
eBook - ePub
Fundamentals of Implant Dentistry, Volume 1
Prosthodontic Principles
- 456 pages
- English
- ePUB (mobile friendly)
- Available on iOS & Android
eBook - ePub
Fundamentals of Implant Dentistry, Volume 1
Prosthodontic Principles
About this book
The authors of this definitive textbook cover the full range of restorative treatment options for edentulous and partially edentulous situations, from relatively simple problems that can be handled by a solo practitioner to those with substantial prosthodontics complexities, periodontal compromise of existing dentition, and significant bone and soft tissue defects.
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Yes, you can access Fundamentals of Implant Dentistry, Volume 1 by John Beumer III,Robert F. Faulkner,Kumar C. Shah,Peter K. Moy in PDF and/or ePUB format, as well as other popular books in Medicine & Dentistry. We have over one million books available in our catalogue for you to explore.
Information

3
Edentulous Patients: Patterns of Bone Resorption and Clinical Outcomes with Implants
Neal Garrett
Ichiro Nishimura
John Beumer III
Ichiro Nishimura
John Beumer III
Many patients are able to function effectively and comfortably with conventional complete dentures, with percentages of patients reporting moderate to high levels of denture satisfaction frequently over 80%.1ā4 However, some patients have difficulty adapting to or accepting conventional dentures (CDs) for a variety of reasons. For certain patients, the existing denture-bearing surfaces do not provide sufficient retention, stability, and support to ensure effective function of the mandible denture. This difficulty with unstable and poorly retained and supported mandibular CDs was a critical factor in the development of predictable dental implants. Even in patients with reasonable denture-bearing surfaces, common mandibular denture movement during oral function may compromise the patientās ability to simultaneously control the mandibular denture and the food bolus, leading to additional impairment in mastication and comfort. Therefore, several essential questions arise regarding implant-retained mandibular overdentures:
ā¢Which patients stand to benefit the most from implant therapy, and how do you identify them?
ā¢Will mandibular implant-retained or -supported prostheses improve the masticatory function of all edentulous patients or just some of them?
ā¢What are the success rates for various implant-based restorations for the edentulous maxilla and mandible?
ā¢Does the nature of implant retention or support (eg, number of implants, types of attachment) impact oral function and patient satisfaction?
ā¢Will the placement of osseointegrated implants prevent the natural processes of ridge resorption associated with denture use?
ā¢Has this service become the validated treatment?
Resorption Patterns
Long-term denture use contributes to resorption of the edentulous mandible.5ā7 Denture use during sleeping hours is especially destructive, particularly if the patient presents with chronic bruxing and grinding habits. Furthermore, in the case of Kellyās combination syndrome,8 the mucoperiosteum of maxillary anterior and mandibular posterior regions is compressed by occlusal forces and precipitates a resorptive remodeling response of the underlying bone.
The molecular mechanisms of compression forceāderived residual ridge resorption have yet to be fully elucidated. Yeh and Rodan9 reported that the application of tensile forces to cells results in the secretion of stress-induced molecules such as prostaglandin E (PGE), a well-known inducer of bone resorption. Tensile stressāinduced PGE may also be involved in orthodontic tooth movement, where compression of periodontal ligament cells leads to production of PGE as well as other bone resorptionāinducing molecules, resulting in resorption of alveolar bone.10 In an experimental model using edentulous rats, mandibular residual ridge resorption was shown to be regulated in part by PGE. The application of a cyclo-oxygenase inhibitor, blocking prostaglandin synthesis, effectively reduced bone resorption by up to 50%.11 Denture-induced residual ridge resorption hence may be explained by the mechanical stress-induced production of bone resorption mediators by the mucoperiosteum.
Following tooth extraction, bone resorption continues but at a reduced rate (Fig 3-1). After Tallgren12 and Atwood13 reported this phenomenon, Carlsson and Persson14 documented its progression (Fig 3-2). The loss of mandibular bone height was most rapid during the first 6 to 8 months after tooth extraction, which was followed by continuous resorption but at a reduced rate. This study also indicated that the rate of residual ridge resorption varies considerably among patients.

