth root for the introduction of masticatory forces into the jaw. Only the introduced masticatory forces initiate the functional remodeling of the tissues, which ensures their lifelong preservation. In the body, only what is functionally defined is preserved. Therefore, with this approach, there is also more of a tendency for a higher number of dental implants. This concept incorporates delicate dentures reduced to single crowns with little metal or other foreign materials, almost a conservative dentistry approach.

In practice, the decision between the two therapeutic approaches is usually relativized by the age of the patients, in that younger and healthy patients tend to be good candidates the regenerative approach, and older and sick patients are better served by the defect prosthetic approach. This is related to the physical resilience, the service life, the baseline situation of the defects, the patient’s hygienic ability, and the desired masticatory function.

1.7 Soft Tissue Augmentation and Management

For didactic reasons, bone augmentation and soft tissue augmentation are often treated in separate lectures and textbooks. In clinical practice, this separation is difficult. This book instead follows a common path for both, because a good implant prognosis requires a mucosal thickness of 3 mm12 and keratinized tissue width of 2 mm,13 which corresponds to the dimensions of the biologic width. Also, bone grafts heal better and undergo less resorption under thick soft tissues than under thin ones. Some of the goals of bone augmentation, such as preventing gray show-through of titanium (Fig 1-14), can also be achieved with soft tissue grafts, but their long-term stability is not as well documented scientifically, with 1- to 3-year data available,14 while 10-year data are available for the same indication in bone.15 However, the soft tissues must also not be too high or overaugmented to avoid the formation of pseudopockets as a space for pathogenic flora. Finally, bone augmentation will only heal without loss if the soft tissue wound above it heals reliably. Good soft tissue management is therefore an inseparable part and a basic requirement of augmentation surgery (see chapter 7).

Fig 1-14 Titanium shows through thin soft tissues.

1.8 Risk Management: SAC Classification

Augmentation surgeries usually have an increased degree of difficulty compared to simple implant placement and belong to groups A and C of the SAC classification16 (Fig 1-15). Augmentation operations place higher demands on the surgeon’s training and equipment than S-level implant procedures:

S

traightforward: No augmentation. This corresponds to a standard treatment without increased surgical anatomical risks and/or prosthetic problems.

A

dvanced: One-stage augmentation. In this situation, there is still enough residual bone for simultaneous implant placement. This refers to a demanding treatment with increased surgical and/or prosthetic risk potential and corresponding equipment and training requirements for the team.

C

omplex: Two-stage augmentation. In this situation, there is not enough bone for simultaneous implant placement. Complex implant treatment at the specialist level with associated risks is required.

Fig 1-15 The SAC classification of the International Team for Implantology (ITI)16 for the surgical and prosthetic aspects of implant treatment.

1.9 Teamwork

Due to the stress and risks of surgical intervention, many patients and dental practitioners decide against implant treatment in cases of bone deficiency, although perhaps both sides would benefit from an osseointegrated prosthesis. By collaborating with surgically specialized colleagues with appropriate expertise, this threshold can be lowered. The discomfort associated with wound healing can be temporarily outsourced to the surgeon by a referring dentist. Subsequent prosthetic treatment is performed back in the home practice. In such a team, the family dentist functions as the architect of the overall treatment, coordinating the individual steps and continuing the patient’s care thereafter.

1.10 References

1. Härle F. Atlas der präprothetischen Operationen. Munich: Hanser, 1989.

2. Schwarz F, Sahm N, Becker J. Impact of the outcome of guided bone regeneration in dehiscence-type defects on the long-term stability of peri-implant health: Clinical observations at 4 years. Clin Oral Implants Res 2012;23:191–196.

3. Iglhaut G, Schwarz F, Winter RR, Mihatovic I, Stimmelmayr M, Schliephake H. Epithelial attachment and downgrowth on dental implant abutments—A comprehensive review. J Esthet Restor Dent 2014;26:324–331.

4. Schwarz F, Giannobile WV, Jung RE. Groups of the 2nd Osteology Foundation Consensus Meeting. Evidence-based knowledge on the aesthetics and maintenance of periimplant soft tissues: Osteology Foundation Consensus Report Part 2-Effects of hard tissue augmentation procedures on the maintenance of peri-implant tissues. Clin Oral Implants Res 2018;29(Suppl 15):11–13.

