Eliades / Katsaros The Ortho-Perio Patient

Clinical Evidence & Therapeutic Guidelines
1. Auflage 2019
ISBN: 978-0-86715-845-8
Verlag: Quintessence Publishing Co, Inc
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 224 Seiten

Although most orthodontic curricula provide courses on interdisciplinary orthodontic-periodontic treatment, there are still surprisingly few resources on the topic. Written by leading scholars in the field, this book provides a broad analysis of the topic from both the periodontal and orthodontic perspectives. The authors systematically analyze the scientific and clinical interactions of these specialties by reviewing all the available evidence and using case studies to demonstrate principles discussed in theory. The result is a text that outlines the treatment fundamentals and shows how to improve the therapeutic outcomes involving orthodontic-periodontic interventions. 346 illus.

Theodore Eliades, DDS, MS, Dr Med Sci, PhD, is Professor and Director of the Clinic of Orthodontics and Pediatric Dentistry at the University of Zurich in Switzerland, where he also serves as Director of Research at the Center of Dental Medicine. Additionally, he is a visiting professor in the Division of Craniofacial Development and Stem Cell Biology at King's College in London. Dr Eliades received his dental degree from the National and Kapodistrian University of Athens in Greece before completing a postgraduate program in orthodontics and a master's degree at Ohio State University; a doctorate in medical science at the University of Athens School of Medicine; and a PhD in biomaterials from the University of Manchester in England. He has published over 260 papers and book chapters and edited 11 books. He is a fellow of the Institute of Materials, Minerals and Mining; the Royal Society of Chemistry; and the Institute of Physics (UK). Dr Eliades has been Editor-in-Chief of the Journal of Dental Biomechanics; Associate Editor of the European Journal of Orthodontics, the American Journal of Orthodontics and Dentofacial Orthopedics, and Progress in Orthodontics; and an editorial board member and reviewer for numerous other journals. He also served as a member of the World Federation of Orthodontists task force for harmonization of worldwide postgraduate orthodontic education. ///////// Christos Katsaros, DDS, Dr med dent, Odont Dr/PhD, is Professor and Chair of the Department of Orthodontics and Dentofacial Orthopedics at the University of Bern in Switzerland, a position he has held since 2008. Prior to that, he served as Associate Professor from 2000 to 2002 and as Professor of Orthodontics from 2002 to 2008 at the Department of Orthodontics and Oral Biology at the Radboud University Nijmegen Medical Centre in The Netherlands. Dr Katsaros received his dental degree from the Aristotle University of Thessaloniki in Greece, and his orthodontic specialty training at the University of Saarland in Homburg/Saar, Germany, where he also completed his doctorate and habilitation. He received his Odont Dr/PhD degree from the University of Gothenburg in Sweden. Dr Katsaros has published over 200 papers and book chapters and edited 2 books. He serves as Associate Editor for the American Journal of Orthodontics and Dentofacial Orthopedics, Section Editor for The Cleft Palate-Craniofacial Journal, and as an editorial board member or reviewer for several international scientific journals. Dr Katsaros previously served as President of the European Orthodontic Society and is an active member of the Angle Society of Europe.

Autoren/Hrsg.

Eliades, Theodore

Katsaros, Christos

Leseproben

Bone Biology and Response to Loading in Adult Orthodontic Patients

Dimitrios Konstantonis

Orthodontic movement is achieved due to the ability of alveolar bone to remodel.1–3 The bone-remodeling process is controlled by an equilibrium between bone formation in the areas of pressure and bone resorption in the areas of tension as the teeth respond to mechanical forces during treatment. The main mediators of mechanical stress to the alveolar bone are the cells of the periodontal ligament (PDL). The PDL consists of a heterogenous cell population comprised by nondifferentiated multipotent mesenchymal cells as well as fibroblasts. The periodontal fibroblasts have the capacity to differentiate into osteoblasts in response to various external mechanical stimuli. This feature of the PDL fibroblasts plays a key role in the regeneration of the alveolar bone and the acceleration of orthodontic movement.

Current research provides scientific data that elucidates the molecular response of the human PDL fibroblasts after mechanical stimulation.4–6 Integrins at focal adhesions function both as cell-adhesion molecules and as intracellular signal receptors. Upon stress application, a series of biochemical responses expressed via signaling pathway cascades, involving GTPases (enzymes that bind and hydrolyze guanosine triphosphate [GTP]), mitogen-activated protein kinases (MAPKs), and transcription factors like activator protein 1 (AP-1) and runt-related transcription factor 2 (Runx2), stimulate DNA binding potential to specific genes, thus leading to osteoblast differentiation. Consecutively, the activation of cytokines like receptor activator of nuclear factor ?B ligand (RANKL) and osteoprotegerin (OPG) regulates osteoclast activity. Despite the importance of these biologic phenomena, the number of reports on the molecular response of human periodontal fibroblasts after mechanical stimulation and on the subsequent activation of signaling pathways is limited.

Age has a considerable impact on the composition and integrity of the periodontal tissues and, according to clinical beliefs and research studies, plays a significant role in the rate of orthodontic tooth movement.7–12 Apart from the observed cellular morphologic changes, the levels of proliferation and differentiation of alveolar bone and PDL cells also diminish with age. At a molecular level, aged human PDL fibroblasts show alterations in signal transduction pathways, leading to a catabolic phenotype displayed by a significantly decreased ability for osteoblastic differentiation, thus affecting tissue development and integrity.13,14 Currently, the difference in molecular response to orthodontic load among different age groups is considered of utmost importance. Still, the clinical application of biologic modifiers to expedite or decrease the rate of orthodontic tooth movement is underway.

