E-Book, Englisch, 220 Seiten
ISBN: 978-3-86867-562-7
Verlag: Quintessenz
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)
This book discusses new developments and innovations in preventive dentistry, from primary "real" prevention to secondary prevention by inactivating initial lesions, and on to tertiary prevention to avoid subsequent progression and
complications of manifest oral disease. This evidence base is then translated into clinical dental practice.
The book addresses everyone interested or involved in dentistry, including students, the whole dental practice team, educators, health scientists, and policy makers, who want to gain insight into these up-to-date clinical practices and future developments. It intends to make an impact on teaching and all fields of clinical dentistry – not by giving cookbook recipes, but by pointing out the rationale behind the changes in our routines.
Presented by an international group of recognized specialists in their fields, the topics include the new understanding and management of caries and periodontal disease, prevention of orthodontic problems, diagnostic approaches, the role of diet and according recommendations for oral health, routes to better oral hygiene, changes in oral disease patterns and their consequences, non- and minimally invasive caries treatment, current fluoride guidelines including the use of silver fluorides, risk management, a common risk-factor approach, facilitating behavior changes, sealants, and probiotics. This broad spectrum is elucidated for the most relevant dental problems from early childhood to seniors to implement preventively oriented dental practice.
Autoren/Hrsg.
Fachgebiete
Weitere Infos & Material
Chapter 01. Understanding caries
Chapter 02. Understanding periodontitis
Chapter 03. Fluoride: How much is needed?
Chapter 04. Nutrition and caries: Sugar is the enemy, but what solutions are offered by preventive dentistry?
Chapter 05. Healthy life, healthy mouth? Interdisciplinary and common risk factor interventions
Chapter 06. Oral hygiene: The best route to a healthy mouth?
Chapter 07. Interdental oral hygiene: To floss, or not to floss?
Chapter 08. Tooth brushing: Myth and science
Chapter 09. Guidance for healthy dental and oral behavior: Multilevel prevention of early childhood caries
Chapter 10. Fissure sealing: Still to be recommended?
Chapter 11. Prebiotics, probiotics, and synbiotics: A revolution in preventive dentistry?
Chapter 12. Silver fluorides: The new magic bullet?
Chapter 13. Self-assembling peptides: A perfectly engineered preventive and therapeutic tool?
Chapter 14. Nonrestorative cavity control: Can nonoperative "preventive" treatment replace restorations?
Chapter 15. Prevention and prophylaxis in orthodontics: Neglected opportunities for successful prevention
Chapter 16. Prevention in elderly and medically compromised patients
Chapter 17. Caries risk or activity: Which should we assess?
2 Understanding periodontitis Daniela Hoedke, Henrik Dommisch Periodontitis is a complex inflammatory human disease. According to the World Health Organization (WHO), periodontitis is considered as a chronic noncommunicable disease (NCD), and it shares social determinants and risk factors with other NCDs such as cardiovascular diseases, diabetes mellitus, cancer, and chronic pulmonary diseases, which account for two-thirds of the worldwide mortality.1 Thus, prevention of periodontal diseases, such as gingivitis and periodontitis, is highly important for each individuum. This chapter will give an overview on the current knowledge of the epidemiology, etiopathogenesis, diagnosis, and preventive as well as therapeutic considerations in relation to periodontitis. Periodontitis is one of the most prevalent oral diseases that can be prevented or treated. Figure 2-1 displays a representative image of a patient with periodontitis. In this specific case, the patient experienced tooth movement, tooth mobility, and generalized bleeding on probing. In addition to the resulting gaps between teeth, plaque deposits and discolored swollen gingival tissue are clearly visible in the interdental regions. Fig 2-1 Representative image of a patient with periodontitis. This image shows the sequelae of periodontal destruction due to periodontitis: tooth movement, tooth mobility, and generalized gingival inflammation. In addition to the resulting gaps between teeth, plaque deposits and discolored swollen gingival tissue are clearly visible in the interdental regions. Epidemiology Gingivitis and periodontitis are considered as two entities of the same biofilm-induced inflammatory disease that affects tissues around teeth.2 While gingivitis is a reversible inflammation of the gingiva around teeth without attachment loss, periodontitis comprises an additional nonreversible degradation of the periodontal apparatus, including the alveolar bone. In the worldwide population, approximately 12% exhibit severe forms of periodontitis, whereas approximately 50% show mild to moderate forms of periodontal disease. It is important to note that periodontitis represents the sixth most common human disease.3,4 According to the increasing world population and high numbers of retained teeth, the global burden due to severe periodontitis increased between 1990 and 2013 by 67%.5 This led to a higher economic load to the health care systems.6 With respect to the distribution of periodontal disease in humans, periodontitis is an age-associated but not age-dependent disease, and the prevalence of periodontitis is strongly elevated between the third and fourth decade of life.3,7 Low socioeconomic status is associated with higher risk for periodontitis, and men suffer more from periodontitis compared to women.8,9 Etiopathogenesis of periodontitis The periodontium is a unique structure in the human body. While body surfaces, such as skin, mucosal tissues, hair, and nails, are constantly renewed, shed, and grow out, respectively, teeth exhibit a nonshedding surface. In addition, the tooth represents a direct connection between bone and the outside microbial