5. Cawood JI. Reconstructive Preprosthetic Surgery and Implantology. In: Härle F, Champy M, Terry BC (eds). Atlas of Craniomaxillofacial Osteosynthesis: Miniplates, Microplates and Screws. Stuttgart: Thieme, 1999:123–136.

6. Cardoso MG, Diniz-Freitas M, Vázquez P, Cerqueiro S, Diz P, Limeres J. Relationship between functional masticatory units and cognitive impairment in elderly persons. J Oral Rehabil 2019;46:417–423.

7. Cawood JI, Howell RA. Reconstructive preprosthetic surgery. I. Anatomical considerations. Int J Oral Maxillofac Surg 1991;20:75–82.

8. Terheyden H. Bone augmentations in implant dentistry. Dtsch Zahnärztl Z 2010;65:320.

9. Cordaro L, Terheyden H. ITI Treatment Guide 7. Ridge Augmentation Procedures in Implant Patients. Berlin: Quintessenz, 2014.

10. Wennström JL, Lindhe J, Sinclair F, Thilander B. Some periodontal tissue reactions to orthodontic tooth movement in monkeys. J Clin Periodontol 1987;14:121–129.

11. Eckert SE. Time to bid adieu to removable dental prostheses. Int J Oral Maxillofac Implants 2014;29:535.

12. Linkevicius T, Puisys A, Steigmann M, Vindasiute E, Linkeviciene L. Influence of vertical soft tissue thickness on crestal bone changes around implants with platform switching: A comparative clinical study. Clin Implant Dent Relat Res 2015;17:1228–1236.

13. Giannobile WV, Jung RE, Schwarz F. Groups of the 2nd Osteology Foundation Consensus Meeting. Evidence-based knowledge on the aesthetics and maintenance of periimplant soft tissues: Osteology Foundation Consensus Report Part 1-Effects of soft tissue augmentation procedures on the maintenance of peri-implant soft tissue health. Clin Oral Implants Res 2018;29(Suppl 15):7–10.

14. Rotundo R, Pagliaro U, Bendinelli E, Esposito M, Buti J. Long-term outcomes of soft tissue augmentation around dental implants on soft and hard tissue stability: A systematic review. Clin Oral Implants Res 2015;26(Suppl 11): 123–138.

15. Chappuis V, Rahman L, Buser R, Janner SFM, Belser UC, Buser D. Effectiveness of contour augmentation with guided bone regeneration: 10-year results. J Dent Res 2018;97: 266–274.

16. Dawson A, Chen S, Buser D, Cordaro L, Martin W, Belser U. The SAC Classification in Dental Implantology. Berlin: Quintessenz, 2011: 19 ff.

2

Biologic Basis of Bone Regeneration and Wound Healing

Unlike machines, the human body does not require space-demanding storage of spare parts; rather, self-repair unfolds on demand from a few pluripotent stem cells. These lie as space-saving pericytes in the walls of the blood vessels, which is practical because neoangiogenesis is already a prerequisite for tissue regeneration for nutritional reasons.

2.1 Bone Tissue Structure

Vascular supply and bone marrow

Bone consists of soft and hard tissue. The soft tissue includes the bone cells, the marrow, and the vessels necessary to supply them. Compact bone is nourished by the central vessels of the haversian system (named after Clopton Havers, English anatomist, 1650–1702) (Fig 2-1). Only the outermost layers are nourished by diffusion from the vessels of the periosteum. After surgical detachment of the periosteum, this part of the bone becomes insufficiently supplied. Among other things, this phenomenon is used as an explanation for why after periosteal detachment, a small surface resorption of the bone of about 0.5 mm is observed.

The maxilla has a rather spongy structure and a peripheral blood supply type. The maxilla is largely peripherally perfused with periosteal vessels via various arterial flow areas (greater palatine artery, anterior and posterior alveolar arteries, nasopalatine artery) through a plexus (Fig 2-2). Thus, the maxillary bone is still nourished via the periosteum even if parts of the internal vascular supply are interrupted, for example, by osteotomies or bone segment formation.

The mandible, on the other hand, has a much more sensitive vascular supply of the central type. Large parts of the horizontal branch are perfused almost exclusively via the central vessel of the inferior alveolar artery. Only the middle portion of the chin arch receives its perfusion through some vessels from the floor of the mouth. The central artery is often occluded as a result of arteriosclerosis, especially in older patients, in which case there is a reversal of flow in the mental artery.1 In addition to the nourishing vessels, the bone houses the hematopoietic tissue in the bone marrow, which is a fluid tissue without inherent stability. Inside the bone, unlike other sites in the body, the bone marrow is located in a place of mechanical rest and external stability. This is also the location of mesenchymal stem cells, which are the origin of bone healing.