Fig 3-1 Continuous ridge resorption following tooth extraction.

Fig 3-2 Residual ridge resorption (RRR). Min, minimum; ave, average; max, maximum. (Data from Carlsson and Persson.14)
Since this observation, numerous studies have addressed the possible causes behind excessive residual ridge resorption seen in selected patients (for a review, see Jahangiri et al15). These studies primarily addressed: (1) anatomical factors, ie, maxilla versus mandible; (2) prosthodontic factors, ie, monoplane teeth versus anatomical teeth; and (3) systemic factors, ie, osteoporosis. Approximately 30% to 40% of women in the United States develop postmenopausal osteoporosis, and many are edentulous. However, most studies examining the effect of osteoporosis (ie, reduced bone mineral index) and the loss of mandibular residual ridge height have repeatedly failed to find any links.7,16ā18 However, Nishimura et al19 reported that postmenopausal osteoporotic women appeared to maintain the height of the edentulous mandible but significantly lost its width, leading to the development of a āknife-edgeā residual ridge (Fig 3-3). The development of the āknife-edgeā morphology was positively correlated with the loss of bone mineral density in cervical vertebral bones. Furthermore, clinical observations of patients with a knife-edge mandibular residual ridge revealed that there was a distinct undercut in the overlying oral mucosa,20 which was not evident in the flat residual ridge (see Fig 3-3). In addition, the edentulous maxilla of some osteoporotic patients exhibits severe bone resorption,21 with the ridge often covered by thin and highly stretched oral mucosa. Therefore, it is conceivable that systemic conditions associated with postmenopausal osteoporosis may affect oral mucoperiosteum remodeling and thus secondarily influence the pattern of residual ridge resorption.

Fig 3-3 Patients with osteoporosis tend to develop a knife-edge ridge with a mucosal undercut in the anterior region. (a) Typical resorption pattern. (b) Resorption pattern of an osteoporotic patient. Note the small maxilla and the knife-edge mandible. (c) Radiograph of a flat residual ridge. (d) Radiograph of a knife-edge residual ridge. (e) Intraoral view of a flat residual ridge. (f) Intraoral view of a knife-edge residual ridge.
Wound closure
Tooth extraction creates a sizable open wound in the oral cavity. While the bony socket is actively filled with newly formed alveolar bone and later remodeled, the gingival flaps undergo rapid contraction toward the center of the extraction socket (Fig 3-4). Longitudinal observations in monkeys reveal that oral mucosa contraction occurred not only during the extraction wound healing but persisted throughout the experimental period of 6 months.22 As a result, the edentulous mucosa tightly adhered to the actively resorbing residual alveolar bone (see Fig 3-4). The tight adherence of overlying oral mucosa to the highly atrophied maxilla and mandible has been described by Muller Devan.23

Fig 3-4 Rapid contraction of the extraction site after 7 days of healing. (a) Extraction site immediately after extraction. (b) Extraction site 1 week later.
Sukotjo et al24 isolated a novel gene from rat gingiva after tooth extraction wounding and called it wound-inducible transcript 3.0 or wit3.0. The expression of wit3.0 in the oral mucosa was significantly activated by tooth extraction in animals24 as well as in humans,25 and the high level of wit3.0 expression appeared to continue after initial healing of the extraction site. Wit3.0 is a small cytoskeleton molecule also called fibroblast growth factor receptor 1 oncogene partner 2 (FGFR1OP2) that contributes to the fibroblast-derived tissue contraction in vitro26 and in vivo.27 The wound-induced overexpression of FGFR1OP2/wit3.0 appeared to be a unique phenomenon for oral mucosa. For example, full-thickness open wounds created in mouse skin do not significantly induce its expression. Therefore, it has been postulated that the wound-induced synthesis of F...
Table of contents
- Cover
- Half Title Page
- Title Page
- Dedication
- Copyright Page
- Contents
- Foreword
- Preface
- Contributors
- Section I Introduction and Biologic Basis
- Section II Restoration of Edentulous Patients
- Section III Restoration of Partially Edentulous Patients
- Section IV Special Topics
- Glossary
- Index