Biology of Tooth Movement

ALVEOLAR BONE

The alveolar bone is the thickened ridge of the jaw that contains the tooth sockets, in which the teeth are embedded. The alveolar process contains a region of compact bone adjacent to the PDL called the lamina dura.15 When viewed on radiographs, it is the uniformly radiopaque part, and it is attached to the cementum of the roots by the PDL. Although the lamina dura is often described as a solid wall, it is in fact a perforated construction through which the compressed fluids of the PDL can be expressed. The permeability of the lamina dura varies depending on its position in the alveolar process and the age of the patient. Under the lamina dura lies the cancellous bone, which appears on radiographs as less bright. The tiny spicules of bone crisscrossing the cancellous bone are the trabeculae and make the bone look spongy. These trabeculae separate the cancellous bone into tiny compartments, which contain the blood-producing marrow.

The alveolar bone or process is divided into the alveolar bone proper and the supporting alveolar bone. Microscopically, both the alveolar bone proper and the supporting alveolar bone have the same components: fibers, cells, intercellular substances, nerves, blood vessels, and lymphatics. The alveolar bone is comprised of calcified organic extracellular matrix containing bone cells. The organic matrix is comprised of collagen fibers and ground substance. The collagen fibers are produced by osteoblasts and consist of 95% collagen type I and 5% collagen type III. The ground substance contains the collagen fibers, glycosaminoglycans, and other proteins. The noncalcified organic matrix is called osteoid. Calcification of the alveolar bone occurs by deposition of carbonated hydroxyapatite crystals around the osteoid and between the collagen fibers. Noncollagenous proteins like osteocalcin and osteonectin also participate in the calcification process.

The cells of the alveolar bone are divided into four types16:

•Osteoblasts: Specialized mesenchymal cells forming bone

•Osteoclasts: Multinucleated cells responsible for bone resorption

•Lining cells: Undifferentiated osteoblastic cells

•Osteocytes: Osteoblasts located within the compact bone

The alveolar bone is an extremely important part of the dentoalveolar device and is the final recipient of forces during mastication and orthodontic treatment. The reaction to these forces include bending of the alveolar socket and subsequent bone resorption and deposition, which depends on the time, magnitude, and duration of the force. Although the biologic mechanisms underlying these cellular changes are not fully known, it seems they resemble those of the body frame, where mechanical loading has osteogenic effects. Despite the similarities between the alveolar and compact bone, the different response to mechanical loading is attributed to the presence of the PDL, a tissue full of undifferentiated mesenchymal cells, which serves as the means through which the signal is transmitted to the alveolar bone.

CONTEMPORARY DATA ON BONE BIOLOGY

Recent studies report interesting findings on bone biology. Bone morphogenetic proteins (BMPs) are a group of growth factors, also known as cytokines, that act on undifferentiated mesenchymal cells to induce osteogenic cell lines and, with the mediation of growth and systemic factors, lead to cell proliferation, osteoblast and chondrocyte differentiation, and subsequently bone and cartilage production.17 Osteoblasts derive from nonhematopoietic sites of bone marrow that contain groups of fibroblast cells, which have the potential to differentiate into bone-type cells known as mesenchymal stem cells, skeletal stem cells derived from bone marrow, bone marrow stromal cells, and multipotent mesenchymal stromal cells.18

Bone is constantly being created and replaced in a process known as remodeling. This ongoing turnover of bone is a process of resorption followed by replacement of bone that results in little change in shape. This is accomplished through osteoblasts and osteoclasts. Cells are stimulated by a variety of signals, and together they are referred to as a remodeling unit. Approximately 10% of the skeletal mass of an adult is remodeled each year.19 The basic multicellular unit (BMU) is a wandering group of cells that dissolves a portion of the surface of the bone and then fills it by new bone deposition20 (Fig 1-1). The osteoblasts are dominant elements of the basic skeletal anatomical structure of the BMU. The BMU consists of bone-forming cells (osteoblasts, osteocytes, and bone-lining cells), bone-resorbing cells (osteoclasts), and their precursor cells and associated cells (endothelial, nerve cells).

Fig 1-1 The basic multicellular unit. Cells are stimulated by a variety of signals in order to start bone remodeling. In the model suggested here, the hematopoietic precursors interact with cells of the osteoblast lineage and along with inflammatory cells (mainly T cells) trigger osteoclast activation. After osteoclast formation, a brief resorption phase followed by a reversal phase begins. In the reversal phase, the bone surface is covered by mononuclear cells. The formation phase lasts considerably longer and implicates the production of matrix by the osteoblasts. Subsequently, the osteoblasts become flat lining cells that are embedded in the bone as osteocytes or go through apoptosis. Through this mechanism, approximately 10% of the skeletal mass of an adult is remodeled each year.

The bone is deposited by osteoblasts producing matrix (collagen) and two further noncollagenous proteins: osteocalcin and osteonectin. Activation of the bone resorption process is initiated by the preosteoclasts, which are induced and differentiated under the influence of cytokines and growth factors into active mature osteoclasts. Osteoclasts break down old bone and bring the end of the resorption process21 (Fig 1-2).

Fig 1-2 Histologic cross section through a PDL under mechanical load. D, dentin; C, cementum; B, alveolar bone. (Courtesy of Dr K. Tosios, National and Kapodistrian University of Athens, Greece.)

The cycle of bone remodeling starts with the regulation of osteoblast growth and differentiation, which is accomplished through the osteogenic signaling pathways. A hierarchy of sequential expression of transcription factors results in the production of bone. Undifferentiated multipotent mesenchymal cells progressively differentiate into mature active osteoblasts expressing osteoblastic phenotypic genes and then...