Fig 2-1 a. Bone is one of the tissues with a strong blood supply. There are cross connections between the central vessels of the osteons, to the periosteum and into the bone marrow. b. In toluidine blue staining, a cross-section through cortical bone looks quite homogeneous (Laboratory MKG Kiel, hard ground section, pig, original magnification ×20). c. A similar preparation to 2-1b after intravital labeling with fluorescent dyes appears much more vivid. It shows the formation of osteons in compact bone. After illumination with UV light, the growth bands are shown by xylenol orange (2 and 3 weeks), calcein green (4 and 5 weeks), and alizarin complexone red (6 and 7 weeks) (Laboratory MKG Kiel, undecalcified hard ground section, pig, original magnification ×20).

Fig 2-2 a. Peripheral blood flow type in the maxilla via multiple periosteal vessels. b. Central circulation type in the mandible via the central vessel of the inferior alveolar artery.

Bone cells

The bone building cells possess progenitor cells (pluripotent mesenchymal stem cells, osteoprogenitor cells), which represent a regenerative reserve. In addition to the bone marrow, it is now known that the pericytes or perivascular cells of the blood vessels are the pluripotent mesenchymal stem cells.2 This is practical because there can be no major bone regeneration without a blood supply. When needed, these cells differentiate into osteoprogenitor cells and finally, after adherence to a matrix, into osteoblasts that build osteoid and then wall themselves into the matrix as osteocytes. Some cover the entire bone surface toward the medullary cavity without gaps as lining cells. If there are gaps in the lining cell layer, eg, due to surgical trauma, this is a signal for osteoclast development. This also explains the surface resorption after periosteal detachment.

Osteoclast function

Osteoclast function is under the influence of osteoblasts. Osteoblasts possess receptors for a wide variety of hormones and messenger substances and can produce RANKL (receptor activator of nuclear factor kappa-beta ligand) under the influence of parathyroid hormone. Together with M-CSF (macrophage colonystimulating factor), they thus control the confluence of monocytic progenitor cells into multinucleated osteoclasts. Osteoclasts are immune cells and, like macrophages, are derived from bloodstream monocytes, which in turn are derived from bone marrow hematopoietic stem cells. At sites where the lining cells detach, osteoclasts attach to the vacant bone sites. The attachment requires the protein osteopontin from the bone matrix, which binds in a ring with integrins from the osteoclasts. This creates a kind of suction cup for the osteoclasts, within which a very strongly acidic environment can be generated by proton pumps without the acid escaping into the rest of the tissue. The acid decalcifies the bone so that its proteins are now exposed for attack by acidic enzymes such as cathepsin. The Howship lacuna is formed (named after John Howship, surgeon and pathological anatomist, London, 1781–1841). By endocytosis, materials in solution in the lacuna are transported to the interior of the cell, where they are further digested. If bacterial lipopolysaccharide is present among these molecules, rapid inflammatory resorption can be initiated by Toll-like receptors,3 which usually leads to very rapid removal of bone or tooth tissue. In contrast to replacement resorption, inflammatory resorption does not fill the bone during bone remodeling; it is incompatible with bone formation due to the proinflammatory wound environment. It leaves defects and sequestra, so the bone surgeon takes preventive measures to ensure a low bacterial presence in the wound.

Basic bone substance

The hard tissue of the bone is a composite material consisting of fibers and filler, with the fibers absorbing tensile loads and the filler absorbing compressive loads. There are many examples of such composites in engineering (eg, reinforced concrete or glass fiber–reinforced plastic in boat building). The bone matrix consists mainly of collagen (fibers) and mineral in the form of hydroxyapatite crystals (filler). This mineral is practically insoluble in water at pH 7.4, but this changes rapidly at an acidic pH (as in caries formation). The mineral can be released from the bone composite by acid treatment to access the proteins of the bone. The bone mineral hydroxyapatite is the model for many bone substitutes; the body accepts certain technologically produced materials as artificial bone matrices, or the bone precursor cells cannot recognize them as foreign due to the lack of protein structures.