environment, only separated by the junctional epithelium and connective tissue fibers. This allows for the dental plaque biofilm to develop and grow along the tooth surface into the gingival crevice, if not disturbed by routine oral hygiene procedures. Microbial factors Although periodontitis is a multifactorial disease, the central role to its pathogenesis refers to the interaction between the dental plaque biofilm, mainly consisting of well-organized bacteria adhering to the dental surface, and the immune inflammatory reaction of the host.10 In this context, periodontal health represents a status of homeostasis associated with a symbiotic biofilm and an appropriate immune-inflammatory reaction of the host, including the presence of neutrophils and the expression of antimicrobial peptides.11,12 The immune response to the periodontal bacteria is different for each individuum and impairs the composition of the bacterial biofilm differentiating from a symbiotic into a dysbiotic composition.13 The change of the relative abundance of pathogenic microorganisms when compared to their abundance in a healthy state leads to alterations within the host-microbial interactions that can further accelerate the inflammatory responses.13 The increasing amount of pathogenic periodontal bacteria, including their virulence factors, leads to an elevation of cellular signal transduction, and subsequently, secretion of pro-inflammatory mediators by various periodontal cell types.14-16 Furthermore, the shift within the microbiota activates the complement system.17 In the course of periodontal inflammation, more immune competent cells, such as macrophages, polymorphonuclear neutrophil granulocytes, T-cells, and B-cells, are present. The synthesis of additional pro-inflammatory mediators, such as interleukins, cell stimulating and receptor activating factors, and proteinases leads to changes of the connective tissue and bone metabolism, and therewith, to periodontal attachment loss.18 Initially, a dysbiosis between an altered biofilm in combination with a dysregulation of the immune reaction of a susceptible host leads to an inflammation of the gingiva (Fig 2-1). Gingivitis is a reversible disease that affects epithelium and connective tissue. The ongoing imbalance between the dysbiotic biofilm and the host-related immune reaction can lead to degradation of connective tissue and alveolar bone.10,12,19-22 In the context of the etiopathogenesis of periodontitis, the role of periodontal bacteria has been investigated for decades, and different plaque hypotheses have been developed.23 Several oral bacterial species, eg Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, have been regarded to be pathogenic. Within the periodontal microbiota, a special role is awarded to P gingivalis, a Gram-negative, anaerobic periodontal bacterium. P gingivalis is considered to be a keystone pathogen in the etiopathogenesis of periodontitis. According to its specifications, P gingivalis can influence the course of the periodontal disease by remodeling a health-associated homeostatic biofilm composition into a dysbiotic biofilm composition, even at very low levels of colonization (< 0.01 % of the bacterial count in an animal model).13,24 Within the framework of inflammatory reaction, intercellular connections of periodontal cells disintegrate, and bacteria and their metabolic products can invade into deeper tissue levels, enter the bloodstream, and, eventually, reach the tissues beyond the oral cavity.25,26 Throughout the body, periodontal bacteria may activate immune cells, which then release pro-inflammatory mediators. In this context, periodontal bacteria are able to modify immune-inflammatory reactions in the whole body. Therefore, it seems to be conceivable that periodontitis may also affect other inflammation-driven diseases, such as diabetes mellitus, cardiovascular diseases, and rheumatoid arthritis (see below). Smoking Smoking is considered to be one of the most important modifiable risk factors for periodontitis, with a clearly documented dose-response relationship.27-29 In this context, smoking affects the composition of the microorganisms within the dental plaque biofilm leading to a higher proportion of pathogenic periodontal bacteria. Moreover, smoking impairs microcirculation and immune response to the bacteria, such as disturbance of the neutrophil function, increased synthesis of pro-inflammatory mediators, and higher levels of activated T-cells.30,31 In the context of periodontitis, the progression of periodontal break down is highly increased in smokers when compared to nonsmoking individuals with periodontitis.32 The importance of the smoking status has now been integrated into the classification system of periodontal diseases.33 In respect to the progression of periodontitis, smoking represents one of the two modifying factors affecting the grading of periodontitis.33 Smoking cessation has positive effects on periodontal conditions, the treatment of periodontitis, and tooth retention.34-38 Nutrition Nutrition and malnutrition, respectively, seem to be of importance in relation to periodontal diseases. It is known that nutrient factors influence inflammatory reactions, and malnutrition may lead to depletion of micronutrients which then increases the susceptibility to periodontitis.39 For example, there is an association between periodontal inflammatory responses and vitamin C depletion. Historically, the relationship between the intake of vitamin C-rich vegetables or fruits and periodontal disease has been described. In the 18th century, during maritime trading and exploratory seafaring, sailors often suffered from a condition called scurvy. Scurvy represents a vitamin C deficiency disease associated with gingival bleeding and tooth mobility caused by altered collagen formation, impaired connective tissue barrier formation, and fibroblast growth.40-42 There are a number of different micronutrients associated with periodontal health and disease. For macronutrients, it has been observed that a higher intake of...