Nonsoluble hard substance proteins

The proteins remaining after dissolution of the mineral are divided into soluble and insoluble bone proteins. Collagen type I is the most important representative of the insoluble proteins in terms of quantity. The stability of bone is determined by its internal structure. This internal structure results from the direction of the collagen fibers, which, like wires, provide internal tensile strength to the bone. The internal direction of the collagen fibers can be visualized in polarized light. The basic building block of the mature cortical bone is the osteon with the central haversian canal. In the lamellar bone, the collagen fibers are wound around the osteon in a parallel, helical pattern in opposite directions, like circular plywood, which explains the high mechanical stability of this bone type. In contrast, the immature woven bone initially forms during wound healing. In woven bone, the collagen fibers are not arranged in parallel but in a braid-like pattern and can thus absorb forces evenly from all directions.

Fig 2-3 Bone components as they can be extracted by stepwise treatment with acids and solvents. On their own, bone morphogenetic protein (BMP) and bone matrix are inactive. Only when the individual components are recombined does an osteoinductive bone substitute material result. For example, recombinant BMP can be combined with bone substitute material to obtain an active graft.

Fig 2-4 The four temporally overlapping phases of wound healing in soft tissue.

Soluble hard substance proteins

The soluble bone proteins can be solubilized from the decalcified bone matrix by the solvent guanidine hydrochloride. The collagenous bone matrix then remains (Fig 2-3). The soluble protein fraction contains, among other things, signal molecules (growth factors and differentiation factors) and about 40 known bone-specific proteins, such as osteopontin, bone sialoprotein, and osteocalcin. The soluble fraction also contains bone morphogenetic proteins (BMPs; about 1 mg per kg bone). Allogeneic bone grafts are sometimes partially decalcified during manufacture so that the natural BMPs are more available in the wound. The material is called demineralized freeze-dried bone allograft (DFDBA).

2.2 Wound Healing

For didactic purposes, wound healing can be divided into four phases: exudative, inflammatory, proliferative, and remodeling. Every wound, whether in bone or soft tissue, passes through these four phases, which overlap in time (Fig 2-4).

Exudative phase (coagulum)

The first phase of wound healing is the exudative phase, which lasts from a few minutes to hours. It is characterized by hemostasis by platelets and polymerization of fibrin, which forms a provisional extracellular matrix. This is necessary for the storage of growth factors and as a scaffold structure for the migration of the wound-healing cells. When the bone is mechanically injured by an implant osteotomy, a defect is created. Bleeding into this defect occurs from the bone marrow. The coagulum adheres to the wound edges, and the wound is mechanically stabilized by coagulation and proteins, eg, fibronectin, in the first hours. Dentists are familiar with the importance of blood coagulum due to the clinical picture of painful fibrinolytic alveolitis (ie, dry socket).

Inflammatory phase (purification)

The granulocytes are followed by the macrophages, which can survive under the oxygen-deficient conditions of a wound margin and here can initiate new vessel formation and thus the next phase by secreting vascular endothelial growth factor (VEGF).

Proliferative phase (healing)

When a wound is clean, macrophages can secrete growth factors such as transforming growth factor-b (TGF-b), insulin-like growth factor (IGF), and VEGF. These factors induce the formation of the granulation tissue that replaces the provisional matrix of the coagulum. The proliferative phase overlaps with the adjacent phases and lasts for days to weeks. Stimulated by VEGF from macrophages, perivascular cells of the adjacent blood vessels detach, divide, and assemble into infiltrates. They coalesce and form tubes that connect to existing blood vessels. They can then be perfused, improving oxygen supply to the defect area. Following the vessels, fibroblasts migrate chemotactically. These encounter the stored growth factors in the extracellular matrix of the blood coagulum and begin collagen formation. Up to this point, wound healing is largely nonspecific and similar in soft and hard tissue wounds. However, the phases that now follow occur much faster in soft tissue than in bone.

BMPs are responsible for the difference between wounds in bone and those in soft tissue. They are stored in the bone and are released when the bone is injured by fracture or osteotomy. An important source is also bone chips (eg, via a bone scraper) or the drill dust in an implant socket, which should therefore preferably not be rinsed out before implant placement. BMP leads to the differentiation of mesenchymal stem cells into bone precursor cells. The resulting osteoblasts can only exist on a firm foundation and anchor themselves to bone structures in their environment, mediated by integrins and osteopontin. When these anchorages signal mechanical quiescence to the cells (mechanoreceptors), they begin expressing bone-specific matrix proteins (osteoid), starting from the injured bone surface.

If the proliferative phase proceeds undisturbed, the matrix mineralizes, and woven bone is formed within a few weeks (Fig 2-5). Bone formation can also proceed on osteoconductive surfaces within reach of osteoblasts. Osteoconductive surfaces are dental implants or bone substitutes (Fig 2-6), which must first be covered with a protein film. The fibronectin contained in this layer is used by osteoblasts for mechanical anchorage. An intermediate stage of cartilage (endochondral ossification), as in the extremities, does not occur in the jawbone, where intramembranous ossification predominates.

Fig 2-5 Initial woven bone formation in the course of a sinus elevation with bone substitute mixture after 6 weeks. Preosteoblasts condense and accumulate around an osteoid matrix, which is already increasingly mineralized in the direction of the right margin of the image (Laboratory MKG Kiel, undecalcified hard section, toluidine blue, pig, original magnification ×200).

Remodeling phase (conversion)

This phase lasts weeks to years in bone. It involves the load-dependent remodeling of immature woven bone (collagen fibers disordered in random direction) into mature lamellar bone (collagen fibers parallel in tensile direction). Freely grafted bone and, within limits, some bone graft substitutes are completely degraded over time and replaced by new bone. This remodeling is also load-dependent because it has been observed that bone is retained on occlusally loaded teeth and dental implants, whereas in unloaded areas of the jaw it is usually quickly degraded again.

Fig 2-6 Particles of xenogeneic bone substitute material (pink) are covered by blue woven bone during healing following sinus elevation and are bonded together and integrated into the bone. The foreign material is osteoconductive; it covers itself with fibronectin, on which osteoblasts attach (Laboratory MKG Kiel, undecalcified hard section, toluidine blue, pig, original magnification ×200).

2.3 Wound Balance: Proinflammatory and Anti-inflammatory Wound Environment

The image of a scale (Fig 2-7) helps the physician to understand wound healing as a quantitative problem, for example, the quantitative depletion of defense cells when bacterial inoculation becomes too high or the quantitative consumption of antibodies when antigens become prevalent.

In the wound environment, a distinction must be made between proinflammatory polarization and anti-inflammatory polarization as the two sides of the scale. Regeneration and tissue formation only occur in the anti-inflammatory milieu, while the proinflammatory milieu ensures degradation of the extracellular matrix of the tissue. The amount of collagen currently present in the tissue is the equilibrium of constant formation and degradation of collagen. When degradative enzymes are secreted by granulocytes, the balance is shifted in the direction of degradation, because the granulocytes make room for themselves in order to be able to move through the tissue more easily. The clinical effect is the bleeding tendency of the inflamed gingiva, which bleeds on probing because collagen has been degraded. The proinflammatory milieu (Fig 2-8) is accompanied by matrix metalloproteinases and other matrix-degrading enzymes and consequently a low content of extracellular matrix and growth factors. Furthermore, proinflammatory cytokines, free radicals, and an acidic environment are found. Acid belongs to inflammation and is part of the bacterial defense mechanism of inflammation. The proinflammatory milieu also includes the urokinase plasminogen activator (uPA), which leads to dissolution of the coagulum and can cause fibrinolytic alveolitis (dry socket). Other examples of non-healing wounds that chronically persist in the proinflammatory mode are leg ulcers or gastric ulcers. Chronic secreting wounds remain in the proinflammatory state.

The anti-inflammatory environment includes the opposite, ie, much extracellular matrix and many growth factors. Important components of the extracellular matrix are fibronectin and proteoglycans. Important tissue growth factors include fibroblast growth factor (FGF), IGF, and TGF. High levels of tissue inhibitors of metalloproteinases (TIMPs) inactivate proteolytic enzymes. The anti-inflammatory environment is slightly basic with the natural tissue pH of 7.4. A basic pH is part of regeneration. Such a wound no longer secretes and heals dry.

The scales of wound healing can therefore tilt in both directions (see Fig 2-8). In both environments, macrophages play the leading role; they can determine the further fate of the wound with their polarization (M1 or M2). M1 polarization promotes the inflammatory milieu by secretion of proinflammatory cytokines.4 The M2 polarized macrophages promote angiogenesis, oxygenation, and extracellular matrix assembly through secretion of growth factors.5

From what has been said, it is clear that tissue regeneration and thus alveolar ridge augmentation and osseointegration of an implant are tied to an antiinflammatory environment. Anything that lowers the pH (eg, decay products of polylactide materials), stimulates the release of proinflammatory cytokines such as IL-1b or tumor necrosis factor-α (TNF-α) (eg, macrophages upon antigen contact), or degrades extracellular matrix (eg, fibrinolysis) stands in the way of bone formation. So the physician should try to shift the wound balance to the anti-inflammatory side. An example of weighing the balance on the anti-inflammatory side is the introduction of extracellular matrix into the wound in the form of collagen membranes, collagen fleece, or collagen powder.6 This acts like a magnet on the hypervalent proteases of the inflammatory environment and causes a substrate inhibition of this enzyme so that the endogenous collagens of the connective tissue are spared.7 This is an additional explanation for the effectiveness of the collagen membrane in guided bone regeneration (see chapter 6).

Fig 2-7 Diagram of wound equilibrium intended to illustrate wound healing as a quantitative process. A non-healing wound contains M1 polarized macrophages of the proinflammatory environment; a healing wound contains M2 polarized macrophages of the anti-inflammatory wound environment. The macrophages are the switch point of the transition from the inflammatory to the regenerative phase. IL-1, interleukin-1; TNF-α, tumor necrosis factor-α.

Fig 2-8 a. The anti-inflammatory wound environment of a healing wound is characterized by a high content of extracellular matrix (fibrin, collagen, fibronectin) and growth factors (VEGF; TGF; FGF, fibroblast growth factor; KGF, keratinocyte growth factor; PDGF, platelet-derived growth factor) and by neoangiogenesis. Tissue inhibitors of metalloproteinases (TIMPs) prevent collagen degradation by inhibiting proteases. b. The proinflammatory or toxic wound environment of a non-healing wound contains cytokines such as TNF-α, many granulocytes, and a weak extracellular matrix with few blood vessels. In the marginal area, hyperemia is present; centrally there is a lack of blood vessels. The toxic wound environment contains oxygen radicals that kill bacteria and somatic cells. Aggressive proteases are also found, which break down collagen and ultimately liquefy the tissue to form pus.

2.4 Bone Remodeling

In the body of young healthy patients there is usually no bone older than 3 to 4 years; later in life the renewal period extends to about 10 years.8 Bone tissue is continuously and abundantly rebuilt. The continuous remodeling explains how, some time after a bone injury, the bone can regain its anatomically correct shape without a visible scar; how bone grafts heal; and how the bone can functionally adapt to the occlusal forces of a dental implant.

The balance between the responsible cells, the osteoclasts and the osteoblasts, is ensured by their molecular coupling, among other things, via the BMPs stored and chemically bound in the bone matrix. The cell complex consisting of degrading and remodeling cells is referred to as the bone multicellular unit (BMU) (Fig 2-9) and is the biologic basis of the equilibrium that keeps bone mass constant despite constant remodeling. At any given time, about 1 to 2 million BMUs are active in the body under healthy conditions.8

In the healing process of a bone block for augmentation, a distinction must be made between resorption from the surface, which costs augmentation height and volume, and internal resorption. Sometimes too much surface resorption of the bone is undesirable, eg, over the facial implant surface or after bone grafting. In contrast, rapid internal resorption with rapid graft remodeling is desirable. The resorption phase in the BMU lasts about 30 to 40 days, followed by reconstruction over approximately 150 days.9 After the bone is degraded by osteoclasts, a rest period of several days occurs during the reversal phase.10 The growth and differentiation factors (BMPs) bound in the bone are exposed on the surface. So-called reversal cells11 clean the cavity and line it with a protein film. This cement line serves as an attachment point for the osteoblasts that subsequently move in. The reversal cells can enzymatically detach the superficial fringe-like proteins protruding from the bone, including the growth factors, by serine proteases.12 The coupling of osteoclasts and osteoblasts, ie, the balance of degradation and attachment, is thought to be regulated by the matrix-bound cytokines such as IGF and BMP, among others.13,14 According to this theory, BMP goes into solution and can now stimulate the receptors of osteoprogenitor cells, which initiates differentiation of the cells into osteoblasts. This differentiation only goes on for so long, as fresh BMP is found and limits itself when the Howship lacuna is replenished. Ideally, osteoclasts and osteoblasts are so precisely balanced by this molecular coupling that neither osteoporosis nor osteopetrosis develops. Similarly, BMPs are also released from the matrix by the dentist crushing autogenous grafts (eg, using a scraper). Thus, bone chips differentiate stem cells into osteoblasts that build new bone.

Fig 2-9